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Antismooth Muscle Antibodies (antismooth + muscle_antibody)
Selected AbstractsAcute generalized exanthematous pustulosis mimicking toxic epidermal necrolysisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2001Arnon D. Cohen MD A 91-year-old patient presented with a nonfebrile, pruritic, widespread eruption that appeared 10 days after starting therapy with cefuroxime tablets, 1000 mg/day, due to stasis dermatitis with secondary infection. The patient was also treated with paracetamol tablets, 500,1000 mg/day, 10 days before the onset of the eruption. Previous diseases included congestive heart disease, hyperglycemia, and ectropion. There was no personal or family history of psoriasis. Additional medications, taken for more than 2 years at the time of the eruption, included indomethacin, captopril, hydrochlorothiazide, isosorbide-5-mononitrate tablets, and a combination drug Laxative®. Examination revealed widespread erythema involving 95% of the total body surface area, with numerous 1,2 mm nonfollicular pustules (Fig. 1). There was no predilection to the body folds. Within 24 h of hospitalization, during intravenous therapy with cefuroxime, the patient's condition worsened and bullae containing clear fluid appeared. Nikolsky's sign was positive on erythematous skin, and eventually skin detachment involved 41% of the total body surface area (Fig. 2). There were no target or target-like lesions and there was no involvement of the mucous membranes. Figure 1. Numerous, 1,2 mm, nonfollicular pustules, with confluence (viewed in the lower left part of the photograph), on erythematous skin Figure 2. Widespread skin detachment An early biopsy from a pustule revealed subcorneal and intraepidermal spongiform pustules, papillary edema, perivascular mononuclear infiltrate with a few eosinophils in the dermis, and leukocytoclastic vasculitis. A later biopsy showed similar findings with no evidence of full-thickness epidermal necrosis or necrotic keratinocytes. Direct immune fluorescence (DIF) taken from erythematous skin was negative. Laboratory studies showed the following results: sedimentation rate, 80 mm/h; white blood cell count, 26,200/mm3 with 87% polymorphonuclears and 1.8% eosinophils; hemoglobin, 13.0 g/dL; albumin, 2.8 g/dL (normal, 3.5,5.5 g/dL); other blood chemistry tests were normal. Immunologic studies for rheumatoid factor, antinuclear antibodies, antismooth muscle antibodies, antiparietal cell antibodies, antimitochondrial antibodies, C3, and C4 were normal or negative. Serology for venereal disease research laboratory (VDRL) test, Epstein,Barr virus, cytomegalovirus, hepatitis B virus, hepatitis C virus, human immunodeficiency virus, and antistreptolysin titer was negative. Chest X-ray was normal. Blood cultures were negative. Swab cultures taken from the pustules revealed Staphylococcus aureus as well as coagulase-negative Staphylococcus. All systemic drugs, including intravenous cefuroxime, were withdrawn with close monitoring for signs of heart failure or infection. Topical therapy consisted of application of wet dressings. Within 10 days, the eruption resolved with re-epithelialization of the erosions and the appearance of widespread post-pustular desquamation (Fig. 3) Figure 3. Post-pustular desquamation on the trunk [source] Improved diagnoses of autoimmune hepatitis using an anti-actin ELISAJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2008Vincent Aubert Abstract The presence of antismooth muscle antibodies is one of the diagnostic criteria of autoimmune hepatitis. We evaluated a new anti-F-actin ELISA test and compared it with indirect immunofluorescence assay (IIFA) for antismooth muscle antibodies (ASMA). Two hundred and nine serum samples (35 autoimmune hepatitis, 174 other hepatopathies and control sera) were tested by IIFA on mouse stomach kidney sections for ASMA and by the Quanta Lite Actin ELISA for anti-F-actin antibodies. ASMA were detected in 26 of 35 sera from autoimmune hepatitis (74%) as compared with 25 (71%) with anti-actin antibodies, as well as in 25 of 49 (51%) samples from viral hepatitis as compared with 7 (14%) with anti-actin antibodies. With regards to autoimmune hepatitis, though sensitivity (74.3 vs 71.4%) and negative predictive value (93.5 vs 93.9%) of ASMA and anti-actin ELISA were comparable, anti-actin ELISA was significantly better than ASMA IIFA in terms of specificity (89.7 vs 74.7%), and positive predictive value (58.1 vs 37.1%). Although frequently positive in HCV samples, a comparable sensitivity but better specificity makes the anti-actin ELISA a useful tool in combination with ASMA IIFA for the screening and diagnosis of autoimmune hepatitis. J. Clin. Lab. Anal. 22:340,345, 2008. © 2008 Wiley-Liss, Inc. [source] Autoimmune hepatitis in the Indian subcontinent: 7 years experienceJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2001Rajesh Gupta Abstract Background: Autoimmune hepatitis (AIH) is presumed to be rare in India. The present prospective study was carried out to determine the prevalence, clinical, biochemical and histological profile of patients with AIH in India. Methods: Consecutive patients with chronic liver disease suspected to be AIH, were screened for antinuclear antibodies (ANA), antismooth muscle antibodies (ASMA), antimitochondrial antibody (AMA), and anti-liver kidney microsomal antibodies (anti-LKM-1). Serum protein electrophoresis and liver biopsy were done. Autoimmune hepatitis was diagnosed according to the International Autoimmune Hepatitis Group criteria. Results: Fifty of 1358 (3.43%) patients with chronic liver disease were diagnosed as autoimmune liver disease; 39 with AIH, two with overlap syndrome, five with primary sclerosing cholangitis, and four with primary biliary cirrhosis. Twenty-nine patients were categorized as definite AIH and 10 as probable AIH. Autoimmune hepatitis was common in females (males : females 1:3), with a mean age of 31 ± 17 years. Patients often presented with fatigue, jaundice and anorexia. Skin lesions (58%), joint symptoms (30%), and menstrual abnormalities (26%) were not uncommon. Mildly elevated alkaline phosphatase and hyper gamma globulinemia were seen in 78 and 91% patients, respectively. Eighty percent of patients were type I AIH, while 20% of cases remained unclassified. Histopathological changes included piecemeal necrosis (100%), plasma cell infiltration (91%), rosette formation (82%), and cirrhosis (76%). Overall mortality was 25% during a mean follow up of 15.7 ± 17.0 months. Conclusions: Our results clearly demonstrate that: (i) AIH is not uncommon in India; and (ii) while the profile and spectrum of AIH resembles that seen in the West, Indian patients present late, often in a cirrhotic state. [source] Fulminant hepatitis associated with hepatitis A virus superinfection in patients with chronic hepatitis CJOURNAL OF VIRAL HEPATITIS, Issue 2000S. Vento There have been conflicting reports of the clinical outcome of acute hepatitis A virus (HAV) infection in patients with chronic hepatitis C virus (HCV) infection. A prospective study evaluated 432 patients with chronic hepatitis C (183 with cirrhosis) over a 7-year period. Of the 17 patients with concurrent HAV infection, seven developed fulminant hepatitis and six died. None of these patients had cirrhosis; however, the HLA phenotype (A1; B8:DR3) appeared to be a significant factor in the development of fulminant hepatitis. Patients with this phenotype had high titres of antinuclear antibodies, antismooth muscle antibodies and antiasialoglycoprotein-receptor antibodies, possibly reflecting the induction of autoimmune hepatitis in this group. The high frequency of fulminant hepatitis in patients with HAV/HCV coinfection contrasts with other surveys, although a large Centers for Disease Control and Prevention (CDC) survey demonstrated that HAV infection in patients with pre-existing chronic liver disease (CLD) is associated with increased mortality. It is likely that CLD has some importance as an underlying factor in the development of fulminant hepatitis following HAV infection. Further prospective studies are needed to clarify this issue. [source] |