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Biomedical subjects

E A Pariente

Publications and source records attributed to E A Pariente.

At least 37 records · Page 2Linked to original sources
PubMed1991

Sinusoidal portal hypertension in hepatic amyloidosis.

Hepatic venous catheterisation and transvenous liver biopsy were performed in five patients with hepatic amyloidosis. In three patients, hepatic venous pressures were normal and histological examination of the liver biopsy specimen showed discrete and sparse perisinusoidal amyloid deposits. In the other two, however, the gradient between wedged and free hepatic venous pressures was increased (12 and 16 mmHg; normal 1-4 mmHg) and amyloid deposits were abundant and diffuse in the Disse's space. This study shows that portal hypertension in patients with hepatic amyloidosis is of the sinusoidal type and is related to the reduction of vascular space of hepatic sinusoids by massive perisinusoidal amyloid deposits. Furthermore, portal hypertension is associated with a poor prognosis in patients with hepatic amyloidosis.

Aged↗
PubMed1990

[Icteric complications related to pregnancy vomiting in the 1st trimester (hyperemesis gravidarum). Review of the literature apropos of a case].

The authors report a case of jaundice occurring secondary to severe vomiting in pregnancy in the first trimester. This is a rare clinical entity (occurring in 0.2-3 cases per thousand) although some people say it does not exist. The physiopathology is still badly understood but it occurs most often between the fourth and eighth week of amenorrhoea. It is characterised by jaundice occurring secondarily to vomiting in the first trimester, with a rise in the bilirubin level in the blood and in the alkaline phosphatases. Sometimes there is a slight rise in the transaminases. The diagnosis can only be arrived at after having excluded all the other possible causes of jaundice which are mentioned in the text. Furthermore the way the condition progresses is an important argument for its aetiology because once vomiting ceases the jaundice goes. The treatment has to be symptomatic with correction of the dehydration.

Adult↗
PubMed1989

[Hepatitis caused by clometacin (Dupéran). Retrospective study of 30 cases. A model of autoimmune drug-induced hepatitis?].

Thirty cases of clometacin-induced hepatitis were retrospectively collected over a nine-year period in hepatogastroenterological units of non university, public hospitals. There was a strong female predominance (90 percent). Clometacin (Dupéran) was taken because of arthritis in 8 out of 10 cases. Administration was continuous in 85 percent of cases and median duration was 445 days. median dose was 450 mg per day. Jaundice, fatigue, and weight loss were the most frequent symptoms, but edema, ascites and palmar erythema were not uncommon. Thrombopenia (38 percent) was the most frequent hematologic abnormality. Renal failure, always with benign course, was present in 1/4 of cases. Biochemical disorders indicated hepatocellular and cholestatic hepatitis in 3/4 and 1/4 of cases respectively. Hypoprothrombinemia below 50 percent was noted in 1 out of 6 cases, and was associated with death in half cases. Gamma-globulins were increased in 80 percent of cases, with a predominant increase of IgG. Antinuclear or anti-smooth muscle antibodies were present in 60 percent of cases, whereas antimitochondrial and antimicrosomes were absent. Histopathological examination of the liver biopsy specimens obtained in 25 patients showed acute hepatitis in 8 and chronic active hepatitis with fibrosis in 17--including 6 patients with cirrhosis; there were no epidemiological, clinical (except ascites), or biochemical differences between these two groups. Four of the 7 patients tested had HLA B8 antigens; they all had chronic active hepatitis, with autoantibodies in 3 cases. Median duration of hospitalization was 21 days. Hepatitis was directly responsible for death in 3 patients; biochemical sequelae (hypergammaglobulinemia or anicteric cholestasis) were present in 8 patients, 2 of whom most likely had cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Fulminant hepatitis due to reactivation of chronic hepatitis B virus infection after allogeneic bone marrow transplantation.

A case of hepatitis B reactivation following bone-marrow transplantation for leukemia in a previously healthy HBsAg carrier is reported. A number of changes in HBV serum markers were contemporary to the acute episode. All of them (increase of HBsAg concentration, conversion from anti-HBe to HBeAg, appearance of anti-HBc IgM and of serum HBV-DNA) were suggestive of a "switching-on" of viral replication. Institution of corticosteroid treatment at the onset of the acute phase did not prevent the fatal outcome.

Adult↗
PubMed1986

[Hepatitis caused by quinidine. Study of a case and review of the literature].

The authors report the case of a 63 year-old woman who developed high-grade fever with chills, nausea, diarrhea, severe pain in the right hypochondrium, and jaundice after one month's treatment with 300 mg of hydroquinidine hydrochloride daily. Serum bilirubin and aminotransferases were slightly increased, while alkaline phosphatases and gamma-glutamyl-transpeptidase serum activities were markedly raised. Histological examination of a liver specimen obtained by the transvenous route showed numerous epithelioid granulomas with giant cell formation and eosinophils in hepatic lobules and portal tracts. Symptoms disappeared three days after withdrawal of the drug, but hepatomegaly and a mild increase in serum gamma-glutamyl-transpeptidase persisted more than eighteen months. Quinidine-induced hepatitis is almost always associated with fever, and, in one-third of the cases, with a pseudo-cholangitis picture. Extrahepatic hypersensitivity manifestations are often present. Histological examination of the liver shows granulomatous or cytolytic hepatitis. Withdrawal of the drug is rapidly followed by a favorable outcome; readministration causes immediate relapse; progression to chronic liver disease has never been reported previously.

Chemical and Drug Induced Liver Injury↗
PubMed1985

Acute effects of captopril on systemic and renal hemodynamics and on renal function in cirrhotic patients with ascites.

The reduction of angiotensin II production by captopril--an angiotensin-converting enzyme inhibitor--could suppress hyperaldosteronism without impairment of renal function and could thereby be useful in the treatment of ascites in patients with cirrhosis. Systemic and renal hemodynamics and renal function were studied in 6 nonazotemic patients with cirrhosis and ascites with a low-sodium diet before and after oral administration of 25 mg of captopril. Cardiac output and renal blood flow did not change significantly after administration of captopril, whereas mean arterial pressure significantly decreased. Systemic and renal vascular resistances were significantly reduced. There was a statistically significant reduction of glomerular filtration rate, filtration fraction, and urinary output. Plasma renin activity significantly increased in all patients after administration of captopril. A statistically significant correlation was found between the decrease in mean arterial pressure and the reduction of glomerular filtration, but no relationship was found between basal values of plasma renin activity and the other observed variations. We concluded that captopril mainly induces hypotension due to an increase in renal vasodilatation in ascitic patients with cirrhosis.

Ascites↗