Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.
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PMID:Disseminated intravascular coagulation complicating aflatoxicosis in dogs. 55 87

Diabetes mellitus was tentatively diagnosed in a black-footed ferret with polyuria, polydipsia, polyphagia, dehydration, and weight loss. Laboratory findings (marked hyperglycemia (724 mg/100 ml), glycosuria, and ketonuria) and the subsequent favorable response to insulin therapy confirmed the diagnosis. Although lesions were not observed in the pancreas, gross and histologic findings concomitant with diabetes mellitus included arteriosclerosis, with calcification of the aorta and other major vessels; mild necrotizing hepatitis; and mild proliferative glomerulonephritis. A perineal adenocarcinoma, with metastasis to an internal iliac lymph node, was an incidental finding. Special stains demonstrated adequate numbers of beta cell granules in the islets of Langerhans. Thus, the diabetes was apparently due to a lack of release of the synthesized insulin or to diminished effectiveness of the secreted insulin.
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PMID:Diabetes mellitus in a black-footed ferret. 92 62

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

Three patients who developed acute nephropathy following ingestion of triphenyltin acetate (TPTA) are described. All of them had significant proteinuria, azotemia, and polyuria. Mild neurological manifestations in all patients were also noted. Hematuria and pyuria were noted in 1 severely poisoned patient. Evidence for hepatitis was present in 2 patients, and for pancreatitis in 1. Renal biopsy showed focal fusion of glomerular cell processes and proximal tubular damage with cellular necrosis. Two patients survived with complete recovery of renal functions. One old patient died of aspiration pneumonia. Acute nephropathy following organotin intoxication appears to result mainly from proximal renal tubular damage with a benign and reversible clinical course.
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PMID:Acute nephropathy of organotin compounds. 834 77

As with most liver diseases, the symptoms of hepatitis in dogs are nearly always aspecific: the dogs eat less, are apathetic, sometimes have polyuria/polydipsia, and sometimes have diarrhoea. Hepatoencephalopathy and ascites only occur with these symptoms in very advanced stages of chronic hepatitis. Only a part of the dogs have jaundice. Because of these aspecific symptoms, the diagnosis hepatitis is often not taken into consideration, even though the presence of a liver disease can be easily detected by measuring plasma concentrations of alkaline phosphatase and bile acids, one or both of which are elevated. The diagnosis is confirmed by histological examination of a liver biopsy sample. The most common forms of hepatitis are non-specific reactive hepatitis, acute hepatitis, and chronic hepatitis. Non-specific reactive hepatitis is a reaction against endotoxin as a result of sepsis or an increased gastrointestinal absorption. Treatment is directed to the primary process. Leptospirosis also causes non-specific reactive hepatitis, but then renal insufficiency is the most prominent feature. The diagnosis is made not on the basis of a liver biopsy but on the basis of increased IgM titres against Leptospira. Immediate treatment with antibiotics and infusions at the first signs (jaundice and uraemia) can save the animal's life. Acute hepatitis can develop as a result of infection, toxins, or liver hypoxia. There is no specific treatment, but adequate recovery often occurs with supportive treatment. Corticosteroids are contraindicated. Chronic hepatitis, which can lead to cirrhosis, is the most common form of hepatitis. It is an autoimmune inflammatory reaction that is usually caused by a virus infection but sometimes by poisoning (intoxication). Long treatment with prednisolone or azathioprine is usually successful, but early recognition of the disease increases the likelihood of success. Nowadays, chronic hepatitis due to hepatic copper accumulation in Beddlington terriers can be detected by DNA tests. Such tests make it possible to distinguish between carriers and non-carriers. Affected animals can be kept symptom-free by life-long treatment with zinc gluconate or penicillamine.
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PMID:[Hepatitis in dogs; a review]. 958 48

India is amidst a demographic transition showing an ageing trend. This will increase non-communicable diseases including diabetes which is already showing an increasing trend. With scanty literature existing on elderly diabetics (> 60 years of age), it was decided to study the clinico-laboratory and complication profile of this group of patients. Fifty consecutive elderly diabetics were studied and evaluated for ECG, chest x-ray, blood sugar, urea, creatinine, lipid profile, proteinuria, motor nerve conduction velocity and autonomic neuropathy. Duration of diabetes varied from one month to 28 years. Fifty-six per cent of the patients presented with classical symptoms of polyuria, polyphagia and polydipsia. Hypertension was present in 40% and cataract in 54% of the patients. Eighteen per cent were obese, 52% had evidence of peripheral neuropathy while 56% had autonomic neuropathy. Background diabetic retinopathy was present in 56%, pre-proliferative retinopathy and maculopathy in 4% each; hypertensive retinopathy in 10% of patients; 44% had microproteinuria and 8% had chronic renal failure. Hypercholesterolaemia was present in 64% and hypertriglyceridaemia in 42% of the patients with 26% having coronary artery disease. Sixty per cent were harbouring infections--20% had foot infections, 14% had tuberculosis and 10% had urinary tract infections. Ninety-two per cent of the patients were aware of their disease but 62% were not aware of the complications and of the need for strict dietary and drug compliance. There was a high prevalence of associated diseases viz, osteoarthritis, cataract, hypertension, hepatitis and parkinsonism. Therefore, this study brings out the need to have a holistic and multidisciplinary approach for management of elderly diabetics who constitute a heterogeneous group with distinct health care problems.
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PMID:Clinical and laboratory profile of diabetes in elderly. 1065 95

An 8-year-old boy presented in 1995 with a 2-year history of hypertransaminasemia and hypergammaglobulinemia. Afterwards the patient displayed onychosis with a positive culture test for Candida albicans (CA). Because of the persistence of hypertransaminasemia, a percutaneous liver biopsy was performed showing 'low grade chronic active autoimmune hepatitis' (AIH), positive for liver-kidney microsomal autoantibodies and antibodies to the hepatic autoantigen cytochrome P450-1A2. Immunosuppressive treatment was initiated. In 2003 he developed Addison's disease resulting in the diagnosis of autoimmune polyendocrinopathy candidiasis-ectodermal dysplasia (APECED) syndrome, also known as autoimmune polyendocrine syndrome type 1 (APS1). Anti-17OH hydroxylase antibodies tested negative, anti-21-OH hydroxylase autoantibodies were positive. Among the other relevant organ- and non organ- specific autoantibodies, aromatic L-amino acid decarboxylase (ADDC) autoantibodies and anti-tryptophan hydroxylase autoantibodies were positive. The patient also presented polyuria and polydypsia with diabetes insipidus. Because of the presence of two diagnostic criteria of APS1, mutations in the autoimmune regulator gene (AIRE) were performed, which revealed the presence of a novel mutation (c1314- 1326 del 13/insGT) in exon 11. In conclusion, the diagnosis of APECED should be suspected in any child with minimal hypertransaminasemia, anti-microsomal autoantibodies and Candida albicans onychosis.
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PMID:An 8-year-old boy with autoimmune hepatitis and Candida onychosis as the first symptoms of autoimmune polyglandular syndrome (APS1): identification of a new homozygous mutation in the autoimmune regulator gene (AIRE). 1789 43

Streptococcus bovis infection was diagnosed in pigeons from 20 lofts submitted for post mortem investigation. Clinical signs were very variable and ranged from hyperacute death to chronic lameness with arthritis. Lesions were generally unspecific except for single cases of muscle necrosis with purulent myositis. Histological examinations demonstrated the septicaemic nature of the infections. Intravenous inoculations of S. bovis resulted in prostration, long lasting loss of weight and polyuria. Microscopically purulent hepatitis and nephritis were the most characteristic lesions. After oral inoculation no clinical signs were seen.
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PMID:Streptococcus bovis infections in pigeons. 1867 55

Fatal hepatic sarcocystosis was diagnosed in a 13-year-old captive black bear (Ursus americanus) with a history of acute onset of vomiting, polyuria, polydipsia, and bilirubinuria. Gross lesions included severe icterus, multisystemic hemorrhage, and gall bladder edema. The most significant microscopic lesion was severe necrotizing hepatitis with intralesional protozoa that reproduced by endopolygeny consistent with a Sarcocystis spp. Infrequent microglial nodules were randomly scattered within the white matter of the cerebral cortices, thalamus, and brainstem, but intralesional protozoal schizonts were not observed. In the liver, immunohistochemistry was positive for Sarcocystis spp. and negative for Toxoplasma gondii and Neospora spp. Positive staining was not observed in the brain. Genus-specific polymerase chain reaction (PCR) amplification of the 18S ribosomal RNA gene was performed on formalin-fixed, paraffin-embedded sections of liver and brain; in both tissues, PCR was positive for Sarcocystis spp. Sequence analysis of the PCR amplicons revealed 100% identity to the published sequences of Sarcocystis canis and Sarcocystis arctosi.
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PMID:Fatal hepatic sarcocystosis in a captive black bear (Ursus americanus) associated with Sarcocystis canis-like infection. 2139 69

A 16-year-old, previously healthy Thai girl presented with DHF grade III. Fifteen hours after the first episode of shock, she had received an excessive amount of crystalloid isotonic solution and 20 ml per kilograms of Dextran-40 however she still had persistently rapid pulse rate and high hematocrit but also had polyuria with more than 4 ml/kg/hr of urine output. She was re-evaluated. Clinical signs showed severe dehydration with some ascites without signs of pleural effusion. Blood gas revealed increased anion gap metabolic acidosis. The cause of polyuria and metabolic acidosis was identified with hyperglycemia, ketouria and glucosuria. Afterwards she was diagnosed and treated as DHF grade III and DKA. Besides insulin administration, fluid resuscitation was very crucial. Intravenous fluid rehydration was needed while the unnecessary extra-volume could cause massive plasma leakage and later on fluid overload. Volume replacement was adjusted to degree of dehydration when signs of volume overload were monitored closely. She was out of DKA at 14 hours after the start of insulin and the intravenous fluid was stopped at 27 hours (36 hours after the first episode of shock). The final diagnosis was DHF grade III, diabetes mellitus with DKA and hepatitis.
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PMID:Dengue hemorrhagic fever grade III with diabetic ketoacidosis: a case report. 2204 83


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