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Acute severe thrombocytopenia is a serious although infrequent complication following abciximab infusion that is usually managed with platelet transfusions. We present a patient who underwent multivessel percutaneous coronary intervention with concomitant abciximab administration. Soon after the procedure the patient developed severe thrombocytopenia that persisted despite multiple platelet transfusions. This patient had been previously diagnosed as having idiopathic thrombocytopenic purpura, although this diagnosis was not recorded in our medical records, and at the time of the intervention the patient had a normal platelet count. He was successfully managed with IgG administration. The clinical and therapeutic implications of this case are discussed.

The platelet function was studied in 23 patients with systemic lupus erythematosus, all of whom met the diagnostic creteria established by the American Rheumatism Association. They were not under any treatment, especially with any drug that might interfere with platelet function. The same study was performed on a control group composed of volunteers donors at a blood bank. The platelet count was definitely lower in the patients with lupus than in the control subjects (p less than 0.0005), although a clear thrombopenia was observed in only two indivduals (8.7 percent). Anti-platelet antibodies were found in only six cases (26 percent). There was a linear correlation between thrombopenia and the presence of hemorrhagic diathesis and low levels of C4 and CH50 components. Plateler adhesiveness was clearly lower in the lupus group than in the control group (p less than 0.0005). The presence of kidney disease determined a greater impairment of the platelet adhesiveness (p less than 0.0025). A notable defect on platelet aggregation was induced by ADP, adrenaline and collagen. This was more apparent in the group of patients exhibiting a higher degree of clinical activity and in those who showed a serum complement decrease. The mechanism responsible for this thrombopathy appears to be an interference in the platelet function due to the presence of circulating immunocomplexes. They adhere to the platelet membrane blocking its function and inhibiting the release of the necessary thrombocytic components for the second phase of the aggregation. This platelet alteration is not usually manifested clinically; for this reason no relationship was found between this platelet defect and the presence of hemorrhagic symptoms in our patients. The condition is reversible and may disappear after therapy with steroids and/or immunosuppresive agents.

On the base of a preestablished protocol, 350 patients from a hospital endocrinological clinic were evaluated to assess the possible role of primary care teams to reduce its possible massification. A comparative evaluation of the causes for consultation was carried out in those patients requiring specialized attention and those which do not need the complexities of hospital organization for their appropriate care and which should be best directed to primary care. It was concluded that there is an overload of hospital clinics, as 34.5% of patients should have been diagnosed and treated in the primary level of care. On the basis of these results, the endocrine diseases requiring primary care would basically be obesity and type II diabetes mellitus, which, in addition, are present in more than 50% of the patients on care.