Altered platelet function

Platelet function Altered platelet function or abnormal results from laboratory studies have occurred in patients taking fluoxetine, paroxetine, or sertraline. 

Ritanserin, another 5-HT2 antagonist, has little or no a-blocking action. It has been reported to alter bleeding time and to reduce thromboxane formation, presumably by altering platelet function. 

Figure 4.2 Although doctors and scientists are not certain about the cause of migraines, many believe they are a result of changes in the release of chemical messengers (such as serotonin or CGRP) from the trigeminal nerve onto cerebral vessels on the surface of the brain. The result is altered platelet function and/or dilation of the cerebral vessels (illustrated here), which somehow produces the symptoms of migraines.

Laffi G, Cominelli F (1988) Altered platelet function in cirrhosis of the liver Impairment of inositol lipid and arachidonic acid metabolism in response to agonists. Elepatology 8 1620-1626. 

In this chapter, literature dealing with altered platelet function in hypertension will be reviewed to develop a better imderstanding of the role of agonist-receptor mediated signal transduction and Ae ensuing biochemical reactions that may be responsible for altered platelet reactivity in hypertension. 

Dextrans, particularly of MW 70 000 (dextran 70), alter platelet function and prolong the bleeding time. Dextrans differ from the other antiplatelet drugs which tend to be used for arterial thrombosis dextran 70 reduces the incidence of postoperative venous thromboembolism if it is given during or just after surgery. The dose should not exceed 10% of the estimated blood volume. They are rarely used. 

Altered platelet numbers and function Platelet dysfunction occurs dose-dependently with carbenicillin, ticarcillin, and, infrequently, other broad-spectrum penicillins (105), but the NMTT cephalosporin moxalactam has also been associated with altered platelet function in both healthy subjects and in patients treated with standard regimens (106-110). In contrast, clinical studies including cefotaxime, ceftizoxime, cefoperazone, and ceftracone did not show platelet dysfunction attributable to these compounds (109-111). There is evidence that beta-lactam-antibiotic-induced platelet dysfunction is at least partially irreversible (112). 

Thrombocytopenia was associated on two consecutive occasions with teicoplanin in a patient with acute myeloid leukemia (28). The exact mechanism for this adverse event is unknown. Teicoplanin does not alter platelet function or blood coagulation (29). 

Thrombotic complications are frequently encountered when blood is exposed to the surfaces of hemodialysis devices, heart-lung machines, arterial grafts, artificial heart components and other prosthetic devices. The blood platelets are particularly vulnerable to these adverse effects which may include a decrease in platelet count, shortened platelet survival and attendant higher platelet turnover, and altered platelet function. However the interaction of platelets with an artificial surface exposed to blood must be preceded by the interaction of the molecular components of plasma, particularly the plasma proteins, with the surface (1,2). This is due to the prepon-... 

D. Salicylates alter platelet function and may also prolong the prothrombin time. 

Altered platelet function probably caused by levetiracetam has been reported in a 75-year-old man with focal epilepsy [196 ]. Platelet aggregation profile normalized 3 weeks after drug discontinuation. 

In a prospective study of 23 children several coagulation disorders were associated with valproate thrombocytopenia n = 2), acquired von Willebrand s disease (6), a significant fall in fibrinogen concentrations (12), and a reduction in factor XIII (4) [373 ]. Thrombelastography showed altered platelet function in 11 and prothrombin time was significantly prolonged, with many other coagulation defects. 

DRUGS THAT ALTER PLATELET FUNCTION [SEDA-33, 637 SEDA-34, 547 SEDA-35, 621] ... 

Although aspirin and sallcyclic acid exhibit half-lives in man of only 13 to 19 min. and 3.5 to 4.5 hrs., respectively,31 the effect of aspirin on platelets Iji vivo has a duration which approximately parallels platelet survival time of 2-7 days. The currently accepted hypothesis to explain this action holds that aspirin Irreversibly alters platelet function by acetylation of a protein component of platelet membrane. A substantial amount of experimental evidence consistent with this hypothesis has accumulated.1 32 Although aspirin does not inhibit ADP-induced aggregation its effect on the release reaction decreases platelet response and abolishes the "second wave" of aggregation in the presence of ADP. It appears that another component of aspirin action is an effect on a plasma cofactor of ADP-induced aggregation.33,34 Evidence has been... 

A distinct impression is emerging from the literature that nutrition plays an important role in haemostasis and thrombosis. Although present knowledge is sketchy and newer information is still needed to place nutritional-thrombotic interrelationships on a firm foundation, recent literature shows that dietary fats alter platelet function and that this might occur as a consequence of alterations of platelet lipids. Thus far, feeding studies in man and animals have shown alterations in platelet factor 3 (PF-3), platelet aggregation, and platelet lipids. 

Tolmetin alters platelet function and prolongs the bleeding time (170 ). It does not appear to interact with the oral anticoagulant phenprocoumon (171 ). 

---