[Silent ischemia in the perioperative period].
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Biomedical subjects
Publications and source records attributed to M Glikson.
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We have reviewed our experience with 14 cases of relapsing hepatitis A (RH-A), as well as 68 cases reported in the literature. Relapse occurs in 3 to 20% of patients with acute hepatitis A, and rarely takes the form of a polyphasic disease (multiple relapses). After a stage of typical hepatitis A, remission phase ensues, with partial or complete resolution of clinical and biochemical manifestations. Relapse usually occurs after a short period (usually less than 3 weeks). Relapse is usually clinically milder than the first phase, with variable liver function abnormalities and a tendency toward more marked cholestatic features. Not uncommonly, immune manifestations occur during this phase, including purpura, nephritis, and arthralgia, with common laboratory findings of rheumatoid factor as well as false-positive reaction to HCV-EIA tests. The clinical course in relapsing hepatitis A is almost always benign, and uneventful recovery is the rule with few exceptions. Steroid treatment, first reported in the present series, resulted in marked clinical improvement. Preliminary results suggest that R-HA is associated with a continuing viremia as well as shedding of virus in stools during the relapse phase. The pathogenesis of R-HA probably involves an interaction between persistent viral infection and immune mechanisms responding to the continuing antigenic stimulation.
A retrospective study was carried out on 36 patients (33 males and 3 females) to determine the incidence of VVI pacemaker dependency following coronary artery bypass surgery. Pacemaker dependency was defined as the presence of pacemaker activity when pacing rate was programmed at 50 beats/min and/or when no hemodynamic adequate rhythm was present during pulse generator replacement. The patients were divided into two groups: (group I) 26 patients with complete atrioventricular (AV) block developing in the early postoperative period. In most of them a pacemaker was implanted up to 3 weeks following surgery (range 2 days to 1 year); (group II) ten patients in whom the indication for pacemaker implantation was sick sinus syndrome with sinus arrest and/or tachy-bradycardia. These patients underwent pacemaker implantation at varying periods of time following surgery (range 12 days to 4 years). Unipolar endocardial leads with VVI programmable pacemakers were implanted in all patients included in this study. Mean follow-up time was 3 years. In group I the pacemaker dependency rate was 65%, whereas in group II it was 30% throughout the follow-up period. It is concluded that the low incidence of pacemaker dependency in patients who undergo pacemaker implantation after coronary bypass surgery necessitates frequent evaluation in the nondependent patient, in order to reassess the need for the pacemaker before pulse generator replacement. Such reassessment should probably include prolonged ambulatory monitoring as well as invasive evaluation of the conduction system, if avoidance of pulse generator replacement is considered.
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Pyridostigmine has a protective effect against organophosphate poisoning when given in a dosage of 30 mg three times daily causing 20-40% cholinesterase inhibition. To test its safety in the human neuromuscular system, a double-blind study on 35 subjects divided into two matched groups was performed. One group was treated with pyridostigmine in a dose of 30 mg three times daily and the other group was treated similarly with placebo, both for a 10-day period. The resultant average cholinesterase inhibition in the treatment group was 23%. Muscle strength and endurance were tested before, during (on the 8th day), and after treatment. Electrodiagnostic studies, including nerve conduction, electromyography, and response to repetitive stimulation, were carried out on four subjects of the treatment group and on two subjects of the placebo group, both before and during treatment (eighth day). Isometric handgrip strength, isokinetic elbow flexor, and extensor strength did not differ between groups as a result of the treatment. Knee flexor and extensor isokinetic strength showed a small (but statistically significant) trend to improve more during placebo treatment, whereas knee extensor endurance decreased slightly in the placebo group. Both these effects are probably due to large fluctuations in performance of the placebo group, whereas the treatment group performance was quite constant. They probably do not represent any adverse effect of pyridostigmine. No electrophysiological changes were found in any of the subjects during treatment. We conclude that pyridostigmine does not cause any significant neuromuscular effect in healthy subjects when taken in a dosage of 90 mg daily for 8 days, causing 20-30% inhibition of cholinesterase.
We report on a 40 year old woman who presented with typical unstable angina pectoris associated with pulmonary oedema, due to poorly controlled hyperthyroidism. No cardiac abnormality was detected by echo-Doppler and nuclear ventriculography. Coronary angiography demonstrated normal coronary arteries. This case represents a new manifestation of the known association of cardiac ischaemia with hyperthyroidism in the presence of normal coronary arteries.
Ectopic GHRH is a relatively uncommon cause of acromegaly, which should be differentiated from pituitary adenoma, in order to avoid damage to the pituitary gland from unnecessary interventions. We report here on a 66-year-old man with acromegaly due to a GHRH-secreting bronchial carcinoid tumour, who recovered completely following removal of the tumour. His hormonal status was studied before and after the operation. Basal GH, GHRH, IGF-I and PRL levels, as well as plasma GH response to glucose load and TRH administration were abnormal before the operation, and became normal thereafter. The somatostatin analogue SMS 201-995 was found to be a potent inhibitor of the ectopic GHRH and the GH secretion (greater than 500 to 42 ng/l and 15.4 micrograms/l to 0.8 microgram/l, respectively). The effect on GHRH proved to be due to direct effect of somatostatin on the tumour cells, as demonstrated in tissue culture studies. A mixed meal was found immediately to suppress GHRH levels without such an effect on GH secretion. We conclude that the neuroendocrine tests usually practised in acromegaly cannot differentiate between ectopic GHRH secretion and pituitary adenoma. High plasma GHRH levels may serve as a diagnostic test for excessive GHRH production, which is almost always ectopic. These high levels are suppressible by somatostatin and a mixed meal.
The occurrence of incessant ventricular arrhythmia with bouts of polymorphous and bidirectional ventricular tachycardia is described in two totally asymptomatic sisters, with structurally normal hearts and no QT prolongation. Familial survey revealed the occurrence of increased ventricular ectopic activity in the father, brother and another sister.
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A 62-year-old woman with CREST syndrome and isolated pulmonary hypertension (without evidence of interstitial lung disease) underwent right heart catheterization to evaluate the effect of steroid and vasodilator treatment on hemodynamic parameters. During 12 weeks of prednisone treatment in a dosage of 40 mg daily, her condition markedly deteriorated clinically and hemodynamically as manifested by pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), mixed venous O2 saturation, and systemic vascular resistance (SVR). Successive trials with various vasodilators demonstrated ineffectiveness of isosorbide dinitrate and phenoxybenzamine, whereas nifedipine was effective in a 15-mg single dose, and prazosin 1 mg was partially effective in reducing PVR, SVR, and increasing CO and mixed venous O2 saturation. The combination of nifedipine 10 mg and prazosin 0.5 mg given alternately every four hours for 48 hours was the most effective in reducing PVR and PAP. Clinical response was favorable as well until treatment with medications was discontinued due to gastrointestinal side effects one month later.
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Two cases of polyarteritis nodosa (PAN) in patients with familial Mediterranean fever (FMF) are reported. These and another 11 cases found in the literature suggest that PAN occurs more commonly in patients with FMF than would be expected in the general population. Perirenal hematoma, which is surprisingly high in patients with FMF, is a life threatening complication of PAN. The diagnosis of PAN in patients with FMF may be delayed due to the similarity of the clinical manifestations of both diseases.
Pulmonary complications of lymphangiography are not uncommon. Clinical manifestations vary from asymptomatic radiological pictures to severe hemorrhagic pneumonitis or a syndrome resembling massive pulmonary embolism. We report a 17-year-old girl with Hodgkin's disease who developed pneumonitis following lymphangiography.
Massive ascites associated with endometriosis is uncommon. Recurrent episodes of bloody ascites as a result of endometriosis occurred in a woman with familial Mediterranean fever, who underwent therapy for induction of ovulation. Ovulatory agents may provoke accumulation of ascites in patients with endometriosis.