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)

A Japanese girl aged 13 years with myeloperoxidase anti-neutrophil cytoplasmic antibodies(MPO-ANCA)-associated glomerulonephritis(GN) progressed to end-stage renal failure after 7 years' clinical observation. She had been suffering from recurrent disease flare associated with serum MPO-ANCA elevation(i.e. 153 EU/ml, 208 EU/ml and 358 EU/ml, maximum at each of the episodes, normal < 10 EU/ml). Each flare was treated successfully with prednisolone combined with cyclophosphamide and azathioprine. However, her renal function gradually deteriorated, and peritoneal dialysis(PD) was initiated 7 years after the onset of the disease. During the clinical course, no extrarenal manifestations were observed. Due to subsidence of the serum MPO-ANCA titer(10 EU/ml) after starting PD, prednisolone and azathioprine were tapered thereafter. Her daily urine volume was preserved at approximately 600 ml at that time. She suddenly developed fatigue with severe anemia, oliguria and hypertension 4 months after discontinuation of immunosuppressive therapy. The serum titer of MPO-ANCA increased to 100 EU/ml. These clinical observation suggests that disease flare may occur in selected patients with MPO-ANCA-associated GN, who develop end-stage renal failure requiring PD. Although recurrent flare associated with an increased serological activity in a proportion of patients with lupus nephritis who have received dialysis has been reported to date, to our knowledge, a similar clinical observation in the MPO-ANCA-associated GN has not been reported. Selected patients with the disease should be followed with close observation after undergoing dialysis.
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PMID:[A case of ANCA-associated glomerulonephritis without extrarenal symptoms with disease flare after starting dialysis]. 1221 82

A 12-year-old boy presented with left shoulder pain during physical exercise and complained of uncommon sweating and fatigue. Diagnostic evaluation revealed a solitary pulmonary nodule in the left upper lobe. All laboratory values were within normal limits, except for an elevated level of antineutrophil cytoplasmic antibodies directed against myeloperoxidase (p-ANCA). Surgery was performed, and pathological examination showed a localized granulomatous vasculitis. Antineutrophil cytoplasmic antibodies directed against affinity purified proteinase 3 (p-ANCA) concentrations returned to baseline within 6 months, and the patient has done well during a follow-up period of 2 years. While nodular vasculitis is known to occur in Wegener's granulomatosis, to the best of our knowledge, this case represents the first c-ANCA negative primary pulmonary vasculitis in childhood.
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PMID:Nodular pulmonary vasculitis in a twelve-year-old boy. 1473 Jun 65

The aim of this study was to compare power output profiles during repeated cycling and running sprints in children and adults. On two separate visits, 12 boys [11.7 (0.5) years] and 13 men [22.1 (2.9) years] performed ten consecutive 10-s sprints interspersed with 15-s recovery intervals on a non-motorised treadmill and cycle ergometer. Peak (PPO) and mean (MPO) power outputs were measured during each sprint. Capillary fingertip blood samples were drawn at rest and 3 min after the final sprint to measure lactate accumulation (Delta[La]). PPO and MPO decreased significantly more in adults compared to children over the ten sprints irrespective of the mode of exercise (P<0.001). PPO decreased by a similar amount during running and cycling in children (-17.7 versus -14.3%, P>0.05, respectively) and adults (-43.3 versus -40.0%, P>0.05, respectively). In contrast, MPO decreased significantly more during running compared to cycling both in children (-28.9 versus -18.7%, P<0.05) and adults (-47.0 versus -36.7%, P<0.05). The greater decrease in MPO during running compared to cycling was accompanied in children by significantly higher Delta[La] values (7.7 versus 4.1 mmol l(-1), P<0.001). In adults, blood lactate accumulation tended to be higher during running than cycling (12.7 versus 10.8 mmol l(-1), P=0.06). To conclude, adults displayed a greater decrement in power output compared to children over the ten repeated running and cycling sprints. Furthermore, children and adults experienced greater fatigue during running compared to cycling. This last result may be attributed to additional muscle recruitment during sprint running.
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PMID:Effects of age and mode of exercise on power output profiles during repeated sprints. 1504 4

A 72-year-old woman with primary biliary cirrhosis (PBC) and antineutrophil cytoplasmic autoantibody (ANCA)-associated rapidly progressive glomerulonephritis is described. She had a 6-year history of PBC diagnosed histologically, with a positive test finding for antimitochondrial antibodies and elevated biliary enzyme activity. The myeloperoxidase-ANCA test result was negative. The patient was treated with ursodeoxycholic acid (600 mg/day) and had been stable for 6 years. She was admitted to our hospital because of general fatigue, exertional dyspnea, and peripheral edema. Her serum level of creatinine was increased (4.4 mg/dL), and her hemoglobin concentration was reduced (8.0 g/dL). The patient was diagnosed as having rapidly progressive glomerulonephritis. Test results for serum antinuclear antibody and myeloperoxidase-ANCA were positive. The diagnosis by renal biopsy was necrotizing crescentic glomerulonephritis. Prednisolone followed by methylprednisolone pulse therapy and cyclophosphamide were administered. The patient underwent plasma exchange twice weekly for 4 weeks. After 4 weeks, her serum creatinine level fell to 1.8 mg/dL, and she recovered renal function without hemodialysis. After 24 weeks, her renal function (serum creatinine level, 1.6 mg/dL) was stable.
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PMID:Antineutrophil cytoplasmic autoantibody-associated rapidly progressive glomerulonephritis in a patient with primary biliary cirrhosis. 1536 78

A 68-year-old-male who was diagnosed as having rheumatoid arthritis (RA) 7 years previously was admitted the Chiba Social Insurance Hospital due to general fatigue, spiking fever, and appetite loss. Blood tests showed extremely high levels of C-reactive protein (CRP, 318.5 mg/dL), and hypergammapathy (IgG 3228 mg/dL, IgA 905 mg/dL, IgM 2537 mg/dL) and high titers of rheumatoid factor (RAPA 40960X). He was diagnosed as having RA with vasculitis, according to interstitial pneumonitis, cutaneous nodules and polyneuropathy. Prednisolone (30 mg/day) was prescribed, however, myeloperoxidase-antineutrophil cytoplasmic antibody proved to be positive (86EU) and cyclophosphamide (50 mg/day) was added one week later. Additionally, IgM K-chain M-protein was revealed and the differentiation between auto-immune and hematologic diseases was required for further drug prescriptions. Therefore, double filtration plasmapheresis (DFPP) was initiated weekly. Hematologic diseases were negated and the hypergammapathy was improved. C-reactive protein and MPO-ANCA decreased to the normal level after three sessions (IgG 1064 mg/dL, IgA 331 mg/dL, IgM 94 mg/dL, CRP 0.04 mg/dL) and the patients symptoms improved. Prednisolone was tapered and he was discharged. It was suggested that the case presented here was quite rare, having an extremely high level of CRP which was successfully managed by DFPP.
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PMID:Double filtration plasmapheresis for the treatment of a rheumatoid arthritis patient with extremely high level of c-reactive protein. 1566 36

A 50-year-old woman was admitted because of high fever and fatigue. Proteinuria, hematuria, and elevated BUN (47.8 mg/dl) and creatinine (3.4 mg/dl) suggested rapidly progressive glomerulonephritis. The serological study revealed all negative results for rheumatoid factor, antinuclear antibody, serum cryoglobulins, MPO-ANCA, PR3-ANCA, and anti-streptolysin O. Antiglomerular basement membrane (GBM) antibody, as assessed by ELISA, was 11 EU (normal, <10). Kidney biopsy on the eighth hospital day demonstrated pauci-immune-type crescentic glomerulonephritis without ANCA. Methylprednisolone pulse therapy (500 mg/day, 3 days) and 45 mg/day prednisolone orally were started. At 3 weeks after kidney biopsy, the anti-GBM antibody value increased from 11 EU/ml to 116 EU/ml, and MPO and PR3-ANCA were still negative. HLA type was DR8 and DR 15(2), with a genotype of HLA-DRB1*08021 and HLA-DRB1*15011. The present case suggests that HLA-DR15 plays an important role on antibody production against alpha 3(IV) NC1 autoantigen after severe nephritis or tissue damage.
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PMID:The increase of antiglomerular basement membrane antibody following pauci-immune-type crescentic glomerulonephritis. 1583 Feb 77

We present a case of classical polyarteritis nodosa (PN) overlapping thrombotic thrombocytopenic purpura (TTP). A 70-year-old woman was transferred to our hospital because of general fatigue and fever. On admission, laboratory findings revealed leukocytosis, normochromic normocytic anemia and renal dysfunction. About one week later, she developed disturbance of consciousness, and laboratory findings revealed rapidly progressive thrombocytopenia and renal dysfunction. We suspected the presence of microscopic polyangiitis (MPA), based on mild elevation of myeloperoxidase (MPO) anti-neutrophil cytoplasmic antibody (ANCA). On post-admission Day 11, renal biopsy was performed but the diagnosis of MPA could not be confirmed because of the absence of glomerular crescent formation or vasculitis. However, the biopsy specimen showed many collapsed glomeruli and interstitial inflammation, indicating the presence of occlusive lesions, such as vasculitis in larger arteries. We instituted methylprednisolone pulse therapy, cyclophosphamide and plasma exchange, because the clinical symptoms also satisfied the criteria of TTP. Despite the intensive treatment, the patient died on 43rd day of hospitalization due to thalamic hemorrhage. Autopsy showed typical findings of classical PN including disruption of arterial walls and fibrinoid necrosis in the medium-sized arteries of the kidneys and colon. We detected reduced activity of von Willebrand factor-cleaving protease (VWF-CP) and the presence of plasma inhibitory IgG against VWF-CP. A better understanding of the mechanisms would be useful.
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PMID:Thrombotic thrombocytopenic purpura associated with polyarteritis nodosa. 1624 Sep 3

Microscopic polyangiitis (MPA) is a systemic necrotizing vasculitis affecting small vessels without necrotizing granulomatous inflammation and is commonly associated with necrotizing glomerulonephritis. Diagnosis is based on typical clinical features, the presence of antimyeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA), and histopathologic findings. Cases of pathologically proven small-vessel vasculitis in nasal biopsy specimens are sparse. Here we report a patient with MPA that was histopathologically confirmed by nasal and paranasal biopsy. A 67-year-old man presented with fever and general fatigue. Laboratory examinations showed severe inflammation and acute progressive renal failure. The serum MPO-ANCA level was elevated. The patient also had nasal polyps that seemed to be nonspecific chronic sinusitis. To obtain a pathologic diagnosis, bilateral ethmoidectomy and nasal polypectomy were performed. Pathological findings revealed vasculitis of small vessels in the mucosal surface. MPA was diagnosed on the basis of clinical symptoms, elevated MPO-ANCA and the pathological findings of the nasal and paranasal surgical specimen.
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PMID:Microscopic polyangiitis histologically confirmed by biopsy from nasal cavity and paranasal sinuses: a case report. 1662 40

A 30 years-old man was administrated with dizziness and fatigue for half month, and the big toe on his left foot got the prolonged bleeding of wound complicated with fever 7 days before the admission. The physical examination (PE) discovered that the case suffered from the anemic appearance, lower part tenderness of sternum, petechiae and purpura on skin of lower extremities, and with remaining not to be remarkable. The examination of blood routine showed WBC 2.3 x 10(9)/L, Hb 60/L, BPC 34 x 10(9)/L and blasts 0. 85. The bone marrow smear indicated markedly the hypercellularity, promyelocytes 89% and strongly positive myeloperoxidase (MPO). The PT and APTT were prolonged, and the FDP and D-dimer were positive. The acute promyelocytic leukemia (APL) with DIC was diagnosed. The patient was administered with all-trans retinoic acid (ATRA) with dosage of 20 mg three times per day. After 14 week treatment, the patient did not get complete remission. Then the tanshinone II A was taken orally with 30mg twice each day. After 8 week treatment of tanshinone II A, the blood routine was restored to normal. Four weeks later, the bone marrow also became normally, and the patient got a complete remission (CR). After more than 3 months of consolidation therapy with tanshinone II A, the patient was relapsed. When the homoharringtonine and cytarabine (HA) were given, the patient was got CR again. Three years later, he was relapsed secondarily, and then died of intracranial hemorrhage. The tanshinone II A could induce CR of APL with ATRA resistance, no side effect was observed; there is a reoccurring possibility from consolidation therapy with tanshinone II A.
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PMID:[Complete remission of acute promyelocytic leukemia resisting all-trans retinoic acid of one case treated by tanshinone II A]. 1723 2

We present the case of a 56-year-old woman with anti-glomerular basement membrane (anti-GBM) antibody disease accompanied by granulomatous reaction in the kidney. Three months prior to admission to our kidney center, she had suffered from interstitial pneumonia and had a slightly elevated level of MPO-ANCA (13 EU). Her serum level of creatinine was normal (0.72 mg/dl) but proteinuria (1+) and hematuria (2+, 1-4/HF) were present. She was admitted to our hospital because of general fatigue, loss of appetite, high fever (over 38.5 degrees C) and a rapid decline in renal function (creatinine 8.50 mg/dl). Hemodialysis therapy was started immediately after admission. The serological study was negative for MPO-ANCA and PR3-ANCA but positive for anti-GBM antibody (139 EU). Renal biopsy demonstrated necrotizing glomeruli, cellular crescents and grauloma formation with multinucleated giant cells. Immunofluorescence microscopy revealed linear staining of IgG and C3. We diagnosed graulomatous, crescentic and necrotizing glomerulonephritis, patho-logically. She was diagnosed as having anti-GBM antibody disease because alveolar hemorrhage was absent. Steroid therapy including methylprednisolone pulse therapy (500 mg/day, 3 days) and 2 courses of plasma exchange were effective in reducing the fever, anti-GBM antibody titer and C-reactive protein level. Her renal function recovered and she was able to quit hemodialysis therapy 68 days after the start of hemodialysis and she has shown no signs of pulmonary alveolar hemorrhage to date. The present case suggests that intensive therapy may restore renal function in anti-GBM disease even though renal function was sufficiently damaged and required hemodialysis therapy and active pathological changes were observed in renal biopsy specimens.
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PMID:Anti-glomerular basement membrane antibody disease with granulomatous lesions on renal biopsy. 1737 97


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