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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infectious mononucleosis (IM) patients, Epstein-Barr virus (EBV)-seropositive and seronegative healthy donors, and patients with other viral infections were tested for lymphocyte blastogenesis (LB) with phytohemagglutinin and six EBV (virus concentrate, culture supernatant, and soluble [S] antigen) or control antigens. Fluorescent antibodies to EBV viral capsid antigen of IgG, IgM, IgA specificities, to nuclear antigen (EBNA), and heterophile antibodies were also assayed. These were correlated with clinical parameters (fever, pharyngitis, adenopathy, hepatitis, splenomegaly, atypical lymphocytes, and total mononuclear cell counts). EBV viral and S antigen-induced LB was significantly greater in seropositive donors. IM patients had antigenspecific LB below that of seropositive donors initially and low responses for the acute phase of illness when clinical symptoms were present and antibody titers were maximal. Specific LB rose to a peak at 3.5 to 9 weeks when the patients had recovered, most laboratory findings had returned to normal, and antibodies had declined. At peak, specific LB in IM patients exceeded that of seropositive donors, but later declined. These results demonstrate specific cell-mediated immunity (CMI) to EBV, and indicate that this develops slowly in IM and contrasts with the evolution of the clinical events and humoral immunity. This correlation supports the hypothesis that CMI is the mechanism of terminating lymphoproliferation in IM.
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PMID:Cellular immunity in infectious mononucleosis. II. Specific reactivity to Epstein-Barr Virus antigens and correlation with clinical and hematologic parameters. 8 Dec 24

Rash, lymphadenopaty, splenomegaly, periorbital edema, and hepatitis occurred in an 18-year-old woman who was taking phenobarbital and hydrochlorothiazide. Tests for fluorescent antinuclear antibody and hepatitis-associated antigen and antibody were negative. Liver biopsy was not characteristic of viral hepatitis. Clinical recovery occurred within two weeks. Treatment consisted of withdrawal of the above drugs plus the administration of methylprednisolone and diphenhydramine.
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PMID:Jaundice and rash associated with the use of phenobarbital and hydrochlorothiazide. 12 22

Liver function abnormalities have been noted in intensively treated hemophiliacs, and have led to less aggressive application of pooled plasma products by some physicians. In a prospective study, liver function was abnormal in 68 of 98 hemophiliacs. The abnormalities of hepatic function tended to persist over a 1-yr study period. There was no correlation between these abnormalities and the age of the patient, the presence of hepatitis-associated antigen or antibody, the presence or absence of splenomegaly (which was found in 26 of 98 patients), the number of infusions of plasma products, the type of hemophilia, or the type of product infused. Titers of antibodies to cytomegalovirus were generally higher in hemophilic patients than in a control group of healthy volunteers. These abnormalities did not suggest that a less aggressive infusion regimen was indicated for the hemophiliac, but did suggest the need for careful long-term observation of such patients.
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PMID:Health of the intensively treated hemophiliac, with special reference to abnormal liver chemistries and splenomegaly. 19 36

This paper gives, in detail, the causes of either liver disease or hepatomegaly in 100 patients, mostly adults, admitted to the medical wards of Angau Memorial Hospital, Lae, during 1968 and 1969. The major findings included liver cell carcinoma, cirrhosis (often with chronic active hepatitis), tropical splenomegaly, pericholangitis and hepatitis. There were 27 with miscellaneous findings including ten with normal, or almost normal, livers despite the definite enlargement. Patients with liver cell carcinoma presented late in the course of their illness and had a poor prognosis. Others, with pericholangitis, had clinical features of portal hypertension indistinguishable from that complicated cirrhosis. There was an unexpected number with chronic active hepatitis and a liver biopsy is essential for such a diagnosis. Hepatic sinusoidal lymphocytosis is almost invariably found in patients with TS but may occasionally be found in those with a non-palpable spleen. Patients with right heart failure of chronic respiratory disease, and jaundice of acute pneumonia were excluded from the study.
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PMID:Liver disease in Papua New Guinea. 19 19

The effect of corticosteroid (or ACTH) therapy on 4 patients with idiopathic granulomatous hepatitis is described. All patients presented with spiking fever and chills and none had jaundice. Only 1 patient had an enlarged tender liver and 3 had splenomegaly. The erythrocyte sedimentation rate was increased in all cases while the white blood cell count was typically normal. Impairment in liver function was insignificant and consisted of a mild elevation of SGOT and alkaline phosphatase activities and prolonged prothrombin time. All patients presented a diagnostic challenge. The diagnosis was established by routine liver biopsies in 3 cases and by laparotomy in the 4th. The etiology could not be established. All patients reacted dramatically to prednisone (or ACTH) after failure of other therapeutic regimens. The disease has, however, been present for 5 years in 1 patient and 10 years in another, Relapses occur after cessation of therapy.
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PMID:Idiopathic granulomatous hepatitis with a prolonged course: effect of corticosteroid therapy. 20 7

In many cases so called neonatal hepatitis of unknown origin nowadays is recognized as a manifestation of alpha1-antitrypsin deficiency. Out of 12 patients with Pi-type ZZ, 5 were diagnosed because of cholestatic jaundice, 2 because of hepato-splenomegaly in the first trimenon, and 3 by family examination. We believe that the affection may be due to a perinataly acquired cytomegalic inclusion disease in one case, in another to a congenital rubella infection. The latter child died at the age of one year because of an esophageal hemorrhage. Over a mean observation time of 3 years the other patients are doing well and show no signs of portal hypertension. The very different course of the hepatopathy is demonstrated. Common bacteria or toxins which do not usually lead to an illness may be realisation factors just as "classical" causes of hepatitis. Up to now it is not known how these factors influence the course of alpha-antitrypsin deficiency.
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PMID:[alpha1-antitrypsin deficiency. Clinical and morphological aspects during childhood (author's transl)]. 21 96

The relationship of chronic hepatitis B and/or liver dysfunction to treatment in 113 hemophiliacs was evaluated by the enzyme tests, SGOT and SGPT, and by the presence of circulating hepatis B surface antigen (HbsAg) or antibody (anti-Hbs). The hemophiliacs were divided into three groups according to treatment pattern. Individuals who had received multiple doses of plasma fractions, derived from four or more commercial lots were placed in tgroup I "large Exposure". Group II "Small Exposure" had been treated with fractions from three or fewer lots and Group III "Cryo" had never received commercial fractions, but had been treated with cryoprecipitate. Abnormal liver function tests (LFT's) were found in 87% of Group I and 76% of Group II, but in only 16% of the "Cryo" group. Differences in LFT's were not great between treated VIII and IX deficient patients. All patients treated with 100,000 units or more showed either persistent or intermittent abnormalities. In the high exposure group, this history of past, overt hepatitis had no influence on observed LFT's. The sera of all patients in the high exposure and all, except one, in the low exposure groups were positive for HbsAg or anti-Hbs by RIA. Splenomegaly was found in 13% of fraction-treated patients. We conclude that there is biochemical evidence of liver disease following large exposure to commercial VIII or IX fractions, which should temper the physician's decision to start treatment with these fractions. On the other hand, evidence that their continued use produces mounting liver dysfunction is insufficient to withdraw this very effective and life-changing treatment from these individuals.
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PMID:Chronic hepatitis in hemophilia. 26 94

Portal hypertension and variceal hemorrhage may be found in the renal transplant patient with chronic liver disease. The development of portal hypertension was found to occur after long-term graft survival without significant rejection. The development of positive cytomegalic virus and negative hepatitis-associated antigen appeared to be common. Splenomegaly and prominent venous collateral were the most frequent physical findings, while ascites and hepatomegaly were less frequent. Portasystemic decompression can be performed successfully, however, the mortality and morbidity appear to be higher for this group than for other cirrhotic patients with comparable hepatic reserve.
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PMID:Portal hypertension following renal transplantation. 35 15

We have evaluated the 133Xenon inhalation method for the determination of splenic blood flow. In twenty-two healthy persons the blood flow was on average 109 +/- 4 mg/100 g X min, which is equivalent to a total blood flow of about 170 ml/min. In patients with chronic fatty liver hepatitis specific blood flow was reduced (81 +/- 10 ml/100 g X min) as it was in patients with cirrhotic liver without splenomegaly (75 +/- 2 ml/100 g X min). With increasing weight of the spleen, the total blood flow rises, although specific blood flow is low. Our results obtained by the 133Xenon inhalation method are similar to results obtained by others using intraarterial injection of tracer gas. The advantages of the inhalation method as a non-traumatic method are: (1) the stress for the patient is very small; (2) blood flow measurements can be repeated within short periods of time. We consider for the present the 133Xenon inhalation method to be the method of choice for the determination of the splenic blood flow.
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PMID:Determination of splenic blood flow by inhalation of radioactive rare gases. 41 64

Classical sex-linked hemophilia (Hemophilia A) has been described as due to deficiency in the synthesis of Factor VIII procoagulant activity (VIII:C). The availability of immunological techniques provided the means of identifying Factor VIII-Related Antigen(VI-IIR:Ag) detectable by rabbit antibodies to F VIII, which is distinct from VIII:C detected by human anti-F VIII available from multitransfused patients. Hemophilia A is lacking in VIII:C but not VIIIR:Ag. Recently, a third function of the F VIII "complex" was discovered with the help of ristocetin (von Willebrand's Factor, VIIIR: RCo). This activity is reduced in von Willebrand's syndrome. Estimation of the titers of VIII:C and VIIIR:Ag provides a method for more accurate detection of hemophilic carriers. Newly available chromogenic substrates perhaps will give rise to more simplified assays of VIII:C. The development of cryoprecipitates and stable lyophilized concentrates of F VIII has greatly simplified and intensified maintenance therapy, and has opened a new era in treatment. Prophylactic therapy has been shown to be very helpful in certain "high risk" cases. The impact and benefits of home care and self-administration has been tremendous. However, the varying quality of cryoprecipitates and the high cost of more purified concentrates are still stumbling blocks in treatment regimes. Other problems exist. Spontaneous bleeding, especially central nervous system bleeding, account for the majority deaths by haemorrhage. Inhibitor kinetics have been well characterized. It is clear that there exists "low" and "high" responders. For the "high" responders, plasmapheresis, immunosuppressives and the infusion of Factor IX concentrates have been utilized with varying success. The prevention of hemophilic arthropathy and its progression by maintenance therapy seems to be still inadequate. The results of trials with more vigorous regimes are awaited. The complications of therapy still remain to be solved. Apart from the well-known complications wuch as hepatitis, haemolytic disease and F VIII inhibitors, the existence of previously unnoticed complications as splenomegaly, hypertension, renal disease and paradoxal bleeding have been recently realized. The role of altered fibrinogen, fibrin degradation products (FDP) and unclassified fibrinogen derivatives (UFD) present in cryoprecipitates and F VIII concentrates in the above complications needs to be further clarified. In conclusion, tremendous progress in various aspects of hemophilia has been achieved in developed countries. Comprehensive care can now be carried out in various centers. On the other hand, developing countries still face a number of basic problems. The concept that hemophilia is a "manageable" disease and that chronic crippling and death from exsanguination can be prevented, should be disseminated widely by various means...
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PMID:Recent advances in hemophilia. 52 46


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