Biomedical subjects
Publications and source records attributed to S Mathur.
Two case reports of patients with myasthenia gravis, premature menopause at ages 18 and 29 years, and evidence of thyroid and ovarian autoimmunity are presented. Both patients had elevated gonadotropins, sex steroid values in the menopausal range, and ovaries without follicular activity. An autoimmune etiology is suggested because of the high titers of antithyroid and antiovarian antibodies.
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Seventeen of 30 patients with chronic vaginal candidiasis (CVC) of at least 5 years duration had varying degrees of menstrual problems and defective T lymphocyte function; 8 developed amenorrhea. In a group of 40 CVC patients, titers of autoantibodies to ovary, thymocytes, a T-cell line (CCRF-CEM), and a B-cell line (RN114) were significantly higher than those in 45 normal females (69 +/- 3 vs. 5 +/- 2, 70 +/- 27 vs. 4 +/- 2, l7 +/- 6, vs. 4 +/ 2, and 73 +/- 24 vs. 8 +/- 5, respectively, mean +/- S.E.). Antibody titers to sperm, T-cell line HSB-2, and B-cell lines RAJI and BALL-1 were within the normal range. Significant correlations were found between anti-Candida, anti-ovarian, and anti-thymocyte antibody titers. Similar results were found for 6 patients with chronic mucocutaneous candidiasis (CMCC) and in serial samples obtained over a one-year period from a representative patient with both CVC and CMCC. The anti-T-lymphocyte antibodies in these patients were directed primarily against non-suppressor (predominately helper) T cells. Absorption of the sera with either Candida cells, ovarian follicle cells, or thymocytes reduced all three antibody titers; absorption with sperm or B-cell lines did not alter the titers. These results suggest the presence of one or more cross-reactive antigens on ovarian follicle, T lymphocytes (especially the helper cell subpopulation), and Candida.
A case of mucinous adenocarcinoma of the renal pelvis occurring in association with staghorn calculus and severe pyelonephritis is reported. The incidence and aetiopathogenesis of this neoplasm is briefly discussed.
Since seminal components can mediate immunosuppression in vitro, it is possible that some antigen(s) may be common to both the reproductive and immunologic systems. In a group of 70 couples with unexplained infertility, 50 "autoimmune" males and 40 "isoimmune" females had lower than normal percentages of total T cells (mean values +/- standard error of the mean 63 +/- 2% and 60 +/- 2% for immune males and females, respectively, versus 77 +/- 2% and 78 +/- 5% for 50 normal males and females, respectively; P < 0.001). Sheep red blood cell (SRBC) rosetting of lymphocytes was significantly reduced when SRBC were preincubated with sperm extracts (61 +/- 4% versus 9 +/- 2%; P < 0.001) but not when SRBC were incubated with normal serum or when lymphocytes were preincubated with sperm extracts. Antisperm antibody titers in the patients' sera (48 +/- 13) were correlated with their antithymocyte antibody titers (18 +/- 3) (P < 0.01). Moreover, antithymocyte antiserum (titer 1024) cross-reacted with sperm extract (titer 128), and vice versa. This cross-reactivity was significantly reduced by absorption of the sera with sperm cells (P < 0.001), thymocytes (P < 0.001), or white blood cells (P < 0.005). Absorption of autoimmune sperm extracts and seminal plasmas with thymocytes or sperm cells reduced the Coombs' titers, especially immunglobulin G (P < 0.01) and immunoglobulin A (P < 0.025). Similar results were obtained in passive hemagglutiation, immunofluorescence, and cytotoxicity assays. We conclude that sperm and T cells share a common antigen(s).
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A new antigenic determinant was discovered with a hemagglutination-inhibition assay system. Designated Hv(1), it is located in the variable region of human immunoglobulin heavy chains of the G, M, and A classes. Pedigree and population analyses suggest that it has an autosomal dominant mode of inheritance. This represents the first description of an allotypic determinant in the variable region of human immunoglobulins.
The effect of changes in progesterone (P) and estradiol (E2) on titres of antibodies to Candida albicans was studied by measurement of these three parameters in the following endocrinologically diverse human groups: normal females, gonadal dysgenetics, users of a sequential oral contraceptive (Oracon) and normal males. In females, C. albicans titres (mean +/- s.e.m.) were significantly higher (P less than 0.05) in the luteal (74 +/- 14) than in the follicular phase (34 +/- 19) of the cycle, and there were similar significant increases in P and E2. In the gonadal dysgenetic group (n = 29), with E2 levels comparable with males, the antibody titres were also equivalent to those in normal males (40 +/- 0.5), but were significantly lower than those of normal females in the follicular phase (P less than 0.05). In contrast, Oracon users, with high blood progestin levels, had C. albicans titres (118 +/- 15) significantly higher (P less than 0.001) than those of control subjects during the follicular phase. A significant correlation (P less than 0.05) was observed between P and C. albicans titres (mainly IgA) in randomly selected samples (n = 112) from normal females during the follicular and luteal phases, and in two subjects from whom blood samples were drawn daily for the entire cycle. In the latter, an increase in E2 but not P in the late follicular phase was accompanied by a marked decrease in C. albicans titres. No changes were observed in total immunoglobulin levels or antibodies to SRBC or Herpes virus in response to the marked changes in hormones. These results indicate that the production of antibodies to C. albicans may be specifically influenced by sex steroid hormones, being enhanced by P and E2 at low levels but depressed by E2 at high levels.
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Titers of serum antibody to Candida albicans were studied in 111 IgA-deficient subjects by the passive hemagglutination method. Circulating antibodies to C. albicans (mean titer, 1:7) were found in only 7.3% of the 111 subjects, as compared with 80% of 137 controls (mean titer, 1:16). However, two IgA-deficient patients with systemic candidiasis were positive for these antibodies (mean titer, 1:64). Indirect immunofluorescence tests indicated that the antibody response in IgA-deficient subjects to superficial or deep-seated infection with C. albicans consists mainly of immunoglobulins of the IgG rather than of the IgM class.
Serum antibody titers to Candida albicans were estimated in 37 women with recurrent vaginal candidiasis and in 148 normal American and Finnish subjects, using the passive-hemagglutination technique. The antibody titers ranged from 0 to 16 in normal individuals and 4 to 256 in vaginal candidiasis patients. Antibodies to C. albicans in the sera of vaginal candidiasis patients were found to be the secretory immunoglobulin A type, as determined by gel filtration and double-diffusion tests. The results were confirmed by the indir-ct fluorescent-antibody technique. Our findings suggest that, in vaginal candidiasis, the antibody response is mainly local, consisting of secretory immunoglobulin A, some of which finds its way into systemic circulation.
Elevated levels of immunoglobulin E anti-Candida antibodies were observed in the sera of patients with systemic and vaginal candidiasis and in cervicovaginal washings of the latter.
The possible influence of sex steroid hormones on circulating IgE levels in general and IgE anti-Candida antibodies in particular was studied by quantification of plasma levels of progesterone, estradiol and IgE (total and anti-Candida-specific) in females during the follicular and luteal phases of the menstrual cycle, and during pregnancy. IgE levels during the follicular and luteal phases were not significantly different, although the mean values for the luteal phase were slightly lower. This trend was apparent in daily samples from two normal females during one menstrual cycle. During pregnancy, when the levels of circulating sex steroids were high, IgE levels were only slightly higher than in the follicular and luteal phases. In men and in gonadal dysgenetics, circulating progesterone levels were similar to those of women during the follicular phase (i.e., lower than in the luteal phase or in pregnancy), but the IgE levels were not different. The apparently low levels of IgE during the luteal phase may therefore be due to physiological factors other than fluctuations in the sex steroid hormones. From the present studies, it is apparent that sex steroid hormones have little or no effect on humoral IgE levels, in marked contrast to previously described correlations for other immunoglobulins, especially anti-Candida antibodies.
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