Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\\n\\n
Seeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\\n\\n
Over these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\\n\\n
We are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\n
Thank you all for being part of the journey. 5,000 times thank you!
\\n\\n
Now with 5,000 titles available Open Access, which one will you read next?
Preparation of Space Experiments edited by international leading expert Dr. Vladimir Pletser, Director of Space Training Operations at Blue Abyss is the 5,000th Open Access book published by IntechOpen and our milestone publication!
\n\n
"This book presents some of the current trends in space microgravity research. The eleven chapters introduce various facets of space research in physical sciences, human physiology and technology developed using the microgravity environment not only to improve our fundamental understanding in these domains but also to adapt this new knowledge for application on earth." says the editor. Listen what else Dr. Pletser has to say...
\n\n\n\n
Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\n\n
Seeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\n\n
Over these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\n\n
We are excited about the present, and we look forward to sharing many more successes in the future.
\n\n
Thank you all for being part of the journey. 5,000 times thank you!
\n\n
Now with 5,000 titles available Open Access, which one will you read next?
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"690",leadTitle:null,fullTitle:"Gamma Knife Radiosurgery",title:"Gamma Knife Radiosurgery",subtitle:null,reviewType:"peer-reviewed",abstract:"Gamma knife radiosurgery is a minimally-invasive treatment alternative for intracranial disorders, including tumors, vascular malformations, facial pain and epilepsy. 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1. Introduction
Tall buildings are common forms of urban settlements, and they involve too many functions with plenty of spaces on a low base area with the advantages of having too many floors. Besides, they have important impacts on local wind characteristics around the near-field urban area. Strong winds are usually accelerated at the roof level within the urban environment around tall buildings, due to particular aerodynamic configurations generally associated with this type of buildings. When it comes to a simple rectangular tall building, it is the flow separated from the windward side edge of the roof which led to shear layers with increasing wind velocities [1]. This flow may result in high wind velocities and turbulent wind conditions. For wind energy harvesting, higher wind speeds are mostly desired to a limit velocity, but higher turbulence levels are mostly not intended since the fluctuations in wind speed reduce the energy extracted from the wind turbine. Besides the turbulence, intensity increases the fatigue loads on the wind turbine. So, the assessment of wind flow around the building is very important for a thorough understanding of the flow characteristics.
Assessment of the wind flow around the buildings is conducted with both experimental and numerical methods. The experimental method ensures reliable information as to airflow in and around buildings; however, the available data is mostly limited due to the expensive experimental processes which require too many sensor locations for high-resolution data. Besides, the approach is not practical for an architect or engineer trying to determine the optimal location of the wind turbine. The parametric tools embodied in CFD codes make it very easy to try different geometrical forms or a principal form with different angle of attacks. However, the experimental method may extend the time consumed on optimization since it requires re-configuration of the experimental setup. In addition, wind tunnel testing has some limitations which CFD overcomes. As stated in [2], CFD does not have scaling problems and similarity constraints since simulations can be conducted at full scale.
The literature as to wind energy harvesting mostly constitutes of the planning and design issues of the wind farms; unfortunately, rare studies have been conducted on wind turbine integration to tall buildings located in dense urban areas. In this chapter, beyond describing wind energy systems of a number of tall buildings, a design methodology from architectural and engineering perspectives is proposed. Within this study, CFD assessment of the wind conditions around a number of tall buildings is given with the estimated amount of the energy generated with the wind turbine. First, the wind turbine integration strategy of these cases is described from the architectural design perspective. Then, brief information about these buildings and their surroundings are explained. Following that, the results of the numerical simulations are given and conclusions are derived.
2. Methodology for the assessment of wind energy potential in an urban area
Wind energy potential assessment mostly starts with climate data analysis. So, a thorough understanding of the local climate which is based on a detailed analysis of long-term (at least 30 years) meteorological data is required [3]. After this data has been achieved, a correlation between terrain roughness of the meteorological station site and the examined urban area is set. For this aim, aerodynamic information of the site and the building are investigated.
Mostly, meteorological stations are located on open areas which have aerodynamic roughness length of y0 = 0.003 m, where wind speed is measured at 10 m height and the mean wind speed values are taken on an hourly basis. To transfer this data to the site examined, a logarithmic wind speed profile can be used since it provides mean wind speed distribution with height taking aerodynamic roughness lengths into consideration. These data are used as the inlet boundary condition for CFD simulation to achieve wind speed velocities at different heights from the ground.
The result of the combination of weather data and the aerodynamic information is used in the CFD simulation as an input to assess wind velocities and turbulence conditions around the building accurately. At this point, it is required to use a convenient mathematical model. The turbulent flow within urban or industrial environments is in general modeled by the Navier-Stokes Equations [4]. In detail, as being an economical solution, steady-state 3D Reynolds-averaged Navier-Stokes (RANS) equations are used mostly. On the other hand, large eddy simulation (LES) undeniably has the potential to provide more accurate and more reliable results than simulations based on the Reynolds-averaged Navier-Stokes (RANS) approach. However, LES entails a higher simulation complexity and a much higher computational cost. The equations in these turbulence models are solved with commercial or open-source CFD codes. The most important point for the architect or engineer who will run the simulation is to comply with the CFD guidelines. The best practices largely advised in the literature are the Architectural Institute of Japan (AIJ) CFD guidelines [5] and the COST 732 Best Practice Guideline for CFD [4] simulation of flows in the urban environment. In both of these guidelines, the grid dependence of the solution is advised to be checked. It should be confirmed that the prediction result does not change significantly with different grid systems. In the best practice guidelines, it is indicated that at least three systematically and substantially refined grids should be used so that the ratio of cells for two consecutive grids should be at least 3.4 [4]. The value of 3.4 means finer grids with 1.5 times the grid number in three dimensions. As a practice, to improve the computational mesh in the necessary regions where solid geometry and fluid field contacts and separation of flow occur is advised.
Criteria for convergence are another important parameter of numerical simulations. For this purpose, as indicated in the Architectural Institute of Japan (AIJ) CFD guidelines, it is important to confirm that the solution does not change by monitoring the variables on specified points or by overlapping the contours among calculation results at different calculation steps [5].
A large computational model needs to be created, and different zones with respect to aerodynamic roughness lengths should be arranged. For instance, in the wind comfort study [6], the nearby area around the analyzed tall building is modeled explicitly (zone 2), and the far field containing an urban area with tall buildings is implicitly modeled (zone 3) using aerodynamic roughness length of y0 = 2 m (Figure 1a). While the whole domain area is 1400 m by 2600 m, the area with explicitly modeled buildings was 400 m by 400 m. An upstream domain extension of 5H and a downstream domain extension of 15H were left in the domain as advised in the guidelines [4]. The site of interest in the center of the computational domain is modeled in detail (zone 1). This zone includes smaller computational cells than the zone at the extension of the explicitly modeled region as illustrated in Figure 1b. A high-quality and high-resolution grid that consists of only cut cells is developed to gain fast convergence.
Figure 1.
Computational domain with zone management (a) and mesh refinement levels of different zones (b) [6].
Once the meshing process was complete, boundary conditions were determined (inlet, outlet, etc.), the appropriate turbulence model and wind velocity profile were selected, and CFD simulations are run. Then the analysis results were examined in detail in a post-processing software, and the necessary conclusions are derived. At the last stage, an appropriate wind turbine model was chosen, and design proposals were developed to integrate the chosen wind turbine system to the case building. Then, the amount of energy that can be produced with the proposed system is calculated. In predicting power output from a wind turbine, a common approach in the literature is to take the power curve provided by the manufacturer and combine it with a wind speed frequency distribution function, such as a Weibull distribution or Rayleigh distribution, and integrating across the range of wind speeds in which generation takes place.
3. Building-integrated wind turbines
In most cases, the energy of the wind is gained through wind farms to supply economical clean power with a renewable energy source. However, the land is restricted in urban and suburban regions, and this is regarded to be a significant limitation on large-scale wind turbine installation. An alternative choice is to use building-integrated wind energy systems [7]. Wind energy installations near buildings have received far less attention [8, 9, 10]. The idea of the on-site generation of micro-wind energy is significant because the energy is being generated near where it is needed. In [8], the authors distinguish between three categories of possibilities for integration of wind energy generation systems into urban environments: (1) locating stand-alone wind turbines in urban locations, (2) retrofitting wind turbines onto existing buildings, and (3) full integration of wind turbines together with architectural form. Categories 2 and 3 are often referred to as building-integrated wind turbines (BIWT). Within the scope of this chapter, category 1 is excluded since to position a stand-alone wind turbine in an urban area is not a form of the building-integrated wind energy system.
As to category 2, there are very few research studies on wind power utilization over existing buildings in urban areas. Table 1 shows examples of recent actual building studies conducted by means of field measurements, wind tunnel experimentation, and CFD. Details of the considered models and test descriptions, as well as key findings, are provided in the table [7].
Lee Shau Kee building (97.4 × 38.7 × 69.9 m) (L, W, H). Kowloon, Hong Kong
RNG k-ε
Minimum height of 1.4 m above the roof is recommended for turbine installations. Building proximity effects can increase the wind power significantly (1.5–5.5 times) at 4 m above the building roof
Field measurements from two locations. CFD field measurements from 10 locations
The building has dimensions of 68.9 × 62.5 × 33.5 m (L, W, H). Central metropolitan Taipei, Taiwan
Nonhomogeneous terrain standard κ-ε. RNG κ-ε. Realizable κ-ε. Computational domain (L, W, H) 16 × 8 × 0.3 km
Recommend increasing the hub height and install microturbines on the windward side of the building. Curved roof edges increase the power density
Table 1.
Examples of recent studies for actual site locations [7].
Category 3 includes aerodynamically designed building forms for full integration of wind turbines. As is well known, in urban environments the mean wind speed is lower than the one in rural areas. The wind speed in urban areas, however, is significantly high at specific locations near to tall buildings. It can be described as micro-generation to produce urban wind energy such as that generated by small-scale wind turbines installed on or around tall buildings. As previously stated, a main benefit of such systems is that the energy generated can be consumed straight at the assembly site, and the building’s user obtains renewable additional energy. The use of wind power for distributed generation in tall buildings is becoming increasingly appealing. Since the theoretically produced energy is a function of the wind speed cube, a tiny rise in wind speed can lead to a significant difference in the generation of wind power. It is therefore of concern to correctly evaluate the wind resource in an urban area and try to improve it through different aerodynamic methods. This is opposite to the traditional strategy of wind engineering where the priority is on decreasing wind speeds and pressures in order to minimize wind-induced lateral loads to secure structural system.
When it comes to building-integrated wind turbines, the Bahrain World Trade Center, the Strata Tower in London, and the Pearl River Tower in Guangzhou, China, are very important examples and pioneers in this field. Therefore, their wind turbine integration strategies are given in the following subsections correspondingly to depict the interdisciplinary approach between architecture and wind engineering.
3.1 Bahrain world trade Center
The Bahrain World Trade Center is the focus of a master scheme to refurbish an existing hotel and shopping mall on a distinguished location overlooking the Arabian Gulf in Manama, Bahrain’s central business district. The two 50-story sail-shaped office towers taper to 240 m high, supporting three horizontal-axis wind turbines with a diameter of 29 m (Figure 2). The elliptical plan forms and sail-like profiles function as airfoils, funneling the onshore breeze between them and producing a negative pressure behind them, thus accelerating the wind speed between the two towers. Vertically, tower form is also a consequence of the airflow dynamics. Their airfoil sections are decreasing in size as they taper upwards [15]. Combined with the increasing onshore breeze velocity at increasing heights, this impact produces a near-equal wind velocity regime on each of the three turbines. Understanding and using this phenomenon is one of the main variables that enabled the practical implementation of wind turbine systems into a design of a tall building. Wind tunnel experimentation verified how the towers’ forms and spatial relationship reshape the airflow, forming a “S”-like flow whereby the center of the wind stream stays almost perpendicular to the turbine within a 45° wind azimuth, either side of the central axis. This improves the power generation capacity of the turbines while at the same time decreasing fatigue on the blades to acceptable levels during wind skewing across the blades [15].
Figure 2.
Wind turbines integrated in between the Bahrain world trade Center towers; elevation view (a) and a general view from the pedestrian level (b) [7].
The horizontal-axis wind turbines placed between the towers are normally pole-mounted and rotate to match the wind direction to maximize the energy output. Therefore, it is very hard to place such turbines to tall buildings located in a climate with variable direction wind conditions. Most architectural projects deploying building-integrated, horizontal-axis turbines, as in the case of the Bahrain World Trade Center, implement the concept of a fixed turbine. It seems more useful to deploy vertical-axis wind turbines since they advantage from the benefit of being fully omnidirectional. However, large-scale verified vertical-axis turbines were not accessible for building applications at the moment of design development for this building. The fixed horizontal turbine suffers the disadvantage of being able to function only with wind from a restricted azimuth range, if issues with blade deflections and stress are to be prevented due to excessive skew flow. The form of the towers was designed from the beginning of this project to catch the upcoming wind and channel it between the towers. Comprehensive wind tunnel testing latterly validated by CFD, illustrations of which are displayed in Figure 3, showed that the upcoming wind is in fact deflected by the towers in the form of a S-shaped streamline that runs through the space between the towers at an angle within the wind skew tolerance of the wind turbine. Engineering projections indicate that the turbine will be capable of operating between 270° and 360° of wind directions, but, to be on the safe side, turbine calculations and initial operating regimes are set on a more limited range between 285° and 345°. The turbine will automatically follow a “standstill” mode in all wind directions outside this range. It is no coincidence that the buildings are oriented towards the prevailing wind which is extremely dominant. The funneling of the towers amplifies the wind speed up to 30% at the turbine position. Together with the form of the towers (bigger impact at ground) and the velocity profile of the wind (lowest at ground), this amplification has the impact of balancing the energy output to the extent that the upper and lower turbines generate 109 and 93% compared to 100% for the turbine at the middle [15].
Figure 3.
CFD images by Ramboll, showing airflow patterns near towers, simulated at the level of the top turbine for different free, undisturbed wind incidence angles with respect to an “x” axis (i.e., horizontal line connecting towers).
3.2 Strata tower, London
Strata Tower is a tall residential building in central London (Figure 4) which was the tallest one when it was constructed in 2005. The architects in the design team of the tower examined the effectiveness of several alternatives to achieve the most suitable lean, clean, and green option. As a residential tower, general energy consumption loads are significantly lower than similar retail or commercial office development, and thus the chance of achieving the required percentage of renewable energy on-site is comparably more possible [16].
The architects initially did not plan to design a building with wind turbines; however, they came through an extensive sequence of design alternatives, assessing each renewable option on their own merits and in the context of the site. For instance, ground source water solutions were thought, but the site’s harsh limitations meant that the water pools would not be far enough from each other to remain feasible. Moreover, energy savings would be reduced by pumping through the entire building’s height. Photovoltaic option was also thought, but the corresponding technology available at that time (2005) would have led to 80% of the southern facade being enclosed with photovoltaic (PV) cells, this too far compromising the amount of glazing needed to provide sufficient daylight into the spaces and views from the apartments. Commercial problems prevailing in 2005 would also have rendered this choice too costly, added to which photovoltaics have a life-span of about 15 years and must be kept carefully clean. This alternative would have had a major impact on service fees. Photovoltaic integration would also negatively affect the facade’s cost per square meter. Similarly, biomass boiler option was also considered, but the ongoing energy costs related with transporting and delivering the fuel, and the availability issues of such fuel, along with the need for a 150-m (492-foot) flue operating the entire building height, meant that this option was marked down. As such, a number of options inevitably lead to a wind energy-based solution [16].
The wind rose for London has a mainly south-westerly axis in summertime; therefore the curved facade was appropriately oriented to catch wind from this prevailing direction (Figure 5).
Once considering the introduction of wind turbines as a site-based renewable energy option, funneling and guiding the wind is a main design element that can considerably improve the wind turbines’ prospective operational production. In fact, the design solution for Strata Tower is another iteration of that taken for the Bahrain World Trade Center also using the concepts of a “Venturi” to direct wind flow, but differently in between the two towers (Figure 6). There are also other significant distinctions—particularly the scale of the project, the reality that the three turbines are installed externally on linking bridges and the hot-humid site which required full air conditioning to help tackle any negative acoustic effects [16].
Figure 6.
Strata tower: Airflow patterns around the wind turbines [13].
The turbines do produce noise, like any other typically roof-mounted piece of plant. The Venturi-like enclosures, however, effectively concentrate the noise away from the flats instantly below into two sound cones. All measures to regulate and minimize noise generation have been discussed, and these measures have actively improved efficiency in some cases. Within the Venturi-like enclosures, careful placement of the turbines on the plan has a significant impact both in general performance and in regulating noise output. Furthermore, in contrast to the more standard three-bladed turbine used on larger versions, opting for a five-bladed turbine provided further noise decreases (Figure 7) [16].
To sum up, the energy output needed for building-integrated wind turbine solution is completely case dependent. The overall production requirement for Strata Tower is 50 megawatt hours of electricity per year in the case of the design load requirement. This is about 8% of the complete energy consumption of the building.
3.3 Pearl River tower, Guangzhou, China
A typical instance of BIWTs and building-integrated photovoltaic (BIPV) in Asia is the Pearl River Tower in Guangzhou, China. It is a 309-m-high 71-story building completed in 2011 and designed to increase velocity through the nozzle effect by making flow openings in the building (Figure 8) [17]. Inside the building are mounted a total of four 8-m-high vertical-axis wind turbines, each at the inner opening on the left and right sides [18]. There are four openings in the Pearl River Tower adjacent to the two-level mechanical floors (Floor 24, from 104 to 111.3 m, and Floor 50, from 205 to 212.7 m), with a bell-mouthed form at both ends of each opening. Opening-1 and opening-2 are at the lower elevation, with opening-1 being placed on the west and opening-2 on the east. Likewise, opening-3 and opening-4 are located in pairs next to the upper mechanical floor (Figure 9). The Pearl River Tower’s orientation is parallel to Guangzhou’s prevailing wind direction, which seeks to maximize turbine power output. Furthermore, the Pearl River Tower is aerodynamically formed with a concave wall on the southern surface and a convex wall on the northern surface that enables better intensification and funneling of the wind through the openings (Figure 9).
Figure 8.
Pearl River tower: Positions of the openings [18].
Figure 9.
Pearl River tower: Airflow patterns around the wind turbines [17].
A helix-shaped vertical-axis wind turbine is installed on the floors inside each of the four openings (Figure 10). These turbines have an 8-kW rated power with 25 m/s rated speed. Such a turbine is designed to generate electricity when there is a wind velocity range of 2.7–40 m/s. This turbine’s swept area is about 10 square meters. It is worth noting that while vertical-axis wind turbines (VAWTs) may usually have lower energy efficiency than widely used horizontal-axis wind turbines (HAWTs), they appear to be particularly favored in urban wind energy development. Due to the lower tip velocity, the noise effect of VAWTs is relatively low, and VAWTs in urban settings can resist high turbulence. Most remarkably, VAWTs are omnidirectional, so wind and turbulence can be extracted more efficiently from all directions with reduced loss of effectiveness. This is particularly appealing for the installation of wind turbines in urban settings where wind direction is extremely variable owing to adjacent buildings and structures’ interference effects [18].
It has been shown through the results of the study [18] that the design of Pearl River Tower makes a good use of the aerodynamic features of the super-tall building, which can result in a significant enhancement of wind speed in the four openings. However, due to the mostly weak wind condition in Guangzhou, the estimated power outputs from the four building-integrated wind turbines are relatively low. Nevertheless, it is expected that the integration of wind turbines into tall buildings will have a remarkable potential to contribute a significant part of the energy requirement of tall buildings in urban areas having high wind velocities.
4. Conclusions and further research
Urban wind energy is the use of wind energy technology in urban and suburban built environment applications. This chapter offers only some opinions on the progress made in the evaluation of wind resources in urban regions, the use of appropriate wind turbines to enhance the utilization of these resources, and the important role of architectural and urban aerodynamics in designing buildings accordingly to increase wind energy output. It is not meant to be comprehensive, but rather it is preferred from the point of view of architects in the context of buildings and cities to provide some perspectives on the abovementioned subjects. It is indicated that while important progress has been made in the field, there is a strong need for additional comprehensive research, especially in the area of urban aerodynamics and wind resource assessment, in order to optimize the generation and utilization of urban wind energy.
It is also concluded that wind conditions can change considerably depending on the building form. Therefore, CFD simulation is required to analyze the effect of the form of the building, accurately. Aerodynamically designing the building leads to improvement in power density and may potentially result in large changes in spatial variability. On the other hand, preliminary comprehensive studies as to the wind resource assessment are very important for the efficiency of a wind turbine system; otherwise, it would not be possible to benefit from this type of system, sufficiently. It is also derived that to accurately position the wind turbine, detailed analyses should be conducted on determining highly turbulent flow areas which can reduce the amount of energy yielded from the wind turbine.
Moreover, it should be noted that research on wind turbine integration to buildings has been mostly conducted by wind engineers. Wind engineering solutions are very crucial in developing building-integrated wind energy systems. The advanced analysis methods that combined with CFD simulations give important aerodynamic information about the building and the nearby field. However, when it comes to proposing aerodynamic form optimization based on the data produced, the solutions should not be free of architectural context, since a very basic change even affects the form of the building. At this point, cooperation with architects is significant when integrating wind energy systems to buildings, since an interdisciplinary approach may fill the gap between the wind engineering solutions and architectural design processes. In collective research, the effect of several factors may be assessed; consequently, this may widen the perspective of the contribution of wind engineering to the improvement of urban wind energy strategies.
The environmental benefits of using a sustainable energy system can be examined, further. For instance, it is very probable to see that using wind turbines leads to a significant decrease in carbon emissions. For this purpose, the elimination of carbon emissions which would be released for the equivalent energy yielded from fossil fuels can be calculated in further studies.
\n',keywords:"building-integrated wind turbines, building aerodynamics, wind energy, computational fluid dynamics (CFD), wind efficient design",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/71418.pdf",chapterXML:"https://mts.intechopen.com/source/xml/71418.xml",downloadPdfUrl:"/chapter/pdf-download/71418",previewPdfUrl:"/chapter/pdf-preview/71418",totalDownloads:188,totalViews:0,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,dateSubmitted:"February 7th 2019",dateReviewed:"February 6th 2020",datePrePublished:null,datePublished:"September 9th 2020",dateFinished:null,readingETA:"0",abstract:"Having a far distance from the ground levels exposed to turbulent wind conditions, tall buildings have the potential of generating wind energy. However, there are many challenges to incorporating wind generation into urban areas. These include planning issues besides visual impacts. So, as to integration, there is a need for a combined approach that considers wind energy harvesting besides these issues. At this point, a multidisciplinary approach can fill the gap between the architectural design and the wind engineering processes. Based on this approach, this chapter presents design strategies from the literature to integrate wind energy to tall buildings using computational fluid dynamics (CFD) simulation. It is intended to guide further researches on wind energy and consequently to contribute to the environmental quality of urban areas and sustainable development of the cities.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/71418",risUrl:"/chapter/ris/71418",book:{slug:"renewable-energy-resources-challenges-and-applications"},signatures:"Ilker Karadag and Izzet Yuksek",authors:[{id:"186397",title:"Dr.",name:"İzzet",middleName:null,surname:"Yüksek",fullName:"İzzet Yüksek",slug:"izzet-yuksek",email:"izzetyuksek@gmail.com",position:null,institution:{name:"Celal Bayar University",institutionURL:null,country:{name:"Turkey"}}},{id:"295400",title:"Dr.",name:"İlker",middleName:null,surname:"Karadağ",fullName:"İlker Karadağ",slug:"ilker-karadag",email:"karadagi@itu.edu.tr",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Methodology for the assessment of wind energy potential in an urban area",level:"1"},{id:"sec_3",title:"3. Building-integrated wind turbines",level:"1"},{id:"sec_3_2",title:"3.1 Bahrain world trade Center",level:"2"},{id:"sec_4_2",title:"3.2 Strata tower, London",level:"2"},{id:"sec_5_2",title:"3.3 Pearl River tower, Guangzhou, China",level:"2"},{id:"sec_7",title:"4. Conclusions and further research",level:"1"}],chapterReferences:[{id:"B1",body:'Stathopoulos T, Blocken B. Pedestrian wind environment around tall buildings. In: Tamura Y, Yoshie R, editors. Advanced Environmental Wind Engineering. Tokyo: Springer; 2016. pp. 101-127'},{id:"B2",body:'Blocken B, Janssen WD, van Hooff T. CFD simulation for pedestrian wind comfort and wind safety in urban areas: General decision framework and case study for the Eindhoven university campus. Environmental Modelling & Software. 2012;30(1):15-34. DOI: 10.1016/j.envsoft.2011.11.009'},{id:"B3",body:'Wu H, Kriksic F. Designing for pedestrian comfort in response to local climate. Journal of Wind Engineering and Industrial Aerodynamics. 2012;104(1):397-407. DOI: 10.1016/j.jweia.2012.02.027'},{id:"B4",body:'Franke J, Hellsten A, Schlünzen H, Carissimo B. The COST 732 best practice guideline for CFD simulation of flows in the urban environment - a summary. International Journal of Environment and Pollution. 2011;44(1–4):419-427. DOI: 10.1504/ijep.2011.038443'},{id:"B5",body:'Tominaga Y, Mochida A, Yoshie R, Kataoka H, Nozu T, Yoshikawa M, et al. AIJ guidelines for practical applications of CFD to pedestrian wind environment around buildings. Journal of Wind Engineering and Industrial Aerodynamics. 2008;96(10–11):1749-1761. DOI: 10.1016/j.jweia.2008.02.058'},{id:"B6",body:'Serteser N, Karadag I. Design for improving pedestrian wind comfort: A case study on a courtyard around a tall building. Architectural Science Review. 2018;61(6):492-499. DOI: 10.1080/00038628.2018.1492899'},{id:"B7",body:'Stathopoulos T, Alrawashdeh H, Al-Quraan A, Blocken B, Dilimulati A, Paraschivoiu M, et al. Urban wind energy: Some views on potential and challenges. Journal of Wind Engineering and Industrial Aerodynamics. 2018;179:146-157. DOI: 10.1016/j.jweia.2018.05.018'},{id:"B8",body:'Stankovic S, Campbell N, Harries A. Urban Wind Energy. London: Taylor & Francis; 2009. DOI: 10.4324/9781849770262'},{id:"B9",body:'Beller C. Urban Wind Energy - State of the Art 2009. Danmarks Tekniske Universitet, Risø Nationallaboratoriet for Bæredygtig Energi. Denmark. Forskningscenter Risoe. Risoe-R; No. 1668(EN); 2009. 43 p'},{id:"B10",body:'Sharpe T, Proven G. Crossflex: Concept and early development of a true building integrated wind turbine. Energy and Buildings. 2010;42(12):2365-2375. DOI: 1016/j.enbuild.2010.07.032'},{id:"B11",body:'Lu L, Sun K. Wind power evaluation and utilization over a reference high-rise building in urban area. Energy Buildings. 2014;68:339-350'},{id:"B12",body:'Tabrizi AB, Whale J, Lyons T, Urmee T. Performance and safety of rooftop wind turbines: Use of CFD to gain insight into inflow conditions. Renewable Energy. 2014;67:242-251'},{id:"B13",body:'Al-Quraan A, Stathopoulos T, Pillay P. Comparison of wind tunnel and on-site measurements for urban wind energy estimation of potential yield. Journal of Wind Engineering and Industrial Aerodynamics. 2016;158:1-10'},{id:"B14",body:'Yang A, Su Y, Wen C, Juan Y, Wang W, Cheng C. Estimation of wind power generation in dense urban area. Applied Energy. 2016;171: 213-230'},{id:"B15",body:'Smith RF, Killa S. Bahrain world trade Center (BWTC): The first large-scale integration of wind turbines in a building. The Structural Design of Tall and Special Buildings. 2007;16(4):429-439. DOI: 10.1002/tal.416'},{id:"B16",body:'Bogle I. Integrating Wind Turbines in Tall Buildings. CTBUH Journal [Internet]. 2011 [cited: 01 September 2019]; 2011(IV):30-34. Available from: http://global.ctbuh.org/resources/papers/download/293-integrating-wind-turbines-in-tall-buildings.pdf'},{id:"B17",body:'Kim H-G, Jeon W-H, Kim D-H. Wind resource assessment for high-rise BIWT using RS-NWP-CFD. Remote Sensing. 2016;8(12):1019. DOI: 10.3390/rs8121019'},{id:"B18",body:'Li QS, Shu ZR, Chen FB. Performance assessment of tall building-integrated wind turbines for power generation. Applied Energy. 2016;165:777-788. DOI: 10.1016/j.apenergy.2015.12.114'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Ilker Karadag",address:"karadagi@itu.edu.tr",affiliation:'
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1. Introduction
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In this chapter, we discuss the groups of disorders classified as systemic sclerosis mimics. Localized and sometimes generalized skin stiffness is typical for this group of diseases. However, quite incongruous pathogenesis, underlying disease mechanisms and distinct organ involvement are significantly different in these conditions. This chapter describes the pathogenesis, clinical manifestation, histopathology findings, and therapeutic possibilities of the most common diseases that may cause difficulties in the differential diagnosis of systemic sclerosis.
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2. Localized scleroderma, morphea
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2.1 Introduction
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Localized scleroderma is a clinically distinct inflammatory disease, primarily of the dermis and also subcutaneous fat [1]. The inflammation leads to scar-like sclerosis. Inflammatory infiltrates and changes of small vessels are similar in morphea and systemic sclerosis (SSc), but morphea has more asymmetric or linear skin localization and distribution than SSc, which has symmetrical distribution. Generalized morphea can prevent and mimic diffuse cutaneous SSc, but this clinical variant does not have Raynaud’s phenomenon, digital sclerosis and lung, and gastrointestinal tract manifestation of the disease. Morphea is responsible for the morbidity of the patient such as skin tightness, joint mobility reduction leading to contractures, growth retardation, and pain [1, 2, 3].
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2.2 Epidemiology
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Morphea typically develops in adults, although morphea can occur at any age. The incidence of morphea is 3 per 100,000 people, and the prevalence of morphea increases with age. The mean age of disease onset is 45 years. Morphea is more prevalent in women than in men (2.6:1), except linear morphea, which has no gender preference [2, 3, 4].
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2.3 Pathogenesis
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The cause of the disease is unknown. Coexistence of various forms of scleroderma and the rare possibility of progression of localized scleroderma into SSc indicate that both types represent different manifestations of the same pathological process. Pathogenesis may be due to participation of environmental influences, immunological disorders, and infections, e.g., association with Borrelia burgdorferi [3]. Sclerosis of the skin is induced by vascular damage, activated T cells, and accented connective tissue production by dermal fibroblasts. Vascular changes represent a reduction in the number of capillaries. Enhanced production of collagen and other extracellular matrix proteins and components is induced by T-cell-derived cytokines, interleukin 4 (IL-4), IL-13, and transforming growth factor beta (TGF-β) [3, 5, 6].
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2.4 Clinical features
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Morphea can be divided into several clinical groups: plaque-type morphea, linear morphea, generalized morphea, deep morphea, nodular morphea, and guttate morphea. Patient with morphea does not have involvement of internal organs and Raynaud’s phenomenon. Some patients may have involvement of muscles, tendons, and joints or neurological or ophthalmological symptoms which depend more likely on anatomical site, e.g., in a patient with linear morphea [2].
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2.5 Plaque-type morphea, circumscribed morphea
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Plaque-type morphea is the most common variant, characterized by a slightly elevated, edematous, erythematous, or violaceous and livid plaque with oval to round or centrifugal distribution (Figure 1). The developmental stage of the disease may influence the clinical features: (i) inflammatory, (ii) sclerotic, and (iii) atrophic [1, 2].
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Figure 1.
Plaque-type morphea, lesion on the right side of the trunk. Plaques are surrounded by a dark red rim on the periphery with a yellowish white color center of the lesion as a result of the increasing deposition of connective tissue.
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In the inflammatory phase, these are delimited striated skin plaques with the accentuated surface by skin pores, which resemble “orange peel” due to the edema of the corium expanding the follicular orifice. Plaques are surrounded by a violaceous rim on the periphery, indicating the active inflammatory stage of the disease. A yellowish-white color develops in the center of the lesion as a result of the increasing deposit of connective tissue [3]. In the sclerotic phase, the inflammatory border is absent. The skin of the lesion is smooth, shiny, and difficult or unable to be shaken. In the final (atrophic) phase, induration disappears; the plaques are soft, slightly sloping for skin and subcutaneous atrophy, and mostly gray-brown pigmented. Circumscribed morphea usually presents as single or multiple skin lesions. It is generally asymptomatic, but the central portion of the progressing lesion starts to get rigid and may be slightly painful [2, 3].
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A different manifestation of morphea can be present. Guttate morphea presents as multiple rather superficial and nummular plaques (Figure 2).
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Figure 2.
Guttate morphea, multiple nummular lesions on the right thigh.
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Deep morphea represents sclerosis that affects the primarily deep parts of the dermis and subcutaneous fat (Figure 3).
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Figure 3.
Deep morphea, the affection of the front of the right thigh, mapping distribution of erythematous and whitish parts with visible scarring.
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2.6 Linear morphea
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Linear morphea is similar in the clinical feature to circumscribed morphea but with a linear distribution. Linear morphea initially starts as a linear erythematous streak or harmless lesion that later forms a scar-like band (Figure 4).
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Figure 4.
Linear morphea, linear distribution of plaques, leading to atrophic changes in the affected limb.
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This scar-like band significantly impairs the mobility of the affected limb. Linear morphea can affect the underlying fascia, the muscle, and tendons. Linear morphea that transcends joints can significantly reduce movement and lead to developmental limb defects in children. Rarely, it can form bizarre configurations when copying Blaschko’s lines [1, 3, 7].
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2.7 “En coup de sabre”
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The “en coup de sabre” represents a linear type of morphea of the head. This morphea is unilateral and extends from the forehead into the frontal scalp (Figure 5).
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Figure 5.
“En coup de sabre” as linear morphea of the head. Linear scarring lesion on the forehead with an erythematous rim spreading to the scalp.
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It usually starts as a small plaque with the surrounding inflammatory erythematous rim. Parry-Romberg syndrome is a rare variant of linear morphea of the forehead and scalp, with progressive loss of subcutaneous fat, with a smaller share of sclerosis [3, 8, 9].
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2.8 Generalized morphea
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Generalized morphea begins as multiple plaque-type morphea on the trunk. This clinical variant is defined by the presence of ≥4 plaques involving at least two different anatomic sites (Figure 6).
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Figure 6.
Generalized morphea begins as multiple-plaque-type morphea on the abdomen, circularly affecting breasts and the neck. In the margins, lesions are with a rim of erythema, indicating the inflammatory stage of the disease.
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In contrast to systemic sclerosis, generalized morphea does not present with sclerosis primarily involving acral skin or sclerodactyly, but this anatomical site can also be affected [10]. Apart from the skin, generalized morphea can also affect the subcutis and fascia, and be accompanied by slight changes in internal organs (especially the gastrointestinal tract and lungs) and the formation of joint contractures with mostly secondary joint involvement and movement limitation [11, 12]. Carapace-like tightening of the chest, can reduce breathing and cause swallowing difficulties.
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2.9 Laboratory findings
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Laboratory abnormalities are typically associated with generalized and linear morphea, but some patients with morphea have elevated antinuclear antibody (ANA). Reported rates of ANA positivity among patients with morphea range from 18 to 68%. Other autoantibodies that are detected less frequently than ANA in patients with morphea include anti-single-stranded DNA (ssDNA), anti-double-stranded DNA (dsDNA), antihistone, anti-topoisomerase IIα, antiphospholipid, and rheumatoid factor [1, 13].
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2.10 Histopathology
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The histopathological findings depend on the stage of the disease and area where the biopsy was taken (inflammatory border or central sclerotic lesion). Biopsy specimens for histology must include subcutaneous fat (Figure 7).
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Figure 7.
Deep skin biopsy to subcutaneous fat after formaldehyde fixation.
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Biopsies performed from inflammatory lesions demonstrate an interstitial and perivascular inflammatory cell infiltrate composed primarily of CD4+ T cells, eosinophils, plasma cells, and mast cells. Inflammation may extend into the subcutaneous tissues. Furthermore, tissue edema, enlarged tortuous vessels, and thickened collagen bundles may be observed. Biopsy from a sclerotic lesion demonstrates homogenization of the papillary dermis and thickened collagen bundles extending into the reticular dermis or beyond (Figure 8). In biopsy from deep morphea, the deep reticular dermis, subcutis, and fascia show sclerotic changes [14].
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Figure 8.
Biopsy from a sclerotic lesion demonstrates homogenization of the papillary dermis and thickened collagen bundles extending into the reticular dermis.
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2.11 Differential diagnosis
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A number of other disorders can present with clinical features that resemble morphea. Generalized morphea is necessary to distinguish from systemic sclerosis or scleredema diabeticorum. In addition to the skin sclerosis, systemic sclerosis generally begins with the Raynaud’s phenomenon, and patients commonly exhibit initial puffiness and eventual sclerosis in the fingertips (sclerodactyly), usually accompanied by nail fold capillary changes. These changes are absent in patients with morphea. The differential diagnosis of plaque-type morphea includes lichen sclerosus, morpheaform basal cell carcinoma, and postirradiation morphea. Furthermore, we need to think of lipodermatosclerosis as fibrosing panniculitis with typical localization on the lower extremities or eosinophilic fasciitis. In some cases of limb involvement, pretibial myxedema or Lyme disease (acrodermatitis atrophicans) must be excluded [1, 13, 14].
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2.12 Treatment
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A variety of treatment options are available for patients with active lesions of morphea; however, evidence in support and success of these therapeutics modalities is limited. The expected outcome of successful therapy for morphea is not a complete healing or normal skin texture. In patients with progressive disease, successful treatment presents stopping the formation of new lesions and limiting the spreading of the disease [1, 15].
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2.13 Topical and intralesional treatment
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Topical therapies are unlikely to be effective for the disease involving the subcutis or deeper tissues and are not useful for preventing the development of new lesions in patients with rapidly progressive disease. Topical tacrolimus as tacrolimus 0.1% ointment may be effective for active, inflammatory morphea [16]. High potency topical and intralesional corticosteroids are widely used for the treatment of morphea; however, no formal studies have documented their efficacy. Topical vitamin D—vitamin D as topical calcipotriene 0.005% ointment—may inhibit effects on fibroblast proliferation, collagen synthesis, and T-cell activation. In some clinical studies, an improvement on this therapy was noted in limited numbers of patients [15, 17].
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Imiquimod is a topical immunomodulator that induces interferon-gamma, a cytokine that inhibits TGF-beta and the production of extracellular matrix proteins. Imiquimod also downregulates the profibrotic cytokine IL-4. Limited data suggest that imiquimod is effective in some patients with plaque-type morphea [18].
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It is possible to use phototherapy in patients with sclerotic diseases like morphea. Longer wavelengths of light as ultraviolet A (UVA) (320–400 nm) are capable of greater depth of penetration into the skin, and most studies of UV phototherapy in sclerotic skin disease have focused on the use of UVA light (320–400 nm). Fewer data are available on the use of PUVA therapy (a combination of UVA and topical or oral use of psoralens) and ultraviolet B (UVB) light (290–320 nm). Phototherapy is unlikely to be effective for morphea with deep involvement (subcutis, fascia, or muscle) and should not be considered as primary therapy alone [19].
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2.14 Systemic treatment
\n
Patients with the progressive disease require systemic therapy with methotrexate or corticosteroids. Methotrexate is the most appropriate systemic therapy for morphea. In patients with acute generalized or rapidly progressive disease, we combine treatment with systemic corticosteroids. Methotrexate is typically given for at least 6–12 months with a weekly dose of 15–25 mg. The systemic corticosteroids are usually tapered and discontinued after 3–4 months or pulse intravenous therapy is used instead (500–1000 mg of intravenous methylprednisolone sodium succinate for 3 consecutive days/month) [15, 20].
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3. Morpheaform inflammatory syndromes/conditions
\n
Some diseases and disorders with acrosclerosis and Raynaud’s phenomenon have a clinical presentation similar to localized scleroderma. The etiology of these disorders is diverse and includes, e.g., secondary sclerosis after exposition to bleomycin, vinyl chloride, L-tryptophan, or toxic oils. Sclerosis can also be induced by endogenous metabolites, by x-irradiation, or during chronic graft-versus-host disease (GVHD) (Figure 9). Morphea-like lesion, eosinophilic fasciitis, and lichen sclerosus can also be observed in these patients [21].
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Figure 9.
Morphea-like lesion in a patient with GVHD. Post-inflammatory hyperpigmentation with whitish areas of sclerotic skin affecting the left thigh.
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3.1 Lipodermatosclerosis
\n
\n
3.1.1 Introduction
\n
Typical changes associated with chronic venous insufficiency include erythema, induration, and hemosiderin pigmentary changes. But a variety of clinical appearances and histopathologic findings also include sclerosis, or sclerosing panniculitis. The various manifestations of this panniculitis have been consolidated under the heading of lipodermatosclerosis or sclerosing panniculitis [22].
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Lipodermatosclerosis typically manifests in patients, usually in women over the age of 40 years with chronic venous insufficiency as a result of chronic hypoxia. Venous hypertension leads to a compromised ability to reduce foot vein pressure during exercise. This change results in increased capillary permeability, with leakage of fibrinogen, with subsequent polymerization leading to formation of fibrin plaques around vessels. There may also be an abnormal regulation of angiogenesis in a patient with lipodermatosclerosis. For example, increased expression of vascular endothelial growth factor receptor 1 (VEGFR-1) can be a result of VEGF-mediated angiogenesis. Another factors may include local stimulation of collagen and obesity [23, 24].
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3.1.2 Clinical features
\n
Sclerosis affects the acral parts of the lower limbs symmetrically. The acute and progressive phase of lipodermatosclerosis presents with pain, erythema, and the formation of induration on the affected area of lower limbs. In the chronic phase, sclerosis of the dermis and subcutis is typically present, and sclerosis results in induration that is more sharply demarcated from the adjacent normal skin (Figure 10). Other gravity dependent sites such as the lower aspect of the abdominal pannus can also develop lipodermatosclerosis. At this point, the changes are relatively diffuse. Hyperpigmentation due to hemosiderin deposition or chronic ulceration of the lower limbs may also be present [22].
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Figure 10.
Lipodermatosclerosis in a patient with chronic venous insufficiency. In this case erythema and sclerotic whitish induration on the medial part of the shank with the border of hemosiderin pigmentary changes are present.
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3.1.3 Histopathology
\n
Early lesions show mid-lobular panniculitis, a lymphocytic infiltrate in the septa, variable degrees of capillary congestion, and extravasation of erythrocytes with hemosiderin deposition. Chronic lesions show septal sclerosis and membranocytic change with a marked reduction in inflammation or lymphocytic infiltrate [25, 26].
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3.1.4 Differential diagnosis
\n
In differential diagnosis, it is necessary to distinguish inflammatory changes such as cellulitis and erysipelas but also erythema nodosum or erythema induratum. As induration develops and progresses, differentiation from morphea and scleromyxedema may be necessary. In morphea, subcutaneous involvement is predominantly septal, and lipophagic and lipodystrophic changes are not typically present [22, 25].
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3.1.5 Treatment
\n
Leg elevation and consistent compression therapy are crucial for the treatment of lipodermatosclerosis. Traditional anti-inflammatory therapies are usually ineffective, but topical or intralesional corticosteroids (e.g., triamcinolone 5–10 mg/cc) may bring relief and improvement with compression therapy [27].
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3.2 Injection of vitamin K
\n
Oil-soluble injection of vitamin K may be responsible for the eosinophilic reaction of the deep part of the dermis and subcutaneous fat, which may resemble localized eosinophilic fasciitis with similar clinical manifestation as deep morphea. This inflammation can result in dermal and subcutaneous atrophy [28].
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3.3 Vaccination-associated morphea
\n
Circumscribed morphea and deep morphea have been described after intramuscular injections of different types of vaccines. The etiology and antigens responsible for this type of inflammation have not been reliably elucidated [29].
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3.4 Paraffin and silicone injections or silicone implants
\n
The leak of silicone from implants and silicone or paraffin injection after reconstructive or plastic surgery induce chronic inflammation that results in localized morphea-like lesion. The contribution to the induction of SSc, eosinophilic fasciitis, or mixed connective tissue disease has also been discussed [30].
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3.5 Porphyrias
\n
Porphyria cutanea tarda can lead to a morphea-like lesion and scarring in the chronic sun (UV)-exposed sites, such as the face, scalp, dorsal part of the hands, and upper part of the chest [31].
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3.6 Radiation-induced morphea
\n
X-irradiation can induce sclerotic, chronic erythematous, and secondary pigmented lesions typically in a patient after irradiation of the chest and axillary region for breast carcinoma (Figure 11). The morphea-like lesions can start several years after radiation [32].
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Figure 11.
Morphea-like lesion in a patient after x-irradiation for breast carcinoma. The erythematous and sclerodermic lesion on the right breast.
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3.7 Differential diagnosis
\n
The differential diagnosis is summarized in this paragraph, but the most important entity in the differential diagnosis of SSc or localized scleroderma is lichen sclerosus et atrophicus and scleromyxedema. Absence of overall symptoms and organ involvement is crucial [21].
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4. Lichen sclerosus
\n
Lichen sclerosus et atrophicus is an inflammatory disease, primarily of the superficial dermis or mucosa, which leads to white scar-like atrophy. Extragenital lichen sclerosus may itch and be cosmetically annoying. Genital lichen sclerosus causes dryness and persistent pruritus. Genital lichen leads to progressive atrophy, and functional impairment, which significantly reduces the quality of life.
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\n
4.1 Epidemiology
\n
Prevalence of lichen sclerosus is unknown. This chronic disease occurs at all ages with a similar incidence in all races. The ratio of occurrence in men and women varies considerably, but in both sexes, the most affected area is the anogenital region (about 85% of patients, in women usually as a vulvar disease) [33, 34].
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4.2 Pathogenesis
\n
Association with the MHC class II antigen HLA-DQ7 was observed, but the specific genetic predisposition is unknown. Unspecific inflammation seems to be essential for the initiation and also the progression of lichen sclerosus. Autoantibodies such as those against the extracellular matrix protein 1 (ECM-1) were found in 80% of patients with lichen sclerosus. Moreover, in female patients with lichen sclerosus, there is a higher prevalence of autoimmune diseases (especially autoimmune thyroid disease) and ANA positivity than in male patients with lichen sclerosus [34, 35, 36].
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4.3 Clinical features
\n
Lichen sclerosus manifests by polygonal, bluish-white, shiny, slightly elevated maculopapules with a pointed follicular bounds of hyperkeratoses, which may be solitary or in groups. This skin lesion can be bounded with an area of erythema. The solitary lesion enlarges to plaques and to the scar-like lesion with a rough surface and skin atrophy (Figure 12).
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Figure 12.
Extragenital lichen sclerosus, slightly elevated plaque with scar-like presentation, with a whitish erythematous rim and skin atrophy.
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More rarely, blistering with possible hemorrhagic content can be present (Figure 13). Extragenital predilection sites include supraclavicular localization, under the breasts, cubit, groin, loose wrist, and cross. Symptoms of extragenital lichen sclerosus are dryness and pruritus.
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Figure 13.
Extragenital lichen sclerosus, whitish plaque with blisters and crusts. Blisters resemble hemorrhagic-like content.
\n
However, lichen sclerosus most frequently affects the anogenital region. In women, it typically affects the vulva and the perianal localization in figure-of-eight configuration (Figure 14). Genital lichen sclerosus begins as slightly elevated lesion of erythema, sometimes with erosions. During the chronic stage of the disease, the skin becomes shiny, sclerotic, and also hypopigmented. The scarring may affect the clitoris and labia, and disability may be significant or even make the sexual intercourse impossible. Although the disease may be symptom-free, it frequently causes severe pruritus and pain is a typical symptom. Another symptom may be dysuria or pain upon defecation [34, 37].
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Figure 14.
Genital lichen sclerosus affects the labia minora, clitoris, and vulval vestibule. Whitish and erythematous plaques are also present in the labia majora, the perineum, and the perianal region.
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4.4 Histopathology
\n
Lichen sclerosus has a specific histopathological pattern. Initially, superficial dermal edema is associated with a band-like lymphocytic infiltrate. The epidermis is thinned and atrophic, with orthohyperkeratosis and vacuolar degeneration of the basal layer. Hyperkeratosis is especially pronounced at follicular openings and may lead to plugging. Vacuolar degeneration of the basal layer and flattening of the rete ridges predispose to the development of blisters, which may become hemorrhagic. The most important changes are found in the superficial dermis with the presence of homogenized collagen (Figure 15). Loss of elastic fibers is typical for lichen sclerosus and is not observed in morphea [38, 39, 40].
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Figure 15.
Skin biopsy of extragenital lichen sclerosus where atrophic thinned epidermis and mild vacuolar degeneration of the basal layer are present. In the superficial dermis, homogenized collagen with perivascular lymphocytic infiltrates can be found.
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4.5 Differential diagnosis
\n
The differential diagnosis of extragenital lichen sclerosus includes morphea, vitiligo, tinea versicolor, anetoderma, or cutaneous lymphoma. In the case of genital lichen sclerosus, erosive lichen planus and erythroplasia of Queyrat must be considered.
\n
Sometimes it is not possible to distinguish morphea from lichen because clinical and especially histopathological findings of both diseases can also be present in one patient or one biopsy [34].
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4.6 Treatment
\n
Topical medications, phototherapy, and systemic therapy have been used for the treatment of lichen sclerosus. The effect of topical corticosteroids was reported especially in genital lichen sclerosus, but mitigation has also been demonstrated in extragenital lichen. Effect of topical corticosteroid therapy has been reported in randomized treatment and retrospective studies. Phototherapy is preferred second-line treatment for patients with limited disease that cannot be effectively treated with topical corticosteroids. An alternative to topical corticosteroids is the use of calcineurin inhibitors pimecrolimus and tacrolimus despite concerns of possible increase of development of squamous cell carcinoma or reactivation of HPV [15, 37, 41].
\n
The use of systemic therapy is limited to a small group of patients with progressive worsening of extragenital lichen sclerosus that failed to respond to a potent topical corticosteroid and phototherapy. For systemic therapy, methotrexate (15–20 mg/week) and systemic corticosteroids (1 g of intravenous methylprednisolone sodium succinate for 3 consecutive days/month) can be used [42].
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5. Eosinophilic fasciitis
\n
Eosinophilic fasciitis is a relatively recently described disease, characterized by fibrosing induration of the extremities and peripheral eosinophilia. In many patients strenuous physical activity precedes the development of this condition.
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5.1 Clinical feature
\n
Initial clinical manifestation includes painful edema of the extremities, which progresses to fibrosis and pseudo-inflammatory appearance (Figure 16). The manifestation of the disease is typically symmetrical on extremities without involvement of the hands, feet, and face [43].
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Figure 16.
Eosinophilic fasciitis with initial clinical manifestation of progressive fibrotic changes with pseudo-inflammatory appearance.
\n
Laboratory findings include elevation of ESR, hypergammaglobulinemia and peripheral eosinophilia which can be present in the early phase of the disease. ANA titer and complement level are usually normal. Pancytopenia, anemia, thrombocytopenia, myeloproliferative disorders, and monoclonal gammopathy have been reported in association with eosinophilic fasciitis. The diagnosis of eosinophilic fasciitis is established via fascial biopsy and/or by MRI [44].
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5.2 Histopathology
\n
Histologically eosinophils and mast cells are present, and dermal fibrosis with patchy infiltrates composed of lymphocytes and plasma cells are also present. In deep biopsy thickening of the fascia is typical, which may be 10–50 times the normal width [44].
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5.3 Treatment
\n
Once the diagnosis of eosinophilic fasciitis is established via fascial biopsy and/or MRI, prompt treatment is essential to preserve mobility and function and prevent joint contractures. Prompt therapy with oral corticosteroids (e.g., prednisone 1–2 mg/kg daily) is usually necessary for reduction or cessation of rapid disease progression and as prevention of mobility reduction and development of joint contractures. The response is typically noted within the first few weeks, and clinical improvement may be seen over several months. Alternatively, hydroxychloroquine, cyclosporine, dapsone, methotrexate, PUVA, or infliximab may be used alone or in combination with prednisone. Phototherapy as UVA1 can also be beneficial [45].
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6. Nephrogenic systemic fibrosis
\n
Nephrogenic systemic fibrosis is most often observed in middle-aged adults but has also been described in children and elderly patients. There is no gender or race predilection. Renal dysfunction and exposure to gadolinium-based contrast medium play a crucial role in the pathogenesis. Although the context use of the gadolinium in a patient with renal dysfunction is irrefutable, the mechanisms of fibrosis are still unknown [46, 47].
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\n
6.1 Clinical features
\n
This disorder presents with large and thick, indurated plaques distributed symmetrically on the extremities and trunk. The skin lesions are irregular and erythematous with a tendency to develop hyperpigmentation. The manifestation on the extremities often results in joint contractures. The condition is frequently associated with considerable pain and loss of mobility. Extracutaneous manifestations include yellow scleral plaques and systemic fibrosis with involvement of the heart, lungs, and also skeletal muscles [48, 49].
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6.2 Histopathology
\n
A deep biopsy is necessary for diagnosis. Histologic features include increased dermal fibroblast-like cells with positivity for CD34 and procollagen I. Haphazard arrangement of thickened collagen bundles is also present. Furthermore, vascular proliferation and mucin deposition may also be present.
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6.3 Treatment
\n
Nephrogenic systemic fibrosis is refractory to treatment with corticosteroids and other immunosuppressive drugs. There have only been case reports of improvement with imatinib, rapamycin, phototherapy UVA1, PUVA, or plasmapheresis. Improvement in renal function after renal transplantation may improve this type of fibrosis [49].
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7. Stiff skin syndrome
\n
This dysfunction may be hereditary as a congenital disorder or acquired during early childhood. Familiar hereditary subtype is caused by heterozygosity for a mutation in the gene that encodes fibrillin-1 (FBN1). Dysfunction of this gene results in the production of giant collagen fibrils in the affected fascia [50].
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\n
7.1 Clinical features
\n
Stiff skin syndrome is characterized by “rock hard” induration and thickening of the skin and subcutaneous tissues. Typical manifestation is on the buttocks and thighs with mild hypertrichosis without affecting the inguinal folds. This disorder does not affect the hands and feet. The condition is stable or slowly progressive, and abnormalities of internal organs are not typically observed. In differential diagnosis the disease may resemble scleredema, deep morphea, or linear scleroderma [51].
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7.2 Histopathology
\n
Histologically, significant thickness of fascia with deposition of hyaline without an associated inflammatory infiltrate can be found. Thickened collagen bundles and mucin deposition may be present in the dermis. The epidermis and papillary dermis are mostly without any pathologies [52].
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7.3 Treatment
\n
Treatment of stiff skin syndrome is very difficult, and no effective treatments have been reported. Physical therapy and regimen measures for the patient can help to prevent progressive joint contractures and immobility [51, 52].
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8. Scleromyxedema
\n
Scleromyxedema is a chronic idiopathic disorder characterized by papules and lesion of induration with dermal mucin deposition and with an increase of dermal collagen resulting in skin sclerosis. Many patients with scleromyxedema have monoclonal gammopathy, with systemic or lethal manifestations. Scleromyxedema represents a generalized variant that needs to be distinguished from localized lichen myxedematosus (variant without sclerosis and paraproteinemia) [53].
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8.1 Pathogenesis
\n
The exact pathogenesis of scleromyxedema is unknown, typically affecting middle-aged adults of both sexes equally. The role of the associated monoclonal gammopathy remains a matter of debate, because, for example, paraprotein levels do not correlate with progression of the disease. But clinical remission of scleromyxedema, during the reduction of paraprotein, that follows after autologous hematopoietic stem cell transplantation was described [53, 54].
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8.2 Clinical features
\n
In the clinical manifestation of scleromyxedema, typically widespread and symmetrically firm, waxy, and closely aligned papules are present (Figure 17).
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Figure 17.
Scleromyxedema. Numerous skin-colored papules of the neck.
\n
Predilection localizations include the head and neck, upper trunk, forearms, and thighs and the proximal parts of fingers. The surrounding skin is shiny with sclerodermoid appearance. Deep longitudinal furrowing is typically involved on the glabella. Strong and rigid infiltrates of the face can result in the face of a lionlike face. As the condition progresses, erythematous and infiltrated plaques may be present with skin stiffening, sclerodactyly, and decreased motility of the mouth and joints.
\n
Scleromyxedema is almost always associated with paraproteinemia. The monoclonal gammopathy is usually IgG and the light chains are more commonly lambda. Patients with scleromyxedema can have a number of internal manifestations, such as dysphagia, proximal muscle weakness due to myositis, peripheral neuropathy, arthropathies, carpal tunnel syndrome, restrictive or obstructive lung disease, and also scleroderma-like renal disease [54].
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8.3 Histopathology
\n
Scleromyxedema is characterized by diffuse deposits of mucin in the upper and middle part of the reticular dermis, increase in collagen deposition in the reticular dermis, and significant proliferation of irregularly distributed fibroblasts. Mucin may fill the walls of myocardial blood vessels as well as vessels of the kidney, the pancreas, adrenal glands, nerves, or lymph nodes [55].
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\n
8.4 Differential diagnosis
\n
The primary differential diagnosis of scleromyxedema includes systemic sclerosis and scleredema. Other conditions in differential diagnosis with possible presence of mucin in the biopsy include nephrogenic systemic sclerosis. Differential diagnosis of leonine facies includes, for example, lepromatous changes, leishmaniasis, cutaneous lymphoma (T cell, rarely B cell), an actinic reticuloid as chronic actinic dermatitis, systemic amyloidosis, nodular mastocytosis, or sarcoidosis [53].
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8.5 Treatment
\n
Recommendations are still based on case reports and open-label small case series. Many chemotherapeutics, primarily melphalan, cyclophosphamide, methotrexate, or chlorambucil, have been tried, with no better results but with the risk of significant side effects. IVIg, alone or in combination with systemic medications such as thalidomide or systemic corticosteroids, may be administered as first-line therapy for cutaneous involvement and also systemic manifestations, including the dermatoneurological syndrome. Additional therapies include PUVA, UVA1, systemic retinoids, cyclosporine, electron beam radiation, plasmapheresis, and extracorporeal photochemotherapy with variable and unpredictable results [56].
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9. Scleredema adultorum of Buschke
\n
Scleredema is typically symmetrical diffuse induration and sclerosis of the upper part of the body especially of the trunk due to thickened dermis with mucin deposition and with relationship to diabetes mellitus.
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\n
9.1 Pathogenesis
\n
Scleredema is a relatively unusual and rare disease that affects patients of all races. The typical form that is associated with diabetes mellitus is more prevalent in men, while other forms are seen more commonly in women. Irreversible glycosylation of collagen and resistance to degradation lead to an accumulation of collagen deposition. Furthermore, stimulation by insulin, microvascular changes and damage, and hypoxia during diabetes mellitus may increase the synthesis of collagen and mucin which result in a dermal deposition of collagen [57].
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9.2 Clinical features
\n
Scleredema adultorum may be divided into three clinical types of scleredema. The first type affects primarily children and middle-aged women. It is preceded by fever, malaise, and an infection (usually streptococcal) of the upper or lower respiratory tract. The localization of this type is the cervicofacial region with extension to the trunk and proximal upper limbs. The cervicofacial region typically affects the perioral localization with difficult opening of the mouth and hindered swallowing. This type usually resolves spontaneously. The second type shares the same clinical features as the first but with very slow manifestation and is more commonly associated with a monoclonal gammopathy [58].
\n
The third type typically affects obese middle-aged men with insulin-dependent diabetes (scleredema diabeticorum). Sclerosis usually starts very slowly and the involvement is persistent. Affected skin is usually erythematous and indurated with typical localization of the posterior region of the neck and the back (Figure 18). The affected skin has peau d’orange appearance. In all three forms, systemic manifestations such as serositis, myositis, dysarthria, dysphagia, parotitis, and ocular and cardiac abnormalities may be present [57, 58, 59].
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Figure 18.
Scleredema adultorum with typical localization of the posterior region of the neck and the back with affected erythematous and indurated skin.
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\n
9.3 Histopathology
\n
The main histopathological feature is the thickening of the reticular dermis, with atypical large collagen bundles. Mucin deposition is also present among separated collagen bundles. There is no increase in the number of fibroblasts, but the elastic fibers are significantly reduced in number. Mucin is also accumulated in the skeletal muscle and in the heart.
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\n
9.4 Treatment
\n
Scleredema which is associated with streptococcal infections is self-limited, thus no therapy is needed. Therapy of scleredema associated with diabetes or a monoclonal gammopathy is more difficult, and no specific treatment is available. Phototherapy as UVA1 or PUVA is the first-line therapy. Systemic and intralesional corticosteroids, intralesional hyaluronidase, antibiotics, methotrexate, cyclosporine, pulse therapy with cyclophosphamide plus oral corticosteroids, tamoxifen, and allopurinol have all been tried, with variable results [58, 59].
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10. Endocrine disorders
\n
Some endocrine disorders like diabetes mellitus and hypothyroidism can be accompanied with skin induration and sclerotic changes and may thus be a diagnostic problem for both systemic sclerosis and its localized forms. Endocrine disorders include sclerodactyly as “diabetic cheiroarthropathy” and myxedema in hypothyroidism.
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\n
10.1 Diabetic cheiroarthropathy
\n
Diabetes mellitus is associated with a wide variety of rheumatologic manifestations which can significantly affect a patient’s quality of life. One of these manifestations includes diabetic cheiroarthropathy which is associated with type I diabetes. Diabetic cheiroarthropathy affects typically the hands. It is postulated to result from increased glycosylation of collagen in the skin and is associated with retinopathy, nephropathy, and duration of the diabetes [60, 61].
\n
\n
10.1.1 Clinical features
\n
Clinical features include thickened skin and limited joint mobility of the hands and fingers, leading to flexion contractures and an inability to approximate the palmar surfaces of the hands and fingers. Sometimes ischemic ulceration and calcinosis cutis can be present.
\n
Treatment relies primarily on glycemic control and on nonsteroidal anti-inflammatory drugs and physical therapy with physiotherapy. With improved glycemic control, the symptoms and signs can be ameliorated and complete reversal is possible [61].
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\n
10.2 Mucinoses associated with thyroid dysfunction
\n
Pretibial myxedema is characterized by cutaneous induration of the shins due to mucin deposition. It is often associated with hyperthyroidism most commonly due to Graves’ disease. Localized myxedema with goiter, exophthalmos, and thyroid acropachy are typical signs of Graves’ disease. Pretibial myxedema is found in 1–5% of patients with Graves’ disease and in up to 25% of those with exophthalmos [62].
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\n
10.2.1 Localized myxedema
\n
\n
10.2.1.1 Clinical features
\n
Localized myxedema presents as erythematous, yellowish or skin-colored waxy induration in a form of a nodulus or plaques. Typical localizations include ventral or anterolateral parts of the lower legs or the feet (Figure 19). In early phases localized myxedema can also present as a diffuse non-pitting edema of the shins or feet that evolves into lymphedema. Even more rarely, localized myxedema affects the face, shoulders, upper extremities, the lower abdomen, scars, or donor graft sites. Large plaques are often painful and pruritic. When present, hypertrichosis and hyperhidrosis are confined to the pretibial myxedematous skin [63, 64].
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Figure 19.
Pretibial myxedema presents as erythematous waxy induration and nodulus on the ventral part of the shank.
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\n
\n
10.2.1.2 Treatment
\n
First-line therapy such as topical corticosteroids or their application under occlusive dressings can be used. In some cases intralesional injection of corticosteroids can be effective. In a patient with lymphedema, medical treatments including IVIg, rituximab, plasmapheresis, and their combination with surgical treatment may have some benefit [63, 65].
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\n
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\n
10.2.2 Generalized myxedema
\n
Generalized myxedema is a manifestation of hypothyroidism where mucin is deposited in the dermis, leading to waxiness of the skin. This condition is caused by a quantitative or functional deficiency of thyroxine. Impaired degradation of mucin and/or increased synthesis is suggested as the main cause.
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\n
10.2.2.1 Clinical features
\n
The typical skin is pale, cool, waxy, and dry. Anhidrosis as an absence of sweating may lead to ichthyosis or eczema “craquelé.” Hair and nails are dry and diffuse non-scaring alopecia is also common. A yellowish hyperkeratosis of the palms may be present. Sometimes purpura on the extremities and skin xanthomas may be observed [66].
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\n
10.2.2.2 Treatment
\n
Early treatment of hypothyroidism is crucial for reduction or cessation of skin involvement and overall symptoms of the disease.
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\n
\n
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\n
\n
11. Amyloidosis
\n
The cutaneous amyloidosis represents a heterogeneous group of conditions in which amyloid, as a fibrillar material that can result from the pathological degradation of various proteins, is deposited in the skin. In primary cutaneous amyloidosis, the deposits are derived from keratin (macular, lichen, biphasic) or immunoglobulin light chains (nodular) [67].
\n
The specific cutaneous lesions of primary systemic amyloidosis are waxy, translucent, or purpuric papules, nodules, and plaques. Amyloid infiltration of the skin may produce thickening and stiffness. Typical localization may be on the limbs but sometimes also on the trunk. This is characteristic of AL amyloid, due to a plasma cell disorder in hematological malignancies. Primary systemic amyloidosis is due to a plasma cell dyscrasia, while secondary systemic amyloidosis arises from chronic inflammatory conditions such as rheumatoid arthritis or in the setting of chronic infections [67, 68].
\n
Skin biopsy reveals accumulation of amyloid with characteristic staining (Congo red) properties under polarizing microscopic examination. Immunofixation of serum or urine is necessary for unambiguous identification of a monoclonal component [69].
\n
Treatment of all forms of amyloidosis is challenging; although the primary cutaneous forms are not life-threatening, primary systemic amyloidosis can carry a poor prognosis for a patient [70].
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\n
12. Conclusion
\n
Systemic sclerosis mimics include a variety of diseases that may resemble systemic connective tissue diseases such as SSc. Above all, the most common diseases are discussed in this chapter.
\n
The basis of proper diagnosis and treatment is the interdisciplinary collaboration of rheumatology and dermatology with the possibility of biopsy tissue collection and histological verification of the disease.
\n
A carefully performed clinical history and physical examination may distinguish these scleroderma mimic syndromes from systemic sclerosis (SSc, scleroderma) and from each other. The distribution and the quality/texture of skin involvement (in SSc typically: sclerodactyly, puffy fingers, ischemic defects/pitting scars/digital ulcers/gangrenes, telangiectasias, calcinosis), the presence of Raynaud’s phenomenon (typically signs of a secondary Raynaud’s phenomenon such as onset after the age of 40, asymmetry, thumb involvement, ischemic pain, history of symptoms <3 years, worsening attacks) or abnormal nail fold capillary microscopy (characteristic scleroderma patterns in SSc), the presence and type of associated systemic manifestations (typical organ involvement characteristic for SSc), and the association with particular concurrent diseases or specific laboratory parameters (SSc-specific autoantibodies such as anti-topoisomerase I, anti-centromere, anti-RNA-polymerase III) can be of substantial help in refining the diagnosis.
\n
In some cases, a full-thickness skin biopsy is helpful to confirm the clinical suspicion. Effective therapies are available for some of these conditions, whereas others are more refractory. For this reason, a prompt diagnosis is important to guide treatment decisions wisely, to spare the patients from ineffective treatments, to facilitate appropriate diagnostic evaluations, and to allow for accurate determination of prognosis [71].
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\n
Acknowledgments
\n
This chapter was supported by NV18-01-00161 A, MHCR 023728 and GAUK 312218.
\n
\n',keywords:"localized scleroderma, lichen sclerosus, eosinophilic fasciitis, nephrogenic systemic fibrosis, scleromyxedema, scleredema",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/68564.pdf",chapterXML:"https://mts.intechopen.com/source/xml/68564.xml",downloadPdfUrl:"/chapter/pdf-download/68564",previewPdfUrl:"/chapter/pdf-preview/68564",totalDownloads:452,totalViews:0,totalCrossrefCites:0,dateSubmitted:"June 26th 2019",dateReviewed:"July 11th 2019",datePrePublished:"August 12th 2019",datePublished:null,dateFinished:null,readingETA:"0",abstract:"Many clinical conditions are presenting with sclerosis of the skin and with tissue fibrosis. These conditions may be confused with systemic sclerosis (SSc, scleroderma). These diseases and disabilities are generally referred to as systemic sclerosis mimics or scleroderma-like syndromes. These disorders have very different etiologies and often an unclear pathogenetic mechanism. Distinct clinical characteristics, skin histology, and disease associations may allow distinguishing these conditions from systemic sclerosis and from each other. A histopathological examination with clinicopathological correlation for diagnosis is important to spare the patients from ineffective treatments and inadequate management. In this chapter, we discussed localized scleroderma, lichen sclerosus, nephrogenic systemic fibrosis, eosinophilic fasciitis, scleromyxedema, and scleredema. These are often detected in the primary care setting and referred to rheumatologists for further evaluation. Rheumatologists, or preferably in collaboration with a dermatologist, must be able to promptly recognize them to provide valuable prognostic information and appropriate treatment options for affected patients.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/68564",risUrl:"/chapter/ris/68564",signatures:"Ondřej Kodet and Sabína Oreská",book:{id:"8269",title:"New Insights into Systemic Sclerosis",subtitle:null,fullTitle:"New Insights into Systemic Sclerosis",slug:"new-insights-into-systemic-sclerosis",publishedDate:"September 18th 2019",bookSignature:"Michal Tomcik",coverURL:"https://cdn.intechopen.com/books/images_new/8269.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"193284",title:"Dr.",name:"Michal",middleName:null,surname:"Tomcik",slug:"michal-tomcik",fullName:"Michal Tomcik"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Localized scleroderma, morphea",level:"1"},{id:"sec_2_2",title:"2.1 Introduction",level:"2"},{id:"sec_3_2",title:"2.2 Epidemiology",level:"2"},{id:"sec_4_2",title:"2.3 Pathogenesis",level:"2"},{id:"sec_5_2",title:"2.4 Clinical features",level:"2"},{id:"sec_6_2",title:"2.5 Plaque-type morphea, circumscribed morphea",level:"2"},{id:"sec_7_2",title:"2.6 Linear morphea",level:"2"},{id:"sec_8_2",title:"2.7 “En coup de sabre”",level:"2"},{id:"sec_9_2",title:"2.8 Generalized morphea",level:"2"},{id:"sec_10_2",title:"2.9 Laboratory findings",level:"2"},{id:"sec_11_2",title:"2.10 Histopathology",level:"2"},{id:"sec_12_2",title:"2.11 Differential diagnosis",level:"2"},{id:"sec_13_2",title:"2.12 Treatment",level:"2"},{id:"sec_14_2",title:"2.13 Topical and intralesional treatment",level:"2"},{id:"sec_15_2",title:"2.14 Systemic treatment",level:"2"},{id:"sec_17",title:"3. Morpheaform inflammatory syndromes/conditions",level:"1"},{id:"sec_17_2",title:"3.1 Lipodermatosclerosis",level:"2"},{id:"sec_17_3",title:"3.1.1 Introduction",level:"3"},{id:"sec_18_3",title:"3.1.2 Clinical features",level:"3"},{id:"sec_19_3",title:"3.1.3 Histopathology",level:"3"},{id:"sec_20_3",title:"3.1.4 Differential diagnosis",level:"3"},{id:"sec_21_3",title:"3.1.5 Treatment",level:"3"},{id:"sec_23_2",title:"3.2 Injection of vitamin K",level:"2"},{id:"sec_24_2",title:"3.3 Vaccination-associated morphea",level:"2"},{id:"sec_25_2",title:"3.4 Paraffin and silicone injections or silicone implants",level:"2"},{id:"sec_26_2",title:"3.5 Porphyrias",level:"2"},{id:"sec_27_2",title:"3.6 Radiation-induced morphea",level:"2"},{id:"sec_27_3",title:"3.7 Differential diagnosis",level:"3"},{id:"sec_30",title:"4. Lichen sclerosus",level:"1"},{id:"sec_30_2",title:"4.1 Epidemiology",level:"2"},{id:"sec_31_2",title:"4.2 Pathogenesis",level:"2"},{id:"sec_32_2",title:"4.3 Clinical features",level:"2"},{id:"sec_33_2",title:"4.4 Histopathology",level:"2"},{id:"sec_34_2",title:"4.5 Differential diagnosis",level:"2"},{id:"sec_35_2",title:"4.6 Treatment",level:"2"},{id:"sec_37",title:"5. Eosinophilic fasciitis",level:"1"},{id:"sec_37_2",title:"5.1 Clinical feature",level:"2"},{id:"sec_38_2",title:"5.2 Histopathology",level:"2"},{id:"sec_39_2",title:"5.3 Treatment",level:"2"},{id:"sec_41",title:"6. Nephrogenic systemic fibrosis",level:"1"},{id:"sec_41_2",title:"6.1 Clinical features",level:"2"},{id:"sec_42_2",title:"6.2 Histopathology",level:"2"},{id:"sec_43_2",title:"6.3 Treatment",level:"2"},{id:"sec_45",title:"7. Stiff skin syndrome",level:"1"},{id:"sec_45_2",title:"7.1 Clinical features",level:"2"},{id:"sec_46_2",title:"7.2 Histopathology",level:"2"},{id:"sec_47_2",title:"7.3 Treatment",level:"2"},{id:"sec_49",title:"8. Scleromyxedema",level:"1"},{id:"sec_49_2",title:"8.1 Pathogenesis",level:"2"},{id:"sec_50_2",title:"8.2 Clinical features",level:"2"},{id:"sec_51_2",title:"8.3 Histopathology",level:"2"},{id:"sec_52_2",title:"8.4 Differential diagnosis",level:"2"},{id:"sec_53_2",title:"8.5 Treatment",level:"2"},{id:"sec_55",title:"9. Scleredema adultorum of Buschke",level:"1"},{id:"sec_55_2",title:"9.1 Pathogenesis",level:"2"},{id:"sec_56_2",title:"9.2 Clinical features",level:"2"},{id:"sec_57_2",title:"9.3 Histopathology",level:"2"},{id:"sec_58_2",title:"9.4 Treatment",level:"2"},{id:"sec_60",title:"10. Endocrine disorders",level:"1"},{id:"sec_60_2",title:"10.1 Diabetic cheiroarthropathy",level:"2"},{id:"sec_60_3",title:"10.1.1 Clinical features",level:"3"},{id:"sec_62_2",title:"10.2 Mucinoses associated with thyroid dysfunction",level:"2"},{id:"sec_62_3",title:"10.2.1 Localized myxedema",level:"3"},{id:"sec_62_4",title:"10.2.1.1 Clinical features",level:"4"},{id:"sec_63_4",title:"10.2.1.2 Treatment",level:"4"},{id:"sec_65_3",title:"10.2.2 Generalized myxedema",level:"3"},{id:"sec_65_4",title:"10.2.2.1 Clinical features",level:"4"},{id:"sec_66_4",title:"10.2.2.2 Treatment",level:"4"},{id:"sec_70",title:"11. Amyloidosis",level:"1"},{id:"sec_71",title:"12. Conclusion",level:"1"},{id:"sec_72",title:"Acknowledgments",level:"1"}],chapterReferences:[{id:"B1",body:'Sehgal VN, Srivastava G, Aggarwal AK, Behl PN, Choudhary M, Bajaj P. Localized scleroderma/morphea. International Journal of Dermatology. 2002;41(8):467-475\n'},{id:"B2",body:'Gabrielli A, Avvedimento EV, Krieg T. Scleroderma. 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International Journal of Dermatology. 2000;39(12):953-954\n'},{id:"B65",body:'Dhaille F, Dadban A, Meziane L, Fessier C, Colta L, Lok C, et al. Elephantiasic pretibial myxoedema with upper-limb involvement, treated with low-dose intravenous immunoglobulins. Clinical and Experimental Dermatology. 2012;37(3):307-308\n'},{id:"B66",body:'Burman KD, McKinley-Grant L. Dermatologic aspects of thyroid disease. Clinics in Dermatology. 2006;24(4):247-255\n'},{id:"B67",body:'Palladini G, Merlini G. Systemic amyloidoses: What an internist should know. European Journal of Internal Medicine. 2013;24(8):729-739\n'},{id:"B68",body:'Schreml S, Szeimies RM, Vogt T, Landthaler M, Schroeder J, Babilas P. Cutaneous amyloidoses and systemic amyloidoses with cutaneous involvement. European Journal of Dermatology. 2010;20(2):152-160\n'},{id:"B69",body:'Nilsson KP, Ikenberg K, Aslund A, Fransson S, Konradsson P, Rocken C, et al. 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Department of Dermatology and Venereology, First Faculty of Medicine, Charles University, Czech Republic
Institute of Anatomy, First Faculty of Medicine, Charles University, Czech Republic
BIOCEV, First Faculty of Medicine, Charles University, Czech Republic
Institute of Rheumatology, Department of Rheumatology, First Faculty of Medicine, Charles University, Czech Republic
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UK Research and Innovation (former Research Councils UK (RCUK) - including AHRC, BBSRC, ESRC, EPSRC, MRC, NERC, STFC.) Processing charges for books/book chapters can be covered through RCUK block grants which are allocated to most universities in the UK, which then handle the OA publication funding requests. It is at the discretion of the university whether it will approve the request.)
UK Research and Innovation (former Research Councils UK (RCUK) - including AHRC, BBSRC, ESRC, EPSRC, MRC, NERC, STFC.) Processing charges for books/book chapters can be covered through RCUK block grants which are allocated to most universities in the UK, which then handle the OA publication funding requests. It is at the discretion of the university whether it will approve the request.)
Wellcome Trust (Funding available only to Wellcome-funded researchers/grantees)
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