SUMMARYA case of cough syncope due to A-V conduction block of the heart is reported in this paper. A-V conduction block and lightheadedness were induced by coughing but not by an Aschner test, carotid sinus massage, Valsalva maneuver, pharyngeal stimulation, and stimulation of systemic baroreceptors. Permanent right-ventricular pacing completely abolished the patient's symptoms. The results suggest that hypersensitivity of a broncho-pulmonary reflex to coughing was responsible for the A-V conduction block and resulting syncopes. Additional Indexing Words: Atrial fibrillationA-V block Tussive syncope OUGH syncope is a conspicuous and well-defined syndrome. Clinically, the fainting fit is always associated with a paroxysm of coughing, often occurring after a few vigorous coughs. A very sudden onset of giddiness is followed by loss of consciousness. While many theories have been advanced concerning the mechanism of this syndrome since the first description of Charcot1) in 1876, recent investigations have paid particular attention to the hypotheses that cough syncope can be attributed to transmission of markedly elevated intrathoracic pressure to the cerebrospinal fluid2) or to reduction in venous return to the heart,3) resulting in cerebral anoxia and syncope. This report describes a patient who presented repeated episodes of loss of consciousness after coughing. Investigations revealed that the mechanism for this patient's syncope is probably a hypersensitive bronchopulmonary reflex which induces a complete A-V conduction block of the heart. Permanent right-
Interferon-gamma (IFN-gamma) was induced from a human peripheral mononuclear fraction by incubation with a streptococcal preparation stabilized with penicillin G (OK432). This IFN-gamma-producing activity was significantly reduced in patients with chronic hepatitis and hepatocellular carcinoma. In patients with liver cirrhosis it was also reduced but not significantly. Serum hepatitis B virus DNA and skin tests for the purified protein derivative of tuberculin, phytohemagglutinin-P and a polysaccharide fraction prepared from streptococcus pyogenes Su strain were determined to have no significant relation to this IFN-gamma-producing activity. Although the addition of interleukin 2 (IL-2) to the culture medium enhanced the IFN-gamma-producing activity, there was no difference in this enhancement between normal control and chronic hepatitis. Therefore reduction of the IFN-gamma-producing activity observed in chronic hepatitis seems to be caused by a decreased number of IFN-gamma-producing activity cells or hypofunction of these cells or both. Since HBeAg became negative in patients whose IFN-gamma-producing activity was increased by the administration of the immunopotentiator OK432 or IFN-beta, the IFN-producing system in the patients with B type hepatitis may contribute to the elimination of HBV. Adenine arabinoside suppressed IFN-gamma-producing activity both in vivo and in vitro.
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