Biomedical subjects
Publications and source records attributed to I Ungi.
A case report of a rare, presumably congenital form of "single coronary artery", is presented. The authors review the classification and clinical significance of the entity with special emphasis with regard to anginal symptoms and the so called sudden unexpected death syndrome. Details and result of surgical intervention (conventional aorto-coronary saphenous bypass) are discussed.
Amanita phalloides-type mushroom poisoning is well recognized as causing acute liver injury and often death. Less is known, however, of whether maternal Amanita poisoning is associated with fetal damage or not. In August 1991 four members of a family were hospitalized with food intoxication caused by Amanita phalloides and Amanita verna. One of them died from hepatic and renal failure. The survivors included a 26-year-old woman in the 23rd week of pregnancy. Her clinical symptoms and blood chemistry data (lowest prothrombin activity 23%) indicated intoxication of medium severity. The management consisted of i.v. hydration, forced diuresis, and administration of silibinin, high-dose penicillin, thioctic acid, hydrocortisone, vitamin K, and fresh frozen plasma. Sonographic and obstetric controls failed to show any fetal abnormalities in the acute phase of poisoning. In the 38th week of pregnancy she gave birth to a healthy baby, who has subsequently undergone an undisturbed development. This observation indicated that severe fetal damage did not occur in maternal Amanita poisoning in the second trimester of pregnancy. Thus, at least from the second trimester on, maternal Amanita poisoning is not necessarily an indication for induced abortion.
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The case-history of a 41-year-old man is reported. He was admitted because of the sudden development of left hemiparesis, loss of consciousness and increasingly deeper coma. The ECG demonstrated second-degree AV block with Wenkebach conduction or episodes with complete AV block. The colour Doppler ultrasound and cranial CT examination revealed occlusion of the right internal carotid artery and a cerebral infarct of the right hemisphere. Within 24 hours patient died from herniation of the brainstem. Postmortem examination revealed a pericardial neoplasm infiltrating both left and right atrium, AV junctional area, interventricular septum and right ventricle. The tumor tissue grew transmurally and protruded into the cavities of the heart. The right internal carotid artery was occluded by a tumor embolism. The histochemical and immunohistochemical results proved that the tumor was a primary malignant pericardial mesothelioma. This kind of cardiac tumor involving the AV node and mimicking stroke is very rare.
The case history of a patient is reported who was treated with a variety of antiarrhythmics over a period of years because of refractory ventricular "bigeminy". As the arrhythmia did not respond to any kind of therapy, amiodarone treatment was started, which the patient received in a maintenance dose of 600-400 mg/day for 4 years. More recently, a bluish-grey hyperpigmentation of the face and other areas of the skin exposed to sunlight developed. A cutaneous biopsy of the hand revealed pigment deposits and lamellated lysosomal inclusions characteristic for amiodarone dermatopathy. The interactive, computer-assisted analysis of the ventricular ectopic activity has clearly demonstrated its innocent, parasystolic nature. The differentiation between ventricular extrasystolic and parasystolic activity is essential, because the latter arrhythmia does not require specific antiarrhythmic pharmacotherapy.
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In anesthetized rats, a marked decrease in CCK-OP activity and, to a far lesser extent, in the pancreatic secretory effect of CCK-33 were found after portal administration, compared to the femoral route. Changes in the biological activity of CCK-OP were further investigated after 30 min incubation with different subcellular liver fractions (1000 X g, 12,000 X g, microsomal fraction with or without NADPH). All the subcellular liver fractions caused an approximately 70% decrease in the CCK-effect, as calculated from dose-response relationships. The inactivation of CCK-OP after incubation with microsomal fractions of thioacetamide (TAA)-induced cirrhotic liver did not differ from that of control rats. The CCK-OP dose-response curves were similar in cirrhotic and control rats, but the pancreatic secretion was sustained to a greater extent and the inhibitory effect of supramaximal stimulation was delayed in cirrhotic rats. It was concluded that CCK-OP can be inactivated by liver proteins present in microsomal fractions, by a NADPH-independent mechanism. This inactivation did not diminish in liver cirrhosis. There were no changes in CCK-OP elimination in cirrhotic rats in vivo, thus pancreatic hypertrophy in experimental cirrhosis must be explained by other mechanisms.
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