Herpes zoster (HZ) is a disease triggered by the reactivation of latent varicella zoster virus (VZV) in spinal or cranial sensory ganglia, and is characterized by a painful vesicular eruption in the affected dermatome. Postherpetic neuralgia (PHN) is a chronic, neuropathic pain that can persist long beyond resolution of visible cutaneous manifestations which is often resistant to current analgesic treatments. The lifetime prevalence of herpes zoster is approximately 20–30% and about 9–34% of these patients develop PHN depending on its definition. Clinical experience has shown that PHN often develops in cases of inadequate initial pain management resulting in increased pain intensity. This review provides an overview of the treatment options for HZ and PHN, focusing on the therapeutic modalities of pain management. The primary objectives of management of HZ are to inhibit viral replication, relieve pain, and prevent associated complications, such as PHN. General treatments for acute HZ are combination of antiviral therapy with a short course of corticosteroids at the onset of the disease in conjunction with an effective control of acute pain, including nonsteroidal anti-inflammatory drugs, acetaminophen, opioids, and anticonvulsants such as gabapentin or pregabalin. Treatment of PHN is often resistant to the current pharmacologic methods. Therefore, a multimodal analgesic treatment regimen including topical lidocaine and capsaicin, systemic therapies, and the interventional treatments is necessary to alleviate pain and its effect on quality of life. As the incidence of HZ increases with age, the number of patients with HZ and PHN may increase in the future considering the gradual aging of the general population. Appropriate management of HZ can reduce the duration and intensity of pain from HZ, and prevent the development of PHN. In addition, prophylactic zoster vaccination can prevent or reduce the incidence of HZ and PHN. Further efforts are needed to minimize pain of the patients suffering from HZ and PHN as it affects the quality of life in the aspect of both physical and psychological impairments.
Part of the book: Pain Management
The aging process in the skin is complex and influenced by more intrinsic and extrinsic factors than any other body organ. The effects of these two types of factors overlap for the most part. The combined effects of these two aging processes also affect dermal matrix alterations. The main clinical signs of skin aging include wrinkling and irregular pigmentation, which are influenced by a combination of intrinsic and extrinsic (e.g., UV radiation, heat, smoking, and pollutants) factors. Histologically, collagen decreases, and the dermis is replaced by abnormal elastic fibers as a cause of wrinkle formation through the loss of skin elasticity. There have been numerous studies of skin aging performed to elucidate the underlying molecular mechanisms and to develop various antiaging therapeutics and preventive strategies. We summarized the molecular mechanisms and treatments of skin aging. Mainly UV radiation induces ROS formation and DNA damage, leading to increased production of MMPs and decreased production of collagen in keratinocytes and fibroblasts, which reflect the central aspects of skin aging. Besides UV radiation exposure, extrinsic factors including tobacco smoking, exposure to environmental pollutants, infrared radiation, and heat contribute to premature skin aging. Like UV radiation, these factors cause ROS formation and increase expression of MMPs, thus accelerating skin aging by inducing extracellular matrix (ECM) degradation. Accumulated collagen fibrils inhibit the new collagen synthesis and account for the further degradation of the ECM through this positive feedback loop. Accumulating evidence for molecular mechanisms of skin aging should provide clinicians with an expanding spectrum of therapeutic targets in the treatment of skin aging.
Part of the book: Molecular Mechanisms of the Aging Process and Rejuvenation