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Clinical manifestations of dengue virus infection vary from unspecified fever, dengue fever (DF) and dengue hemorrhagic fever (DHF). The fundamental difference in the diagnosis between DF and DHF is plasma leakage, hypotension, thrombocytopenia and hemorrhagic diathesis in DHF. The objectives of the study were to determine the lowest platelet, haematocrit increase, and TNF-α levels in DF and DHF patients as an indication of severity of dengue virus infection. The cross-sectional study was conducted by taking 54 blood samples of patients aged 26-45 years who were infected by dengue virus and grouped into two groups: DF patient group (27 blood samples) and DHF group (27 blood samples). The lowest platelets and hematocrit rise were determined by Hematology Analyzer and the TNF-α levels were determined by ELISA. The data obtained were statistically analyzed by independent Mann-Whitney test. The results showed that the lowest mean platelet counts of DF patients were significantly (p

Acute promyelocytic leukemia often manifests with hemorrhagic diathesis, thrombotic events being much rarer. This is the case of a 59-year-old patient with thrombotic cerebro-vascular complications as the onset manifestation of acute promyelocytic leukemia.

Dammar resin is a natural food additive and flavoring substance present in many foods and drinks. The present study evaluates the chronic toxicity and carcinogenicity of dietary dammar resin in F344 rats. Dietary concentrations in the 52-week chronic toxicity study were 0, 0.03, 0.125, 0.5, or 2%. The major treatment-related deleterious effects were body weight suppression, increased relative liver weight, and low hemoglobin levels in males and females. Foci of cellular alteration in the liver were observed in the male 2% group, but not in any other group. The no-observed-adverse-effect level for chronic toxicity was 0.125% for males (200.4 mg/kg b.w./day) and females (241.9 mg/kg b.w./day). Dietary concentrations in the 104-week carcinogenicity study were 0, 0.03, 0.5, or 2%. Dammar resin induced hemorrhagic diathesis in males and females, possibly via the inhibition of extrinsic and intrinsic coagulation pathways. Incidences of hepatocellular adenomas and carcinomas were significantly increased in the male 2% group, but not in any other group. In the 4-week subacute toxicity study, the livers of male rat-fed diet-containing 2% dammar resin had increased levels of protein oxidation and increased the expression of two anti-apoptotic and seven cytochrome P450 (CYP) genes. There was also an increased tendency of oxidative DNA damage. These findings demonstrate that dammar resin is hepatocarcinogenic in male F344 rats and underlines the roles of inhibition of apoptosis, induction of CYP enzymes, and oxidative stress in dammar resin-induced hepatocarcinogenesis.

WOS: 000316239000008, PubMed ID: 24385752, Objective: von Willebrand disease (vWD) is the most common hereditary bleeding disorder. The purpose of this investigation was to determine the prevalence of vWD among adolescents in Izmir and to assess the sensitivity and specificity of PFA-100 as a screening method in detecting this disease. Material and Methods: Our study was conducted on adolescents in the city of Izmir between October 2006 and March 2007. A total of approximately 1500 high school students between 14 and 19 years of age were planned to be included in the investigation. Survey forms prepared for assessing hemorrhagic diathesis were completed by 1339 individuals (512 males, 827 females). The necessary laboratory tests were performed after having obtained written informed consent from 40 individuals suspected to have hemorrhagic diathesis. Results: Based on the von Willebrand factor antigen (vWF:Ag) and ristocetin cofactor activity (vWF:RCo) levels and bleeding symptoms, vWD type-1 was diagnosed in 14 individuals (4 males, 10 females; prevalence: 1.04%). The most common bleeding symptom in these patients was found to be epistaxis (10/14). Screening with PFA-100 revealed prolongation in both cartridges (Col/ADP and Col/Epi) in 3 of the 14 patients. PFA-100 was determined to exhibit 21.4% sensitivity and 100% specificity in the diagnosis of vWD. Conclusion: The PFA-100 device was found to have high specificity but to have exhibited low sensitivity. Therefore, its utilization as a screening test may be problematic in patients with mild type-1 vWD. Specific tests (vWF:RCo, vWF:Ag) are required for the definite diagnosis of vWD. However, further studies with a large number of patients are needed.

The presence of asymptomatic antiphospholipid antibodies (aAPA) creates many difficult diagnostic and clinical problems - they might be a cause either of incorrect hemorrhagic diathesis recognition or an unnecessary anticoagulant therapy. Patients with aAPA should be counseled individually regarding potential thrombotic and/or obstetric complications. An increased risk of these complications is particularly high when lupus anticoagulant (LAC) and IgG anti-beta2 glycoprotein antibodies coexist. The approaches to the diagnosis and management of treatment of patients with aAPA are also discussed.

Ethylenediaminetetraacetic acid (EDTA)-dependent pseudothrombocytopenia (PTCP) is the phenomenon of a spurious low platelet count due to antiplatelet antibodies that cause platelet clumping in blood anticoagulated with EDTA. The aggregation of platelets in EDTA-dependent PTCP is usually prevented by other anticoagulants, such as sodium citrate or heparin. EDTA-dependent PTCP has never been associated with hemorrhagic diathesis or platelet dysfunction. In this article, a 10-year-old boy with EDTA- and heparin-dependent PTCP is presented because of rare presentation. We report that EDTA and heparin can induce platelet clumping, and thus spuriously low platelet counts. However, aggregation of platelets was not detected in blood samples with sodium citrate, and platelet count was normal.

Excerpt In 1926 von Willebrand1described a familial bleeding tendency affecting both sexes and characterized by a prolonged bleeding time, accompanied by a normal coagulation time and platelet coun...

Eine 57-jahrige Patientin mit Belastungsdyspnoe, Schwache sowie subkutanen Blutungen an beiden Oberschenkeln wurde zur stationaren Abklarung eingewiesen. Es bestand eine ausgepragte Gingivitis. Rontgenologisch, sonographisch, elektro- und echokardiographisch ergaben sich keine diagnostisch wegweisenden Befunde. Im Labor war der Vitamin-C-Serumspiegel deutlich erniedrigt. Bei gezieltem Befragen gab die Patientin an, aus Angst vor allergischen Reaktionen (Migranesymptomatik) im Rahmen einer fruher diagnostizierten Nahrungsmittelallergie Vitamin-C-haltige Nahrungsmittel zu meiden. Die therapeutische Substitution von Vitamin C fuhrte zu einer klinischen Befundbesserung. Differentialdiagnostisch muss auch heute das Krankheitsbild eines Skorbuts erwogen werden. Insbesondere bei pathologisch veranderten Ernahrungsgewohnheiten kann ein alimentarer Vitamin-C-Mangel auftreten.

The present study has intended to contribute to the elucidation of the pathogenic mechanisms, involved in the thrombocytopenia and in the bleeding diathesis seen in the course of Leptospirosis. The group of cases included in the present prospective study consisted of 30 patients with Leptospirosis, admitted to the Infectious and Parasitic Diseases Ward, Hospital das Clínicas, Faculty of Medicine, University of São Paulo. The following possible mechanisms of thrombocytopenia have been considered and therefore investigated: platelet consumption, due to disseminated intravascular coagulation; immune-mediated platelet destruction, due to platelet-associated antibodies and an inhibited platelet production in the bone marrow. Thrombocytopenia occurred in 86.6% of 30 patients and did not seem to be immune-mediated by platelet-associated antibodies. Furthermore it did not seem to be due to a disseminated intravascular coagulation consumption. Although there was a statistically-significant correlation between bone marrow platelet production and platelet counts we think that the static microscopic examination of a bone marrow aspirate cannot accurately depict the dynamic mechanisms of platelet production when these cells are being consumed in peripheral blood. Vasculitis should be considered as the most important factor for the pathogenesis of the bleeding disturbances in Leptospirosis. However, we believe that thrombocytopenia, uremia and coagulation disorders, individually or as a group, should be included among the contributing factors that lead to and worsen bleeding episodes, which represent the leading cause of death in this disease. O propósito do presente trabalho é colaborar para o estudo da patogenia da plaquetopenia que ocorre na Leptospirose. A pesquisa foi feita de maneira prospectiva e o grupo de casos foi constituído por 30 pacientes internados com hipótese diagnostica de Leptospirose na Clínica de Doenças Infecciosas e Parasitárias do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo. Investigou-se a possibilidade de haver consumo de plaquetas por coagulação intravascular disseminada, ou a possibilidade de destruição periférica de plaquetas por anticorpos e, se poderia haver inibição da produção de plaquetas em nível medular. Para a investigação desejada foram utilizados os seguintes exames: contagem de plaquetas, tempo de protrombina, tempo de recalcificação, tempo de trombina, tempo de tromboplastia parcial ativada, dosagem do fibrinogênio, dosagem do fator V, dosagem do fator VIII, dosagem dos produtos de degradação da fibrina, dosagem da antitrombina III, mielograma e pesquisa de anticorpos antiplaquetas. Foram ainda estudados o hemograma, a dosagem de uréia, a dosagem de creatinina, a dosagem das enzimas hepáticas (aspartatoaminotransferase, alaninaaminotransferase, desidrogenase láctica, gamaglutamiltranspeptidade e fosfatase alcalina), e a dosagem das bilirrubinas. A análise dos dados obtidos no presente trabalho permitiu-se chegar às seguintes constatações e conclusões: 1ª) A plaquetopenia é freqüentemente encontrada na forma grave de Leptospirose ocorrida em nosso meio (86,6%). 2ª) A plaquetopenia da Leptospirose não parece ser mediada por anticorpos antiplaquetas. 3ª) A avaliação dos dados obtidos não mostrou haver evidências clínicas e laboratoriais de ocorrência de coagulação intravascular disseminada. 4ª) Verificou-se existência da relação de dependência entre a plaquetogênese medular e a contagem de plaquetas no sangue periférico (P = 0,0261). A possibilidade de haver inibição da plaquetogênese medular por algum produto bacteriano (toxina) não pode ser totalmente afastada, porém acreditamos que o exame estático da medula óssea não pode dar-nos uma idéia precisa do mecanismo dinâmico da formação de plaquetas na presença de "consumo periférico". 5ª) Embora a plaquetopenia possa representar um fator contribuinte para a síndrome hemorrágica, não chegamos a uma diferença estatisticamente significativa entre a contagem das plaquetas nos pacientes plaquetopênicos que sangraram e nos que não apresentaram sangramento. 6ª) Na maioria dos casos (86,3%) a normalização da contagem das plaquetas ocorreu no período de sete dias após a internação. 7ª) Não houve diferença significativa entre as médias dos tempos de normalização da contagem de plaquetas nos pacientes que apresentaram e nos que não apresentaram sangramento. 8ª) Houve diferença significativa, entre as médias das contagens das plaquetas nos pacientes de níveis séricos menores e os níveis séricos mais elevados de uréia, sendo maior no primeiro grupo (t22 = 1,818 > t22:0.05 = 1,717). 9ª) A média do nível sérico dos pacientes que apresentaram sangramento foi maior do que a média do nível sérico de uréia dos pacientes que não sangraram, podendo-se afirmar que a uremia contribui para agravar o quadro hemorrágico na Leptospirose. A vasculite deve ser considerada como fator mais importante na patogênese dos distúrbios hemorrágicos da Leptospirose1,2,8,23, porém, acreditamos que a trombocitopenia, a uremia e os distúrbios da coagulação, isoladamente ou em conjunto, devem ser incluídos entre os fatores que agravam o quadro hemorrágico o qual representa hoje a principal causa de óbito na doença.

The current status of knowledge of the uremic hemorrhagic diathesis is reviewed. Discussions of clinical features, classification and pathogenesis, retention products and hemostatic defects, and therapy are included.

Peptic ulcer disease remains the most common upper GI hemorrhagic diathesis, except, of course, for esophageal varices. But mucosal lesions such as vascular ectasias and superficial ulcers of Dieulafoy's disease are being increasingly recognized. Therapeutic endoscopic techniques, notably laser coagulation and injection sclerotherapy, may obviate surgery.

FIBRINOLYTIC therapy is a major advance in the treatment of occlusive vascular disease. Problems remain, however, including resistance to fibrinolytic therapy, delays in reperfusion, reocclusion after successful thrombolysis, and serious hemorrhage.1 2 3 Increasing evidence indicates that platelets have an important role in both delaying reperfusion and mediating reocclusion. In addition, preliminary data suggest that some thrombi resist lysis because they are rich in platelets and that platelet dysfunction contributes to the hemorrhagic diathesis associated with thrombolytic therapy. It is worthwhile, therefore, to review the complex interrelations between platelets and fibrinolysis, with emphasis on the therapeutic potential (and risks) of combining thrombolytic . . .

Myelodysplastic syndrome is a blood disorder characterized by anemia, neutropenia, thrombocytopenia, and morphological abnormalities of blood cells. And the bone marrow is normo-or hypercellular.A 54-year-old male with this syndrome was referred to our clinic, complaining of oral bleeding. All wound sealings were successfully performed using the fibrin adhesion system (Beriplas® P) for local hemostasis. Excellent results were obtained in the present case.

Immunoglobulin therapy combined with prednisolon proved to be an appropriate therapy of acquired VW syndrome in order to enable invasive diagnostic procedures but not sufficient in order to control bleeding disorders.

Until recently, anti-platelet/coagulation therapy had not been recommended for patients with cirrhosis. Although venous thrombosis is one of the representative complications of cirrhosis and ischemic disorders associated with atherosclerosis are not infrequent in cirrhotic patients, many clinicians have tended to hesitate to introduce anti-platelet/coagulation therapy to their patients. Undoubtedly, this is due to the increased risk of hemorrhagic diathesis in cirrhotic patients. However, accumulating evidence has revealed the benefits of anti-platelet/coagulation therapy for cirrhotic patients. In addition to the safety of the therapy carried out against cardiovascular diseases in cirrhotic patients, some clinical data have indicated its preventive effect on venous thrombosis. Moreover, the efficacy of anti-platelet/coagulation therapy against cirrhosis itself has been demonstrated both clinically and experimentally. The conceptual basis for application of anti-platelet/coagulation therapy against cirrhosis was constructed through two pathologic studies on intrahepatic thrombosis in cirrhotic livers. It may be better to use thrombopoietin-receptor agonists, which have been tested as a treatment for cirrhosis-related thrombocytopenia, in combination with anti-platelet drugs to reduce the risk of venous thrombosis. During the last decade, the World Journal of Gastroenterology, a sister journal of World Journal of Hepatology, has been one of the main platforms of active discussion of this theme.

Factor XIII inhibitor, a rare cause of coagulopathy, is usually not detected by screening tests, e.g. activated partial thromboplastin time (aPTT) and thromboplastin time (PT) (1). The following report describes the case of a patient with known Coombs-reactive red cell autoantibodies. Factor XIII inhibitor was detected with delay because severe hemorrhagic diathesis was initially attributed to heavy trauma.

A heterozygote for congenital deficiency of plasma plasmin inhibitor had hemorrhagic episodes repeatedly after the age of 79. Before the age of 79, he had not exhibited any hemorrhgic tendency and did not have abnormal bleeding even after surgical operations. Although heterozygotes for congenital deficiency of this inhibitor usually have no or only a mild hemorrhagic tendency, this case suggests that they may exhibit severe hemorrhagic tendency when they reach advanced ages because of age-related vascular changes producing hemostatic imbalance.

A study of 565 Puerto Rican patients with storage pool deficient (SPD) Hermansky-Pudlak syndrome (HPS) demonstrated that most HPS patients had minor bleeding episodes while others had repeated, severe hemorrhagic episodes requiring transfusion. The severity of bleeding in these latter patients could not be attributed to their SPD alone. As swine with SPD platelets and low von Willebrand factor antigen (vWF:Ag) have more severe hemorrhages than pigs with either defect alone, 146 albino patients and 46 normally pigmented patients were examined for their level of vWF:Ag. The risk of SPD HPS patients having severe, repeated bleeding episodes increased when vWF:Ag fell below 70 U/dL. Family studies indicated that low vWF:Ag levels were more frequently associated with O blood group than from a gene suppressing production or release of vWF1. HPS patients should be tested for vWF:Ag levels.

Patients with acute or chronic renal failure exhibit an increased tendency to bleed. The severity of the hemorrhagic diathesis is not always correlated with the severity of uremia. Hemorrhagic episodes remain a major contributory factor to the morbidity and mortality associated with renal failure (1).

A case is reported in which progressive liver symptoms with rise in bilirubin concentration, hemorrhagic diathesis, and signs of portal hypertension developed three years before death in liver coma. The pathologic and neuropathologic findings are described. The case was clarified after dimethylnitrosamine was demonstrated in food intended for the patient and after it was established that small amounts of nitrosamine could have been repeatedly ingested by the patient over a period of years. Comparable cases of human dimethylnitrosamine poisonings published in the literature are presented. The relatively typical morphologic alterations in the liver are described. Problems involved in the histological interpretation of such liver changes as well as the forensic conclusions to be drawn are discussed.

Hemorrhagic diathesis was investiqated in 147 cases consisting of 12 acute hepatitis, 22 chronic hepatitis, inactive form, 27 chronic hepatitis, active form, 43 liver cirrhosis, 7 cholecystopathy and 36 other miscellaeous hepato-biliary diseases.Eight labolatory tests detecting bleeding tendency were performed: bleeding time clotting time, clot retraction, Rumpel-Leede phenomenon, platelet count, thrombotest, normotest and plasma prothrombin time. Bleeding time longer than 5min. was observed in 46 out of 120 (33%) cases, clotting time longer than 15min.; in 1 out of 140 (1%), incomplete clot retraction; in 29 out of 132 (22%), over two positive Rumpel-Leede phenomenon; in 24 out of 136 (18%), platelet count less than 120, 000; in 34 out of 146 (23%), thrombotest less than 70%; in 85 out of 135 (63%), normotest less than 70%; in 35 out of 70 (50%) and plasma plothrombin time longer than 15sec.; in 27 out of 137 (20%).In liver cirrhosis, following tests showed abnormal values more often than in other diseases: Rumpel-Leede phenomenon (14 out of 41 (34%) cirrhosis, 10 out of 95 (11%) other diseases), platelet count (20 out of 43 (47%), 14 out of 103 (14%)), thrombotest (35 out of 41 (85%), 50 out of 94 (53%)), normotest (24 out of 28 (86%), 11 out of 42 (26%)), and plasma prothrombin time (19 out of 42 (45%), 8 out of 95 (8%)). Clot retraction is one of the most reliable test to avoid the bleeding after liver biopsy. There is no difference, however, in various liver diseases of the impaired retractions rates.Hemorrhagic diathesis was often observed in acute hepatitis and chronic hepatitis as well as in liver cirrhosis. Therefore, previous to peritoneoscopy and liver biopsy, it is necessary to check hemorrhagic diathesis. And if there is bleeding tendency, it should be treated beforehand.

The discovery of a severe factor VII deficiency with increased bleeding tendency resulted in investigations of 22 members of the family. In the propositus and in two of his siblings a severe hypoproconvertinemia was demonstrated, a partial deficiency was found in ten persons. Studies of the family confirmed that this disorder is transmitted by an autosomal gene with intermediate penetrance. The mutated gene produces a severe deficiency in the homozygote and a partial deficiency in the heterozygote. The parents of the homozygote patients were consanguineous. Hemorrhagic diathesis was noted only in patients with a severe factor VII deficiency. Causes for the variability of the clinical manifestations are discussed.

A carrier of hemophilia B was found to have an unusually low factor IX level of 13 per cent. Her history of previous bleeding and the hospital course following elective dental extractions were consistent with a mild hemorrhagic diathesis. The patient is a member of a rare kindred of hemophiliacs. The mean level of factor IX in 12 carriers in this kindred was 42 per cent, with a range of 13 to 100 per cent. This patient represents the sixth reported case in which a female carrier of factor IX deficiency was symptomatic.

SummaryIntravenous heparin will correct the enhanced thromboplastin generation of oxalated plasma obtained from the human arteriosclerotic patient. It will not,however, correct the deficiency of antithromboplastin activity in non-oxalated plasma obtained from the pathological subject. This deficiency of antithromboplastin disappears if oxalate ion is introduced into the heparinized plasma.

A case of gingival hemorrhage secondary to uremia has been reported, and the unsuccessful attempt at local control has been described. The probable mechanism of the hemorrhagic diathesis of uremia has also been described. This bleeding tendency is due to an altered pathway of urea metabolism with consequently increased levels of GSA, which inhibits platelet function. In view of the increased number of persons with chronic renal disease who are surviving as a result of repeated dialyses on the artificial kidney, the dentist must be acutely aware of the possible consequences of uremia.