Biomedical subjects

T F Nikolai

Publications and source records attributed to T F Nikolai.

At least 19 recordsLinked to original sources

PubMed1990

Linkage of the multiple endocrine neoplasia type 2B gene (MEN2B) to chromosome 10 markers linked to MEN2A.

The syndrome of multiple endocrine neoplasia type 2B (MEN 2B) resembles that of MEN 2A in that both include medullary carcinoma of the thyroid, pheochromocytoma, and autosomal dominant inheritance, but is distinct in that MEN 2B patients have neuromas of the mucous membranes. MEN2A has been linked to RBP3, D10S5, FNRB, D10S15, and D10Z1 near the centromere of chromosome 10. We examined linkage between MEN2B and RFLPs on chromosome 10 in all available members in two or three generations of 14 kindreds. The centromere marker D10Z1 was linked to MEN2B with a peak lod score of 5.42 at theta = 0.02. One possible recombinant was observed between D10Z1 and MEN2B. Multipoint analysis of RFLPs at FNRB, D10Z1, RBP3, and D10S15 gave a peak lod score of 7.12 at the midpoint between D10Z1 and RBP3 on the long arm (band q11). The most likely gene order FNRB-D10Z1-MEN2B was 27 times more likely than MEN2B-FNRB-D10Z1 and 31/2 times more likely than FNRB-MEN2B-D10Z1. Additional data will be required to establish the order of these loci with confidence.

Chromosomes, Human, Pair 10↗

PubMed1990

Thyroid function and treatment in premenstrual syndrome.

In 1986 it was reported that a high percentage of women with premenstrual syndrome (PMS) were found to have thyroid hypofunction (TH), mostly subclinical hypothyroidism, as defined by an augmented response of TSH to TRH, and that all affected women had complete relief of PMS symptoms with L-T4 therapy. We studied baseline thyroid function (T4, T3 uptake, T3, TSH, and TSH response to TRH) in 15 normal women (group 1) and 44 women with PMS and treated 22 of the PMS women with L-T4 (group 2; 1.6 micrograms L-T4/kg dose) and the other half with placebo (group 3) for 2 months in a double blinded protocol. We found no evidence of thyroid dysfunction in group 2 or 3, except for 1 subject with slightly elevated TSH (6.2 microIU/mL) and moderate augmented response to TRH (change in TSH, 65 microIU/mL). During the treatment phase we found a complete relief of symptoms in 6 (27%), a partial relief of symptoms in 6 (27%), and some relief of symptoms in 12 (54%) in group 2. Whereas in group 3, 10 (45%) had complete relief, 5 (23%) had partial relief, and 15 (68%) had some relief of symptoms. These results show that 1) there is no significant thyroid disease in PMS; and 2) L-T4 is no better than placebo in treatment of PMS. We conclude that the high incidence of thyroid hypofunction previously reported in PMS is due to an unusually low TSH level for the limit of the normal range for the TRH stimulation test.

Adult↗

PubMed1989

Recovery of thyroid function in primary hypothyroidism.

In recent years transient primary hypothyroidism has reported with increasing frequency. Physicians are often unsure whether withdrawal of thyroid hormone to identify the transient hypothyroidism is indicated and cost-effective and in which patients this should be done. To study these questions, thyroid hormone therapy was withdrawn from 63 patients with proven primary hypothyroidism at 6 months and again at 1 and 3 years to determine if there was recovery of thyroid function. Of the 49 patients with primary hypothyroidism (PH) that was not attributable to such causes as drug therapy, surgery, iodine-131 therapy, or silent or subacute thyroiditis, only two patients recovered thyroid function. In the other 14 patients, hypothyroidism developed within 6 months postpartum. Nine of these 14 recovered thyroid function. Therefore, it appears that when PH is not related to certain specific causes or states, it is likely to be permanent. Furthermore, withdrawal of thyroid hormone therapy to assess recovery of thyroid function is unnecessary and not cost-effective.

Female↗

PubMed1987

Postpartum lymphocytic thyroiditis. Prevalence, clinical course, and long-term follow-up.

A group of 238 women were surveyed for thyroid disease at six and 12 weeks post partum. Twenty-seven (11.3%) of 238 entered into the study were found to have thyroid disease. Fifteen (56%) of 27 had positive microsomal hemagglutinin antibody titers. A spectrum of thyroid disease was found: persistent hypothyroidism (two patients), transient thyrotoxicosis followed by persistent hypothyroidism (one) or transient hypothyroidism (three), euthyroid goiter (five), transient thyrotoxicosis (seven), transient hypothyroidism (three), high-normal thyroxine levels (five), and low-normal thyroxine levels (one). All nine patients who underwent biopsy had active lymphocytic thyroiditis. Three-year follow-up of 25 of the 27 affected individuals revealed that 12 (48%) still had thyroid disease. This study demonstrates that there is a high incidence of postpartum thyroid disease, usually of a transient nature, and that only about one fourth of the cases are detected or clinically obvious.

Cross-Sectional Studies↗

PubMed1986

Functional activities and nonenzymatic glycosylation of plasma proteinase inhibitors in diabetes.

The functional activity of three of the major plasma protease inhibitors, alpha 1-proteinase inhibitor, antithrombin III and alpha 2-antiplasmin, has been measured in a series of persons with diabetes mellitus and compared with healthy controls. The mean specific functional activity of both diabetic plasma antithrombin III (50.8 +/- 7.0 U/mg) and alpha 1-proteinase inhibitor (35.3 +/- 5.6 mU/mg) was found to be significantly lower than in healthy controls (57.9 +/- 6.0 U/mg) and (42.2 +/- 10.7 mU/mg). No difference was detected in alpha 2-antiplasmin activity or levels. The glycosylated protein fraction of 83% of diabetic plasmas showed the presence of less than 1% of the total alpha 1-proteinase inhibitor when isolated by phenylboronate affinity chromatography. Incubation of normal plasma with 250 nmol/l glucose (a level approximately 6 X higher than encountered in uncontrolled diabetes) resulted in a 17% and 6% decrease in antithrombin III and alpha 1-proteinase inhibitor activities. We conclude that the decrease in specific activity of alpha 1-proteinase inhibitor is not related to nonenzymatic glycosylation, but the decrease in antithrombin III specific activity may be related.

Adult↗

PubMed1986

Reduced trypsin binding capacity of alpha 2-macroglobulin in diabetes.

The plasma proteinase inhibitor, alpha 2-macroglobulin, is usually elevated in diabetes. The trypsin binding capacity and the concentration of alpha 2-macroglobulin in 90 diabetics sera were compared with 30 age- and sex-matched normal sera. The mean alpha 2-macroglobulin concentration determined by radial immunodiffusion was 313 mg/dl for the diabetics as compared to 240 mg/dl for the healthy subjects (significantly higher, p less than 0.01). The mean of the ratio, mol trypsin bound/mol alpha 2-macroglobulin (molar binding ratio) for the Type I diabetics (n = 54), 0.82, was significantly lower than the mean of the healthy subjects, 0.87, or the mean of the Type II diabetics, 0.87. No relationship between the molar binding ratios and the levels of glycosylated hemoglobin was found. The alpha 2-macroglobulin was isolated from the plasma of 11 Type I diabetics and 7 normals. The maximum molar trypsin binding capacities of the diabetic alpha 2-macroglobulin were significantly lower. The mean for the diabetic alpha 2-macroglobulin was 1.72 vs. 1.97 for the normal alpha 2-macroglobulin. These results indicate that the trypsin binding function of alpha 2-macroglobulin is moderately impaired in diabetes. No differences were found in the extent of proteolytic cleavage of the 'bait region' of diabetic alpha 2-macroglobulin, autolytic cleavage or the methylamine reaction at the thiolester site between diabetic and normal alpha 2-macroglobulin. Nonenzymatic glucosylation of normal alpha 2-macroglobulin did not lower the trypsin binding capacity. The nature of the modification of alpha 2-macroglobulin leading to reduced trypsin binding capacity or the physiological significance is not yet known.

Adult↗

PubMed1986

Goitrous Hashimoto's thyroiditis. Lack of association with HLA antigens.

We studied HLA antigen frequency in 54 carefully selected patients with goitrous Hashimoto's thyroiditis. All had an appropriate clinical course, positive family history, antithyroid antibodies and/or a needle biopsy indicating chronic lymphocytic thyroiditis. We found no statistically significant association with any HLA-A, -B, -C or DR specificity.

Female↗

PubMed1980