Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten Kenyan patients with visceral leishmaniasis unresponsive to sodium stibogluconate, at a dose of 16 to 20 mg Sb/kg body-weight/day given for 30 to 98 days, were treated with 20 mg Sb/kg bw given every eight hours. This regimen was modified or abandoned in six patients because of suspected toxicity, although toxicity was difficult to assess because of intercurrent illness. Toxic effects included lethargy, anorexia, vomiting, electrocardiographic changes, fall in haemoglobin and rise in liver enzymes. One patient died, probably from a cardiac arrhythmia. Two patients were cured, four responded partially and four showed no response. Pentamidine, at a dose of 4 mg/kg body-weight given one to 3 times per week for 5 to 39 weeks, was given as initial treatment in one patient and after failure of sodium stibogluconate in seven. Toxic effects included nephritis, hepatitis, transient diabetes and subcutaneous abscesses. Two patients were cured, two responded partially, three showed no response and one, after apparent cure, relapsed and was unresponsive to additional pentamidine treatment. Low-frequency, long-duration pentamidine was often useful in maintaining any improvement made during treatment with the less well tolerated high-dose, high frequency sodium stibogluconate. We observed the step-wise development of resistance to both sodium stibogluconate and pentamidine. The problems of managing patients with visceral leishmaniasis which is unresponsive to conventional doses of pentavalent antimonials are discussed and some tentative suggestions put forward.
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PMID:Visceral leishmaniasis unresponsive to antimonial drugs. II. Response to high dosage sodium stibogluconate or prolonged treatment with pentamidine. 300 95

The historic, physical, laboratory, and histologic findings for 74 cats with chronic renal disease were reviewed. Most cats were older, and no breed or sex predilection was detected. This most common clinical signs detected by owners were lethargy, anorexia, and weight loss. Dehydration and emaciation were common physical examination findings. Common laboratory findings were nonregenerative anemia, lymphopenia, azotemia, hypercholesterolemia, metabolic acidosis, hyperphosphatemia, and isosthenuria. The most common morphologic diagnosis was chronic tubulointerstitial nephritis of unknown cause. The other pathologic diagnoses were renal lymphosarcoma, renal amyloidosis, chronic pyelonephritis, chronic glomerulonephritis, polycystic renal disease, and pyogranulomatous nephritis secondary to feline infectious peritonitis.
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PMID:Clinicopathologic findings associated with chronic renal disease in cats: 74 cases (1973-1984). 358 99

A 49-year old woman developed non-oliguric acute renal failure accompanied by bilateral acute anterior uveitis, following a three weeks' period of lethargy, anorexia and temporary fever. Kidney biopsy revealed acute interstitial nephritis with interstitial infiltrations of lymphocytes and monocytes, as well as multiple perivascular epithelioid granulomas. A substantial improvement of renal function was achieved under treatment with systemic corticosteroids. The uveitis resolved completely under additional topical treatment. During a follow-up period of 9 months, there has been no relapse of nephritis or uveitis. The disease of this patient resembles the so-called TINU syndrome of unknown aetiology. Remarkable features of the present case are the histological diagnosis of granulomatous acute interstitial nephritis in the absence of systemic granulomatous disease, as well as a possible association with the administration of non-steroidal antiinflammatory drugs.
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PMID:[Acute granulomatous interstitial nephritis with iritis. Possible induction by non-steroidal antiphlogistics]. 381 94

Renal impairment in sarcoidosis is usually due to hypercalcaemia and nephrocalcinosis but can also be caused by granulomatous nephritis or interstitial nephritis without sarcoid granulomata. A variety of types of glomerulonephritis have also been described in sarcoidosis but these rarely cause impaired renal function. Renal failure as an isolated manifestation of sarcoidosis is uncommon. A 66-year-old woman presented with a 1-year history of lethargy, polyuria and nocturia. Clinical examination was unremarkable and she had impaired renal function (urea 18 mmol/l (108 mg%) and creatinine 380 mumol/l (4.3 mg%)). As her kidneys were normal in size, she underwent renal biopsy, which revealed granulomatous interstitial nephritis. Reevaluation showed no other evidence of sarcoidosis and she had impaired urinary acidification and concentrating capacities. Therapy with corticosteroids produced a marked improvement in symptoms and renal function. This case confirms the view that granulomatous sarcoid nephritis is steroid sensitive and that full recovery can be expected provided interstitial fibrosis and scarring do not occur.
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PMID:Reversible renal failure due to isolated renal sarcoidosis. 646 14

A 6-day-old female (Bison bison) was inoculated with 10 million sporocysts of the B1 isolate of Sarcocystis cruzi originally obtained by feeding heart of a naturally infected cow (Bos taurus) to a laboratory-raised coyote. The bison became febrile, lethargic, and anorectic at about 25 days after inoculation of the sporocysts, and was euthanatized 3 days later. There were widespread hemorrhages, hepatitis, myocarditis, nephritis, and enteritis; intravascular meronts were found in the adrenal cortex and lamina propria of the small intestine. Another 7-day-old male bison was inoculated with 100,000 sporocysts of the same B1 isolate of S cruzi. Except for mild fever and transient diarrhea, the bison remained clinically normal. Sarcocysts were found at necropsy on day 76 after inoculation. It was concluded that S cruzi of cattle is transmissible to bison.
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PMID:Sarcocystosis in neonatal bison fed Sarcocystis cruzi sporocysts derived from cattle. 681 77

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

Eastern Screech Owls (EASOs) were experimentally infected with the pathogenic New York 1999 strain of West Nile virus (WNV) by subcutaneous injection or per os. Two of nine subcutaneously inoculated birds died or were euthanatized on 8 or 9 days postinfection (DPI) after <24 hr of lethargy and recumbency. All subcutaneously inoculated birds developed levels of viremia that are likely infectious to mosquitoes, with peak viremia levels ranging from 10(5.0) to 10(9.6) plaque-forming units/ml. Despite the viremia, the remaining seven birds did not display signs of illness. All birds alive beyond 5 DPI seroconverted, although the morbid birds demonstrated significantly lower antibody titers than the clinically normal birds. Cagemates of infected birds did not become infected. One of five orally exposed EASOs became viremic and seroconverted, whereas WNV infection in the remaining four birds was not evident. All infected birds shed virus via the oral and cloacal route. Early during infection, WNV targeted skin, spleen, esophagus, and skeletal muscle. The two morbid owls had myocardial and skeletal muscle necrosis and mild encephalitis and nephritis, whereas some of the clinically healthy birds that were sacrificed on 14 DPI had myocardial arteritis and renal phlebitis. WNV is a significant pathogen of EASOs, causing pathologic lesions with varying clinical outcomes.
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PMID:Experimental West Nile virus infection in Eastern Screech Owls (Megascops asio). 1686 76

Canine Lyme disease is caused by the spirochete Borrelia burgdorferi after transmission by an Ixodes tick, typically resulting in joint pain, fever and lethargy. Lyme nephritis is a poorly characterized syndrome associated with severe glomerular and tubular renal injury and poor clinical outcome in young to middle-aged dogs positive for exposure to B. burgdorferi. The aims of this study were to identify associations between natural exposure to B. burgdorferi and the presence of microalbuminuria in nonclinical young Labrador and Golden Retrievers and to compare two commonly used serologic tests available to document B. burgdorferi exposure: the Western blot and the commercial point-of-care C6 peptide enzyme-linked immunosorbent assay (ELISA) tests. Microalbuminuria was assessed using a commercial point-of-care ELISA specific for canine albumin. Blood and urine samples from 268 asymptomatic Labrador and Golden Retrievers were included. Of these, 18.7% were positive for B. burgdorferi exposure according to the C6 ELISA; 21.2% were positive for natural exposure to B. burgdorferi and 11.5% for vaccinal antibodies according to the Western blot. The agreement rate was 93% between the two tests (kappa = 0.78, P < 0.0001) for natural exposure. Urine from 6.1% of the dogs was positive for microalbuminuria. There was no association between microalbuminuria and exposure to B. burgdorferi based on results of a Western blot (P = 0.57) or C6 ELISA (P = 0.53). Microalbuminuria is likely not a consequence of B. burgdorferi exposure in young nonclinical Labrador and Golden Retrievers.
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PMID:Microalbuminuria and comparison of serologic testing for exposure to Borrelia burgdorferi in nonclinical Labrador and Golden Retrievers. 1745 61

A 16-yr-old, captive-born, female California sea lion (Zalophus californianus) was evaluated for intermittent lethargy, partial anorexia, and polydipsia of 2 wk duration. The animal was immobilized for physical examination. It was in thin body condition, with multifocal mucosal ulcerations over the caudal and ventral tongue. Blood was collected for hematology, serum chemistry, and leptospirosis serology. Serum chemistry revealed severe azotemia, mild hyperglycemia, and severe hyperphosphatemia. The animal went into cardiac arrest during recovery from anesthesia and died. On histopathology, abundant amorphous, finely fibrillar, eosinophilic material was deposited in the kidneys, and smaller amounts of the same material were found in the splenic and pancreatic vessels; these findings are consistent with systemic secondary amyloidosis. The animal also had chronic nephritis, which, coupled with renal amyloidosis, resulted in renal failure and death. Systemic amyloidosis should be considered as an additional differential diagnosis for renal failure in California sea lions.
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PMID:Secondary amyloidosis and renal failure in a captive California sea lion (Zalophus californianus). 1863 24

Mice fed 1.5 mg ochratoxin A (OTA) per kg body weight and infected with Trypanosoma brucei rhodesiense were compared with trypanosome-infected placebo-fed and uninfected OTA-fed controls. Uninfected OTA-fed mice showed fever, lethargy, facial and eyelid oedemas, mild hepatitis and nephritis, and high survival. Infected placebo-fed controls had mean pre-patent period (PPP) of 3.26 days, lethargy, dyspnoea, fever, facial and scrotal oedema, survival of 33-65 days, reduced red cell counts (RCC: 10.96-6.87x106 cells/microl of blood), packed cell volume (PCV: 43.19-26.36%), haemoglobin levels (Hb: 13.37-7.92 g/dL) and mean corpuscular volume (MCV) of 37.96-41.31 fL, hepatosplenomegaly, generalized oedemas, heart congestion, hepatitis and nephritis. Compared to infected placebo-fed controls, infected OTA-fed mice had significantly (P<0.05) shorter mean PPP (2.58 days), reduced survival (6-47 days), more pronounced fever and dyspnoea. The latter had significantly (P<0.05) reduced RCC (10.74-4.56x106 cells/microl of blood), PCV (43.90-20.78%), Hb (13.06-5.74 g/dL), increased MCV (39.10-43.97 fL), severe generalized oedemas, haemorrhages, congestion, hepatic haemosiderosis, hepatitis, nephritis, endocarditis, pericarditis and exclusively, splenic macrophage and giant cell hyperplasia, expanded red pulp and splenic erythrophagocytosis. It was concluded that OTA aggravated the pathogenesis of T. b. rhodesiense infection in mice, and should therefore be taken into consideration during trypanosomosis control programmes.
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PMID:Aggravation of pathogenesis mediated by ochratoxin A in mice infected with Trypanosoma brucei rhodesiense. 1915 50


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