Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven patients, 4 girls and 3 boys, aged 3 to 12 years /X = 7.14/ affected by haemorrhagic fever with renal syndrome /HFRS/., were hospitalized at the University Children's Hospital in Belgrade during the last two years /January 1988-January 1990/. The diagnosis was established on the basis of clinical features, epidemiological data and autopsy findings in one patient while in the others the diagnosis of HFRS was confirmed serologically by indirect immunoflorescence tests on Vero E 6 cells. A significant increase in antibody titre against Hantaan virus was found in all serologically tested patients. Three of them had also significant increase of antibody titre against Soeul and one against Puumale virus. In four patients the disease appeared as family outbreak at the end of January 1988 while the others were sporadical cases. All patients but one mentioned contact with rodents at home or in fields. The predominant slynical symptom were: sudden onset of febrile condition with headache, generalized malaise, myalgia, abdominal pain, vomiting, diarrhoea, oliguria and oedema. All patients had haematuria and only one had other severe haemorrhagic manifestations. Four patients were hypertensive. Two patients had renal insufficiency, but only one required haemodialysis. Five patients recovered after 2 to 8 weeks without sequellae, one patient was still /7 months after the beginning of the disease/ in mild renal insufficiency and one patient died. Autopsy findings showed tubular necrosis in the kidney, myocarditis, massive pneumonia with hydrothorax and jejunal haemorrhagia.
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PMID:[Hemorrhagic fever with renal syndrome in children]. 168 34

Adenovirus (AV) infection usually has a benign course in normal hosts; however, in immunocompromised patients, AV may cause pneumonia, cystitis, or disseminated disease with substantial morbidity and even mortality. Although pulmonic AV involvement is common, infection of the kidney is unusual. The histologic findings previously described include tubular necrosis with interstitial inflammation and glomerulonephritis. We report a case of an AV-induced unilateral mass lesion in the kidney of a patient with Hodgkin's disease (HD) following bone marrow transplantation.
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PMID:Adenovirus infection of the kidney: mass formation in a patient with Hodgkin's disease. 192 70

Foscarnet is a pyrophosphate analogue that has been successfully used in severe cytomegalovirus (CMV) infections. Little is known of the incidence and mechanisms of foscarnet-induced nephrotoxicity as most data comes from recipients of renal allografts or from patients with severe underlying disease or with other nephrotoxic drugs. We have retrospectively analyzed the evolution of renal function after 56 courses of foscarnet. In addition, we have prospectively studied the protective effects of hydration on foscarnet nephrotoxicity (2.5 liters of saline/day during the night before the foscarnet therapy and throughout the course of treatment). Foscarnet-induced acute renal failure was defined as a rise in serum creatinine of at least 25% from the basal value. An increase in serum creatinine occurred in 37 cases out of the 56 courses of foscarnet (66%). The mean serum creatinine prior to foscarnet was 80.5 +/- 3.3 mumol/l and the mean increase was 190 +/- 28.3 mumol/l (range 80-1,000). Peak serum creatinine was higher than 200 and 300 mumol/l in 16 and 13 patients, respectively. Kidney obtained at autopsy from a 30-year-old male with AIDS, CMV pneumonitis and acute renal failure secondary to foscarnet administration showed an extensive tubular necrosis. In the group which was prospectively hydrated only 1 patient had an acute renal failure. The mean serum creatinine at the peak (96 +/- 4 mumol/l) and at the end of the treatment (83 +/- 4 mumol/l) was significantly lower (p less than 0.05) than in non hydrated patients. In conclusion, foscarnet is a highly nephrotoxic drug which induces acute tubular necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Foscarnet nephrotoxicity: mechanism, incidence and prevention. 255 31

Captopril protects rat lung from radiation-induced pneumonitis and fibrosis and preserves function and survival in experimental radiation nephropathy. This study determined the structural benefit of captopril used preventively in radiation nephropathy. Twenty-eight Wag/RijMCW rats, divided in six groups, received 0 to 17 Gray total body irradiation followed by syngeneic bone marrow transplant. Captopril 0, 62.5, 125, 250, or 500 mg/l was given in the drinking water from the time of irradiation, and the rats were killed at 20 weeks. Using light and electron microscopy, kidneys of irradiated no-drug rats showed glomerular tuft capsular adhesions and hyalinization, focal tubular necrosis, severe interstitial fibrosis, and marked thickening and hyaline degeneration of the wall of interlobular arteries and arterioles, with intimal proliferation and periadventitial edema and inflammation. Lumens of the smaller arteries were often occluded. Significant collagen deposition was present in glomeruli, interstitium, and adventitia of interlobular arteries. Marked reduction of glomerular, tubular, vascular, and interstitial damage was seen in irradiated, captopril-treated animals, with only mild focal tubular interstitial injury and fibrosis seen. alpha smooth muscle actin-positive cells, probably myofibroblasts, were enhanced in the irradiated kidneys, and this expression was reduced in a dose-related fashion by captopril. There was also reduction in the arteriolar wall thickening, luminal occlusion, and collagen deposition in captopril-treated animals. The presence of elastin was not affected by radiation or drug treatment. Blood pressure and azotemia were lower and survival was higher in irradiated drug-treated rats compared with irradiated no-drug rats. We conclude that captopril exerts significant functional and structural protection against renal radiation injury. There was notable reduction in radiation-induced fibrosis in captopril-treated animals in this model, as in experimental lung radiation injury.
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PMID:Captopril preserves function and ultrastructure in experimental radiation nephropathy. 880 58

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

The use of zinc in metal alloys and medicinal lotions dates back before the time of Christ. Currently, most of the commercial production of zinc involves the galvanizing of iron and the manufacture of brass. Some studies support the use of zinc gluconate lozenges to treat the common cold, but there are insufficient data at this time to recommend the routine use of these lozenges. Zinc is an essential co-factor in a variety of cellular processes including DNA synthesis, behavioral responses, reproduction, bone formation, growth, and wound healing. Zinc is a relatively common metal with an average concentration of 50 mg/kg soil and a range of 10-300 mg/kg soil. Meat, seafood, dairy products, nuts, legumes, and whole grains contain relatively high concentrations of zinc. The mobility of zinc in anaerobic environments is poor and therefore severe zinc contamination occurs primarily near points sources of zinc release. The recommended daily allowance for adults is 15 mg zinc. The ingestion of 1-2 g zinc sulfate produces emesis. Zinc compounds can produce irritation and corrosion of the gastrointestinal tract, along with acute renal tubular necrosis and interstitial nephritis. Inhalation of high concentrations of zinc chloride from smoke bombs detonated in closed spaces may cause chemical pneumonitis and adult respiratory distress syndrome. In the occupational setting inhalation of fumes from zinc oxide is the most common cause of metal fume fever (fatigue, chills, fever, myalgias, cough, dyspnea, leukocytosis, thirst, metallic taste, salivation). Zinc compounds are not suspected carcinogens. Treatment of zinc toxicity is supportive. Calcium disodium ethylenediaminetetraacetate (CaNa2EDTA) is the chelator of choice based on case reports that demonstrate normalization of zinc concentrations, but there are few clinical data to confirm the efficacy of this agent.
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PMID:Zinc. 1038 62

We encountered a case of acute gasoline intoxication at the scene of washing the inner wall of a petrol tank. The decedent was a 50-year-old male, who was the supervisor. Two young workers wearing mask respirators began to wash the inner wall of the gasoline tank under poor ventilation. About 1 h later, because one of the workers lost consciousness, the supervisor entered the tank, without a mask respirator, to rescue the worker. However, the supervisor immediately fainted, and died 26 h after the accident. In the autopsy, blisters were observed on the skin of the face, neck, anterior chest, upper extremities, and back. The heart contained hemolyzed blood. Histologically, hemorrhagic pulmonary edema, pneumonia, and proximal tubular necrosis were found. In the toxicological analyzes, toluene, xylene, and trimethylbenzene were detected in the blood, brain, and gastric contents. Toluene concentrations in the blood and brain were 0.3 mug/ml and 3.7 mug/g, respectively. Since pathological findings were consistent with the reported findings concerning gasoline intoxication, and constituents of gasoline were in the body, death was attributed to acute gasoline intoxication. It was considered that sufficient ventilation and proper use of a mask respirator were essential for this kind of work.
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PMID:A case of acute gasoline intoxication at the scene of washing a petrol tank. 1456 77

The broad spectrum of heat-related injury (HRI) and its associated lesions is well described in the human literature, with rare reports of similar findings in farm animals. In the current case series, lesions from 4 of 8 lambs that presented with clinical signs of heat stress are reported. Gross lesions at necropsy consisted of acute renal swelling and pallor in 2 of 4 lambs, muscle pallor in 2 of 4 lambs, and chronic bronchointerstitial pneumonia in each of the 4 lambs. Histological lesions considered heat-related included acute renal tubular necrosis, pigment casts, tubular epithelial regeneration, multifocal myocyte degeneration, necrosis, and dropout with histiocytic influx and regeneration. Chronic, bronchointerstitial pneumonia, present in each lamb, was considered a condition predisposing to HRI. Compatibility between observed lesions and those reported in human beings with injury secondary to elevated body temperatures established a diagnosis of HRI in these animals. Diagnostic pathologists should consider HRI in lambs with histological evidence of renal tubular necrosis and/or rhabdomyolysis and even in cases where the clinical picture is strongly suggestive but lesions are not demonstrable.
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PMID:Heat-related injury in lambs. 2258 57

A retrospective examination of gross and histologic reports was performed to find common lesions in young and adult captive rock hyrax ( Procavia capensis ) from multiple zoo populations. One hundred and thirty-seven reports were analyzed from specimens that were submitted to Northwest ZooPath from 1997 to 2013. Histologic findings from necropsy and biopsy reports and causes of mortality only from necropsy reports were compiled to determine the most common findings. Within the study population, 41 (30%) were male, 62 (45%) were female, and the remainder (34, 25%) were of undetermined sex. Of the 111 necropsies, 87 (78%) died naturally, and 24 (22%) were euthanatized. There were 26 (19%) biopsies with no known status of the animal. The most frequent causes of death or reason for euthanasia were bacterial septicemia (n = 29, 21%) and degenerative cardiomyopathy (n = 29, 21%). The other most prevalent lesions were hemosiderosis (n = 55, 40%), pancreatic islet and interstitial fibrosis (n = 36, 26%), pneumonia of undetermined cause (n = 26, 19%), enteritis/colitis (n = 24, 18%), and renal tubular necrosis (n = 20, 15%). In many animals of this study population (n = 115, 84%), multiple lesions affecting multiple organs were found.
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PMID:A RETROSPECTIVE STUDY OF PATHOLOGIC FINDINGS IN CAPTIVE ROCK HYRAX (PROCAVIA CAPENSIS) IN THE UNITED STATES. 2666 36

In mid-July 2013, an outbreak of peste des petits ruminants (PPR) was observed in a herd of camels after they were imported from Kuwait to the Khuzestan province in southwest of Iran. The clinical signs of the affected animals included sudden death, fever, oral erosion, and ecthyma like lesions, yellowish diarrhea, pneumonia and respiratory distress, enlargement of lymph node, severe dehydration, dermatitis, ulcerative keratitis, and conjunctivitis. Necropsy findings included keratoconjunctivitis, congestion and consolidation of the lung, paleness of the liver, and enlargement and edema of lymph nodes. Histopathological exam revealed degeneration and acute hyperemia of the lungs, fatty change and necrotic foci in the liver, tubular necrosis in the kidneys, and necrotic dermatitis. We used immunocapture enzyme linked immunosorbent assay (ELISA) to confirm peste des petits ruminants virus (PPRV) and differentiate it from rinderpest virus. Then virus genome was studied by molecular analysis for detecting of strain and substrain of the virus. Immunocapture ELISA of all specimens reacted positively against PPRV antigens. Also, reverse transcription polymerase chain reaction (RT-PCR) results in the lung and lymph nodes of the dead camels consolidated the cause of disease to be PPRV. The present study is the first report of the PPRV outbreak in camels in Iran.
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PMID:The first report of peste des petits ruminants (PPR) in camels (Camelus dromedarius) in Iran. 2715 51


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