Chemotherapy-induced thrombosis.

Viral infections are associated with coagulation disorders. All aspects of the coagulation cascade, primary hemostasis, coagulation, and fibrinolysis, can be affected. As a consequence, thrombosis and disseminated intravascular coagulation, hemorrhage, or both, may occur. Investigation of coagulation disorders as a consequence of different viral infections have not been performed uniformly. Common pathways are therefore not fully elucidated. In many severe viral infections there is no treatment other than supportive measures. A better understanding of the pathophysiology behind the association of viral infections and coagulation disorders is crucial for developing therapeutic strategies. This is of special importance in case of severe complications, such as those seen in hemorrhagic viral infections, the incidence of which is increasing worldwide. To date, only a few promising targets have been discovered, meaning the implementation in a clinical context is still hampered. This review discusses non-hemorrhagic and hemorrhagic viruses for which sufficient data on the association with hemostasis and related clinical features is available. This will enable clinicians to interpret research data and place them into a perspective.

/pdf/review-viral-infections-and-mechanisms-of-thrombosis-and-3v0bpkxwua.pdf

Review: Viral infections and mechanisms of thrombosis and bleeding.

Background
The incidence and determinants of hepatic decompensation have been incompletely examined among HIV/hepatitis C virus (HCV)-coinfected patients in the antiretroviral therapy (ART) era, and few studies have compared rates of outcomes to those of patients with chronic HCV alone.

/pdf/hepatic-decompensation-in-antiretroviral-treated-patients-co-310l5v5387.pdf

Hepatic Decompensation in Antiretroviral-Treated Patients Co-Infected With HIV and Hepatitis C Virus Compared With Hepatitis C Virus–Monoinfected Patients: A Cohort Study

Thrombosis and disseminated intravascular coagulation (DIC) are common complications in cancer. Patients with malignancy have a prothrombotic state due to the ability of almost all type of cancer cells to activate the coagulation system. However, none of the haemostatic markers of coagulation has any predictive value for the occurrence of the thrombotic events in one individual patient. The pathogenesis of the prothrombotic state in cancer is complex and, probably, multifactorial. Prothrombotic factors in malignancy include the tumour production of procoagulants (i.e., tissue factor (TF) and cancer procoagulant (CP)) and inflammatory cytokines, and the interaction between tumour cells and blood (i.e., monocytes/macrophages, platelets) and endothelial cells. Other mechanisms of thrombus promotion include some general responses of the host to the tumour (i.e., acute phase, inflammation, angiogenesis), decreased levels of inhibitors of coagulation, and impaired fibrinolysis. In addition, the prothrombotic tendency of cancer patients is enhanced by anticancer therapy, such as surgery, chemotherapy, hormone therapy and radiotherapy, by indwelling central venous catheter, and by haemodinamic compromise (i.e., stasis). However, not all of the mechanisms allowing the prothrombotic state of cancer are entirely understood. Therefore, it is presently difficult to rank the relative weight of these multiple interactions on the basis of the well-recognised clinical evidences of enhanced thrombotic episodes in patients with cancer. In this review we attempt to describe the current proposed mechanisms for the pathogenesis of the prothrombotic state in cancer patient. A better understanding of these mechanisms could help clinicians in the developments of more targeted treatment to prevent thromboembolic complications in cancer patient.

The prothrombotic state in cancer: pathogenic mechanisms.

Background: The exact incidence of venous thromboembolism (VTE) in cancer patients is unknown, partly because of confounding factors. Prophylactic treatment is warranted in surgical patients with cancer because of a high incidence of VTE. We performed a retrospective study to evaluate if the same applies for cancer patients treated with chemotherapy. Methods: The medical records of 206 consecutive patientswithmalignancy,treatedwithchemotherapy,were identified. The kind of malignancy and chemotherapeutic treatment were recorded, as was the date of treatment. The records were reviewed for other risk factors for VTE, and were searched for proved deep venous thrombosis or pulmonary embolism. Results: Of those 206 patients, 15 (7.3%) had proved VTE during or within 3 months after chemotherapeutic treatment. The annual incidence was 10.9%. The incidence of VTE was specifically high in the 39 patients treated with a combination of fluorouracil and leucovorin calcium because of colorectal cancer (6 [15%] of the patients were affected). The occurrence of VTE in the latter group of patients was not influenced by factors such as surgery, central venous catheters, or tumor load. Conclusions: The annual incidence of VTE in patients treated with chemotherapy was high, specifically in patients with colorectal cancer treated with fluorouracilleucovorin. If these observations are confirmed, trials to evaluate the use of prophylactic anticoagulant treatment should be conducted.

Symptomatic Venous Thromboembolism in Cancer Patients Treated With Chemotherapy

Recent reports have documented an increase of thrombotic complications in patients with carcinoma of the breast receiving chemotherapy regimens containing cyclophosphamide, methotrexate, and 5-fluorouracil. The authors studied blood from nine such patients screening for abnormalities that might predispose to thrombosis or indicate that the coagulation cascade had been activated. Six of the patients were in the adjuvant setting, and three had metastatic disease. Samples were collected from each patient before, during, and after completion of the chemotherapy in question. In each patient a statistically significant decline in functional protein C activity (P = 0.001) was demonstrated at midtherapy. In seven of nine patients functional protein C level normalized after the cessation of therapy. No other positive results were found. The authors conclude that the combination of cyclophosphamide, methotrexate, and 5-fluorouracil, when administered to patients with a diagnosis of carcinoma of the breast, causes a reversible decline in the activity of protein C.

Acquired protein C deficiency in patients with breast cancer receiving cyclophosphamide, methotrexate, and 5-fluorouracil.

True thymic hyperplasia is rare in adults. The authors have encountered this entity in two patients who were deemed disease-free following combination chemotherapy for malignant disease. It cannot be assumed that the development of a mediastinal mass or its persistence following chemotherapy is due to recurrent or residual disease. The interrelationship between the immunosuppressive effects of neoplasia and chemotherapy with the resultant thymic overgrowth remains to be clarified.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%2819851001%2956%3A7%3C1526%3A%3AAID-CNCR2820560709%3E3.0.CO%3B2-X

Thymic hyperplasia following successful chemotherapy. A report of two cases and review of the literature

AMINOCAPROIC acid is a useful agent in the management of hemophilia, particularly following extensive dental manipulations. The drug is widely used, in large measure because toxic reactions, including gastrointenstinal disturbances, dizziness, tinnitus, malaise, headache, rash, and conjunctival and nasal suffusion, are mild and rarely encountered. We report the case of a patient who experienced several of these side effects after aminocaproic acid infusion, then promptly progressed to a grand mal seizure, a toxic reaction not previously described. Report of a Case A 32-year-old man with mild hemophilia (factor VIII levels ranging from 10% to 15%) was admitted for dental scaling and prophylaxis. The patient's hemophilia had been identified two years prior to this admission, when he had bled excessively after dental extraction. At that time, von Willebrand's disease had been excluded by a normal bleeding time and ristocetin aggregation study. He had a long history of dental problems and had

Seizure after infusion of aminocaproic acid.

A 63-year-old man presented with fever, easy bruisability, splenomegaly and pancytopenia. Bone marrow aspiration was unsuccessful, and marrow biopsy revealed crowding by sheets of mononuclear cells; a diagnosis of leukemic reticuloendotheliosis (LRE) was made and the patient underwent splenectomy. There was no hematologic improvement, and the patient continued to have a significant requirement for erythrocytes and platelet transfusions. Within two months of beginning oxymetholone therapy (50 mg orally three times a day) the patient's platelet count had normalized, followed by improved erythrocyte and leukocyte counts. When the drug was discontinued, the peripheral blood counts deteriorated drastically; he again demonstrated hematologic improvement when oxymetholone therapy was reinstated. We feel that by demonstrating a hematologic response to oxymetholone, relapse when it was withdrawn, and another remission upon readministration, that we have provided stronger evidence than previously reported for the efficacy of this drug in LRE.

A case of leukemic reticuloendotheliosis responding to oxymetholone.

We investigated the etiology of thrombocytopenia, with or without platelet thrombi, occurring while patients are receiving parenteral heparin We used two in vitro methods to detect possible humoral factors in the sera of patients who became thrombocytopenic while receiving heparin In the presence of heparin, four of four such patients' serum caused platelet aggregation Only serum from the patient most severely affected clinically caused release of platelet factor 3 (PF3) All control sera gave negative results by both methods We propose that platelet aggregation studies may be a sensitive and reliable method of confirming that thrombocytopenia occurring during heparin therapy is due to a humoral factor requiring the presence of heparin

In vitro detection of heparin-induced humoral antiplatelet activity.

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