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Biomedical subjects

E A Pariente

Publications and source records attributed to E A Pariente.

At least 19 recordsLinked to original sources
PubMed1992

Internal radiation therapy for hepatocellular carcinoma. Results of a French multicenter phase II trial of transarterial injection of iodine 131-labeled Lipiodol.

Preliminary Phase I trials have shown iodine 131 (131I)-Lipiodol (ethiodized oil; Laboratoires Guerbet, Aulnaysous-Bois, France) to be well tolerated and most likely effective in the treatment of hepatocellular carcinoma (HCC). In this multicenter Phase II trial, the authors tested the feasibility and reproducibility of this treatment in other medical institutions and evaluated its efficacy in 50 patients with unresectable Stage I or II HCC, by the classification of Okuda et al. The authors studied 47 men and 3 women (63.9 +/- 7.1 years old) with Stage I (n = 18) or II (n = 32) HCC, by the classification of Okuda et al., which was verified by histologic findings (n = 25), cytologic findings (n = 11), or association of a tumor with alpha-fetoprotein serum values greater than 500 micrograms/l (n = 14). This multicenter trial (1) confirmed that the 131I-Lipiodol treatment is well tolerated; (2) showed that there is a high reproducibility of results with respect to other institutions and an objective tumor response in 40% of the cases; and (3) indicated the necessity of performing a randomized controlled study.

Adult↗
PubMed1992

Fipexide-induced fulminant hepatitis. Report of three cases with emergency liver transplantation.

Fipexide belongs to a new class of cognition activators and is noted for its lack of amphetamin-like side effects. We describe three patients who developed fulminant hepatic failure less than 2 months after beginning fipexide administration. The mean interval from the onset of jaundice to the onset of encephalopathy was 8 days. Emergency liver transplantation was undertaken when factor V was 20% of normal or less and coma developed. All patients were transplanted less than 1 week after the onset of encephalopathy. Two survived and one died immediately after transplantation. Histologic examination of the livers revealed massive liver cell necrosis, predominantly centrilobular, and a moderate inflammatory infiltrate within the portal spaces. We conclude that fipexide can induce massive liver cell necrosis and fulminant liver failure. As a result of this life-threatening complication, reconsideration of the indications for this drug is warranted.

Adolescent↗
PubMed1992

[Portal vein thrombosis and hereditary protein C deficiency. Presentation of a case and review of the literature].

The authors report the case of a 51 year-old man, without any personal or familial history of thromboembolism, presenting with abdominal pain. Portal vein thrombosis was demonstrated by ultrasonography and arteriography. The patient had neither esophageal varices or congestive gastropathy. No cause for portal vein thrombosis was detected. Type I protein C deficiency was demonstrated in this patient as well as in his asymptomatic sister. The presence of a (fortuitously?) associated increase in platelet aggregability initially led to a trial regimen of aspirin (300 mg per day); abdominal pain resolved, and a partial regression of portal vein thrombosis was demonstrated on ultrasonograms six months later; no further complications occurred during the 4-year follow-up period. The 13 previously published cases of protein C deficiency-associated portal vein thrombosis are reviewed.

Aspirin↗
PubMed1991

[Physiopathology of inflammatory bowel diseases].

The author presents a brief review of the main pathophysiological hypotheses put forward to explain the formation of lesions of inflammatory bowel diseases (ulcerative colitis and Crohn's disease). No infectious or alimentary cause has been found. Immunological abnormalities are numerous, but none of them seems to be primary. The effector role of inflammation mediators is better known and leads to new developments in therapeutics. The study of healthy relatives is an interesting means of looking for abnormalities that pre-exist the disease, as seems to be the case with intestinal permeability. The french contribution of fundamental research on inflammatory bowel diseases is insufficient and must be stimulated.

Colitis, Ulcerative↗
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↗