A 17-year-old man with the Kleine-Levin syndrome died unexpectedly of cardiopulmonary arrest during a period of autonomic instability that followed an episode of megaphagia. At autopsy, the only pertinent finding was mild depigmentation of the locus ceruleus and substantia nigra. Premortem CSF levels of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels were elevated. These findings indicate that many symptoms of the Kleine-Levin syndrome are a result of a neurotransmitter imbalance in the serotonergic pathway of the brainstem.
In laboratory animals, the administration of sodium nitrite (NaNOa) together with secondary amines or alkylureas can induce tumors, and this is attributed to the acidcatalyzed in t ragast ric for mat ion of N-nji t roso compounds, i.e., nitrosamines and nitrosamides [reviewed in ( 1) 1. This process could conceivably occur in the human stomach and be involved in the etiology of some human cancers ( 2 ) . In chemical experiments, ascorbate blocked the formation of N-nitroso compounds from nitrite plus amines and ureas, presumably because ascorbate reacted with nitrite and hence made it unavailable for the formation of N-nlitroso compounds ( 1). Therefore, we suggested that ascorbate might be administered together with nitrosatable drugs, to lessen the possibility of in vivo formation of N-nitroso compounds. Subsequently, we found that the induction of lung adenomas in strain A mice by chronic treatment with piperazine in the food and NaN02 in the drinking water was inhibited when ascorbate was included in the food (3).Intragastric administration of high doses of dimethylamine (DMA) plus NaNOa to mice produced acute liver necrosis, which was attributed to the intragastric formation of dimethylnitrosamine (DMN) (4). Similar administration of aminopyrine plus NaNOz to rats also produced acute liver necrosis and an elevation in serum glutamic-pyruvic transaminase (GPT) levels, attributed to in vivo formation of DMN (5). We report here the effect of sodium ascorbate on the liver necrosis and the elevation in serum GPT and glu-
S!CIHIE:~IIC COMPLICATIONS related to dopamine therapy have been reported in adults administered relatively high doses (greater than 10 mcg/ kgjmir'c).1 Usually these patients had pre-existing vascular disease, such as diabetes mellitus, Raynaud's disease, frostbite, or arteriosclerosis. Peripheral gangrene has been reported with tow to medium dose dopamine infusion in patients whose clinical course was complicated by shock, fever, blood loss, disseminated coagulation or pre-existing vascular disease. 2-5 However, the specific effects of these clinical findings on the peripheral adrenergic neural effector mechanism have not been stressed.The present report describes an unusual case off peripheral gangrene developing in a child that received a low to medium dose (between 4 and 9 mcg/ kg/min) intravenous dopamine infusion. This patient's clinical course was complicated by congestive heart failure, respiratory distress, oliguria, and mild disseminated intravascular coagulation. The clinical features of the case are described and the physiologic relationship of these clinical findings to function of the peripheral alpha adrenergic mechanism are discussed. Case ReportThe patient was a 23-month-old Caucasian male with a clinical and cardiac catheterization diagnosis of pentalogy of Fallot. A ~vaterston-Cc~oley shunt was performed at age 12 months. At age 23 months he underwent definitive repair of the pentalogy and takedown of the previous ivaterston shunt.The initial 24 hours postoperatively were marked by congestive heart failure, hypotension, hypoxia, and oliguria. Abnormal right ventricular compliance was reflected by high filling pressures in the right atrium (15-20 mm Hg). Left atrial pressures were lour (2-8 mm Hg), reflecting pulmonary pooling and poor right sided cardiac output. Although a low Pa02 of 33 mm Hg was recorded, the average Poz was 48 mm Hg. The disparity of blood How between the right and left lungs was visible roentgenographically. This was due to the marked disparity between the size of the pulmonary arteries in the shunted and unshunted lungs. This roentgenographic difference disappeared over the intervening days, and the P02 values improved. The mean aortic blood pressure reached a low of 36 mm Hg for less than one hour and then resumed its mean pressure of 50 to 65 mm Hg with the institution of dopamine. Mildly elevated liver enzymes were consistent with congestive heart failure. Hypofibrinogenemia, 123 n~g/dl (normal 15Q-400 mg/dl) and abnormal elevation of fibrin split products 74 mcg/ml (normal less than 10 mg/ dl) were also present. Total fluid volume in the first FIG. 1. Gangrene of fingers, sharply demarcated with proximal interphalangeal joints to the tips.
A variant creatine kinase (CK) isoenzyme was identified in the sera of some patients who had advanced adenocarcinoma of the breast, stomach, and large intestine. A similar variant isoenzyme, together with a high concentration of CK-BB isoenzyme, was identified in some breast tumor cytosols. The variant creatine kinase activity in both sera and tumor cytosols was unaffected by antibodies specific for both the CK-M and DK-B subunits. This indicates that DK-MB isoenzyme determinations are currently best performed by electrophoretic rather than immunologic technics.
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