In the present retrospective study we determined the frequency of glucose intolerance in active untreated acromegaly, and searched for risk factors possibly supporting the emergence of the diabetic condition. Among 43 patients, 8 (19%; 95% CI: 8-33%) had diabetes mellitus and 2 (5%; 1-16%) impaired glucose tolerance. No impaired fasting glycemia was demonstrable. The frequency of diabetes was on average 4.5 times higher than in the general Slovak population. Ten factors suspected to support progression to glucose intolerance were studied by comparing the frequency of glucose intolerance between patients with present and absent risk factors. A family history of diabetes and arterial hypertension proved to have a significant promoting effect (P<0.05, chi-square test). A significant association with female gender was demonstrated only after pooling our data with literature data. Concomitant prolactin hypersecretion had a nonsignificant promoting effect. In conclusion, the association of active untreated acromegaly with each of the three categories of glucose intolerance (including impaired fasting glycemia, not yet studied in this connection) was defined as a confidence interval, thus permitting a sound comparison with the findings of future studies. Besides a family history of diabetes, female gender and arterial hypertension were defined as additional, not yet described risk factors.
Objective: To evaluate whether long-term exposure to heavy environmental pollution with polychlorinated biphenyls (PCBs) could result in impairment of thyroid status as evaluated by an epidemiological field survey. Methods: Thyroid volume (ThV) was measured by ultrasound in 238 employees of a factory (EMP) which previously produced PCBs and 454 adolescents from the surrounding area polluted by PCBs. Controls (C) were 572 adults and 965 adolescents from much less polluted areas. In the 238 EMP and various numbers (shown in parentheses) of adult C the levels of thyroid-stimulating hormone (TSH) (n ¼ 498), thyroxine (n ¼ 498), thyroglobulin (n ¼ 278) and thyroid antibodies (anti-peroxidase (TPO Ab), n ¼ 517; anti-thyroglobulin (Tg Ab), n ¼ 455; anti-TSH receptor (TSHR Ab), n ¼ 238) were estimated in serum, while only TSH and TPO Ab were measured in 269 and 171 adolescents from polluted and control areas respectively. In several subjects in whom thyroid disease was suspected, total tri-iodothyronine or free thyroxine and tri-iodothyronine were measured. In a total of 362 adults and adolescents the urinary iodine was estimated. Results: Using the Mann-Whitney test, ThV in EMP (mean Ϯ S.E. ¼ 18.85 Ϯ 0.69 ml, median ¼ 17.3 ml, upper quartile ¼ 22.9 ml, n ¼ 238) was significantly higher (P < 0.001) than that in C (13.47 Ϯ 0.48 ml, 11.5 ml, 15.3 ml, n ¼ 486 respectively). Similarly, ThV in adolescents from the polluted area (9.37 Ϯ 0.17 ml, 8.9 ml, 11.0 ml, n ¼ 454 respectively) was significantly higher (P < 0.001) than that in C (8.07 Ϯ 0.10 ml, 7.6 ml, 9.6 ml, n ¼ 965 respectively).In adults, a significantly increased prevalence of TPO Ab (P<0.05) was found (using the chi-square test) in EMP women of all ages (54/190) vs C women (70/282), in EMP women aged 31-50 years (40/117 vs 70/282 respectively) and those aged 41-50 years (28/77 vs 54/215 respectively). Compared with C, there was also a higher prevalence of Tg Ab in EMP women aged 31-60 years (36/169 vs 50/342 respectively) and of TSHR Ab (P < 0.001) in the group of EMP men and women (25/238) vs sex-and age-matched C (6/238).No difference between EMP and C was found in the level of thyroxine (mean Ϯ S.D. ¼ 116.1 Ϯ 31.2 nmol/l, n ¼ 238 vs 112.2 Ϯ 37.0 nmol/l, n ¼ 460 respectively), TSH in the range 0.1-4.5 mU/l (1.56 Ϯ 0.86 mU/l, n ¼ 219 vs 1.51 Ϯ 0.84 mU/l, n ¼ 460 respectively), prevalence of TSH >4.5 (14/238 vs 28/498 respectively) and <0.1 mU/l (5/238 vs 10/498 respectively). The prevalence of individuals without any defined clinical or laboratory signs of thyroid disorders among EMP who had worked in the factory for 21-35 years (43/128, 33.6%) was significantly lower than that in twice as many matched C (118/256, 46.1%, P < 0.025) or in EMP who had worked for only 11-20 years (36/73, 49.3%, P < 0.05).In adolescents, no difference was found in the prevalence of TPO Ab or TSH >4.5 mU/l between the polluted (17/269, 6.3% and 2/243, 0.8% respectively) and C areas (15/171, 8.5% and 4/140, 2.8% respectively). The median values of urinary iodine were in the op...
X-linked adrenal hypoplasia congenita (AHC) is a rare developmental disorder associated with primary adrenal insufficiency and combined primary and secondary male hypogonadism. It is caused by deletions or mutations of the NR0B1 (DAX1) gene encoding DAX1, an atypical orphan member of the nuclear receptor superfamily. The continuous molecular genetic analysis of male patients with primary adrenal insufficiency revealed 13 novel mutations within the coding region of the NR0B1 gene which are predicted to inactivate the DAX1 function. These were three nonsense mutations (c.312C>A, p.Cys104X, c.670C>T, p.Gln224X; and c.873G>A, p.Trp291X), five duplications (c.269_270dup, c.421_422dup, c.895_896dup, c.989dup, c.999_1000dup), and five deletions (c.483del, c.745_746del, c.734_740del, c.1092del, and c.1346del). All of the mutations resulted in a premature stop codon destroying the ligand binding domain of the predictive DAX1 protein.
Taking the mean -2 SD result as a threshold, FP value of 500 nmol/L can be consider as cut-off at 30 min in the LDT for defining the intact adrenocortical function, independently of age and body weight, body surface area.
A specific radioimmunoassay of llß4iydroxy-4-androstene-3,17-dione, an androgen of exclusively adrenal origin, is described and evaluated. The antiserum was raised in rabbits using 6ß,llß-dihydroxy-4-androstene-3,17-dione-6ß-hemisuccinate:bovine serumalbumin conjugate äs an immunogen. The method has been used for determination of the plasma levels of the hormone in healthy subjects, including children, with regard to the possibility its use äs a laboratory marker for monitoring corticoid therapy in patients with congenital adrenal hyperplasia and in patients with various endocrine disorders, under basal conditions and after dynamic tests. The plasma levels of llß-hydroxyandrostenedione (means ± s.d.) in healthy persons at 8 a. m. were 8.69 ± 2.88 (men), 7.72 ± 2.85 (women), 8.73 ± 5.13 (boys) and 7.88 ± 5.23 (girls) nmol/L respectively. The hormone cöncentrations followed the pattern of circadian rhythm of Cortisol, they were increased markedly after cprticotropin and suppressed by dexamethasone. t*. -sone, and its pattern of production is independent of the menstrual cycle in women (2, 3). It originales llß-Hydroxy-4-androstene-3,17-dione (llß-hydroxy-frorn adrenal 11 ß-hydroxylation of androstenedione androstenedione) is believed to be an androgen of rather than from side chain cleavage of Cortisol (4). exclusively adrenal origin, measurement of which In the study of its dynamics, its metabolic clearance could serve äs an indicator of adrenal contribution rate, the main distribution volumes and both blood to an overall androgen production (1-3). This is levels and urinary secretion rates were determined (5). sustained by the observations that llß^hydroxyan-Values close to those of its precursor androstenedione drostenedione levels follow the circadian rhythm of were obtained, the blood production rate being howcortisol, its production is stimulated by both cortico-ever lower than that of androstenedione, in agreetropin and corticoliberin but not by human chorionic ment with the fact that a portion of the latter origigonadotropin and supresses markedly by dexametha-nates from the gonads.
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