Endoperoxidation, hyperprostaglandinemia, and hyperlipidemia in a case of erythrophagocytic lymphohistiocytosis. Reversal with VP‐16 and indomethacin

Clinicopathologic and histopathologic evidence of both endoperoxidation with hyperprostaglandinemia and hyperlipidemia in a 5‐week‐old infant with a hemophagocytic syndrome is reported. Institution of histiocytolytic (VP‐16) and cyclo‐oxygenase inhibitor (indomethacin) therapies returned the prostag...

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Bibliographic Details
Published in:Cancer 1987-11, Vol.60 (10), p.2388-2393
Main Authors: Brown, R. E., Bowman, W. P., D'Cruzmd, C. A., Pick, T. E., Champion, J. E.
Format: Article
Language:English
Subjects:
Dinoprost
Dinoprostone
Etoposide - therapeutic use
Glucose - therapeutic use
Histiocytes - pathology
Humans
Hyperlipidemias - drug therapy
Hyperlipidemias - etiology
Indomethacin - therapeutic use
Infant
Lipid Peroxides - blood
Liver - pathology
Lymphatic Diseases - complications
Lymphocytosis - complications
Male
Phagocytosis
Prostaglandins E - blood
Prostaglandins F - blood
Vitamin E - therapeutic use
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Summary:Clinicopathologic and histopathologic evidence of both endoperoxidation with hyperprostaglandinemia and hyperlipidemia in a 5‐week‐old infant with a hemophagocytic syndrome is reported. Institution of histiocytolytic (VP‐16) and cyclo‐oxygenase inhibitor (indomethacin) therapies returned the prostaglandin levels and lipid profile to a nearly normal state coincidental with clinical recovery. It appears that by reducing the cell mass of histiocytes and controlling the over‐production of prostaglandins, some types of hemophagocytic syndrome can be reversed.
ISSN:0008-543X
1097-0142
DOI:10.1002/1097-0142(19871115)60:10<2388::AID-CNCR2820601007>3.0.CO;2-A