CELLULAR SOURCE OF SERUM LACTATE-DEHYDROGENASE ELEVATION IN PATIENTS WITH THROMBOTIC THROMBOCYTOPENIC PURPURA

Elevated serum lactate dehydrogenase (LDH) is a characteristic finding in patients with thrombotic thrombocytopenic purpura (TTP). It is wid ely accepted that total serum LDH principally rises due to the release of red blood cell LDH as a consequence of intravascular hemolysis. To identify the cellular source of serum LDH in TTP, we prospectively an alyzed total serum LDH and LDH isoenzyme profiles in 10 consecutive pa tients with classic, acute idiopathic TTP within 5 days of clinical pr esentation. Total LDH was quantitated on a Hitachi 911 Analyzer (India napolis, IN), using the lactate to pyruvate reaction. LDH isoenzymes w ere measured by serum protein electrophoresis, using the Beckman LDH I soenzyme Kit (Anabeim, CA). Isoenzymes attributable to erythrocytes (L DH1, LDH2) were not disproportionately elevated in 9 of 10 patients. L DH3 was below or within normal limits for all 10 patients, and one pat ient showed a slightly increased LDH4. Serum LDH5, the isoenzyme deriv ed primarily from liver and skeletal muscle, was elevated 1-2 times no rmal in all patients. Evidence supporting hemolysis as the major contr ibution to the elevated total serum LDH frequently encountered in acut e TTP was not identified in this study. The isoenzyme fractions LDH1 a nd LDH2 elevated by erythrocyte injury were not disproportionately ele vated in this series. LDH 5, the isoenzyme found in skeletal muscle an d liver, was consistently 1- to 2-fold greater than normal in all pati ents. We propose that the elevation of serum LDH seen in patients with TTP is due to release of LDH from a variety of tissues damaged as a r esult of systemic ischemia. (C) 1998 Wiley-Liss, Inc.