Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polymyalgia rheumatica (PMR) is a common clinical syndrome that is characterized by pain and stiffness in neck, shoulder girdle and pelvic girdle. The aetiology is unknown. However, recent studies have documented an association with HLA antigens and infectious agents. It occurs mostly after the age of 50 years and is often accompanied by systemic features such as fever, asthenia, hyporexia and weight loss. An erythrocyte sedimentation rate (ESR) of at least 40 mm/hour has been considered diagnostic criterion. Nevertheless, a normal ESR accounted for up to 20% of cases of PMR. A dramatic and prompt response to corticosteroid treatment is characteristic. Giant cell arteritis/temporal arteritis (GCA) has been found in 0-80% of cases of PMR. Temporal biopsy could initially be deferred in patients with PMR younger than 70 years with no cranial symptoms, in which the risk of GCA is very low.
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PMID:[Rheumatic polymyalgia]. 1073 Apr 6

The presence of circulating autoantibodies to gut enterocytes has been very rarely described in adults and is considered a possible cause of refractory sprue. Our aims was to describe the case of an adult patient with serum anti-enterocyte autoantibodies associated with a clinical picture characterized by involvement of both the small intestine and colon. A female, age 50, had suffered from diarrhea with mucus and blood, abdominal pain, thinness, anemia, and leukopenia since the age of 20. She also suffered from HCV infection and had mild chronic hepatitis. Family history was positive for autoimmunity. Symptoms were reported to worsen after eating gluten-containing foods, but anti-transglutaminase and anti-endomysial antibodies were negative. Intestinal histology showed mild, patch villous atrophy with a high intraepithelial lymphocyte count, but a normal number of intraepithelial lymphocytes carrying the gamma/delta+ receptor. HLA was: A11, A31 (19), B52 (5), DR 15 (2), DR 14 (6), DR 51, DR 52, DQ1. Colonoscopy did not show ulcerations or erosions and colon histology showed a moderate inflammatory infiltrate without minor crypt distortion or granuloma. RAST tests were positive for lactalbumin, lactoglobulin, casein, egg, and gliadin. After commencement of an oligoantigenic diet, stool frequency initially decreased, but the presence of mucus in the stools persisted, with episodes of bloody diarrhea. After one year of diet, nutritional parameters were low and anemia associated with a low leukocyte count persisted. Upper and lower gastrointestinal endoscopy and histology of the small intestine and colon were virtually unchanged. Consequently, natural autoantibodies and enterocyte autoantibodies were assayed. The patient was positive for IgG class enterocyte autoantibodies at a titer of 1:34. No other organ-specific or non-organ-specific autoantibodies were positive. Prednisolone treatment was started and the symptoms improved. After one year of this treatment plus elimination diet she was reevaluated. Bowel movement frequency was normal, body weight increased, and the asthenia had completely regressed. IgG anti-enterocyte autoantibodies were absent. Histology of the distal duodenum showed a normal villus/crypt ratio and IEL infiltration was reduced. Colon histology showed a reduction in inflammatory infiltrate in the lamina propria. In conclusion, we report a case of generalized gut disorder in an adult patient, affecting both the small intestine and the colon and characterized by the presence of circulating anti-enterocyte autoantibodies. Systematic testing for enterocyte autoantibodies should be performed not only in patients with refractory sprue, but also in subjects with upper and lower intestinal symptoms who have not been definitively diagnosed.
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PMID:Autoimmune enteropathy and colitis in an adult patient. 1292 54

Hyperacute rejection is rare among ABO-compatible liver transplantations. The mechanism is donor preformed antibodies causing graft loss within a few days. Herein, we have described a case of an ABO-compatible liver transplantation that underwent hyperacute rejection, needing retransplantation for treatment. A 27-year-old man of blood group A positive who displayed fulminant hepatic failure due to hepatitis B (in agreement with the O'Grady criteria), received an ABO-compatible graft. He developed significant asthenia, fever, hypotension, oliguria, and coagulopathy. Ultrasonography revealed total thrombosis of the portal vein and absence of dilatation of bile ducts. The patient was priorized for retransplantation and underwent a good subsequent evolution. On anatomopathologic exam the explant revealed thrombosis of the intrahepatic branches of the portal vein with venous and ischemic infarcts compatible with a diagnosis of hyperacute rejection. The clinical findings of hyperacute rejection were characterized by progressive elevation of bilirubin and thrombocytopenia associated with signs of hepatic failure during the first days after transplantation. In this case, the histological exam was compatible with hyperacute rejection, excluding the diagnoses of hepatic artery thrombosis or biliary obstruction, despite the negative test for anti-HLA antibodies. The diagnosis of hyperacute rejection could be made associated with a short ischemic time and a good response after retransplantation.
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PMID:Antibody-mediated rejection: hyperacute rejection reality in liver transplantation? A case report. 1845 39

Multiple extraintestinal diseases are present in 0.3- 4.5 % of inflammatory bowel disease patients. A 39-year-old woman was admitted with a 3 months history of cervicalgia with functional incapacity, asthenia, tibio-tarsal bilateral arthritis and bloody diarrhoea. She had ferropenic anemia, SR-120 mm, creatinine clearance-42 mL/min, proteinuria-1.2 g/24h. Colonoscopy with biopsy showed active ulcerative rectossigmoiditis. She had bilateral sacroileitis more pronounced at the right side which was suggestive of ankylosing spondylitis. HLA B27 was positive. Because of colestasis, colangio-MRI and CPRE were done and were suggestive of primary sclerosing colangitis. Renal disease was interpreted as an analgesic nephropathy versus glomerulonephritis associated with ulcerative colitis. Cardiac ecodoppler showed pericardial thickening with a thin pericardial effusion. Full improvement of gastrointestinal complaints was observed with 5-ASA topic enemas, sulfassalazine, corticosteroids and azathioprine and full remission of ankylosing spondylitis with adalimumab. This case illustrates extraintestinal wide involvement as the initial presentation of ulcerative colitis, remarking its systemic nature.
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PMID:[Ulcerative colitis initial presentation with multiple extra-intestinal manifestations]. 2068 1

Fibromyalgia (FM) syndrome is a disabling clinical condition of unknown cause, and only symptomatic treatment with limited benefit is available. Gluten sensitivity that does not fulfill the diagnostic criteria for celiac disease (CD) is increasingly recognized as a frequent and treatable condition with a wide spectrum of manifestations that overlap with the manifestations of FM, including chronic musculoskeletal pain, asthenia, and irritable bowel syndrome. The aim of this report was to describe 20 selected patients with FM without CD who improved when placed on a gluten-free diet. An anti-transglutaminase assay, duodenal biopsy, and HLA typing were performed in all cases. CD was ruled out by negative anti-transglutaminase assay results and absence of villous atrophy in the duodenal biopsy. All patients had intraepithelial lymphocytosis without villous atrophy. Clinical response was defined as achieving at least one of the following scenarios: remission of FM pain criteria, return to work, return to normal life, or the discontinuation of opioids. The mean follow-up period was 16 months (range 5-31). This observation supports the hypothesis that non-celiac gluten sensitivity may be an underlying cause of FM syndrome.
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PMID:Fibromyalgia and non-celiac gluten sensitivity: a description with remission of fibromyalgia. 2472 27

Drug-induced liver injury (DILI) to flucloxacillin is rare and is classified as idiosyncratic, as it is dependent on individual susceptibility, unpredictable, and dose-independent. The authors present the case of a 74 - year - old man with a history of monoclonal gammopathy under investigation and alcoholic habits of 24 g/day, with asthenia, anorexia, nausea, abdominal discomfort, and fever with three days of evolution. He was treated with two courses of antibiotic therapy with flucloxacillin to erysipelas previously (3 months and 2 weeks before admission). Lab tests showed serum AST levels of 349 U/L, ALT 646 U/L, alkaline phosphatase 302 U/L, GGT 652 U/L, total bilirubin 3.3 mg/dL and direct bilirubin 2.72 mg/dL. Infectious, autoimmune, and metabolic causes were ruled out. Magnetic resonance cholangiopancreatography showed normal results. Liver biopsy showed mild multifocal (predominantly microvesicular) steatosis; marked changes in the centrilobular areas (sinusoidal dilatation, marked congestion, hemorrhage, and multifocal hepatocyte collapse); expansion of the portal areas with the formation of bridges; proliferated bile ducts and inflammatory infiltrate of variable density, predominantly mononuclear type. The HLA-B*5701 screening test was positive. Hepatic biochemical tests remain abnormal with a significative increase in total bilirubin, which reached levels of 24.1 mg/dL, with the development of jaundice, pruritus, and choluria. DILI was assumed, and the patient was treated with ursodeoxycholic acid. There was favorable evolution, without evidence of blood coagulation dysfunction or encephalopathy. The analytic normalization was, however, slow, with evolution to chronicity. The authors present this case to remind the possibility of moderate/severe drug-induced liver injury to flucloxacillin, an antibiotic commonly used in clinical practice and association with the HLA-B * 5701 allele reported in the literature.
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PMID:Flucloxacillin-Induced Hepatotoxicity - Association with HLA-B*5701. 3213 Mar 75