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Microangiopathic Haemolytic Anaemia Associated with Hypercakaemia in an Experimental Rat Tumour
Author(s) -
Hilgard Peter,
Hohage Roderich,
Schmitt Werner,
Köhle Walter
Publication year - 1973
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1973.tb05745.x
Subject(s) - fibrin , fibrinogen , coagulation , platelet , disseminated intravascular coagulation , fibrinolysis , medicine , hypercalcaemia , pathology , endocrinology , immunology , calcium
S ummary . A severe microangiopathic haemolytic anaemia develops during the course of tumour growth in rats bearing the solid Walker carcinosarcoma 256. Early changes of blood coagulation are the prolongation of the clotting and clot‐forming time in the thrombelastogram, a reduction of factor‐VIII activity and impaired platelet aggregation. Subsequent decrease of plasma fibrinogen and blood platelets indicate intravascular coagulation as the cause of the haematological changes. Fibrinogen turnover studies with homologous 131 I‐fibrinogen showed a significantly shortened half time. Concomitant with the alterations of the clotting mechanism a decrease of plasminogen level as well as an increasingly prolonged euglobulin lysis time were found; these may be interpreted as the result of the fibrinolytic response to intravascular fibrin deposition. Histological examination of the animals’ organs demonstrated fibrin strands and large fibrin thrombi exclusively in the capillaries of the tumour. Simultaneously with the intravascular coagulation syndrome the animals develop a hypercalcaemia caused by a parathyroid hormone‐like substance elaborated by the tumour tissue. Since clinical reports point to an interrelation between thrombotic disorders and hyperpara‐thyroidism, the possible role of hypercalcaemia in triggering intravascular coagulation is briefly reviewed.