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)

Alterations of the gallbladder wall is a well known sonographic sign of acute cholecystitis. But thickening of the gallbladder wall is also found in patients without intrinsic gallbladder disease. We present our experience on this regard in patients with cirrhosis, acute viral hepatitis, infectious mononucleosis, halothane hepatitis, fulminant hepatic failure, malaria due to plasmodium falciparum, heart failure, severe malnutrition due to gastric obstruction, septicemia, pyogenic hepatic abscess, amoebic hepatic abscess and in a 14 years old patient with fracture of the skull-acute anemia-shock. Most of these diseases affected the liver directly or indirectly. Knowledge of these alterations of the gallbladder wall in these circumstances are important in order to avoid a the erroneous diagnosis of acute cholecystitis.
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PMID:[Ultrasonographic changes in the gallbladder wall in non-gallbladder diseases]. 253 57

We have defined the clinical presentation and course of X-linked agammaglobulinemia (X-LA) by means of a multi-center retrospective survey of 96 patients. Infections were the most common presenting feature of patients with X-LA. The most frequent infections involved the upper respiratory tract (75%), lower respiratory tract (65%), gastrointestinal tract (35%), skin (28%), and central nervous system (16%). Clinical clues to the diagnosis of X-LA were the chronic or recurrent nature of infections, a family history of immunodeficiency, and infections at more than one anatomic location. Infections remained a significant problem after the diagnosis of X-LA was made and gamma-globulin prophylaxis had been instituted. One or more chronic infectious diseases occurred in 71% of patients. The respiratory tract was the most common site of disease, and the gastrointestinal tract was relatively spared. Patients died at a mean age of 17 years. The two major causes of death were chronic pulmonary disease with resultant cardiac failure, and disseminated viral infections which characteristically caused a dermatomyositis-like syndrome, hepatitis, pneumonitis, and meningoencephalitis.
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PMID:X-linked agammaglobulinemia: an analysis of 96 patients. 258 Nov 10

Fifty one patients (pts) with various heart diseases and 6 normal subjects (N) were studied. Four of the 51 pts showed unusually high GOT values (greater than 3000 IU) without preceding evidence of acute heart failure, myocardial infarction, or hepatitis. Of these 4 pts, either ventricular tachyarrhythmias, marked bradycardia, or rapid ventricular response with atrial fibrillation (af) were evident a few days prior to the GOT elevation. GOT values returned to below 100 IU within a few days, but hypotension and frequent arrhythmias were sustained in 3 of the 4 pts and these 3 pts died about one month later. The symptoms of the remaining one improved but he too died 9 months later of ventricular fibrillation. A postmortem histological examination revealed centrilobular necrosis of the liver cells. Thus, abnormal GOT elevation may result from hepatic cell necrosis, which is probably due to tissue hypoperfusion caused by severe arrhythmias. Hepatic venous flow velocity (HFV) was measured in the remaining 47 pts and 6N using a pulsed doppler echocardiogram. The HFV curve was biphasic, with the first curve corresponding to the forward flow velocity during ventricular systole (s-HFV) and the second corresponding to ventricular diastole (d-HFV). The ratio of the area under s-HFV curve to the sum of areas under s-HFV and d-HFV curves was defined as the VI ratio. In N, the VI ratio was 0.7 +/- 0.06 whereas the VI ratio in pts in sinus rhythm tended to be above 0.7. This indicated that s-HFV is greater than d-HFV in N while s-HFV is less than d-HFV in pts in sinus rhythm. There was a good negative correlation (n = 15: r = -0.70) between VI ratio and cardiac index (CI) in these pts, suggesting that the contribution of s-HFV to the venous return becomes greater as the cardiac function becomes more impaired. In pts with af, the VI ratio was below 0.5 and there was a good positive correlation (n = 14: r = 0.82) between the VI ratio and CI. This suggested that the s-HFV may be reduced due to a lack of atrial contribution in af so that contribution of d-HFV to venous return becomes greater as the cardiac function becomes more impaired. Thus, the HFV pattern may reflect the abnormality of the cardiac pump function in human beings.
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PMID:Liver function in congestive heart failure: abnormal elevation of serum hepatic enzyme and hepatic venous flow velocity. 271 78

Previous investigations have shown that antibodies in sera from patients with halothane hepatitis recognize neoantigens, expressed in livers of halothane-exposed rabbits and rats, which consist of a halothane metabolite bound covalently to specific microsomal proteins. These studies have suggested that the patients' antibodies may play a role in the pathogenesis of the hepatitis. In the present investigation, human liver biopsy samples were analyzed using an immunoblotting method to seek evidence for expression of halothane-induced neoantigens in humans. Sera from four patients with halothane hepatitis, which recognized halothane-induced rabbit liver neoantigens of 100, 76 and 57 kD, reacted strongly with antigens of very similar molecular weights that were expressed in livers from two patients who had died of cardiac failure following recent anesthesia with halothane. The antigens were not expressed in normal human liver or in livers from three patients who died of cardiac failure following anesthesia with agents other than halothane. The human antigens were not recognized by antibodies present in various control sera. Recognition of the 100- and 76-kD human antigens by the patients' antibodies was greatly reduced by absorption of sera with liver microsomes from halothane-exposed rabbits, but not by absorption of sera with control rabbit microsomes. These results indicate that humans exposed to halothane express liver neoantigens which are analogous to the halothane metabolite-protein neoantigens characterized previously in halothane-exposed animals.
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PMID:Evidence for expression in human liver of halothane-induced neoantigens recognized by antibodies in sera from patients with halothane hepatitis. 319 77

Of 511 cases of brucellosis studied between December 1983 and February 1986, four (0.8%) had sternoclavicular (STCL) arthritis. Two were male and two female, and only one was younger than 50 years old. All four cases had significantly high specific IgG antibody titres (1 of 1280), measured by the indirect immunofluorescent (IIF) test, and two had Brucella melitensis isolated from their blood. In two cases, STCL arthritis was the presenting problem, and it was associated in one with ankle arthritis, hepatitis, renal impairment, orogenital ulcers and a haematological picture of myelodysplasia; in the other it was a relapsing STCL arthritis. In the remaining two cases, STCL arthritis was part of an extensive osteoarticular disease, which was associated in one with cachexia, liver cirrhosis, heart failure and prostatitis with urine retention, and in the other with severe thrombocytopenia. Excellent results were obtained from six to eight weeks' therapy with streptomycin, rifampicin and cotrimoxazole or tetracycline.
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PMID:Brucellar sternoclavicular arthritis, the forgotten complication. 325 Mar 41

The long-term follow-up of 80 heart transplant patients (70 men, 10 women) from January 1982 to July 1985 who had received cyclosporine (CsA) showed a high incidence of mild to severe liver dysfunction. Fifty patients (62.5%) had long-lasting postoperative biological disturbances (alanine amino transferase greater than 2N and/or alkaline phosphatase greater than 1.5N for 3 months or more). Most patients were asymptomatic; eight were icteric, and one had arthralgia. The most common biological feature consisted of isolated elevation of ALAT (27 cases). Assessment of causes led to a definite etiology in 42 patients: 7 cardiac failure, 13 HBsAg-positive liver disease (26%) (chronic persistent hepatitis 8, chronic active hepatitis 2, subacute necrosis 2). Fourteen patients (28%) sustained non-A, non-B (NANB) hepatitis (chronic persistent hepatitis 5, chronic active hepatitis 1, cirrhosis 1), and 7 (14%) sustained a drug-related hepatitis. Liver biopsy and complete virus screening was contributive to the diagnosis in nearly all patients. Additionally, prolonged impairment of liver function tests occurred in 62% of heart transplant recipients, mostly during the first 6 postoperative months. Hepatitis B virus (HBV) and NANB hepatitis accounted for 26% and 28% of the cases of liver dysfunction, respectively; drug-induced hepatitis may have been involved in 14% of the cases. Complete hepatitis virus screening should be performed before heart transplant and in any case of abnormal liver function posttransplantation. HBV vaccination prior to heart transplant is recommended in HBsAg- and HBcAb-negative candidates for heart replacement. Long-term follow-up of these patients is mandatory to assess the severity of these liver dysfunctions.
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PMID:Prevalence and causes of long-lasting hepatic dysfunction after heart transplantation: a series of 80 patients. 329 31

Sixty-six children aged between 8 months and 15 years (average age 5.5 +/- 3.8 years) underwent mitral reconstructive operations for congenital mitral regurgitation between June 1969 and February 1987. The pathologic findings of the mitral valves were annular dilatation in 37 patients, cleft of the leaflet in eight, hypoplasia of the leaflet in 44, perforation of the leaflet in one, chordal elongation in 22, chordal absence in 16, and chordal shortening in seven. The methods of repair consisted of asymmetric annuloplasty (Kay-Reed method) in 61 patients, De Vega-type annuloplasty in one, plication of redundant leaflet in 15, and closure of cleft or perforation in nine. The single operative death (1.5%) was due to heart block. Follow-up data were available over 373.8 patient-years (average 5.7 years). The four late deaths (6.0%) were due to heart failure in two patients, pneumonia in one, and hepatitis in one. The actuarial survival rate was 93.1% +/- 3.1% at 7 years and 88.4% +/- 5.1% after 17 years. Valvuloplasty failed in 19 of the long-term survivors. One of these patients underwent mitral valve replacement 11 years after initial operation. The rate of freedom from reoperation was 86% +/- 10% after 17 years. The rate of freedom from valvuloplasty failure was 80% +/- 6.7% after 5 years, 67% +/- 7.2% after 10 years, and 44% +/- 11.9% after 15 years.
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PMID:Early and late results of reconstructive operation for congenital mitral regurgitation in pediatric age group. 339 49

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38

Patients with chronic heart failure (CHF) can often develop such diseases as hepatitis of viral etiology, alcoholic hepatitis, drug affection of the liver and other diseases masked as congestive liver. In most cases CHF concomitant liver diseases have an atypical course with a tendency to a chronic course. CHF is one of the important pathogenetic mechanisms lying in the basis of chronicity of concomitant liver diseases. Refractory CHF, inconsistency of the hemodynamic indices of persistent hepatomegaly must lead a physician to the detection of probable independent liver diseases complicating the syndrome of heart failure. CHF is a factor causing an enhanced fibrosing liver reaction. An important diagnostic test of fibrinogenesis lying in the basis of chronicity of liver diseases, is the determination of enzymatic markers reflecting synthesis and catabolism of the main substance of connective tissue. Change in the levels of haptoglobin, ceruloplasmin and glutamic acid dehydrogenase is an indirect sign of damage of the liver parenchymal endoplasmic reticulum. These indices can serve as differential criteria of the prevalence of cardiovascular disorders in the liver or concomitant independent liver diseases.
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PMID:[Pathogenetic mechanisms of chronicity in liver diseases in patients with circulatory failure]. 361 41

The critical care environment may be characterized by invasive monitoring, vasoactive drugs, and major interventions which may have adverse effects on gastrointestinal function. Furthermore, conditions such as heart failure or sepsis may compromise oxygen delivery to gastrointestinal organs. Life threatening illness from a variety of causes may produce endoscopically evident gastritis or ulceration in up to 100% of patients, and clinically evident bleeding in 20%. Clinical studies suggest that antacids or H2 receptor blockers may reduce the frequency of this complication. Other conditions are associated with a spectrum of hepatic dysfunction ranging from the cholestatic jaundice of reactive hepatopathy during sepsis to centrilobular necrosis and hepatitis of shock liver. Additionally, many drugs used in the critical care setting may adversely affect mesenteric oxygen delivery and result in ischemia or infarction of the bowel. An increased awareness and understanding of these and other gastrointestinal complications in critically ill patients will, it is hoped, lead to earlier detection and better therapy than is now available.
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PMID:Gastrointestinal complications in critically ill patients: the intensivists' overview. 396 47


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