Splenectomy in Myelofibrosis

Jensen, Mogens Krogh

doi:10.1111/j.0954-6820.1964.tb00605.x

Cited by 21 publications

(1 citation statement)

References 24 publications

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“…This observation, confirmed by the autopsy findings, is in agreement with the findings of Merskey (1947), Bastrup-Madsen (1952), Hickling (1953), SchaEer & Stodpart (1953), Beyreder & Rieder (1956 and Ward & Block (1971). Marked enlargement of the liver was observed in 3 patients who survived more than 10 months after splenectomy, as reported previously by Bukh & With (1945), Laster & Miller (1953), Asher (1955), Cartwright et a1 (1955), Rohr (1956) and Jensen (1964). Abdominal pain or discomfort related to the enlarged liver were not reported.…”

Section: Clinical Manifestations Of Liver Involvementsupporting

confidence: 81%

Nature and Incidence of Liver Involvement in Agnogenic Myeloid Metaplasia

Ligumski

Polliack

1978

Scandinavian Journal of Haematology

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Clinical, biochemical and histopathological data of 33 patients with agnogenic myeloid metaplasia (AMM) were examined with reference to liver disease and dysfunction. Clinical manifestations of hepatic or portal system involvement included hepatomegaly, jaundice, hepatitis, gall stones, ascites and bleeding esophageal varices. The liver was smooth and firm; it became larger with progression of the disease, but to a lesser degree than the spleen. Mild indirect bilirubinaemia occurred in the course of the disease in about half of the patients. Hepatitis was diagnosed in 5 (15 %) patients and in 3 (10 %) cases it was the cause of death. Cholelithiasis was found in 4 (12 %) patients. Biochemical liver dysfunction occurred in 22 (66 %) patients. A progressive increase in serum alkaline phosphatase and a gradual decrease in serum albumin were observed in 4 patients, who were followed for 5 to 15 years. Hepatic myeloid metaplasia was found in all 20 patients examined histologically. The liver architecture was grossly distorted in 4 cases: in 2 this was due to impaction of the sinusoid with haemopoietic cells, and in the remaining 2 to necrosis and haemorrhage following viral hepatitis. Periportal fibrosis was observed in 6 (30 %) of the liver specimens. Ascites, portal hypertension, or both, were found in 7 (64 %) of the 11 autopsies and in 5 (22 %) of the remaining patients. Liver histology, examined in 11 patients, revealed periportal fibrosis in 5 cases and myeloid metaplasia only, in the remaining 5. Patients with ascites or portal hypertension exhibited more frequently increased levels of serum alkaline phosphatase and vitamin B12, and lower levels of plasma prothrombin and serum albumin. The pathogenesis of the hepatic and portal system involvement in agnogenic myeloid metaplasia (AMM) remains uncertain. Mechanical pressure by foci of myeloid metaplasia, chronic passive congestion, hepatitis or combinations of the above may lead to atrophy or necrosis of the parenchyma, followed by reparative fibrosis. Portal hypertension and ascites, a common complication of advanced AMM, could be due to the combined effect of an increased blood flow in the portal system, hypoalbuminaemia and sinusoidal obstruction.

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