The frequency of smoking-induced nasopharyngeal lymphoid hyperplasia in heavy smokers and its potential clinical implications are still unknown. Precise criteria to differentiate this entity from other types of nasopharyngeal lymphoid hyperplasia are needed. A prospective clinicopathological study of smoking-induced nasopharyngeal lymphoid hyperplasia was conducted in 17 heavy smokers. Ten nonsmoking patients, five of them with chronic sinusitis, three with adult-onset adenoid hypertrophy, and two children with adenoidal hypertrophy served as a control group. Both in smokers and in nonsmokers, lymphocytic infiltration of the mucosa was characterized immunohistochemically as T cells. In smokers, semithin (1 micron) sections revealed deformed and migrating cytotoxic lymphocytes in the nasopharyngeal mucosa. The lymphocytes were attached to epithelial, ciliated, and goblet cells, resulting in cell damage. Transmission electron microscopy of biopsies from smokers revealed emperipolesis, characterized by mucosal invasion and epithelial cell damage by an unusual population of migrating T lymphocytes that penetrate them. These findings confirm a direct effect of smoking on the nasopharyngeal lymphoid tissue, which forms part of the immune system. It is concluded that the diagnostic evaluation and therapeutic approach of heavy smokers with otological and airway symptoms should be based on thorough endoscopic examination of the nasopharynx. When the diagnosis is not clear-cut, selective tele-endoscopic biopsy and electron microscopic examination are recommended. This entity should be added to the list of known clinical manifestations of the smoking habit.

A syndrome of primary copper deficiency in a 6-month-old premature baby is described. Features which can be ascribed to lack of copper, include (1) a sideroblastic anemia resistant to other therapy, with vacuolation of erythroid and myeloid bone marrow cells, and iron deposition in the vacuoles and in some mitochondria; (2) neutropenia, especially segmentopenia, which was common and prominent; (3) long-bone changes on radiological examination, particularly osteoporosis with blurring and cupping of the metaphyses; (4) depigmentation of skin and hair, with distended blood vessels due to changes in the elastin of the vessel walls; and (5) central nervous system abnormalities including hypotonia, psychomotor retardation, and difficulties with sight. Besides this small premature infant, who had received a relatively copper-deficient milk diet for at least three months, a second case has been seen in a 2,100-gm premature infant, after three months of intravenous alimenation necessitated by neonatal bowel surgery. Treatment with oral copper, 1 to 3 mg/day, dramatically cured both patients. It is recommended that 100 to 500µg/day of copper be added to the diet of small premature infants until they are receiving other foods beside milk, and to prolonged intravenous alimentation beginning in the newborn period.

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A patient with lymphosarcoma treated with weekly injections of vincristine developed an acute myocardial infarction immediately after the second injection of vincristine. After he recovered from the infarction, the treatment was continued and he developed an additional myocardial infarction. I n vivo and in vitro studies have not revealed any effect of vincristine on the clotting mechanism. T h e possible causes for the association of vincristine-treated lymphoma and myocardial infarction are discussed.Cancer 36:1979-1982, 1975. H E TOXIC EFFECT OF VINCRISTINE IS MAINLYT neurologic,4 manifesting as muscle weakness, paresthesia, loss of deep tendon reflexes, ptosis, diplopia, a n d hoarseness. Alopecia a n d constipation commonly occur. O t h e r rare side effects are inappropriate ADH secretion9 orthostatic hypotension,z a n d thrombocytosis.8To the best of o u r knowledge, myocardial infarction has n o t been mentioned i n t h e literature as a complication of vincristine administration.In this study we describe n case of myocardial infarction which developed i n a patient with lymphosarcoma after vincristine administration. CASE REPORTF.Z., a 58-year-old male originating from Rumania, was admitted to the Department because of lymphadenopathy and weakness of 1 month's duration. Two years previously, he had suffered a myocardial infarction and since then from mild angina pectoris. On physical examination the patient was found to be in good general condition, weighing 76 kg. He had no fever. Enlarged lymph T h e authors thank Miss van-der-Lyjn for her excellent technical assistance.Received for publication March 25. 1975. nodes, u p to 2 cm in diameter, firm, nontender, and nonadherent to skin were palpated in the neck and inguinal areas. T h e spleen and liver were not palpable. All laboratory findings, including complete blood count, renal and liver function tests were within normal limits. Electrocardiogram (ECG) on admission showed an absence of R waves in leads V, V, and Q wave in leads L,, aVF ( Fig. 1). A lymph node was hiopsied and the diagnosis of lymphosarcoma was established.Treatment with weekly injections of vincristine, according to an increasing dose schedule, was started. T h e first weekly injection of 3.8 mg was tolerated well. One hour after the second intravenous injection of 7.6 mg vincristine (0.1 mg/kg body weight) the patient complained of severe pressing precordial pain radiating to the left arm which lasted for 2 hours. His blood pressure was 130/80 mm mercury, the pulse rate 100 per minute with occasional extrasystoles. An ECG recording revealed T wave inversion in leads L, L,, aVL, V,V,, S T depression in V,-V,, S T elevation in L,, and premature ventricular contractions (Fig. 2).Examination of blood enzyme levels showed serum creatin phosphokinase (CPK) 5.0 Menashe-Gaist units (normal 0.9-3.0 units), lactic dehydrogenase (LDH) 476 King units (normal 100-250 units), and serum glutamic oxnloacetic transaminase (SGOT) 28 Sigms units (normal 15-40 units).T h e possibility of a vincrist...

The effect of 30% Urografin on platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and arachidonic acid was examined. In vivo and in vitro experiments in 10 nondiabetic subjects and in vitro experiments in 7 diabetic-uremic patients showed a statistically significant decrease in platelet aggregation 20 minutes after in vitro incubation or in vivo infusion with Urografin. Urografin concentration was about 2.4-2.5%. The possibility of bleeding induced by contrast media and the connection with acute renal failure in diabetic-uremic patients are discussed.