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Intriguingly treatment uti infection generic thyroxine 75 mcg free shipping, nonpathogenic species of African trypanosomes may be killed by the human high-density-lipoprotein particles astonishingly subverting a parasite pathway for heme uptake schedule 8 medicines cheap thyroxine 200 mcg line. The complex of haptoglobin-related protein and apolipoprotein L-1 (apoL1) are taken up into the parasite by a parasite glycoprotein receptor medicine vs dentistry buy 100mcg thyroxine visa, which binds the haptoglobin-hemoglobin complex treatment ulcer buy thyroxine australia. In children the disease is more rapidly progressive, and epileptic seizures and psychomotor retardation are the principal features of the disease. Hematologic and Laboratory Features the main hematologic features are a normocytic, normochromic anemia and moderate thrombocytopenia. Hemodilution, hemolysis, and dyserythropoiesis or ineffective erythropoiesis all contribute to the pathogenesis. Hemolysis may be caused directly by lytic factors released by trypanosomes or indirectly by deposition of immune complexes and subsequent clearance of coated erythrocytes. In vitro studies have suggested that the variant surface glycoprotein from trypanosomes may be shed and taken up onto the erythrocyte membrane, where antibody and complement deposition could contribute to hemolysis. Bone marrow response is inadequate, and although the nature of the defect is unclear, there is failure in incorporation of iron into erythroid precursors as is seen in many forms of the anemia of chronic disease. Trypanosomes multiply in the lymphatic system for 6 to 14 days before causing patent infection in the blood, characterized by waves of parasitemia and fever. Serum IgM levels may be elevated to four times normal and with raised IgG levels cause an increased erythrocyte sedimentation rate. The white blood cell count may be elevated with monocytosis, lymphocytosis, and circulating plasma cells, but eosinophilia is absent. Plasma cells with eosinophilic inclusion or Mott morular cells may occasionally be seen. Petechia and purpura may be secondary to vascular injury, thrombocytopenia, and a complex but poorly defined coagulopathy. Functionally both thrombosis and fibrinolysis are increased, and fibrin degradation products (D dimers) are raised in acute disease, and in T. However, anemia and endocrine dysfunction, including amenorrhea, reduced libido, and impotence become apparent. Aspirated fluid can be examined under a coverslip, and motile trypanosomes are typically seen at the edges of the coverslip. Trypanosomes can be seen in wet smears, where a drop of blood is placed on a slide and examined under a coverslip. Alternatively, thick or thin Giemsa-stained blood films are made as for malaria diagnosis. The sensitivity of detection with these methods ranges from 104 per mL for wet smears to 102 per mL for ion-exchange columns and centrifugation. Inoculation of the aspirate or samples into susceptible animals or in vitro culture has been used to detect low-level parasitemia. Trypanosomes may be detected in lymph node aspirates and in wet and thick blood smears. Serology Serologic tests are used for passive population screening in control programs (for review see reference 201). It is quite sensitive (>95%) but lacks specificity due to cross-reactivities with animal Trypanosoma spp. A single organism is seen in this sample taken from cerebrospinal fluid filtered in a "minicolumn. Some patients may have false-negative results using this test if they are infected by parasites that do not express this variant antigen. At 1: 16 serum dilution, test specificity was 99%, whereas sensitivity ranged from 83. If neuropathy is suspected, melarsoprol should be stopped immediately and thiamine (100 mg, three times a day) given until symptoms subside. Hemolytic anemia, agranulocytosis, and thrombocytopenia have been reported as side effects. Combination therapies of the antitrypanosomal drugs nifurtimox and eflornithine and also the combination of melarsoprol and nifurtimox are under trial for the treatment of second-stage disease to increase the efficacy of treatment and to overcome increasing drug resistance. Asymptomatic or early-stage patients with trypanosomiasis are clearly a threat to the blood supply. Patients are excluded in the United Kingdom, Europe, and North America by the general donor queries relating to fever and constitutional symptoms. Occasional patients may become severely ill and have complex hematologic abnormalities. Treatment Treatment of trypanosomiasis depends on the subspecies of trypanosome present. The drugs may be difficult to source and are toxic, so treatment requires expert help. Hematologic side effects include neutropenia, and more general side effects include hypotension, hypercalcemia, hyperkalemia, renal failure, and hyperglycemia. It causes dose-dependent bone marrow suppression with anemia, neutropenia, and thrombocytopenia in the majority of patients. Melarsoprol is a trivalent organic arsenical compound and is more toxic but cheaper than eflornithine. Melarsoprol causes a secondary encephalopathy in 5% to 10% of treated cases and is fatal in half of these. Prior treatment of blood-stage disease with pentamidine may reduce antigen levels and possibly adverse events. This flagellated protozoon is transmitted by the triatomine insects, the reduviid bugs.

Disulfide bonds (-S-S-) critical to the integrity of the two-chain zymogens or active forms are presented treatment brown recluse spider bite cheap thyroxine. The Ca2+ binding association with this modification is also the basis for the anticoagulant activity of sodium citrate medication 3 checks purchase discount thyroxine on line, a calcium chelator treatment uti infection order thyroxine 100mcg overnight delivery, found in the blue top vacuum tubes used for clinical laboratory testing of clotting activity medicine zoloft thyroxine 50mcg fast delivery. The level of inhibition achieved with the same dose of warfarin varies among patients. Increased sensitivity to warfarin has been identified in patients when started after surgery. Each complex is composed of a serine protease enzyme, a cofactor that functions as a surface receptor or enhancer for the enzyme Ca2+, and a negatively charged membrane surface provided by activated or damaged cells. Three procoagulant complexes (extrinsic tenase, intrinsic tenase, and prothrombinase) and one anticoagulant complex (protein Case) are illustrated. Tissue factor is composed of an extracellular domain (residues 1-219), a transmembrane domain (residues 220-242), and a cytoplasmic domain (residues 243-263). Thrombomodulin is an endothelial cell-surface glycoprotein composed of five distinct domains. Thrombomodulin functions as the cofactor in the protein Case complex and assists in the generation of activated protein C. Presentation of tissue factor to the circulation is the event that triggers the primary procoagulant pathway of coagulation31-33. There are no known mutations or deficiencies of human tissue factor, and tissue factor deletion in mice is lethal during embryonic development,34 leading to the speculation that tissue factor is essential for life. The commonly accepted sources of functional tissue factor are the subendothelium exposed upon vascular damage or monocytes stimulated by cytokines. However, there is controversy regarding the source and presentation of active tissue factor and whether functional tissue factor circulates in blood in healthy and pathologic states. Thrombomodulin is a high-affinity receptor for all thrombin forms and acts as a cofactor for the thrombin-dependent activation of protein C. Thrombomodulin activity on the surface of endothelial cells is decreased by inflammatory cytokines,57,58 and this decrease may contribute to the hypercoagulation characteristic of inflammatory states. Von Willebrand factor von Willebrand factor has several key roles in coagulation and is also contained in the -granules of human platelets. Cleaved factor VaLeiden retains limited cofactor activity and continues to promote thrombin generation. The identification, role in coagulation, and overall importance of factor V in hemostasis have been described in numerous reviews. Together specific and broad-spectrum inhibitors function to localize, limit, and control hemostasis (see Chapter 129). Antithrombin Proteinase inhibitors Proteinases, enzymes that hydrolyze peptide bonds, are found in a wide array of biologic systems, including the blood coagulation process (clot formation and fibrinolysis), digestive system, apoptotic cascades, and the immune system. To keep these systems in balance between activation and inhibition, a complex system of proteinase inhibitors has evolved. In blood, proteinase inhibitors constitute a significant percentage of circulating proteins. In general, proteinases that activate the coagulation and fibrinolytic cascades have highly defined substrate specificities. Congenital antithrombin deficiency exhibits an autosomal dominant pattern of inheritance, with an incidence of 1 in 2000 to 1 in 5000. Antithrombin has a broad spectrum of inhibitory activity with most of its target proteases participating in the coagulation cascade. When antithrombin is complexed with heparin, its rate of inhibition of several coagulation proteases is accelerated by up to 10,000-fold. The general mechanism of inhibition involves reaction of the active site of the enzyme with a peptide loop structure (the reactive center loop) of antithrombin, forming a tight, equimolar (1: 1) complex. Inactivation proceeds through covalent bond formation between antithrombin and the protease followed by inactivating structural rearrangements of both antithrombin and the protease. Cleavage sites for activation are identified with an arrow, and with the specific amino acid residues of the site shown. It circulates in plasma as a heterogeneous collection of partially proteolyzed forms144-147 (see Table 128-1 and. It is distinctive in its capacity to inhibit members from each of four mechanistic classes of proteinases (serine, cysteine, and aspartic proteinases and metalloproteinases). Reduced levels of 2-macroglobulin in humans have been observed in individuals with chronic obstructive lung disease213 and metastatic cancer. Inactivation of the 2-macroglobulin gene in mice has no obvious phenotype, but the mice are resistant to endotoxin challenge. Multiple processes involving components of the vessel wall, circulating platelets, and plasma protein moieties interact to maintain blood fluidity. These must be precisely choreographed to allow the vasculature to perform its myriad complex physiologic activities. The endothelium, the thin layer of cells that lines the interior of blood and lymphatic vessels, plays a key role because of its strategic interface among organs, tissues, and circulating blood. The cells that form the endothelium are called endothelial cells, those in direct contact with blood are called vascular endothelial cells, and those in direct contact with lymph are known as lymphatic endothelial cells. Vascular endothelial cells line the entire circulatory system (from the heart to the capillaries).

It is a novel technology and not analogous to the bleeding time or light transmission platelet aggregometry treatment borderline personality disorder purchase thyroxine overnight delivery. Platelet function is measured as a function of the time needed to occlude the aperture medicine 0031 purchase thyroxine 150mcg, termed "closure time medications descriptions purchase discount thyroxine online. Each laboratory that uses this technology must determine its own normal values because of influences of different collection tubes and anticoagulant concen trations medications bad for kidneys cheap thyroxine online. Of note, von Willebrand disease or platelet function defects leading to bleeding can be present even with normal results for one or both of the screening assays. At present, no screen ing assay can exclude the diagnosis of von Willebrand disease or a platelet function defect. If the clinical history is compelling but the screening test results are normal, more definitive von Willebrand factor or platelet function testing is needed. Likewise, if screening test results for platelet function abnormalities are abnormal, the consult ing physician has the onus to diagnose or exclude von Willebrand disease or a platelet function defect. Thus once medication or non prescription drug use is excluded, more sophisticated, specifically diagnostic studies for von Willebrand disease and a platelet function defect are needed for most patients requiring invasive procedures. If clinically appropriate, complete von Willebrand factor and platelet function studies are performed. In general, 1 of 10 patients in this diagnostic category have a platelet function defect. Its diagnosis is made by abnormal results for studies of von Willebrand antigen, von Willebrand factor activity (ristocetin cofactor assay and collagen binding assay), and von Willebrand factor multimers. Two forms of platelet aggrega tion studies are available: light transmission aggregometry in plateletrich plasma and impedance aggregometry in plateletrich plasma or whole blood. Light transmission aggregometry in platelet rich plasma is the gold standard of platelet function testing71; imped ance aggregometry is less well characterized. Platelet storage pool disorders can be diagnosed if platelet light transmission aggregometry is performed simultaneously with studies that include measurement of proteins within or released from platelet granules or dense gran ules or measurement of granule membrane proteins. Platelet activation defects, such as that induced by aspirin, can be diagnosed as well using this combination of techniques (see Chapter 132). Finally, with appropriate monoclonal antibodies, flow cytometry is used to com pletely examine the surface expression of platelet glycoproteins and the activation state of the cell. In individuals with idiopathic thrombosis, recognition of a specific molecular or protein defect may be important in deter mining the duration of anticoagulant therapy. Finally, 18% of patients without a family history of thrombosis and 30% to 40% of patients with a family history may have an identifiable molecular or protein risk factor for venous thrombosis. Monitoring of activated coagulation states and their amelioration with treatment is another activity of the specialized hemostatic labo ratory. The two forms of clinical presentation are an acute form that is a hyperfibrinolytic state and a subacute form that is more indolent. Assay results are positive in patients in postoperative states, with resolving hematomas, and after largevessel or pulmonary thrombosis. Positive results of a Ddimer assay also have become an adjunct to the clinical diagnosis of pulmonary embolism. Physicians may find that monitoring the degree of the activated blood coagulation state is useful as a guide to therapy. In addition to the Ddimer, other assays that could be used to monitor an activated blood coagulation state include prothrombin fragment 1. Finally, heparininduced thrombocytopenia presents unique opportunities to coagulation laboratory testing for both diagnosis and monitoring of the activated blood coagulation state. Laboratory diag nosis and monitoring the effectiveness of therapy for heparininduced thrombocytopenia is discussed in detail in Chapter 135. H58-A-Platelet Function Testing by Aggregometry: Approved guideline, Wayne, Pa, 2008, Clinical and Laboratory Standards Institute. Monitoring Acute Hemostatic and Thrombotic Conditions In addition to the diagnosis of hemostatic and thrombotic disorders, the coagulation laboratory has the function of monitoring patient therapy. This section is divided into two parts: monitoring of anticoagulation therapy and measurement of activated coagulation. Anticoagulation monitoring is an increasingly larger activity of hemostasis laboratories. This monitoring is especially important in patients who are obese, in those who have renal function compro mise, and in patients before elective surgery. MacFarland D: An enzyme cascade in the blood clotting mechanism, and its functions as a biochemical amplifier. Potzsch B, Hund S, Madlener K, et al: Monitoring of recombinant hirudin: Assessment of a plasmabased ecarin clotting time assay. Anstey A, Mayne K, Winter M, et al: Platelet and coagulation studies in EhlersDanlos syndrome. Fressinaud E, Veyradier A, Truchaud F, et al: Screening for von Wille brand disease with a new analyzer using high shear stress: A study of 60 cases. H58A-platelet function testing by aggregometry: Approved guideline, Wayne, Pa, 2008, Clinical and Laboratory Standards Institute. The clinical challenge in evaluating acquired disorders of platelet function is to determine whether observed derangements in platelet function pose a threat to the patient. Although platelet function can be altered to predispose to either hemostatic or thrombotic disorders, this chapter deals primarily, but not exclusively, with platelet disorders that may compromise hemostasis.

Although these cell line experiments often produce elegant results regarding mechanism of observed in vitro action medications used for fibromyalgia purchase generic thyroxine, whether the phytonutrients have the same benefits in humans consuming the whole foodstuffs or concentrated supplements remains uncertain medicine man dr dre discount 50mcg thyroxine visa. This recommendation is primarily based on the absence of convincing data supporting therapeutic benefit symptoms emphysema thyroxine 150mcg without prescription. Concurrent use of a supplement medications given for uti order 100 mcg thyroxine free shipping, particularly a botanical, with chemotherapy could lead to a clinically important interaction that could yield an increase or decrease in the effects of either component. In a classic pharmacokinetic interaction study, 10 healthy volunteers were administered a single 400-mg oral dose of imatinib before and after 2 weeks of treatment with 300 mg of St. The investigators found that the pharmacokinetics of imatinib were significantly altered by St. It is generally recommended that cancer patients receiving any intervention avoid taking St. Patients with hematologic malignancies are often at increased risk for bleeding problems. There has been a long-standing tendency to attribute thrombocytopenias of unclear etiology in cancer patients to botanical supplements that they are taking, particularly traditional Chinese medicine herbs. Warfarin is a frequently prescribed anticoagulant, itself derived from a botanical, which can be impacted in a number of ways by diet and dietary supplements. Inappropriate control of anticoagulation because of fluctuation in warfarin effect exposes the patient to risks of increased bleeding or thromboembolic complications. Finally, the anticoagulant effect of warfarin can be antagonized by vitamin K intake. Patients prescribed warfarin are often advised not to eat green leafy and cruciferous vegetables or to consume green tea because they are rich in vitamin K and might interfere with the anticoagulant effect. Vitamin D3 Vitamin D is one of the few remaining vitamins that has not been shown to be ineffective in protecting against malignant disease. An ongoing randomized clinical trial is currently looking at a two-by-two factorial design of omega-3 fatty acids and vitamin D3 supplementation in older adults to assess cancer risk reduction, among other endpoints. At the same time, increasing evidence suggests that vitamin D deficiency may be related to the risk of a number of solid tumors, particularly breast, colon, prostate, and pancreas. One proposed explanation for this unexpected finding is that sun exposure is actually a surrogate marker of vitamin D status, and it is actually vitamin D sufficiency that is protective against lymphoma. Hence, it may be appropriate in view of the widespread incidence of vitamin D insufficiency, especially in older adults, for integrative oncologists to measure 25-hydroxy-vitamin D levels in patients with hematologic malignancies and supplement with a fatsoluble vitamin D3 preparation to bring the levels into sufficient or optimal range. Green Tea Omega-3 Fatty Acids Green tea (Camellia sinensis) is an increasingly consumed beverage being sought after for multiple potential beneficial health effects. Patients with multiple myeloma are now frequently advised by their oncologists not to consume green tea at all because of its potential to negate the treatment effects of bortezomib, found in mouse studies. Omega-3 fatty acids have been reported in isolated cases to potentiate the anticoagulant effects of warfarin. These factors, which make the omega-3s attractive as antiinflammatory and cardiovascular agents, need to be borne in mind in patients on warfarin therapy. Taken in the absence of warfarin, omega-3s are not believed to be a significant cause of bleeding at doses of less than 4000 mg/day. Epidemiologic data suggest an inverse relationship between the intake of marine omega-3 fatty acids and the development of a number of hematologic malignancies and the good risk-to-benefit profile. They are among the most common classes of supplements used by patients with hematologic malignancies. Their use is directed for cytotoxic effects, for synergy with conventional therapy, or to lessen the toxicity of conventional therapy. Estimates of antioxidant use by patients with cancer have varied considerably, with rates ranging from 13% to 87% depending on the survey, the type of disease studied, and a variety of other individual Chapter 158 Integrative Therapies in Patients With Hematologic Diseases 2189 and demographic factors. Evidence supporting the potential role of antioxidants in preventing and treating disease include preclinical studies. These studies have correlated oxidative stress and an antioxidant-depleted diet with the development of diseases, including cancer. In addition, decreases in antioxidant enzymes or the micronutrients, thiol, vitamin E, vitamin C, beta-carotene, or zinc and increases in the production of reactive oxygen species have been reported in leukemia patients. These types of data have led many patients with hematologic malignancies to take antioxidant supplements primarily in conjunction with conventional cancer treatment. Much of the controversy surrounding antioxidants and cancer therapy has arisen because radiation therapy and certain classes of chemotherapy agents exert some of their anticancer effects through the generation of reactive oxygen species or free radicals. The theoretical concern is that antioxidants might somehow interfere with or counteract the activities of these anticancer agents. However, to date, preclinical experiments and clinical studies have not definitively shown impact on treatment outcome. Vitamin C, at orally achievable concentrations (equivalent to 1 g/day, a dose frequently used by patients), inhibited the in vitro multiple myeloma cell cytotoxicity of bortezomib and blocked its inhibitory effect on 20S proteasome activity. In addition, green tee polyphenols and dietary supplements carrying hydroxyl groups, including flavonoid compounds such as quercetin, bind and inhibit the activity of bortezomib on malignant B cells and multiple myeloma cells in vitro, although by mechanisms independent of their antioxidant activity. Taken together, these studies suggest that antioxidant supplements should be avoided in patients taking bortezomib and other boronic acid proteasome inhibitor therapy. The precise role of antioxidant supplementation in the patients with hematologic malignancies remains to be determined. Studies adequately evaluating the impact of supplementation on toxicity and disease free survival have not yet adequately demonstrated that the benefits of supplementation clearly outweigh the risks; therefore, the possibility of harm must be strongly considered.

Local activation of coagulation in the bronchoalveolar compartment may contribute to acute lung injury in these patients medicine 81 order thyroxine 75 mcg. In addition treatment urinary retention purchase generic thyroxine canada, there was a striking activation of white blood cells symptoms 5dpiui buy generic thyroxine 150mcg line, as demonstrated by 2-integrin upregulation and increased production of reactive oxygen species medicine to stop vomiting purchase thyroxine with amex. There was a marked correlation between the extent of inflammation and coagulation activation and the clinical severity of the heatstroke. Cancer procoagulant is an endopeptidase that can be found in extracts of neoplastic cells but also in the plasma of patients with solid tumors. Interactions of P- and L-selectins with mucin from mucinous adenocarcinoma can induce formation of platelet microthrombi and probably constitute one-third mechanism of cancer-related thrombosis. Disseminated Intravascular Coagulation in Obstetric Complications Placental abruption is a leading cause of perinatal death. Amniotic fluid embolism is a rare but serious complication of pregnancy and delivery. A maternal mortality rate of 86% was reported in a 1979 review of 272 cases, but in a more recent population-based study, the maternal mortality rate (26. Patients predisposed to amniotic fluid embolism are multiparous women whose pregnancies are postmature with large fetuses and women undergoing a tumultuous labor after pharmacologic or surgical induction. Apparently, amniotic fluid is introduced into the maternal circulation through tears in the chorioamniotic membranes, rupture of the uterus, and injury of uterine veins. The extensive occlusion of the pulmonary arteries and an acute anaphylactoid response reminiscent of severe systemic inflammatory response syndrome provoke sudden dyspnea, cyanosis, acute cor pulmonale, left ventricular dysfunction, shock, and convulsions. These symptoms are followed within minutes to several hours by severe bleeding in 37% of patients. Hemorrhage is particularly severe from the atonic uterus, puncture sites, gastrointestinal tract, and other organs. In a large series of patients, a good correlation was noted between the clinical severity and abnormalities in platelet counts and fibrin(ogen) degradation products. With some large aortic aneurysms, localized consumption of platelets and fibrinogen can produce coagulation abnormalities and bleeding. Localized pain may occur, likely from thrombosis of vascular channels within the hemangiomas, and there may be bleeding after trauma or surgery because of the consumptive process. Patients with this syndrome exhibit accelerated platelet turnover and accumulation of labeled platelets and fibrinogen in the hemangiomas. Kasabach and Merritt were the first to describe bleeding in association with giant cavernous hemangiomas, benign tumors found in newborns or children that can evolve into convoluted masses of abnormal vascular channels that sequester and consume platelets and fibrinogen. Hemangiomas may regress spontaneously, and some respond to radiation or laser therapy. Disseminated Intravascular Coagulation With Liver Disease the levels of most coagulation factors, endogenous anticoagulants, and major components of the fibrinolytic system are reduced in patients with severe liver disease, reflecting reduced synthesis. Thrombocytopenia is common because of hypersplenism and decreased hepatic production of thrombopoietin. They include a reduced half-life of radiolabeled fibrinogen that is reversed by heparin administration, failure of replacement therapy to significantly increase the levels of hemostatic factors (suggesting ongoing consumption), and increased levels of markers of activation of coagulation. Other tests are specifically aimed at the detection of neoantigens on degraded cross-linked fibrin. One of such tests detects an epitope related to plasmindegraded cross-linked chain, resulting in fragment D-dimer. The only problem so far is that a reliable test is not available for quantitating soluble fibrin in plasma. Venoms of these snakes contain enzymes or peptides that (1) release fibrinopeptide A (Agkistrodon rhodostoma); (2) activate prothrombin even in the absence of calcium (E. In patients with meningococcal septicemia, very low plasma levels of protein C are observed, and this may play a pivotal role in the occurrence of purpura fulminans in these patients. Observations in patients with severe gramnegative septicemia indeed confirmed the downregulation of thrombomodulin in vivo and impaired activation of protein C. Antithrombin is the principal inhibitor of thrombin and may be readily exhausted during continuous thrombin generation. By using receiver-operating characteristics curves, an optimal cutoff for a quantitative D-dimer assay was determined, thereby optimizing sensitivity and the negative predictive value of the system. Because of the relatively low plasma concentration of 2-antiplasmin, the determination of this protease inhibitor is a helpful test for judging the dynamics of fibrinolysis. However, because the concentration of 2-antiplasmin is relatively low and therefore sensitive to relatively rapid exhaustion, this test may underestimate total fibrinolytic activity. Diagnostic Algorithm for the Diagnosis of Overt Disseminated Intravascular Coagulation* 1. The major difference between the international and Japanese scoring systems seems to be a slightly higher sensitivity of the Japanese algorithm, although this may be attributable to different patient populations because Japanese series typically include relatively large numbers of patients with hematologic malignancies. Sepsis itself is a clear risk factor for thrombocytopenia in critically ill patients, and the severity of sepsis correlates with the decrease in platelet count. The principal factors that contribute to thrombocytopenia in patients with sepsis are impaired platelet production, increased consumption or destruction, or sequestration platelets in the spleen or along the endothelial surface. These cytokines and growth factors should theoretically stimulate megakaryopoiesis in the bone marrow. However, in a substantial number of patients with sepsis, marked hemophagocytosis may occur. This may result in massive platelet activation and as a consequence a consumptive thrombocytopenia and arterial and venous thrombosis occur.

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