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)

Amiodarone is a class III antiarrhythmic medication used extensively to treat ventricular arrhythmias. It is pharmacologically classified as a cationic amphiphilic drug due to its polar and apolar components. During the past few years, amiodarone has proved to be an effective treatment therapy for patients with ventricular dysfunctions, regardless of the etiology, and in particular ventricular arrhythmia associated with Chagas disease. Nevertheless, despite its hemodynamic and electrophysiological benefits, amiodarone produces serious collateral effects such as a bluish skin discoloration, photosensitivity, thyroid dysfunction, corneal deposit, peripheral neuropathy, bone marrow suppression, hepatitis, heart blocks, pneumonitis, among others. The objective of this case report is to discuss one of the most serious complications related to amiodarone, pulmonary toxicity, which is described as a differential diagnosis for a chagasic patient that was on the waiting list for a heart transplant. Amiodarone pneumonitis is a relevant differential diagnosis for heart failure (HF) patients using amiodarone that are admitted to the emergency ward with dyspnea.
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PMID:The importance of amiodarone pulmonary toxicity in the differential diagnosis of a patient with dyspnea awaiting a heart transplant. 1705 13

Bentazone is a herbicide widely used in the agrochemical field and acts by interference in photosynthesis in plants. Case reports of bentazone poisoning in humans are rare, but hepatorenal damage and death have been described, though the mechanism of toxicity remains speculative. We describe 2 cases of acute bentazone poisoning and compare these with other literature reports. The clinical picture included nausea, vomiting, diarrhea, abdominal pain with gastrointestinal corrosive injury, dyspnea and acute hepatorenal dysfunction. Respiratory failure, acute hepatitis, acute renal failure requiring hemodialysis, and death occurred following a large ingested dose of 1,764 mg/kg. Bentazone may have direct organ toxicity, especially in liver and kidney, in subjects with renal hypoperfusion, rhabdomyolysis, preexisting renal disease or concomitant nephrotoxic drug consumption. Aggressive supportive therapy, hydration and measures to prevent renal hypoperfusion are essential to reverse acute renal failure.
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PMID:Acute renal failure induced by bentazone: 2 case reports and a comprehensive review. 1844 22

Alpha-1-antitrypsin deficiency (AATD) is a genetic disorder that manifests as pulmonary emphysema, liver cirrhosis and, rarely, as the skin disease panniculitis, and is characterized by low serum levels of AAT, the main protease inhibitor (PI) in human serum. The prevalence in Western Europe and in the USA is estimated at approximately 1 in 2,500 and 1 : 5,000 newborns, and is highly dependent on the Scandinavian descent within the population. The most common deficiency alleles in North Europe are PI Z and PI S, and the majority of individuals with severe AATD are PI type ZZ. The clinical manifestations may widely vary between patients, ranging from asymptomatic in some to fatal liver or lung disease in others. Type ZZ and SZ AATD are risk factors for the development of respiratory symptoms (dyspnoea, coughing), early onset emphysema, and airflow obstruction early in adult life. Environmental factors such as cigarette smoking, and dust exposure are additional risk factors and have been linked to an accelerated progression of this condition. Type ZZ AATD may also lead to the development of acute or chronic liver disease in childhood or adulthood: prolonged jaundice after birth with conjugated hyperbilirubinemia and abnormal liver enzymes are characteristic clinical signs. Cirrhotic liver failure may occur around age 50. In very rare cases, necrotizing panniculitis and secondary vasculitis may occur. AATD is caused by mutations in the SERPINA1 gene encoding AAT, and is inherited as an autosomal recessive trait. The diagnosis can be established by detection of low serum levels of AAT and isoelectric focusing. Differential diagnoses should exclude bleeding disorders or jaundice, viral infection, hemochromatosis, Wilson's disease and autoimmune hepatitis. For treatment of lung disease, intravenous alpha-1-antitrypsin augmentation therapy, annual flu vaccination and a pneumococcal vaccine every 5 years are recommended. Relief of breathlessness may be obtained with long-acting bronchodilators and inhaled corticosteroids. The end-stage liver and lung disease can be treated by organ transplantation. In AATD patients with cirrhosis, prognosis is generally grave.
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PMID:Hereditary alpha-1-antitrypsin deficiency and its clinical consequences. 1856 11

A 46-year-old woman presented with arthralgia. She had a history of fluctuating liver function impairment for 6 months. Laboratory investigations revealed elevated liver function test results, positive antinuclear antibodies and elevated serum IgG. The histological findings of a liver biopsy were interface hepatitis accompanied by plasmocytic infiltration with bridging fibrosis. There was no evidence of cirrhosis on pathological examination and no portal hypertension on endoscopic and radiographic studies. Autoimmune hepatitis was diagnosed, and treatment with prednisolone improved the liver dysfunction. After 6 months, she complained of dyspnea. Doppler echocardiography showed a dilated right ventricle, severe tricuspid insufficiency, and systolic pulmonary arterial pressure indicative of pulmonary arterial hypertension. We report this rare case of autoimmune hepatitis with pulmonary arterial hypertension.
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PMID:Autoimmune hepatitis associated with pulmonary arterial hypertension. 1901 10

Varicella zoster virus (VZV) seronegative patients under immunosuppressive therapy are at risk for severe life-threatening varicella. A 25-year-old male patient presented with rash and hepatitis. He had been known to suffer from Crohn's disease and received immunosuppressive treatment with azathioprine. The patient showed dyspnoea, and presented with a generalized rash with vesicular lesions typical for herpesvirus infections. He was started immediately on acyclovir therapy. Varicella infection was determined in this VZV seronegative patient in rash vesicles, blood and tracheal secretions and a high VZV viral load was detected in these specimens. The causative agent was genotyped by sequencing of several genes as a variant of the European genotype E2 containing several unique single nucleotide polymorphisms. Despite all measures, there was progressive septic shock, and the patient died due to multi-organ failure. Immunocompromised adults without varicella history are at high risk to develop life-threatening complications of varicella. Antiviral therapy with acyclovir can only be successful when administered as early as possible on suspicion of varicella infection in this group of patients. The most effective method to prevent severe varicella in immunocompromised patients is active immunization prior to immunosuppressive therapy.
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PMID:Fatal varicella in an immunocompromised adult associated with a European genotype E2 variant of varicella zoster virus. 1905 12

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

We describe a 65-year-old man who had liver involvement with Churg-Strauss syndrome. He was admitted to the hospital because of fever, weight loss, dyspnea, abdominal pain, skin lesions and paraesthesias. His past medical history revealed a diagnosis of acalculous cholecystitis that had been made eight months earlier. Microscopic examination of a gall bladder biopsy specimen obtained at that time revealed an increase in extravascular eosinophils. There was evidence of a new bilateral pulmonary disease with bronchoconstriction and a transient infiltrated lesion in the right upper lung. The patient's white cell count was 14 620 per cubic millimetre, with 39% eosinophils (5800 per cubic millimetre) and 39% neutrophils. IgE was 503 g/L (normal range, 0 to 100 g/L). Liver function tests were mildly elevated. Fine needle liver biopsy showed active interface hepatitis. A diagnosis of Churg-Strauss syndrome was made. In this patient the syndrome occurred in a rare association with hepatitis, likely due to immunologic events in the liver. The patient was successfully treated with 60 mg/day of prednisolone monotherapy.
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PMID:Churg-Strauss syndrome associated with acalculous cholecystitis and liver involvement. 1919 81

A 5-year-old male, drowsy, jaundiced child presented with fulminant hepatitis and had HAV and HEV infection. He had hepatic encephalopathy grade 1, fever, pallor, hypotension, crepitations in his right lung base and hepatosplenomegaly with dyspnoea. He had highly raised liver enzymes and hypoalbuminemia (2.8 g/dl) but anemia (hemoglobin of 7.7 g/dl and 5.7 g/dl 2 days later), reticulocytopenia and severe thrombocytopenia (44 x 10(9)/l) were unexplained. Parvovirus B19-specific IgM antibodies and B19 DNA were found in the serum of the child. Chest X-ray showed pleural effusion and bronchopneumonia, while blood culture isolated coagulase-negative staphylococci (BACTEC 9120) and he had low oxygen saturation. Hence, he was treated with IV amoxicillin+ clavulinic acid and oxygen inhalation. He had seizures and cardiac arrest but was revived. On the third day his condition worsened and the child died despite intensive care. Hence it is concluded that his anemia and thrombocytopenia were B19 induced and this might have aggravated or caused fulminant hepatitis.
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PMID:Parvovirus B19-induced thrombocytopenia and anemia in a child with fatal fulminant hepatic failure coinfected with hepatitis A and E viruses. 1920 89

Alpha(1)-antitrypsin deficiency is characterized by a pathologic reduction of the serum concentration of alpha(1)-antitrypsin, the most important antiprotease in man. It is one of the most common hereditary diseases in Caucasians. Approximately 2% of obstructive airway diseases are caused by alpha(1)-antitrypsin deficiency. Patients above 35 years may develop lung emphysema, especially in the lower lobes. Symptoms are those of chronic obstructive pulmonary disease such as cough, sputum expectoration, and progressive dyspnoea. Patients with homozygous defect often develop cholestatic hepatitis in the neonatal period. However, only few adult patients develop chronic liver disease up to liver cirrhosis with an elevated risk for malignant liver tumors. The diagnostic hallmark is the reduced serum concentration of alpha(1)-antitrypsin while genetic testing proves the defect. An early recognition of the disease is decisive for prophylactic and therapeutic measures. Smoking should be stopped immediately. Treatment of lung disease includes physiotherapy, antiobstructive and antiinflammatory medication, augmentation with human alpha(1)-antitrypsin and lung surgery including lung transplantation. Liver toxins should be avoided. Besides experimental therapeutic approaches, liver disease can only be treated by liver transplantation.
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PMID:[Alpha1-antitrypsin deficiency]. 2013 85

A two-year-old Large White boar from a pig breeding stock in an indoor farm in Switzerland presented anorexia, reduced general condition and fever. Despite antibiotic and anti-inflammatory treatment, the boar developed severe dyspnoea and cyanosis, and died after 4 days. At necropsy, no gross lesions were observed. Histopathologically, multifocal degeneration and necrosis of myocardial fibers with interstitial edema, severe multifocal non-suppurative myocarditis and hepatitis, and non-suppurative interstitial nephritis were observed. In heart samples, groups of organisms resembling apicomplexan tachyzoites were seen associated with the lesions. A PCR using the primers COC1-COC2 that target a conserved region of the small-subunit rRNA gene of Apicomplexa was performed with DNA from paraffin-embedded tissues. An amplification product of about 350 bp was obtained from heart samples. A sequence analysis showed 100% identities with GenBank sequences reported for Sarcocystis miescheriana. The histopathological observations and molecular findings in combination with the clinical signs, and absence of other pathologic agents highly suggested that an acute infection with S. miescheriana was the cause of death in this boar. To our knowledge, this the first report of fatal acute sarcocystosis after natural infection in a pig breeding herd.
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PMID:First report of naturally acquired clinical sarcocystosis in a pig breeding stock. 2114 59


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