Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient, a 28 year-old-man, was admitted to a hospital because of general fatigue and fever. He was pointed out renal dysfunction and was transferred to Nagasaki University Hospital. The laboratory data on admission showed moderate azotemia (BUN 43 mg/dl, Cr 5.4 mg/dl). A percutaneous renal biopsy on admission revealed a diffuse crescentic glomerulonephritis. A direct immunofluorescence of renal biopsy showed a linear pattern for IgG along the glomerular basement membrane. Radioimmunoassay of his serum for circulating anti-GBM antibody was strongly positive. Aggressive treatment with pulse therapy (methylprednisolone), plasmapheresis, and continuous heparin infusion was performed. He had markedly recovered from renal failure and escaped hemodialysis. The patient is making satisfactory process after 3 years.
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PMID:[Anti-glomerular basement membrane antibody-mediated glomerulonephritis remarkably improved by pulse therapy with methylprednisolone, plasmapheresis and continuous heparin infusion]. 262 42

Data for 26 patients with membranoproliferative glomerulonephritis, type I (MPGN I) and 22 with membranoproliferative glomerulonephritis, type III (MPGN III), as distinguished by glomerular ultrastructure, were analyzed to determine differences in presentation, complement perturbation, and glomerular morphology by light microscopy. MPGN III was detected with greater frequency by the chance discovery of hematuria and proteinuria in the otherwise healthy individual (MPGN III, 63%; MPGN I, 30%; P = .01) and never, in the absence of renal failure, presented with systemic symptoms such as ease of fatigue, weight loss, and pallor, as may patients with MPGN I. The more frequent detection of MPGN III by chance is evidence that its onset is insidious and that for long periods it produces no symptoms or signs. Glomerular proliferation is also less than in MPGN I. Further, in MPGN III, the complement perturbation and glomerular immunofluorescence give no evidence of classical pathway activation, for which there is abundant evidence in MPGN I. Even with severe hypocomplementemia in MPGN III, C3 nephritic factor, another cause of hypocomplementemia, is rarely detectable and then in very low concentration. The cause of the complement perturbation in MPGN III has so far escaped identification. Although these observations give evidence that MPGN III is distinct from MPGN I, there is compelling evidence from other studies that a predisposition to both types is inherited and that similar genetic factors are operative in the two types. Because their genetic basis appears to be the same, it must be concluded that despite their differences, types I and III are variants of the same disease.
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PMID:Differences between membranoproliferative glomerulonephritis types I and III in clinical presentation, glomerular morphology, and complement perturbation. 382 60

In the past 10 years we have examined 20 children with inflammatory liver disease associated with high serum titers of anti-liver-kidney microsome antibody (anti-LKM). The first hepatic symptoms were progressive fatigue and jaundice, the fortuitous finding of hepatomegaly or splenomegaly with raised transaminase activity, or an acute hepatitis-like illness. At the time of diagnosis, hepatomegaly was present in 18 children, splenomegaly in 16, jaundice in nine, and ascites in two. Serum alanine transferase activities were elevated in all but two, who had already received steroids. Serum total gammaglobulin values were greater than 2.0 gm/dl in 16 children, prothrombin activity less than or equal to 60% in six, and serum titer of anti-LKM between 1:100 and 1:100,000. All children but one had cirrhosis, and histologic signs of aggressivity were present in 14. In 11 children one or more extrahepatic diseases were present, including type 1 diabetes, vitiligo, glomerulonephritis, autoimmune hemolytic anemia, hypoglycemia with hyperinsulinism, autoimmune thyroiditis, chronic mucocutaneous candidiasis with hypoparathyroidism, and multiple cutaneous and visceral telangiectasias. Treatment with prednisone and azathioprine improved the liver condition in 16 of the 18 patients given treatment. In eight of them discontinuation of treatment resulted in rapid relapse; 14 are still receiving treatment and have stable hepatic function with follow-up from 8 months to 6 1/2 years. Only two are free of treatment. Four children died, two in spite of immunosuppressive therapy, one during a relapse, and one of extrahepatic disease. These results indicate that this autoimmune inflammatory liver disease may have onset early in life, with several clinical patterns; is frequently associated with certain types of extrahepatic manifestations of autoimmune origin; and is a potentially fatal disease for which immunosuppressive treatment must be started early.
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PMID:Liver disease associated with anti-liver-kidney microsome antibody in children. 395 Aug 19

Segmental Mediolytic Arteritis (SMA) is a very rare arterial lesion which is limited in adults to the involvement of the intra-abdominal muscular arteries. The pathology is characterized by segmental disruption of the arterial media which leads segmental mediolysis, with subsequent dissecting aneurysm or rupture. A 73-year-old man was admitted to a hospital because of high fever, general fatigue and weight loss. These symptoms were resistant to antibiotic therapy, and soon after, renal insufficiency developed. Three months after the onset of symptoms, he died suddenly of hemorrhagic shock. Autopsy revealed rupture of the splenic artery and systemic necrotizing arteritis in the small-sized arteries of liver, pancreas and kidneys, as well as in the connective tissues around the adrenal glands. Histopathology of the splenic artery was consistent with SMA, and that of the systemic vascular lesions, with microscopic polyarteritis nodosa. Focal glomerular lesions characteristic of crescentic and/or granulomatous glomerulonephritis were present. A developmental mechanism for SMA is discussed with respect to this case together with a review of previous reports of this disease.
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PMID:[An autopsy case of segmental mediolytic arteritis (SMA) accompanied with microscopic polyarteritis nodosa]. 748 68

A 53 year old man first presented with a mild anti-neutrophil cytoplasmic antibody (ANCA), type (MPO-ANCA) associated microscopic polyangiitis. Approximately one year later, he presented with fatigue, fever, cough, sore muscles and erythrocyturia. At admission he was uraemic. Kidney biopsy showed in LM extracapillary glomerulonephritis and in immunofluorescence microscopy linear deposition of IgG along the glomerular basement membrane (GBM). MPO-ANCA was still positive, but antibodies against GBM were now also present. Retrospective analysis revealed the presence of anti-GBM antibodies nine months before clinical illness. Pr3-ANCA (C-ANCA) was negative during the whole course. In spite of decreasing anti-GBM antibody levels during treatment, his condition aggravated, and he died from complications. Thus, coexisting anti-GBM antibodies may explain suddenly deteriorating renal function in patients with ANCA associated vasculitis.
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PMID:[Rapidly progressing glomerulonephritis. Microangiitis associated with antibodies against the glomerula membrane]. 757 Nov 13

A previously healthy 51-year-old man, hospitalized because of fatigue and joint complaints, was found to have left-sided diffuse pulmonary infiltration and a rapid rise in creatinine concentration. Anti-neutrophil cytoplasmic antibodies (cANCA) and anti-glomerular basement antibodies (anti-GBM) were found in serum. Renal biopsy revealed extracapillary glomerulonephritis with diffuse half-moon formations. Immunohistology showed a diffuse granular pattern for immunoglobulin G, M and complement C3, without linear deposits. Immunosuppressive treatment combined with plasmapheresis brought about rapid clinical improvement and normalization of the lung involvement and renal function, as well as a fall in the cANCA titre. During a follow-up period of 5 years there has been no recurrence of symptoms, although the anti-GBM titre remained strongly positive and the cANCA titre twice rose to abnormal levels.
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PMID:[Unilateral diffuse pulmonary involvement in vasculitis with anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibodies]. 791 84

A 49-year-old man was admitted because of general fatigue, cough and hematuria. During the hospital course, acute renal failure, hemoptysis and dyspnea developed. A percutaneous renal biopsy revealed a diffuse crescentic glomerulonephritis, and direct immunofluorescence showed a linear pattern of IgG along the glomerular basement membrane. Although serum anti-glomerular basement membrane (anti-GBM) antibody was not detected. Goodpasture's-like syndrome was suspected, and methylprednisolone pulse therapy and plasmapheresis were administered. Concomitantly, extracorporeal membrane oxygenation (ECMO) was instituted because of deterioration in respiratory status due to a severe pulmonary hemorrhage despite maximal ventilatory support. Temporarily, the patient improved and ECMO was discontinued. ECMO may be a useful therapeutic support for hypoxia resulting from pulmonary hemorrhage in Goodpasture's syndrome (GPS) and Goodpasture's-like syndrome.
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PMID:Goodpasture's-like syndrome and effect of extracorporeal membrane oxygenator support. 800 Jan 12

Recently group A Streptococcus toxic shock like syndrome (TSLS) has been reported, but as for group B streptococcus (S. agalactiae) infection, there have been little documentation in the literature. We report a case of fluminant septic shock due to Streptococcus agalactiae (S. agalactiae). A 72-year-old male was admitted to our hospital because of general fatigue and azotemia. He was diagnosed as having MPO-ANCA related glomerulonephritis and treated with steroid therapy. Gradually he was doing well. On the 228th hospital day, he suddenly had tachypnea, transient conscious disturbance, and profound hypotension. About 16 hours later, he died despite intensive treatment. S. agalactiae was isolated from the blood. Autopsy revealed bilateral bronchopneumonia and shock liver. To our knowledge, this is the first report of septic shock caused by S. agalactiae.
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PMID:[A case of fluminant septic shock due to Streptococcus agalactiae in a patient with MPO-ANCA related glomerulonephritis]. 898 74

A 74-year-old man was admitted to our hospital because of edema of the lower legs, fever, and increasing fatigue. Laboratory evaluation revealed proteinuria, microhematuria, leukocytosis, thrombocytosis, anemia, a high level of C-reactive protein. A test for myeloperoxidase-antineutrophil cytoplasmic antibodies was highly positive. Microscopic polyarteritis nodosa was diagnosed and therapy with prednisolone was begun. Examination of a renal biopsy sample showed necrotizing crescentic glomerulonephritis. A chest roentgenogram and CT scan disclosed bilateral basilar interstitial changes. Six months later, the patient was admitted again because of disturbance of consciousness, malnutrition, and hyponatremia. After admission, alveolar infiltrates developed in the right lung and the patient died on the 5th hospital day as a result of respiratory failure. An autopsy revealed Candida pneumonia of the right lung and massive intra-alveolar hemorrhage, which was believed to have caused the respiratory failure. Other findings were usual interstitial pneumonia, cellular small-vessel angiitis in the lungs, and healed angiitis in the kidneys and liver. In this case of microscopic polyangiitis and chronic interstitial pneumonia, steroid therapy was effective against the angiitis, but the patient died of an opportunistic infection and alveolar hemorrhage.
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PMID:[Microscopic polyangiitis and pulmonary fibrosis in a patient who died of Candida pneumonia and intra-alveolar hemorrhage]. 936 70

In this case-report we describe the fatal outcome of systemic vasculitis. A 51-year-old man was hospitalised with constant abdominal pain, chest pain, anorexia, fatigue, weight loss, dyspeptic complaints, and a period of high fever at home. Bilateral adrenal enlargement was found without a plausible cause. Endoscopy revealed a reflux oesophagitis grade I, which was treated with famotidine. His complaints disappeared without further treatment. Five days after release from hospital the patient was re-admitted with subfebrile temperature followed by an Addison's crisis due to primary adrenal failure. Laboratory tests for systemic illness were all negative. He was treated with high-dose corticosteroids. Right adrenal biopsy revealed haemorrhage, possibly of older age. After 10 days he returned with severe kidney and heart failure. He was transported to another hospital for haemodialysis. Unfortunately the patient passed away because of cardiac arrhythmias. Postmortem investigation revealed inflammation of middle-sized and small arteries in the adrenal glands, heart, lung and thyroid. In the kidneys, mesangio-proliferative glomerulonephritis was found. A definite classification of the vasculitis could not be made because of the high-dose corticosteroids therapy. Possibly, the haemorrhage of both adrenal glands was caused by venous thrombosis due to the hypercoagulable state, which is often observed in vasculitis.
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PMID:Bilateral adrenal enlargement as a first sign of systemic vasculitis. 944 26


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