Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019087 (hemorrhagic diathesis)
 678 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daunomycin (rubidomycin, daunorubicin), an anthracycline antimetabolite used in the therapy of acute leukemia, is highly toxic to both normal and malignant cells. Treatment with daunomycin may produce thrombocytopenia and bleeding which have been attributed to bone marrow toxicity. We have examined daunomycin to determine if a direct drug effect on platelet structure and function could contribute to a hemorrhagic diathesis in some patients on therapy. Normal citrated platelet-rich plasma was reacted in vitro with daunomycin and/or collagen with structural assessment by phase and electron microscopy and functional studies by platelet aggregation, [2-14C]5-hydroxytryptamine release studies and assays for released cytoplasmic marker enzyme, lactic dehydrogenase, in the supernatant fluid. High [greater than 0.04 mg/ml (greater than 0.07 mM)] concentrations of daunomycin were associated with structural changes, specifically by platelet swelling, vacuole formation and mitochondrial swelling with interruption of the trilaminar membrane. Platelets, exposed to low doses of daunomycin, 0.001 to 0.01 mg/ml (0.00177-0.0177 mM) of platelet-rich plasma, were dysfunctional with decreased aggregation with collagen and decreased [2-14C]5-hydroxytryptamine release. These studies indicate that daunomycin has a direct effect on platelets in vitro which may explain certain instances of bleeding observed in some patients undergoing therapy.
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PMID:The effect of daunomycin on platelets in vitro. 261 25

Assessment of animals with a suspected hemorrhagic diathesis of unknown cause(s) should be methodical. Most acquired coagulopathies result from thrombocytopenia. A platelet estimate (from a blood smear) and/or a platelet count on a fresh blood sample therefore are useful first steps in case evaluation. If thrombocytopenia is present, the most likely causes are immune-mediated destruction of platelets, DIC, or megakaryocytic hypoplasia. These diagnoses can be pursued by further test, including antiplatelet antibody assays (for example, the platelet factor 3 tests or an ELISA test), measurement of FDP, and bone marrow biopsy, respectively. If the platelet count is normal, a buccal mucosa bleeding time test is a useful second step. If this is prolonged, most likely causes are vWD or a thrombocytopathy (functional platelet defect). von Willebrand's disease can be diagnosed by measurement of vWf concentration or activity. A normal bleeding time does not exclude a diagnosis of vWD, but suggests that the functional activity of vWf is not compromised markedly. If the bleeding time is normal, APTT and PT should be measured. A prolonged APTT with normal PT, in the clinical setting, implies a deficiency of factor XI, IX, or VIII. A prolonged PT with normal APTT indicates factor VII deficiency. Prolongation of both APTT and PT usually is caused by a deficiency of several factors and is seen most often in cases with vitamin K deficiency or antagonism. Obviously, if a particular cause is suspected from the case history or for other reasons, appropriate tests should be evaluated at the beginning. If these do not confirm the provisional diagnosis, the just-described protocol might be a useful one to follow.
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PMID:Laboratory evaluation of hemorrhagic coagulopathies in small animal practice. 267 37

Between 1981 and 1988, we recorded 11 patients presenting a neoplastic microangiopathy. All patients suffered from adenocarcinoma, except one with an undifferentiated lung carcinoma; the origin of the tumor was mammary in 5 cases and gastric in 3. In our study, microangiopathy was the first manifestation of the neoplastic disease on 3 occasions; on 7 occasions it was a complication of an advanced stage of a known oncological disease; and on 1 occasion it occurred during a course of intra-arterial chemotherapy. Regenerative anemia (mean 9.5 g/dl hemoglobin), thrombocytopenia (mean 42,000 platelets/mm3), and an elevated LDH value (mean 1,268 U/l) characterized these patients. Disseminated intravascular coagulopathy (DIC) was found in half the cases in which it was sought. In spite of aggressive antitumoral treatment, the course was disastrous with an average survival of 13.6 days. The most frequent causes of death were renal insufficiency or hemorrhagic diathesis. These data corroborate those cited in the literature since 1979, and are consistent with those reported by Antman during the period 1962-1979.
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PMID:Eleven cases of neoplastic microangiopathy. 269 95

The authors summarize the operative experiences performed with CO2 laser in 352 cases of oral surgery with special regard to the hemostatic effect. One of the patients suffered from hemophilia, 5 from thrombocytopenia and 5 from hypoprothrombinemia. Of the alterations to be eliminated 128 were especially inclined to hemorrhage (hemangioma, epulis, granuloma fissuratum). The operations were carried out with out-patients in local anesthesia. Due to the hemostatic effect of the laser the surgery could be performed in dry operative areas, the laser knife coagulates in the course of cutting the small vessels. Both in the group of patients with hemorrhagic diathesis and in the group of operation of alterations inclined to bleeding the experiences were highly favourable. No significant differences were found between the group of patients with hemorrhagic diathesis and other patients in the respect of the duration of operation, degree of bleeding, healing of the wound and complication. CO2 laser of high energy was found to be well applicable in the field of oral surgery owing to its excellent hemostatic effect, especially in operations where the patient or the alteration to be removed (possibly both) are disposed to bleeding.
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PMID:[Significance of the hemostatic effect of lasers in oral surgery]. 281 53

An otherwise healthy woman developed a hemorrhagic diathesis with fluctuating clinical symptoms and laboratory findings, but without thrombocytopenia, over 8 years. In periods of bad clinical condition, a platelet defect, characteristic of thrombasthenia, was found. In contrast to classic thrombasthenia, electrophoresis of the patient's platelet membranes revealed normal amounts of glycoproteins IIb alpha, IIb beta, and IIIa in the normal positions. Monoclonal antibodies, specific for GPIIIa and GPIIb/IIIa, respectively, bound normally to the P1A1-positive platelets from the patient. Although no antibody and no platelet function inhibitor were evident in the autologous plasma, an IgG1 antibody that was bound to the patient's platelets and was directed against GPIIb/IIIa could be demonstrated. After elution from the patient's platelets, this antibody immunoprecipitated GPIIb (both subunits), IIIa, and a 200-kilodalton (kd) band (probably undissociated GPIIb/IIIa complex) from solubilized normal platelets, but did not react with thrombasthenic platelets. Adding the eluate from the patient's platelets to normal platelet-rich plasma immediately caused concentration-dependent inhibition of adenosine diphosphate (ADP)-induced and collagen-induced aggregation and also strong inhibition of ADP-stimulated fibrinogen binding. Because it was very unlikely from the patient's medical history that the antibody was caused by alloimmunization, the hemorrhagic diathesis must be interpreted as acquired thrombasthenia due to an anti-GPIIb/IIIa autoantibody.
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PMID:Acquired thrombasthenia due to GPIIb/IIIa-specific platelet autoantibodies. 301 87

A 68-year-old male who suffered from thrombocytopenia and mild splenomegaly for 18 years was found to present agranular gray platelets on peripheral blood smear. Bone biopsy revealed a mild, diffuse, reticular fibrosis with no collagen, and electron microscopy of the platelets showed an absence of almost all the alpha-granules. Platelet thrombospondin and fibronectin analysed by SDS-polyacrylamide gel electrophoresis and Rocket immunoelectrophoresis were absent. Follow-up of 4 years showed the same parameters with no evidence of active myeloproliferative or dysmyelopoietic disorders. Hemorrhagic diathesis was limited to ecchymoses and postprostatectomy bleeding, necessitating platelet transfusion. This led us to conclude that our patient probably had a constitutional primary alpha-granule deficiency or gray platelet syndrome. This extremely rare defect has been described in less than 10 patients, all of them very young. Our observation shows that these patients may have a long, uneventful survival.
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PMID:Gray platelet syndrome in the elderly. 341 74

A 71-year-old male with disseminated intravascular coagulation (DIC) caused by abdominal aortic aneurysm was successfully treated surgically. He had aortic regurgitation, an old myocardial infarction, and nephrotic syndrome. The infrarenal part of the inferior vena cava, which was on the left side of the aneurysm, was temporarily transected during the surgical procedure. Preoperative heparin therapy was insufficient, but infusion of blood components during the operation and minimal dissection of the aneurysm were effective in controlling intraoperative hemorrhage. Hypofibrinogenemia and thrombocytopenia were normalized immediately after operation, and hemorrhagic diathesis was completely cured. In this case, the definitive treatment of DIC caused by an abdominal aortic aneurysm war removal of the lesion and the infusion of coagulation factors during the operation was effective in minimizing blood loss.
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PMID:Disseminated intravascular coagulation caused by abdominal aortic aneurysm. 341 54

The case is presented of a 26-year-old male patient suffering from chronic anemia since infancy. At age 12 (1972), congenital dyserythropoietic anemia (CDA) was diagnosed which could not be grouped with one of the three known variants of CDA. From onset the disease was complicated by thrombocytopenia with severe hemorrhagic diathesis. After splenectomy (1972) an extremely enlarged accessory spleen was removed in 1985 disclosing, histologically, excessively developed extramedullary hematopoiesis. Since bone marrow biopsy showed massive hyperplasia, the cellular phase of a myeloproliferative syndrome could not be excluded by histology alone.--Only a few cases of CDA with involvement of granulocytes and megakaryocytes have been reported so far. It is not clear whether or not they should be classed with CDA. In any event, involvement of granulopoiesis and/or thrombopoiesis indicates a genetic lesion of very early precursors, perhaps stem cells. It is proposed that such variants would be more correctly designated "congenital dyshematopoietic syndromes".
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PMID:[Atypical congenital dyserythropoietic anemia]. 342 66

We report the case of a 38-year-old woman with hemorrhagic diathesis. Since early childhood she has suffered from epistaxis, gingival bleeding, ecchymoses and, since puberty, very frequent menorrhagia. Prolongation of bleeding time and thrombocytopenia (100,000 platelets/microliter) with giant platelets were observed. Since idiopathic thrombopenic purpura was suspected, splenectomy was performed. Neither this nor steroid treatment caused any improvement. The patient was able to give birth to an unaffected child, but delivery was followed by a major hemorrhage. In 1986, hysterectomy was considered because of frequent menorrhagia and, therefore, the patient's hemostasis was reinvestigated. The aforementioned abnormalities were confirmed and complementary examinations by electron microscope revealed giant platelets without granular abnormalities. While von Willebrand factor was normal, ristocetin agglutination was defective and analysis of platelet membrane glycoproteins showed absence of glycoprotein Ib. - These observations prompted the diagnosis of Bernard-Soulier syndrome. The study of the family demonstrated that 6 family members were heterozygote. This is believed to be the first large Bernard-Soulier family reported in Switzerland.
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PMID:[Bernard-Soulier syndrome in a Swiss family]. 342 69

Septicemia is frequently accompanied by changes in the plasmatic as well as cellular coagulation systems and by microclot formation. The occurrence of a hemorrhagic diathesis and microthrombosis is best explained by the syndrome disseminated intravascular coagulation (= consumption coagulopathy). Disseminated intravascular coagulation can be initiated by different agents and by different pathways. The activation of coagulation by endotoxin is well studied; it is mediated by synthesis of tissue factor by monocytes and endothelial cells. The formation of microthrombi is caused by the precipitation of circulating soluble fibrin under the influence of localizing factors, and it is observed under conditions of reduced fibrinolysis activation. Furthermore, thrombocytopenia, thrombocytopathy and endothelial cell damage caused by a direct effect of the toxic agent contribute to the bleeding diathesis.
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PMID:[Sepsis and blood coagulation]. 371 2


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