Hair loss in women is

Hair loss in women is polygenic and multifactorial with the additional influence of environmental factors. Several studies focused on the importance of several genes related to alopecia (Carey et al., 1993, Hillmer et al., 2008, Randall, 2008). FPHL involves progressive hair follicle miniaturization and subsequently the conversion of terminal follicles into vellus-like follicles. These vellus-like follicles have a shortened hair cycle because of a reduction in the anagen phase, which leads to the production of short and fine hair shafts. Unlike in men, the miniaturization is not uniform and intense in women; therefore, there are no complete areas of baldness except in very rare cases (Birch et al., 2001). Moreover, the miniaturization process may be accompanied by a mild-to-moderate lympho-histiocytic inflammatory infiltrate in the peri-infundibular region. The term “microinflamation” has been used to differentiate this infiltrate from the inflammation that occurs in scarring alopecia (Stefanato, 2010). FPHL and male balding share a final common pathway of follicular regression but current knowledge suggests that the etiology is not necessarily the same in both sexes. Androgens are a key driver of male balding and also involved in the etiology of pattern hair loss in some women. However, other nonandrogenic factors that are still unidentified likely play a role in causing FPHL (Herskovitz and Tosti, 2013).
Comorbidities The most common endocrinologic comorbidity that is associated with FPHL is polycystic ovarian syndrome (El Sayed et al., 2016). Metabolic syndrome, which is characterized by obesity, insulin resistance, hypertension, hyperprolactinemia, and raised Streptomycin sulfate mg levels, also appears to be frequently associated with FPHL (El Sayed et al., 2016). An increased risk of carotid and coronary artery diseases have also been reported (Arias-Santiago et al., 2010). To further clarify the comorbidity profile of FPHL, systematic studies in larger population-based samples are needed. An association between ferritin levels and FPHL is controversial. Some studies have demonstrated lower ferritin levels in patients with FPHL compared with controls and antiandrogen therapy seem to work better in patients with ferritin levels >40 μg/l (Ramos and Miot, 2015).
Diagnosis
Differential diagnosis A differential diagnosis of FPHL includes TE, postpartum hair loss, cicatricial alopecia in pattern distribution, and alopecia areata (diffuse or incognita; Asz-Sigall et al., 2016). As discussed, dermoscopy is a very useful complementary tool to get the right diagnosis, especially in the early stages of the disease.
Treatment
Topical therapy
Conclusions
Progression of chronic kidney disease (CKD) toward end-stage renal failure (ESRF) is a prominent problem in clinical nephrology. The incidence of CKD is rising, but effective therapies to halt progression of disease remain elusive. Progression of CKD results from a complex interplay of pathologies that involve all constituents of the kidney, which makes Spontaneous mutation difficult to single out targets for effective therapeutic strategies. The extent of so-called tubulointerstitial fibrosis is often considered to be the rate-limiting step in progression of CKD. This idea is founded on histopathological analysis of large cohorts of kidney biopsies, which demonstrated that only tubulointerstitial fibrosis (which at the time was determined as the relative volume of the interstitium within a kidney biopsy section) correlates with and also predicts progression of CKD toward ESRF, irrespective of the underlying primary disease., , , Widening of the tubulointerstitium, which is referred to as tubulointerstitial fibrosis, is caused by a composite of extracellular matrix (ECM) accumulation, sterile inflammation, accumulation of activated fibroblasts, and rarefaction of microvessels. Although the relevance of each of these events to progression of fibrosis and CKD is hotly debated, this knowledge led to the concept that tubulointerstitial fibrosis is a common pathway of all chronic progressive kidney diseases and that effective antifibrotic therapies could potentially halt progression of CKD irrespective of the underlying disease. However, such therapies are not yet available.