Faculty Bibliography

Heparin-induced thrombocytopenia and thrombosis syndrome was diagnosed in a 63-year-old woman 11 days after coronary artery bypass grafting. Her only presenting complaints were incisional leg pain and vague chest discomfort. The syndrome was suspected when her platelet count was found to be 37,000/microL. A subsequent ventilation-perfusion lung scan showed findings highly probable for pulmonary embolism. An inferior venacavogram obtained before a pulmonary angiogram revealed a large retrohepatic thrombus at the right atrial junction. The patient was successfully treated with the defibrinogenating agent ancrod (Arvin). A diagnosis of heparin-induced thrombocytopenia and thrombosis syndrome should be considered and heparin therapy should be avoided in patients with low platelet counts who have been previously treated with heparin

High-dose intravenous gammaglobulin (IVIgG) was given to 12 children and adults with chronic idiopathic thrombocytopenic purpura (ITP) to avoid splenectomy or because they either failed to respond to or required maintenance with high doses of steroids and/or immunosuppressives. The average platelet count increase to initial therapy was 239,500/microliters (range 23,000-790,000). A concomitant IgG Fc receptor blockade, measured by IgG-sensitized 51Cr-labeled autologous erythrocytes, was seen in 11 of 11 patients tested, both splenectomized and not splenectomized, lasting 3-4 wk. Six or more months after treatment, 2 children are in remission, 2 children and 2 adults are stable requiring no therapy with platelet counts of approximately 50,000 and 30,000, respectively, 3 children require maintenance IVIgG therapy at 2-10-wk intervals, and 1 child and 2 adults have become refractory to further IVIgG. Splenectomy was not performed in 4 children. Two adults were able to discontinue daily prednisone. The 3 patients who became unresponsive to Swiss Red Cross gamma-globulin (IgSRK) therapy did so in conjunction with a markedly elevated platelet-associated IgG and IgM. Serum IgM increased an average of 103 mg/dl after the IVIgG infusions. No significant side effects were seen

Purified Fab fragments of digoxin-specific antibodies obtained from sheep were used to treat 26 patients with advanced, life-threatening digoxin (23 cases) or digitoxin (3 cases) toxicity. These patients had advanced cardiac arrhythmias, and in some cases hyperkalemia, which were resistant to conventional treatment. All patients had an initial favorable response to doses of Fab fragments calculated (in most cases) to be equivalent, on a molar basis, to the amount of cardiac glycoside in the patient's body. In four patients treated after prolonged hypotension and low cardiac output, death ensued from cerebral or myocardial hypoperfusion. In one case the available Fab fragment supply was inadequate to reverse a massive suicidal ingestion of digoxin, and the patient died after recurrent ventricular arrhythmias. In the remaining 21 patients, cardiac rhythm disturbances and hyperkalemia were rapidly reversed, and full recovery ensued. There were no adverse reactions to the treatment. We conclude that the use of purified digoxin-specific Fab fragments is a safe and effective means to reverse advanced, life-threatening digitalis intoxication

We have investigated the case of a woman, 44 years of age, who presented with erythrocytosis, thrombocytopenia and a right axial myxoma. Surgical removal of the tumor allowed correction of all hematologic abnormalities. A serum erythropoietin level obtained from the right atrium of the patient during pre-operative cardiac catheterization was twice those of 4 control patients (250 MIU vs. 131 MIU). Renal vein erythropoietin levels were normal. This implicates atrial myxomas as another tumor capable of erythropoietin production, and explains the heretofore mysterious polycythemia frequently reported to be associated with this tumor

Systolic time intervals, echocardiographic indexes of left ventricular contractile function and serum triiodothyronine and thyroxine levels were measured before treatment in nine patients with hyperthyroidism, and again every 2 weeks for the first 2 months after therapy and then every 4 weeks until the subjects were clinically and chemically euthyroid. Six of the nine became transiently hypothyroid. Although the preejection period corrected for heart rate (preejection period index) increased as the patients became euthyroid, the change was not significant. Preejection period index increased dramatically in the patients becoming hypothyroid (p less than 0.005). Corrected left ventricular ejection time (left ventricular ejection time index) also increased as the patients became euthyroid (p less than 0.001), and increased again with the appearance of hypothyroidism (p less than 0.05). There was a linear correlation between velocity of circumferential fiber shortening and serum triiodothyronine level (r - 0.77) and between velocity of circumferential fiber shortening and serum thyroxine level (r = 0.70) at all stages of thyroid function. Thus thyroid hormone definitely enhances left ventricular function in human beings, and both excess and deficiency cause predictable reversible changes in myocardial contractile function. Thus thyroid hormone definitely enhances left ventricular function in human beings, and both excess and deficiency cause predictable reversible changes in myocardial contractile function. Furthermore echocardiographic measurements of velocity of circumferential fiber shortening provide rapid estimates of the chemical status of thyrotoxic patients before and after treatment