Mitogen Induced Production of Polyclonal IgG is Decreased in Women With Severe Endometriosis

PROBLEM: The etiology and/or pathogenesis of endometriosis may involve aspects of both humoral and cellular immunity. METHOD: In this investigation, we analyzed the ability of B lymphocytes from distinct patient groups for production of IgGl, IgG2, and IgG3 following in vitro stimulation with polyclonal B-cell mitogens (pokeweed mitogen and Staphylococcus aureus Cowan strain I) after in vitro stimulation with polyclonal B-cell activators. RESULTS: We observed that the in vitro production of IgGl, IgG2, and IgG3 was identical among fertile controls (no endometriosis; N = 22), infertile women without endometriosis (N = 22), infertile women without endometriosis (N = 20) and patietns with stage 1 or 2 endometriosis (N = 31). In contrast, in vitro IgG2 production was significantly reduced among women with stage 3 or 4 endometriosis (N = 11) compared to controls (P < 0.001). CONCLUSION: Since the number of circulating B cells was similar in each patient group studied, the reduced production of IgG2 in patients with stage 3 or 4 disease was not merely due to fewer antibody producing cells in those subjects, and we speculate that the observed decrease in polyclonal IgG2 production among these patients is due to a primary defect. In additional studies, we observed that polyclonal IgG2 production was normal among stage 3 or 4 patients treated with danazol (N=ll), but significantly reduced in patients treated with gonadotropin releasing hormone agonists (N = 8). Although not conclusive, these data suggest that danazol may have the capacity to correct the defective production of polyclonal IgG2 in patients with severe endometriosis.     

Role of Cardiac Electrophysiologic Studies in Patients with Unexplained Recurrent Syncope

Cardiac electrophysiologic studies (EPS) with programmed electrical stimulation (PES) were performed in 30 patients with recurrent syncope to uncover possible arrhythmic etiology. All patients had undergone thorough medical and neurologic evaluation prior to EPS without finding a definitive cause for syncope. In the majority of patients an arrhythmic etiology for syncope was suspected but could not be documented utilizing the 12-lead surface ECG, extended in-hospital and/or ambulatory monitoring (for ≥ 48 hours) and exercise testing prior to the EPS. The studies provided a clue to the possible underlying rhythm disturbance which could have caused syncope in 16/30 patients. Sustained or nonsustained ventricular tachycardia and/or ventricular fibrillation was induced in 11/30, sinus node dysfunction in 4/30 and intra-His block in the remaining one. Fourteen of the 16 have remained free of symptoms following therapy based on results of EPS during a follow-up period ranging from 6–30 months (mean 16.5 ± 7.8). In 2/16 syncope recurred (one arrhythmic and one non-arrhythmic) despite pacemaker therapy for sinus node dysfunction detected during EPS. In the remaining 14/30 patients, EPS and PES did not induce arrhythmia which could account for patient symptomatology and therefore no specific therapy could be recommended. Eleven of these 14 patients experienced a recurrence of symptoms within a 6–25 month period (mean 16.2 ± 6.8). Of the 16 patients with inducible arrhythmias considered clinically significant, 15 had associated structural heart disease. On the other hand, of the 14 patients without clinically significant arrhythmias, structural heart disease could be detected in only three. It is concluded that cardiac arrhythmias constitute a common cause of unexplained syncope, particularly in patients with structural heart disease, and that EPS with PES can uncover the type of arrhythmic disturbance in a significant number of cases.