Notes

Impulsive Iliopsoas Muscles Hemorrhage-Predictors regarding Connected Fatality.
We have provided a systematic review of the literature of this new and challenging entity of cutaneous IgG4-RD.Macular arteritis (MA) has a striking discordance between the clinical presentation of hyperpigmented macules and the histopathologic findings of a lymphocytic arteritis with intraluminal hyalinized fibrin ring and thrombosis. It has been proposed that MA represents the chronic, indolent, lymphocytic form of the neutrophil-predominant cutaneous polyarteritis nodosa. MA usually affects middle-aged women asymptomatically on the legs. There is also a slightly more severe variant with more infiltrated plaques and livedo racemosa, termed lymphocytic thrombophilic arteritis. MA and lymphocytic thrombophilic arteritis have similar histologic features, both with a largely intact vascular elastic lamina, despite the abundant fibrin and endarteritis obliterans. There is no evidence for progression from MA to lymphocytic thrombophilic arteritis to cutaneous polyarteritis nodosa, and aggressive therapy should be avoided in MA, given the indolent, benign disease course.New and emerging types of cutaneous vascular (capillary) proliferations have been described or better categorized in the last few years. They include reactive angioendotheliomatosis, acroangiodermatitis (pseudo-Kaposi sarcoma), diffuse dermal angiomatosis, intravascular histiocytosis, glomeruloid angioendotheliomatosis, and angiopericytomatosis (angiomatosis with cryoproteins). Clinically, they are characterized by multiple, red violaceous, and purpuric patches and plaques, sometimes evolving toward necrosis and ulceration with a wide distribution but a propensity to involve the extremities. Histologically, they are characterized by different patterns of intravascular or extravascular lobular or diffuse hyperplasia of endothelial cells, pericytes, and sometimes histiocytes. Although these angioproliferations can histologically have a pseudoangiosarcomatous pattern, they are reactive in that they originate from the (sub)occlusion of vascular lumina by different localized or systemic disorders. The vascular proliferation stops after the inducing hypoxic stimulus has been withdrawn. Among them, diffuse dermal angiomatosis of the breast is a variant of diffuse dermal angiomatosis involving middle-aged women with macromastia, obesity, smoking, and vasculopathic disorders, considered a distinct disorder in the spectrum of cutaneous reactive angiomatoses. It presents with reticulated erythematous to purple patches with sometimes a tendency to ulcerate and bleeding, appearing on large, pendulous breasts. The pathogenesis is related to tissue hypoxemia resulting from subclinical torsion, compression, and increased venous hydrostatic pressure due to the macromastia, aggravated by the associated ischemic conditions such as hypertension and diabetes. selleckchem There is no evidence-based therapy, but reduction mammoplasty is a viable treatment option. This should be evaluated in all patients who fail conservative therapy.Neutrophilic dermatoses (NDs) are a group of reactive, noninfectious autoinflammatory diseases characterized by (1) infiltration of the epidermis, dermis, and or/hypodermis by neutrophils; (2) their association with distinct diseases (eg, hematologic malignancy and chronic inflammatory diseases); (3) potential extracutaneous involvement; and (4) response to anti-inflammatory drugs, such as corticosteroids, dapsone, colchicine, and novel biologic therapies, such as the anti-interleukin-1 blockade. Although distinct NDs have been described, transitional forms with overlapping features are often identified. These justify a simplified classification of NDs with three major forms superficial (epidermal or pustular) NDs, dermal (en plaques) NDs, and deep NDs. We review selected or novel variants of NDs, including subcorneal pustular dermatosis, the group of immunoglobulin A neutrophilic dermatoses, amicrobial pustular dermatosis of the folds, and neutrophilic urticarial dermatosis, as well as atypical forms of Sweet syndrome and pyoderma gangrenosum closely mimicking severe infectious diseases. Knowledge of these variants is essential for proper diagnosis, adequate management, and avoidance of a dangerous escalation of therapy, such as unnecessary immunosuppression or extensive surgery.Aquagenic palmoplantar keratoderma (APK) is an uncommon hereditary or sporadic condition that is characterized by edematous flat-topped papules appearing on palmar skin with wrinkling after brief water exposure. APK has been associated with cystic fibrosis (CF), presenting with the same mutations found in CF (usually ΔF508 of the CFTR gene), either homozygous or heterozygous. APK may be idiopathic or drug-induced. The diagnosis is easily made if one is aware of this entity. Topical aluminum hydroxide and botulinum toxin injections are the most commonly used treatments. The sporadic form may have a shorter course compared with the hereditary one, resolving spontaneously after a few years. The condition should no longer be considered a true keratoderma but rather a pseudo keratoderma, and in spite of the many different names found in the literature, the term "aquagenic (pseudo) keratoderma" seems to be the most appropriate one.Papuloerythroderma of Ofuji (PEO) is a rare skin condition first described in 1984 and characterized by diffuse erythroderma composed of papules coalescing into plaques with sparing of skin folds, known as the deck-chair sign. The disease is almost exclusively seen in the elderly and affects men more frequently than women. Common laboratory findings include peripheral and tissue eosinophilia, elevated levels of immunoglobulin E, and lymphopenia. The diagnosis entails exclusion of potentially causative pathologies, including drug intake, atopy, malignancy, and infection. These factors have frequently been found in association with PEO, but their role in the etiopathogenesis of the disease is poorly understood. A dysregulated immune system, with particular involvement of T-helper (Th)2 and Th22 cells, seems to be important in the development of PEO. Controversy exists as to whether PEO exists as an independent entity or as a clinical pattern of a variety of distinct conditions. Treatment necessitates first addressing any coexisting circumstances that may have a causal relationship with PEO.
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