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This article discusses the prevalence of depression in patients with intracranial hemorrhage (ICH) and the relationship of selective serotonin reuptake inhibitor (SSRI) use with bleeding risk. A detailed account of the patient's psychiatric history and current hospital admission is also provided. This article then further explores the pathophysiological mechanisms that contribute to depression in ICH patients, the effect of SSRIs on outcomes in patients with ICH, and ways to treat depression in ICH patients. Based on the literature, the conclusion is that practitioners should avoid SSRIs in ICH patients with certain genetic markers and treat depression as seriously as one would treat a physical ailment. Ultimately, more research is necessary to explore how to treat depression in this patient population.

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Two insulin-dependent diabetic patients with advanced nonproliferative and early proliferative retinopathy showed regression of diabetic retinopathy after three weeks of intensive plasmapheresis. Because of the sudden unexplained death in one patient, the study was stopped. However, these observations in this pilot study suggest that factors mediated through plasma contribute to the pathogenesis of diabetic microangiopathy.

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A high incidence of anaphylactic reactions has been observed in patients undergoing therapeutic plasma exchange. In three of 22 patients who underwent multiple exchanges, urticaria, bronchospasm, and hypotension developed during a course of plasma exchange that responded to treatment with steroids, antihistamines, and epinephrine. Fatal pulmonary microvascular occlusion with platelets and granulocytes developed in an additional patient eight hours following an apheresis procedure involving albumin replacement. The mechanism for the latter complication is not known but did not appear to invoke complement activation. This unexpectedly high risk of potentially fatal complications must be considered when a course of therapeutic apheresis, particularly involving treatment of a chronic disease, is planned.

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Current concepts of atherogenesis, based on animal models, suggest a role for platelets in the development of atherosclerotic lesions, possibly through the release of alpha granule constituents. Platelets may also contribute to the development of vascular spasm through thromboxane A2 production. Platelet activation in the coronary circulation in patients with coronary artery disease (CAD) should occur if these hypotheses apply clinically. We measured aortic and coronary sinus plasma levels of the platelet alpha granule constituent beta-thromboglobulin (B-TG) and thromboxane B2 (TX B2) by radioimmunoassay in 15 patients with severe atherosclerotic CAD, seven patients with angiographically normal coronaries, and five patients undergoing evaluation for coronary artery spasm (CAS). Compared with the controls, CAD patients had significantly greater transmyocardial release of B-TG (11.1 +/- 8.1 ng/ml, mean +/- SEM vs 62.5 17.2, p less than 0.05 by rank sum test); TX B2 gradients showed a similar trend but the difference was not statistically significant (-0.08 +/- 0.03 ng/ml vs 0.22 +/- 0.02, 0.05 less than p less than 0.10). Three of the five patients studied developed CAS which was associated with acute elevation in coronary sinus TX B2; the two non-CAS patients with drug provocation had undetectable coronary sinus TX B2. We conclude that abnormal platelet activation takes place in the coronary circulation of CAD patients, and that production of acute myocardial ischemia by CAS occurs with increased coronary sinus TX B2.

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Plasma beta-thromboglobulin (beta-TG), a platelet-specific protein, is a marker of intravascular platelet degranulation. We measured plasma beta-thromboglobulin by radioimmunoassay in 13 patients with thrombocytopenia of various etiologies to determine whether or not the test is clinically useful in the differential diagnosis of thrombocytopenia. Four patients with intravascular platelet consumption (three with thrombotic thrombocytopenic purpura and one with vasculitis) had significantly higher plasma beta-thromboglobulin levels than four patients with extravascular platelet destruction due to idiopathic thrombocytopenic purpura. Five patients with thrombocytopenia and decreased numbers of megakaryocytes in the bone marrow also had beta-thromboglobulin levels that were not elevated. Two patients with thrombotic thrombocytopenic purpura achieved clinical remission associated with a decrease in beta-TG level to the normal range. Plasma beta-thromboglobulin determination can be useful in determining the mechanism of thrombocytopenia when bone marrow examination demonstrates adequate megakaryocyte numbers.

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A 45-year-old-woman was presented with fever, microangiopathic hemolytic anemia, thrombocytopenia, purpura, and mental status changes. She was diagnosed as having thrombotic thrombocytopenic purpura (TPP). She was treated with daily plasma exchange and antiplatelet drugs, steroids, and vincristine. This patient had a remarkable course with 18 days of coma on full therapy followed by essentially complete recovery coincident with an increase of the plasma exchange dose to two plasma volumes processed per procedure. The patient has remained well with discontinuation of plasma exchange. We conclude that prolonged coma without evidence of major central nervous system structural lesions in TTP should be treated vigorously and continuously with plasma exchange.

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Thrombosis is a well-recognized complication of atherosclerosis and may be a factor in initial lesion formation. Experimental endothelial cell injury results in activation of the coagulation mechanism and therefore may be a critical aspect of the pathogenesis of occlusive vascular disease. If this is so, then risk factors for atherosclerosis should affect the endothelium either by causing cell injury, inhibiting repair mechanisms, or altering its thromboresistant properties. To test this, we studied the effect of several risk factors on endothelial cell behavior in vitro. Since the smooth muscle cell is the major cellular component of human atherosclerotic plaque and since a primary smooth muscle cell lesion is suggested by the clonal nature of human plaque, we also studied the effect of risk factors on arterial smooth muscle behavior. We have found that homocysteine directly injures human endothelium, which may account for the premature arterial disease in homocystinuria. Serum from patients with familial hypercholesterolemia inhibits the critical function of endothelial cell migration, as well as arterial smooth muscle cell migration. Moderate hypoxia has no effect on endothelial cell or smooth muscle cell viability, proliferation, or migration. Platelet factors are shown to affect human smooth muscle cell proliferation and both endothelial cell and smooth muscle cell migration. Preliminary study of platelet activation in diabetes with retinopathy suggests a relation to glucose control, but might reflect underlying vessel disease rather than direct platelet effect.

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