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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 10 women and five men with papulonecrotic tuberculid, an uncommon form of cutaneous tuberculosis (TB). The mean age was 22.6 years (range, 2 1/2-35 years) at presentation. The Mantoux test was strongly positive in 13 patients. Five patients showed presumptive evidence of associated TB; in one case, the presence of TB was proven by culture. Response to anti-TB was dramatic in all cases. Clinical findings were similar to those previously published. We emphasize the simultaneous occurrence of erythema induratum, associated Takayasu's disease, possible associated phlebitic tuberculid, and clinical mimicry of acute bacterial endocarditis. The main histopathological findings obtained from 27 biopsy specimens included dermal necrosis (26 of 27 cases), a poorly formed granulomatous infiltrate (27 of 27 cases), vasculitis (11 of 27 cases), perivascular spongy edema (11 of 27 cases), and follicular necrosis or suppuration (five of 27 cases). A Ziehl-Neelsen stain was negative in all biopsy specimens. Immunohistochemical labeling revealed a preponderance of T-lymphocytes (UCHL-1+), monocytes-macrophages (S-100+), and Langerhans cells (ACT+), indicative of a type IV hypersensitivity reaction. B-lymphocytes (L26+) were sparse. Conditions that may be confused with PNT on clinical or histopathological ground include pityriasis lichenoides et varioliformis acuta, papular urticaria, papulopustular syphilide, miliary TB, septicemia, perforating granuloma annulare, chondrodermatitis nodularis, reactive perforating collagenosis, allergic granulomatosis, suppurative folliculitis, and infectious causes of palisading granulomas. Papulonecrotic tuberculid has distinct clinical, histopathological, and immunohistochemical features. Awareness of this entity is important since an appropriate diagnosis is necessary for the institution of timely curative treatment.
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PMID:Papulonecrotic tuberculid. A clinical, histopathological, and immunohistochemical study of 15 patients. 780 63

Chronic urticaria includes several different subsets with distinct pathophysiologies, and with important implications for investigation and treatment. Chronic 'idiopathic' urticaria represents a special challenge, which, until recently, was not taken up by dermatological or immunological investigators. However, it has now emerged that at least 30% of patients possess histamine-releasing autoantibodies against Fc epsilon R1, or less commonly IgE itself. These autoantibodies are causative. Recent work implicates complement activation in most cases. Functional (i.e. histamine releasing) autoantibodies are specific to chronic urticaria. However, immunoreactive (non-histamine-releasing) anti-Fc epsilon R1 autoantibodies can be found in sera of patients with physical urticarias and with autoimmune connective tissue and bullous diseases. The reason for the occurrence of this disease type in some individuals but not others is unclear. One possibility is the development, in genetically predisposed persons, of autoantibodies by molecular mimicry - perhaps against lipopolysaccharide of Helicobacter pylori, an organism frequently infecting the upper gastrointestinal tract of chronic urticaria patients.
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PMID:Pathophysiology of chronic urticaria. 1189 48

Since the discovery of Helicobacter pylori (H. pylori), numerous studies have considered the possibility that it plays a role in different extragastric diseases. Most of these studies may be classified as epidemiological studies or investigations of H. pylori eradication, but there are also case reports and in vitro studies. This review reveals the limitations common to most of them. Idiopathic thrombocytopenic purpura is the disease for which the strongest association with H. pylori infection has been shown. Data are also accumulating about the role of H. pylori infection in idiopathic iron deficiency anemia and chronic idiopathic urticaria. Interesting results show that H. pylori infection affects atherosclerosis and is weakly associated with ischemic heart disease and stroke. Moreover, CagA-positive H. pylori strains may play a role in the natural history of atherosclerotic stroke. Recent studies suggest a link between H. pylori and Parkinson's disease. Preliminary data indicate that H. pylori infection impairs gastric ghrelin production and may influence nutritional status. The association between H. pylori infection and other extragastric diseases remains controversial. H. pylori infection may cause extragastric manifestations directly or indirectly, by various mechanisms including atrophic gastritis, the release of inflammatory mediators, molecular mimicry, and systemic immune response. Evidence suggests that anti-H. pylori therapy improves idiopathic thrombocytopenic purpura (significant increase of platelet count in half of the cases), iron-deficiency anemia, and chronic urticaria (30% remission rate), but the data from randomized controlled trials are insufficient to confirm these positive effects.
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PMID:[Does Helicobacter pylori infection play a role in extragastric diseases?]. 1824 21