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At least 37 records · Page 2Linked to original sources
PubMed1976

Hemorrhagic diathesis in Weber-Christian disease.

A case of a 21-year-old woman with Weber-Christian disease, associated with consumption coagulopathy and adequately controlled over the past year or more by corticosteroid and heparin therapy, has been described. Through the study on this case, it was concluded that a hemorrhagic diathesis complicating Weber-Christian disease, at least in advanced cases, was characterized by consumption coagulopathy associated with enhanced blood coagulability which arises from hyperlipemia due to abnormal lipid metabolism and further, that the consumption coagulopathy was modified by diminished synthesis of clotting factors and activation of the fibrinolytic system due to the secondary hepatic impairment. It might also be likely that systemic vascular changes contribute to the activation of the clotting system as a trigger of clotting factor consumption. The complex pathophysiology of a hemorrhagic diathesis in this disease seemed to be brought about by a complex combination of such a variety of factors. In addition, decreased erythrocyte sedimentation rate observed characteristically during hemorrhage might probably have a direct correlation with hypofibrinogenemia due to consumption coagulopathy in advanced cases.

Adult↗
PubMed1974

A hemorrhagic diathesis with involvement of hypothalamus produced in rats by cyclophosphamide.

Large doses of cyclophosphamide caused a hemorrhagic diathesis related to bone marrow destruction and thrombocytopenia. Although several organs had hemorrhages, there was a striking predilection for the hypothalamus, ileum and mesentery of adult rats. The reasons for this localization are not known, but involvement of hypothalamus may be related to known functional effects of the drug on the neuroendocrine system. There were hemorrhages in choroid plexus, ciliary body and urinary bladder also, but these localizations were due to prior direct toxic injury to these structures by cyclophosphamide.

Animals↗
PubMed1984

Hemorrhagic diathesis in multiple myeloma.

Hemorrhage occurs during the clinical course in 15% of patients with multiple myeloma. We recently treated a patient with myeloma who had postoperative bleeding and hematuria despite normal coagulation parameters and platelet count. Platelet function studies revealed markedly abnormal aggregation to all stimulants. Plasma exchange successfully reversed in vitro and in vivo bleeding abnormalities.

Blood Platelet Disorders↗
PubMed1990

Non-specific therapy of a hemorrhagic diathesis after a bite by a young Bothrops asper (barba amarilla): a case report.

Hemorrhagic diathesis developed 4 hr after a bite by one fang of a two-month-old specimen of Bothrops asper. Severe allergy to horse serum contraindicated the use of horse antivenom, and a substitution therapy was started 20 hr after the bite. During the following 4 days the patient was treated with infusions of 8 g human fibrinogen, 2500 U of cryoprecipitate, 1000 ml of human plasma and vitamin K in several portions. By means of plasmapheresis 1800 ml of plasma was exchanged. Until plasmapheresis on the third day the treatment resulted in short remission and diminution of the spontaneous bleeding, which ceased on the 5th day. Coagulation tests relevant to disseminated intravascular coagulation and consumption coagulopathy were performed for 12 days. Fibrinogen levels started to rise on the 8th day and normalized 12 days after the bite. Analysis of the venoms from juvenile and adult Bothrops asper snakes revealed that the former has a strong prothrombin-converting activity, the latter contained mainly a thrombin-like, fibrinogen-converting enzyme.

Age Factors↗
PubMed1988

A combination therapy of vitamin K1 and bile acid on hemorrhagic diathesis in patients with decompensated liver cirrhosis.

This paper presents a study of treatment involving vitamin K1 (VK1) accompanied by bile acids for hemorrhagic diathesis that was applied 42 times in 35 patients with decompensated liver cirrhosis. The hepaplastin test (HPT) value showed no change during the administration of VK1 alone. The HPT value elevated significantly, however, after the administration of VK1 with bile acid, especially when using ursodeoxycholic acid (UDCA). The HPT value in patients treated with VK1 in addition to UDCA before treatment with 53.2% +/- 10.2% (mean +/- SD) and after that for 2.1 +/- 1.1 months (mean +/- SD) with 74.7 +/- 16.8% showed a significant difference (p less than 0.001). On the other hand, no significant difference was noted between the HPT value of 57.2 +/- 13.6% before and that of 62.9 +/- 13.9% after the treatment in patients treated using VK1 in conjunction with chenodeoxycholic acid (CDCA). These results indicate that the therapy incorporating VK1 and bile acid, especially UDCA, is useful for reducing the hemorrhagic tendency in patients with decompensated liver cirrhosis who show no improvement using VK1 alone.

Chenodeoxycholic Acid↗