Nodular regenerative hyperplasia of the liver in hematologic disorders: a possible response to obliterative portal venopathy. A morphometric study of nine cases with an hypothesis on the pathogenesis.

Wanless Ir, Godwin Ta, AARON FEDER

PubMed · 1980 · 235 citations · 0 references

Concepts

TL;DR

The study proposes that thrombi, mainly platelet aggregates formed in the portal venous system or spleen, embolize to the liver, causing obliterative vascular lesions. These emboli lead to portal vein obstruction, triggering atrophy and regenerative nodule formation in the liver. Nine patients with hematologic disorders exhibited nodular regenerative hyperplasia, with portal hypertension suspected in three, hypersplenism in four, and morphometric analysis revealing frequent lesions in portal veins ≤0.2 mm, more common than in elderly controls. References 2 and 3.

Abstract

Nodular regenerative hyperplasia was found in nine patients who had hematological disease including polycythemia vera, agnogenic myeloid metaplasia, primary thrombocythemia, rheumatoid arthritis with thrombocytosis, multiple myeloma, and erythrocytosis associated with polycystic renal disease. Portal hypertension was suspected in three and features of hypersplenism were present in four. 2. Nodular regenerative hyperplasia occurred in livers which had widespread obliteration of portal vein radicals (obliterative portal venopathy). Morphometric analysis indicated that the portal vein lesions were predominately located in veins up to 0.2 mm in diameter and were significantly more frequent than similar lesions occurring in elderly persons. 3. The following pathogenesis of nodular regenerative hyperplasia is proposed: Thrombi, perhaps largely composed of platelet aggregates formed in the portal venous circulation or spleen, embolize to the liver and results in obliterative vascular lesions. Atrophy and regenerative nodule formation occur in response to the interruption of the portal blood supply.