Irinel Parepa

By Elvira Craiu, Lucia Cojocaru, Andrei Rusali, Razvan Maxim and Irinel Parepa

Part of the book: Recent Advances in Cardiovascular Risk Factors

By Andra‐Iulia Suceveanu, Adrian‐Paul Suceveanu, Irinel‐Raluca Parepa, Felix Voinea and Laura Mazilu

The prevalence of hepatopulmonary syndrome (HPS) in the setting of cirrhosis ranges between 4 and 47% and its presence increases the mortality rate, especially when hypoxemia is present. Our study aim was to fix whether there is a correlation of results between two simple and non‐invasive procedures such as transthoracic contrast‐enhanced ultrasound (CEUS) and pulse oximetry, used for early detection of HPS in patients with liver cirrhosis, having as endpoint the improvement in their outcome. The rapid lung enhancement and delayed left ventricle enhancement of the saline solution, after at least three systolic beats during CEUS and pulse oximetry showing a SaO2 < 95%, were correlated and considered positive for the diagnosis of HPS. One hundred and sixty‐five (44%) of the total of 375 patients diagnosed with liver cirrhosis enrolled in the current study, with or without respiratory symptoms (dyspnea, clubbing, distal cyanosis, cough and/or spider angioma), showed positive criteria for HPS diagnosis during CEUS. SaO2 < 95% and PaO2 < 70 mmHg were found in 123 patients (33%) during pulse oximetry investigation. Pearson correlation index showed a good correlation between lung and heart CEUS findings and pulse oximetry (r = 0.97) for HPS diagnosis. CEUS and pulse oximetry results correlate and rapidly diagnose HPS, a highly fatal complication of liver cirrhosis (LC), guiding the future treatment by speeding up orthotopic liver transplant OLT recommendations to improve the survival rates.

Part of the book: Liver Cirrhosis

By Andra Iulia Suceveanu, Roxana Popoiag, Laura Mazilu, Irinel Raluca Parepa, Andreea Gheorghe, Anca Pantea Stoian, Felix Voinea, Claudia Voinea and Adrian Paul Suceveanu

Advanced liver cirrhosis requiring hospitalization is frequently associated with electrolytic disturbances, the most common finding being serum hyponatremia. The goal of treatment in patients with decompensated liver cirrhosis complicated with severe hyponatremia is to normalize the increased amount of water in the body and to improve the sodium concentration. Fluid restriction is recommended at 1.5 L/day to prevent sodium depletion in the serum, but the lack of efficacy is probably due to a poor patient compliance. Discontinuation or adjustments of diuretic dosages are sometimes required. Albumin associated with vasoconstrictors as midodrine can increase the effective arterial blood volume and seems to improve the serum sodium concentration. A promising therapeutic option targeting the pathophysiological mechanism of hyponatremia consists of improving solute-free water excretion, which is markedly impaired in these patients. The use of agents such as k opioid agonists has been attempted, but has been dropped due to the severe side effects. Recently, a new therapeutic class called vaptans has taken an important place in the treatment of hypervolemic hyponatremia. The main side effects during the administration of these drugs in patients with liver cirrhosis are reversible after discontinuing therapy. Therefore, it is recommended to use vaptans for short periods of time.

Part of the book: Management of Chronic Liver Diseases

By Laura Mazilu, Dana Stanculeanu, Andreea Gheorghe, Adrian-Paul Suceveanu, Irinel Parepa, Felix Voinea, Doina Catrinoiu and Andra-Iulia Suceveanu

Metformin has been used for almost half a century as the first line of treatment for type 2 diabetes. Mechanisms of action are still incompletely known, recent studies have shown that metformin exerts its effects through several mechanisms, including the stimulation of AMP-activated protein kinase, decreasing production of cyclic AMP, inhibition of mitochondrial complex I of the electron transport chain, targeting glycerophosphate dehydrogenase and altering gut microbiota. In recent years, studies have shown that patients with type 2 diabetes mellitus have a lower risk of developing cancer, and patients with cancer and type 2 diabetes have a lower mortality. Experimental studies have demonstrated that metformin has anti-tumor activity by inhibiting mTORC1 signaling pathway and mitochondrial complex, inhibiting tumor growth and proliferation, and inducing cellular apoptosis. There are multiple studies showing that combination of metformin with different types of anti-cancer therapies may reduce toxicities and tumor resistance. This chapter is focused on the progress made in understanding the anti-tumor effect of metformin and its association with cancer therapy.

Part of the book: Metformin

By Andra Iulia-Suceveanu, Sergiu Ioan Micu, Claudia Voinea, Madalina Elena Manea, Doina Catrinoiu, Laura Mazilu, Anca Pantea Stoian, Irinel Parepa, Roxana Adriana Stoica and Adrian-Paul Suceveanu

The human gastrointestinal tract presents a vastly population of microorganisms, called the microbiota. The presence of these microorganisms offers many benefits to the host, through a range of physiological functions. However, there is a potential for these mechanisms to be disrupted condition, known as dysbiosis. Recent results are showing important associations between diabetes and the gut microbiota and how the intestinal flora can influence the prognosis of this illness. Microbial intestinal imbalance has been linked to alterations in insulin sensitivity and in glucose metabolism and may play an important role in the development of diabetes. Metformin is one of the most important and widely used first-line medications for the management of type 2 diabetes (T2D). It is a complex drug with multiple sites of action and multiple molecular mechanisms. In recent years, attention has been directed to other modes of action, other than the classic ones, with increasing evidence of a major key role of the intestine. By analysing the effects of metformin on the homeostasis of the microbiota of diabetes patients, our present topic becomes one of the major importance in understanding how metformin therapy can improve gut microbiota dysbiosis and thus provide a better outcome for this illness.

Part of the book: Metformin

By Andra-Iulia Suceveanu, Andrada Dumitru, Marilena Musat, Claudia Voinea, Felix Voinea, Irinel Parepa, Anca Pantea Stoian, Laura Mazilu and Adrian Paul Suceveanu

Ulcerative colitis and Crohn’s disease represent the major groups of idiopathic disorders in inflammatory bowel disease (IBD). The etiology includes environmental factors, genetic factors, and immune responses. The pathogenesis is diversified; however, no guaranteed curative therapeutic regimen has been developed so far. This review contains information related to pathophysiology and current treatment options for IBD. It is known that IBD is caused by tissue-disruptive inflammatory reactions of the gut wall; that is why downregulation of the immune responses allows the healing of the damaged mucosa and allows the resetting of the physiological functions of the gut back to normal. The main treatment options are still corticosteroids, immunomodulators, antibiotics, probiotics, and a series of new agents. Their effects include modulation of cytokines, neutrophil-derived factors, adhesion molecules, and reactive oxygen/nitrogen metabolites. The monoclonal antitumor necrosis factor as infliximab recombinant anti-inflammatory cytokines or related gene therapy is also used nowadays. Still, the fecal microbiota transplantation (FMT) is considered to revolutionize the therapy in IBD, considering the abnormal inflammatory response due to the complicated relationship between microbiota and the immune system. It is imperative to mention the critical role dysbiosis may have in the pathogenesis of IBDs. This review summarizes the available literature concerning the efficacy of FMT in IBDs.

Part of the book: Human Microbiome