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Portal hypertension in lymphoproliferative and myeloproliferative disorders: Hemodynamic and histological correlations
Author(s) -
Dubois Alain,
Dauzat Michel,
Pignodel Christine,
PomierLayrargues Gilles,
MartyDouble Christiane,
Lopez FrançoisMichel,
Janbon Charles
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840170214
Subject(s) - medicine , portal venous pressure , portal hypertension , gastroenterology , hemodynamics , splenic vein , hepatic fibrosis , blood flow , pathology , right gastric vein , hepatology , vein , vascular disease , cardiology , fibrosis , cirrhosis
The pathogenesis of portal hypertension in patients with lymphoproliferative and myeloproliferative disorders is not fully understood. We investigated 20 patients with myeloproliferative disease and 47 patients with lymphoproliferative disease. Transvenous liver biopsies and hepatic vein pressure gradient measurements were performed in all patients, and portal vein blood flow was measured by pulsed Doppler sonography in 31 of these patients and in 22 normal volunteers. The hepatic vein pressure gradient was significantly higher in patients with hepatic infiltrates, fibrosis or both than in patients without hepatic lesions (8.3 ± 5.0 mm Hg vs. 4.1 ± 2.3 mm Hg; p < 0.01). Portal vein blood flow was significantly higher in patients with hematological disease than in normal volunteers (31.2 ± 15.5 ml/min · kg vs. 14.2 ± 4.6 ml/min · kg; p < 0.01). In 81.8% of patients with hepatic infiltrates, fibrosis or both and increased portal vein blood flow, the hepatic vein pressure gradient was greater than 6 mm Hg. Although we saw a significant correlation between splenic vein blood flow and portal vein blood flow (n = 20; p < 0.01), we found no significant correlation between splenic vein blood flow and hepatic vein pressure gradient or spleen size. Hepatic infiltration and fibrosis appear to be major determinants of increased hepatic vein pressure gradient, probably because they increase intrahepatic vascular resistance. The role of increased splenic blood flow is probably not determinant. However, because portal pressure was not measured directly in this study, the incidence of portal hypertension may have been underestimated. (H EPATOLOGY 1993;17:246–250.)