Gene/Protein Disease Symptom Drug Enzyme Compound
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A review of the medical records of 123 persons with Legionnaires' disease hospitalized in the 1976 Philadelphia epidemic showed that the manifestations of infection ranged from mild grippe to a severe pneumonia that also involved other organ systems. Early in the illness, constitutional symptoms predominated. Fever, malaise, myalgia, rigors, confusion, headache, and diarrhea were usually followed by nonproductive cough and dyspnea. Physical examination showed few abnormalities other than rales. Moderate leukocytosis with left shift, elevated erythrocyte sedimentation rate, elevation of serum levels of liver enzymes, and hematuria and proteinuria were characteristic. Chest radiograph showed patchy, often nodular, areas of consolidation. Progression of pneumonia led to respiratory failure and the need for mechanical ventilatory assistance for 19 patients; renal failure, primarily after shock, occurred in 18 persons. Twenty-six patients died. Treatment with erythromycin or tetracycline resulted in the lowest case-fatality ratios, but the associations were not statistically significant.
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PMID:Legionnaires' disease: clinical features of the epidemic in Philadelphia. 43 27

A 38-year-old man was hospitalized for proteinuria, and pitting edema. He had noticed Raynaud's phenomenon at about age fifteen. One month prior to admission, his urine contained protein and the serum creatinine was 3.0 mg/dl. On admission, sclerodactylia, digital pitting scar of fingertips, digital bone absorption and pulmonary fibrosis were observed and a diagnosis of progressive systemic sclerosis (PSS) was made. Laboratory investigations revealed: 24-hour urine protein excretion 3 g; serum creatinine 5.6 mg/dl; creatinine clearance 13.5 ml/min; antinuclear factor strongly positive in a speckled pattern; antibodies to nRNP positive with a titer of 1: 20, 480; antibodies to DNA, Sm, SS-A, SS-B, Scl-70, centromere and Jo-1 negative; serum complement normal. A renal biopsy revealed focal and segmental necrotizing glomerulonephritis with 70% crescents but no vascular changes. Circulating antiglomerular basement membrane antibodies were negative. Immunofluorescence disclosed granular deposits of IgM and C3 in the mesangium and along the capillary walls. Treatment was begun with methylprednisolone pulse therapy. After 5 month, serum creatine and creatinine clearance were 1.9 mg/dl and 35 ml/min, respectively. A year after the discharge, he was readmitted for hemoptysis and worsening of proteinuria and microhematuria. A chest radiograph demonstrated bilateral alveolar consolidation. Serum creatinine was elevated to 3.5 mg/dl. The continuous hemoptysis resulted in a severe dyspnea associated with a rapid fall in the hemoglobin. On the fourth hospital day, the PaO2 was 41 Torr on oxygen by mask that necessitated mechanical ventilation and pulse therapy was started. However, the patient died on the ninth hospital day of respiratory failure due to pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis complicated by crescentic glomerulonephritis and diffuse pulmonary hemorrhage]. 147 23

Renal biopsies were carried out in 29 patients with scleroderma to study the early vascular lesions and their eventual clinical significance. Haemolytic acute renal failure was present in 9 patients. The biopsies showed early vascular lesions on interlobar arteries. The main biological change was proliferative or fibrous endarteritis. Mucoid infiltration was found in 3 biopsies. The arterioles were spared or only slightly affected without major fibrinoid necrosis. These lesions were therefore distinct from those of malignant hypertension. However, at autopsy of 2 of these cases, the vascular lesions were undistinguishable from those of malignant hypertension. The biopsies in 13 out of 14 patients with scleroderma without obvious renal involvement (9 cases) or with moderate proteinuria and/or hypertension without renal failure (5 cases) showed interlobar endarteritis with associated mucoid infiltration in 3 patients. This lesion was isolated but sometimes extensive even in young patients without hypertension. One patient died within one year, of disseminated colonic carcinoma, and 4 of cardio-respiratory failure due to scleroderma without hypertension, renal failure or proteinuria. Eight of the 9 remaining patients were traced 6 to 16 years after biopsy. Two were moderately hypertensive but none had renal failure. Cutaneous and internal organ scleroderma had regressed in the majority and proteinuria had disappeared in 3 cases.
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PMID:[Renal involvement in scleroderma]. 652 54

The protean manifestations of Legionnaires' disease are described in an analysis of 12 sporadic cases. Two forms of the disease have been delineated. One variant (Group A) consisted of six patients who had a mild form of non-progressive pneumonia with minimum extra-pulmonary involvement. Six patients (Group B) were differentiated by rapidly progressive pulmonary infiltrates, severe hypoxia and respiratory failure, plus a higher frequency of band neutrophils and extra-pulmonary manifestations. Particularly notable were evidence of severe myositis (elevated creatinine phosphokinase and lactate dehydrogenase), anaemia, and neurological findings which included alterations in the sensorium, meningitis, and convulsions. Cerebrospinal fluid (CSF) abnormalities were seen frequently in patients with neurological manifestations, and necropsy findings in one patient suggested that the Legionnaires' bacillus was capable of producing a fatal leucoencephalitis. Renal findings included haematuria, proteinuria and oliguric renal failure. Hepatic transaminases (SGPT, SGOT) were elevated in six patients and serum bilirubin was abnormal in five. Alkaline phosphatase values were normal to minimally elevated. The gastrointestinal symptoms commonly considered to be a frequent initial manifestation of Legionnaires' disease were rare in this series. Recommendations for instituting empirical therapy, based upon recognition of a clinical syndrome which should suggest the diagnosis of Legionnaires' disease, are included.
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PMID:The protean manifestations of Legionnaires' disease. 663 Oct 29

Eight patients with Legionnaires' disease were seen at one hospital in the summer of 1979. They presented in the same 12-day period with an illness of rapid onset characterized by fever, chills, malaise, profuse sweating and neurologic symptoms. Neutrophilia, a high erythrocyte sedimentation rate, proteinuria, hypoalbuminemia, hyponatremia, hypochloremia and abnormal liver enzyme levels in the serum were usually noted. The roentgenographic findings in the lungs ranged from segmental interstitial infiltration to panlobar pneumonia. Seven patients responded to erythromycin treatment, though one died suddenly, presumably of unrelated cardiac disease. The other patient died of a combination of renal and respiratory failure, with pulmonary edema.
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PMID:Eight cases of Legionnaires' disease. 700 76

Over the past 50 years, survival has improved in patients with systemic lupus erythematosus and associated nephritis. Yet, there are few long-term outcome studies in patients with well-defined nephropathy. We examined the outcome of 439 patients with lupus nephritis who were seen at the Mayo Clinic between 1964 and 1986 in whom renal biopsies were assessed using the World Health Organization (WHO) classification. There were 341 women and 98 men (mean +/- s.d., age 33.5 +/- 14 years); 200 (46%) patients were hypertensive and 249 (57%) had impaired renal function at renal biopsy. All WHO morphologic classes were represented and 339 (77%) patients had class III, IV and V (the more severe forms of nephritis). Follow-up averaged 10.2 years per patient. At last contact, 286 (65%) patients were alive and 153 (35%) were dead. Overall patient survival was 80%, 69% and 53% at 5, 10 and 20 years after biopsy that was significantly worse than expected survival (P < 0.001). Ten-year cumulative patient survival improved comparing earlier to more recent time spans: 64% in 231 patients seen during 1964-75; 76% in 2089 patients studied during 1976-86 (P = 0.03). Survival free of renal failure was 83%, 74% and 64% at 5, 10 and 20 years, and survival was unfavorably influenced by progressive WHO class, hypertension, impaired renal function, nephrotic range proteinuria, hypoalbuminemia and anemia. Multivariate analysis found impaired renal function, increased urine protein, anemia and younger age to be independent predictors of renal failure. WHO class was not a significant predictor when adjusted for these four factors. Cardiovascular events accounted for 48% of the known deaths and were equally distributed across all WHO classes, followed by infections, renal failure, malignancy, respiratory failure and gastrointestinal bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic determinants in lupus nephritis: a long-term clinicopathologic study. 779 13

A 73-year old man was admitted to the hospital because of dyspnea. His proteinuria was pointed out in 1981. He felt dyspnea after exertion and abnormal chest X-ray shadow was pointed out in 1984. He was admitted to our hospital for further examination for the first time in 1988. He was diagnosed as IgA nephropathy by renal biopsy, and idiopathic interstitial pneumonia (IIP) by transbronchial lung biopsy. Then steroid therapy was begun because of progression of renal dysfunction in November 1990. But thereafter dyspnea, hypoxia and fine diffuse reticulonodular shadow on chest X-ray film was exacerbated. And he died because of respiratory failure. In this case, progression of IgA nephropathy seemed associated with exacerbation of IIP.
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PMID:[IgA nephropathy with acute exacerbation of idiopathic interstitial pneumonia: an autopsy case]. 843 77

We report here a case of Cogan's syndrome associated with systemic vasculitis as well as myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis. A 71-year-old woman with the diagnosis of aortitis syndrome and pulmonary fibrosis for 7 years, complained of vertigo and hearing impairment. A diagnosis of serous otitis media was made. Although steroid therapy was effective, the symptoms relapsed several times. Seven months after the first manifestation of aural symptoms, she developed painful red eyes bilaterally and proteinuria. On admission, perinuclear ANCA without cytoplasmic ANCA was detected by indirect immunofluorescence assay and MOP-ANCA was detected by enzyme linked immunosorbent assay using the 363 ELISA Unit. Renal biopsy showed necrotizing crescentic glomerulonephritis without immune deposits. A diagnosis of atypical Cogan's syndrome with systemic vasculitis and pulmonary fibrosis was made from the clinical and histological findings. As nephrotic syndrome progressed after admission, she was started on high-dose corticosteroid administration. Urinary protein and other symptoms, except for hearing acuity, improved in parallel with a decrease in the MPO-ANCA titer to normal values. While tapering the dose of corticosteroid, the MPO-ANCA titer increased again and dyspnea occurred. Although pulse methylpredonisolone therapy was performed, the patient died of respiratory failure complicated with sepsis. Postmortem lung biopsy showed pulmonary fibrosis and massive alveolar hemorrhage. The findings of this case study suggest that MPO-ANCA may be closely related to the pathogenesis of Cogan's syndrome.
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PMID:[A case of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis associated with Cogan's syndrome]. 891 96

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

1,1-Dichloroethane (DCE) is a solvent that is often found as a contaminant of drinking water and a pollutant at hazardous waste sites. Information on its short- and long-term toxicity is so limited that the U.S. EPA and ATSDR have not established oral reference doses or minimal risk levels for the volatile organic chemical (VOC). The acute oral LD(50) in male Sprague-Dawley (S-D) rats was estimated in the present study to be 8.2 g/kg of body weight (bw). Deaths appeared to be due to CNS depression and respiratory failure. In an acute/subacute experiment, male S-D rats were given 0, 1, 2, 4, or 8 g DCE/kg in corn oil by gavage for 1, 5, or 10 consecutive days. The animals were housed in metabolism cages for collection of urine and sacrificed for blood and tissue sampling 24 h after their last dose. There were decreases in body weight gain and relative liver weight at all dosage levels, as well as increased renal nonprotein sulfhydryl levels at 2 and 4 g/kg after 5 and 10 days. Elevated serum enzyme levels, histopathological changes, and abnormal urinalyses were not manifest. For the subchronic study, adult male S-D rats were gavaged with 0.5, 1, 2, or 4 g DCE/kg 5 times weekly for up to 13 weeks. Animals receiving 4 g/kg exhibited pronounced CNS depression, with more than one-half dying by week 11. The 2-g/kg rats exhibited moderate CNS depression. One 2-g/kg rat died during week 6. There were very few manifestations of organ damage in animals that succumbed or in survivors at any dosage level. Decreases in bw gain and transient increases in enzymuria were noted at 2 and 4 g/kg. Serum enzyme levels and blood urea nitrogen were not elevated, nor were glycosuria or proteinuria present. Chemically induced histological changes were not seen in the liver, kidney, lung, brain, adrenal, spleen, stomach, epididymis, or testis. Hepatic microsomal cytochrome P450 experiments revealed that single, high oral doses of DCE did not alter total P450 levels, but did induce CYP2E1 levels and activity and inhibit CYP1A1 activity. These effects were reversible and regressed with repeated DCE exposure. There was no apparent progression of organ damage during the 13-week subchronic study, nor appearance of adverse effects not seen in the short-term exposures. One g/kg orally (po) was found to be the acute, subacute, and subchronic LOAEL for DCE, under the conditions of this investigation. In each instance, 0.5 g/kg was the NOAEL.
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PMID:Acute, subacute, and subchronic oral toxicity studies of 1,1-dichloroethane in rats: application to risk evaluation. 1160 9


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