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Biomedical subjects

L J Valenta

Publications and source records attributed to L J Valenta.

At least 55 records · Page 3Linked to original sources
PubMed1982

Correlation of the HLA-A1,B8 haplotypes with circulating autoantibodies in a family with increased incidence of autoimmune disease.

Two cases of Addison's disease, two cases of scleroderma, three cases of primary hypothyroidism possibly due to Hashimoto's thyroiditis, three cases of diabetes mellitus, and two cases of ovarian failure and secondary amenorrhoea were diagnosed in a single family. In 44 members of four generations of the family including all the diseased, we have performed HLA typing and measurement of circulating autoantibodies. All diseased patients were older than 12 years, all possessed HLA B8 antigen, and all but two showed specific autoantibodies in their serum. In contrast, none of the family members without HLA B8 developed any of the autoimmune diseases in spite of the fact that in 13 of them some circulating autoantibodies were demonstrable in the serum. It is concluded that genetic factors play an essential role in the development of autoimmunity in the studied family. The individuals acquire circulating autoantibodies as they develop the disease. Environmental factors play a secondary role as evident from the age dependence. HLA typing can become an important diagnostic tool in identifying the individuals at a risk of autoimmune disease. Detection of circulating serum autoantibodies alone correlated poorly with the autoimmune disease.

Addison Disease↗
PubMed1982

Immunological aberration in primary hyperparathyroidism.

Altered immunological reactivity in primary hyperparathyroidism is suggested by the strong association between this disorder and malignancy. The present study was carried out to determine whether altered lymphocyte proliferation in response to common mitogens (PHA, Con-A, PWM) exists in primary hyperparathyroidism, and, if so, whether the abnormality resides in the lymphocytes or in humoral factors present in the plasma of patients with hyperparathyroidism. Ficoll-Hypaque purified lymphocytes from 6 patients with primary hyperparathyroidism and 4 normal volunteers were stimulated with PHA, Con-A and PWM in the presence of plasma from patients with primary hyperparathyroidism and normal AB+ plasma. The incorporation of [3H]thymidine in unstimulated (control) and stimulated cultures was determined. The results demonstrate that lymphocyte proliferation was significantly higher when both patients' and normal lymphocytes were stimulated with mitogens in the presence of patients' plasma. These findings suggest that plasma from patients with primary hyperparathyroidism contains a potentiator of lymphocyte mitogenesis, or, alternatively lacks an inhibitor of lymphocyte activation that is present in normal plasma.

Adult↗
PubMed1982

Pseudo-Cushing's syndrome: the role of alcohol.

The mechanisms responsible for the genesis of pseudo-Cushing's syndrome are poorly understood. We studied the effect of acute ethanol administration on the hypothalamic-pituitary-adrenal axis in five chronic alcoholic patients and three normal volunteers. Ethanol was administered alone and together with beta 1-24 ACTH given intravenously. Baseline plasma ACTH and cortisol concentrations were significantly higher in the patients than in normal controls (p less than 0.05). Acute ethanol administration produced no significant change in the mean plasma ACTH concentration, failed to augment the effect of exogenous ACTH on the adrenal gland, and produced similar changes in the serum cortisol and aldosterone concentration in both the normal controls and the alcoholic patients. We speculate that pseudo-Cushing's syndrome may represent a state of stress-induced hypercortisolemia secondary to multiple episodes of subacute withdrawal from ethanol.

Adrenocorticotropic Hormone↗
PubMed1982

Modulatory role of gamma-aminobutyric acid (GABA) in the regulation of gonadotropin secretion in patients with chronic renal failure.

The role of gamma-aminobutyric acid (GABA) in the regulation of gonadotropin secretion in renal failure, was studied in 5 patients with chronic renal failure who were on maintenance dialysis. Di-n-propylacetic acid (valproic acid-VA), a GABA-transaminase inhibitor which has been shown to increase brain GABA levels, was used in the study. VA produced no significant change in the basal serum LH and FSH concentrations, or in E2 or T concentrations in the renal failure patients, or the E2 and P concentrations in normal controls, but augmented the delta LH (maximum increment above baseline) and delta FSH response to LH-RH. delta LH rose from 30.4 +/- 12.7 mIU/ml (mean +/- SD) to 41.1 +/- 16.8 mIU/ml (p less than 0.01) after VA, while delta FSH rose from 2.8 +/- 1.8 mIU/ml to 3.8 +/- 1.6 mIU/ml (p less than 0.05). The findings support a modulatory role for GABA in gonadotropin secretion in chronic renal failure.

Adult↗
PubMed1981

Effect of di-N-propylacetic acid (valproic acid) on the TSH response to TRH--a presumptive role for gamma aminobutyric acid.

The effect of di-n-propylacetic acid (valproic acid), an inhibitor of gamma aminobutyric acid (GABA) transaminase, was studied with reference to its effect on the serum concentration of thyroid hormones, baseline serum TSH concentration and TRH stimulated TSH release, in seven normal controls and six patients with primary hypothyroidism. All volunteers took 250 mg of valproic acid administered orally, four times daily for 3 days. Baseline serum T4 and TSH concentrations were unaffected by valproic acid administration (p less than 0.05) while serum T3 concentrations fell in all volunteers (p less than 0.001). Serum T3 concentration (mean +/- SD) fell from 116.3 +/- 18 ng/dl to 101.7 +/- 15 ng/dl in the control group and from 94.2 +/- 47.9 ng/dl to 81.5 +/- 43.2 ng/dl in the hypothyroid group. Valproic acid produced a decline in stimulated serum TSH concentrations (delta TSH--maximum increment above baseline) in all controls and patients studied (p less than 0.01). delta TSH (mean +/- SD) declined from 16.1 +/- 4.7 microunits/ml to 10.5 +/- 5.8 microunits/ml in the control subjects and from 43.1 +/- 25.4 microunits/ml to 29.7 +/- 18 microunits/ml in the hypothyroid patients. Based on the data presented, it is postulated that GABA plays an inhibitory role either by acting directly on the pituitary gland inhibiting TSH release, or by inducing the secretion of a hypothalamic TSH-inhibitory factor. The data do not exclude a direct pharmacological effect of valproic acid on pituitary TSH release. Decrease in serum T3 following valproic acid may be due to peripheral mechanisms.

4-Aminobutyrate Transaminase↗
PubMed1981

Effects of valproic acid, naloxone and hydrocortisone in Nelson's syndrome and cushing's disease.

Two patients with Nelson's syndrome and one patient after bilateral adrenalectomy for Cushing's disease, without any evidence of Nelson's syndrome, were studied with respect to the effect of hydrocortisone, naloxone and valproic acid (a GABA transaminase inhibitor) on ACTH secretion. Hydrocortisone suppressed plasma ACTH concentrations to normal in the patient without Nelson's syndrome, but failed to do so in the two patients with Nelson's syndrome. Naloxone and valproic acid caused a decline in plasma ACTH concentrations in the patients with Nelson's syndrome, but produced no change in the patient without Nelson's syndrome. Secretion of ACTH may thus be influenced by both opiate peptide and by gamma aminobutyric acid, as well as by the cortisol concentration, these agents may act at different sites to inhibit ACTH release by the tumour.

Adrenalectomy↗
PubMed1981

Hyperthyroidism and propylthiouracil-induced agranulocytosis during chronic lithium carbonate therapy.

The authors describe the case of a 49-year-old woman who developed a goiter, mild symptoms of hyperthyroidism, and grossly elevated thyroid function tests after 2 years of treatment with lithium carbonate. Thyroid microsomal autoantibodies were also present. She was retreated with propylthiouracil and improved, but within 3 months she developed agranulocytosis. Propylthiouracil was discontinued, and the patient was treated with antibiotics and recovered. She was then given 131I to control her hyperthyroidism. The case is an example of the rare association of hyperthyroidism with lithium, which usually suppresses thyroid function, and demonstrates that lithium carbonate cannot prevent agranulocytosis caused by propylthiouracil.

Agranulocytosis↗
PubMed1981

Effect of calcium and potassium on basal and gonadotrophin-releasing hormone (GnRH) stimulated release of luteinizing hormone (LH).

LH release from the anterior pituitary was studied by the method of an in vitro superfusion of bovine anterior pituitary tissue slices. LH release was stimulated by increased potassium concentration (23 and 59 mM) and by synthetic GnRH (1 and 4 ng/ml). While the potassium effect was completely dependent on extracellular calcium, that of GnRH was only partially dependent. Additive effect was observed when GnRH followed enhanced potassium infusion but not vice versa. This suggested that the mechanism responding to potassium may be contained within the stimulatory pathway of GnRH. There was a difference in the dynamics of the LH response: maximum response was attained in about 10 min of potassium infusion while infusion of GnRH resulted mostly in multiphasic stepwise release of LH reaching a plateau in 60 to 90 min only. It is speculated that the potassium effect involves the K+, Na+ dependent ATPase.

Animals↗
PubMed1980

Gonadotropin-releasing hormone receptor binding in bovine anterior pituitary.

Synthetic gonadotropin-releasing hormone (GnRH) was monoiodinated at a high specific radioactivity with 125I. The iodinated hormone retained full biological activity as assessed by the release of luteinizing hormone in vitro from bovine anterior pituitary tissue slices. Specific binding of 125I-labeled gonadotropin-releasing hormone of high affinity and low capacity was obtained using dispersed bovine anterior pituitary cells. The binding had sigmoid characteristics, compatible with the presence of more than one binding site. The subcellular fraction responsible for binding was identified with the plasma membranes. However, significant binding also occurred in the secretory granules fraction. The plasma membranes were solubilized with sodium dodecyl sulfate. Using gonadotropin-releasing hormone covalently coupled to a solid phase, a protein was purified by an affinity technique from the solubilized plasma membrane preparation which possessed similar binding propperties as plasma membranes, both intact and solubilized. The protein migrated as a single component on polyacrylamide gel in sodium dodecyl sulfate and the estimated molecular weight was 60 000. The character of the gonadotropin-releasing hormone concentration dependence binding as well as association kinetics were multiphasic and suggested the presence of more than one binding site. When analyzed by the Hill plot, the Hill coefficient of all binding curves was always greater than one which is compatible with positive cooperativity. This was further supported by the dissociation studies where the dissociation rate was inversely proportionate to both the gonadotropin-releasing hormone concentration and the time interval during which the gonadotropin-releasing hormone-gonadotropin-releasing hormone receptor protein complex was formed. Using difference chromatography, aggregation of the purified gonadotropin-releasing hormone receptor protein was demonstrated to occur upon its exposure to gonadotropin-releasing hormone. The formed macromolecular complexes bound preferentially 125I-labeled gonadotropin-releasing hormone. It is concluded that a single receptor protein is responsible for gonadotropin-releasing hormone binding in the bovine anterior pituitary. It is a part of the plasma membranes. Its interaction with gonadotropin-releasing hormone provokes transitions of the protein into different allosteric forms and this may be related to the biological effect of gonadotropin-releasing hormone on gonadotropin secretion.

Animals↗
PubMed1980

Post-traumatic hypopituitarism due to a hypothalamic lesion.

Two patients were studied who suffered from severe head trauma with skull fracture. Hypopituitarism developed in both. Because of elevated serum prolactin levels and because of preserved response of some of the pituitary hormones to exogenous thyrotropin and gonadotropin-releasing hormones, the responsible lesion in both cases was most likely suprasellar. Findings of interest included slightly elevated thyroid-stimulating hormone (TSH) levels in the presence of hypothyroidism in one of the patients, and dissociation of the luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responsiveness to both gonadotropin-releasing hormone and clomiphene citrate in the other patient. It is suggested that the diagnosis of post-traumatic hypopituitarism be considered in patients with head trauma and that periodically appropriate laboratory testing be performed to confirm the diagnosis.

Adolescent↗
PubMed1980

Colonic mucosal potential differences in the management of 21-hydroxylase deficiency.

Use of the colonic potential difference as a means of assessing the efficacy of different suppressive steroid regimens was explored in a patient with incomplete 21-hydroxylase deficiency. Changes in the potential difference were found to closely reflect changes in the plasma concentration of hormones such as aldosterone, androstenedione, dehydroepiandrosterone, and dehydroepiandrosterone sulfate. Dexamethasone, which produced the most marked change in the potential difference, also produced the most suppression of the plasma steroid concentrations. It is suggested that the colonic potential difference can be used as a simple alternate means of assessing the efficacy of suppressive steroid therapy in some patients with 21-hydroxylase deficiency.

Action Potentials↗
PubMed1979

Esophageal motor function in Graves' disease.

Esophageal motor function was studied in 10 patients with untreated Graves' disease and 15 healthy volunteers who served as controls. A noncompliant recording system with a triple-lumen assembly was used. Resting upper- and lower-esophageal-sphincter pressures, amplitude, duration, and velocity of peristaltic contractions in the body of the esophagus, and the number of repetitive and simultaneous contractions were measured. There was no significant difference in peristaltic amplitude and duration between the controls and the patients with Graves' disease. However, there was a significant increase in velocity of contractions in Graves' disease as compared with controls. On restudy of 5 patients who became euthyroid after treatment with 131I, all the measured parameters were unchanged except for velocity of the peristaltic contractions. The value for this measurement decreased essentially to the same as that found in the control subjects. It is concluded that: (1) thyrotoxicosis increases the propagation velocity of esophageal contraction, and (2) thyroid hormones may play a physiologic role in the control of esophageal motor function.

Adult↗
PubMed1979

Thyroid function studies in the nephrotic syndrome.

Total serum and urinary thyroxine (T4), triiodothyronine (T3), and thyroxine-binding globulin (TBG) as well as serum free T4, thyroid-stimulating hormone (TSH), and T3 resin uptake (T3RU) were measured in seven patients with the nephrotic syndrome. The nephrotic syndrome was defined by proteinuria exceeding 3 g/24 h. All patients were clinically euthyroid. Most values for total serum T4, free T4, T3, T3RU, TBG, and TSH were within normal limits. However, the mean serum T3 and TBG values were significantly lower in patients compared with the control group. The values (mean +/- 2 SD) for urinary T4 were 24.3 +/- 20.3 in the patient group and 1.5 +/- 0.7 microgram/24 h in the control group. Urinary T3 values for patients and the control group were 2100 +/- 856 and 848 +/- 253 ng/24 h respectively. Urinary TBG was 2.1 +/- 1.8 mg/24 h in the patients and undetectable in the control group. There was no correlation between daily urinary T3 and T4 and urinary TBG. There was a weak correlation between daily urinary protein excretion and urinary T4 (r = 0.5).

Adult↗