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Biomedical subjects

B A Lamberg

Publications and source records attributed to B A Lamberg.

At least 19 recordsLinked to original sources
PubMed1992

The value of visual evoked potentials in optic neuropathy of Graves' disease.

Visual evoked potentials (VEP) were tested in patients with ophthalmopathy (OP) of Graves' disease (GD) before treatment and half-a-year and 5-7 yr after orbital decompression (7 patients) or retrobulbar irradiation (3 patients). Five patients not requiring treatment for OP and 16 healthy subjects served as controls. Treatment of OP was given on clinical grounds including decreased visual acuity (VA) indicating optic neuropathy. Before treatment VA was decreased in 5 out of 19 eyes whereas VEP were abnormal in all. The mean latency at N60 both in the operated (83.1 +/- 21.6 ms) and in the irradiated groups (80.9 +/- 7.0 ms) was significantly different from that in the untreated group (62.6 +/- 8.2 ms; p < 0.001) and the healthy subjects (58.9 +/- 6.3; p < 0.001). At P120 only the latency of the operated group differed significantly from that of the other groups (p < 0.001). There was a relationship between the eye muscle changes seen on CT scans and the ophthalmopathy score (according to the classification of the American Thyroid Association) and the latency both at N60 and P120. A change from a V-shape to a W-shape of the waves occurred more often in the treated patients before therapy than in the other groups. Two patients had multiphase VEP in both eyes which improved after treatment. After adequate clinical response the visual acuity improved in one of the 5 patients with initially depressed VA. VEP, initially abnormal in all, improved in 7 of the 19 eyes (37%) but further deterioration was observed in 8 (42%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Visual evoked potentials in Basedow's ophthalmopathy before and after orbital decompression or retrobulbar irradiation.

VEP are an objective and a more sensitive sign of optical neuropathy in Graves' ophthalmopathy than is visual acuity. A correlation exists between VEP and the changes in the external eye muscles as visualized on CT scans. VEP should always be registered if CT changes are present. Improvement of optic neuropathy as evaluated from VEP seems to be remarkably infrequent.

Evoked Potentials, Visual↗
PubMed1991

Endemic goitre--iodine deficiency disorders.

Endemic goitre occurs when the prevalence of thyroid enlargement in the population of an area exceeds 10%. With few exceptions its cause is iodine deficiency superimposed on other goitrogenic factors normally present and responsible for sporadic goitre. Iodine deficiency causes significant health problems and so, the term iodine deficiency disorders (IDD) has been introduced. The earliest sign of IDD is goitre, but these disorders also include cretinism, neonatal hypothyroidism and congenital defects, as well as retardation of mental and physical development etc. IDD are a worldwide problem: WHO estimates that substantially more than 800 million people are at risk and more than 190 millions suffer from IDD; over 3 million people have cretinism and in the largest and worst affected areas many millions suffer from mental and physical developmental defects. IDD can be totally eliminated by prophylaxis using iodine administered in salt, oil or some other vehicle. Problems over preventing iodine deficiency relate to difficulties in the handling and distribution of the iodized vehicle in some parts of the world and on the political will to introduce preventive schemes. In only a very few areas does the presence of goitrogenic agents in the environment cause endemic goitre despite adequate iodine supply. In a limited number of places excessive iodine from seaweed used as staple food results in endemic goitre.

Adult↗
PubMed1979

Thyroid hormones and TSH, prolactin and LH responses to repeated TRH and LRH injections in depressed patients.

Twelve patients with unipolar depressive disorders received 600 microgram of synthetic TRH or LRH, in a random order, for 3 days each. Placebo injections were given as two 3-day courses prior to and between the active treatments. Serum TSH, prolactin (Prl) and LH were measured by radioimmunoassays prior to the experiment as well as immediately before and 20 min after each injection. Serum T4 and T3 were determined by radioimmunoassays before the treatments and 24 h after the first two TRH injections. Serum T4 level in depressed patients did not differ from controls. Serum T3 level in depressed patients was significantly below, and the reverse T3 level was slightly above the normal mean. However, the latter difference was not statistically significant due to the large variation of rT3 levels among the depressed patients. The TSH responses did not differ from that of controls after the first injection but the responses after the second injection were lower than in a control study. The Prl responses to TRH were sub-normal in seven out of eight patients. Blunted LH responses to LRH were seen in three patients.

Adult↗
PubMed1979

Suppression of the TSH response to TRH by thyroxine therapy in differentiated thyroid carcinoma patients.

Absent response of serum thyrotrophin (TSH) after stimulation with 200 micrograms synthetic thyrotrophin-releasing hormone (TRH) was used as a criterion of adequate suppression of TSH in the treatment of thyroid carcinoma patients with thyroxine. The mean causing total suppression of the response was 223 micrograms of thyroxine per day. At this dose level about 40% of the patients had serum thyroxine concentrations above the upper reference interval and only 10% had elevated triiodothyronine concentrations. In some patients the TSH response to TRH varied between absent and low normal when tested at long intervals. The ideal dose of thyroxine is obviously slightly higher than the smallest one causing total suppression of the TSH response to TRH, i.e. about 250 micrograms a day. The individual dose must be found using the TRH stimulation test because serum thyroid hormone levels cannot be used as a guideline for adequate dosage. In some patients the thyroid remnant of apparently normal thyroid tissue was not totally suppressed although the thyroxine dose was definitely above the level causing suppression of the response to TRH.

Adenocarcinoma↗
PubMed1979

Primary hypothyroidism preceding thyrotoxicosis: a report of 2 cases and a review of the literature.

Two cases are reported in whom primary hypothyroidism preceded thyrotoxic Graves' disease. The hypothesis is advanced that this sequence of events was mediated by spontaneous changes in the patient's autoimmune reactions to thyroid. In particular, it may reflect a spontaneous alteration in the balance between blocking antibodies reactive at or near the TSH receptor or cytotoxic thyroid autoimmune mechanisms on the one hand, and thyroid stimulating autoantibodies on the other.

Antibodies↗
PubMed1978

Nuclear binding of triiodothyronine and thyroxine in lymphocytes from subjects with hyperthyroidism, hypothyroidism and resistance to thyroid hormones.

Binding of triiodothyronine (T3) and thyroxine (T4) to nuclei of intact human lymphocytes was studied. The binding characteristics were analysed by Scatchard's method. In lymphocytes from euthyroid healthy subjects there was a single set of saturable nuclear T3 and T4 binding sites with an apparent mean equilibrium association constant of 3.3 X 10(10) l/mol and 1.7 X 10(10) l/mol, respectively. The estimated mean maximal specific binding capacity for T3 was 50 fmol/mg DNA and for T4 was 55 fmol/mg DNA, indicating that these two hormones may have a common receptor. In hyperthyroid and hypothyroid patients nuclear affinity for T3 and T4 was very similar to that for euthyroid reference subjects. In hyperthyroidism, T3 and T4 binding capacity was unaltered, whereas in hypothyroidism it was nearly twice as high as in euthyroidism. Lymphocytes from three members of a family with hereditary peripheral resistance to thyroid hormone action were studied. One set of saturable T3 and T4 nuclear binding sites with affinity constants similar to those in the euthyroid group was found. However, in these subjects the estimated binding capacity for T3 and T4 was rather low, indicating that the biochemical defect in this family might be a mild deficiency of nuclear receptor protein. Incubation with diphenylhydantoin and salicylate added in vitro did not alter the binding of T3 and T4 to lymphocyte nuclei. Nuclear binding was also not affected in patients receiving therapeutic amounts of diphenylhydantoin.

Adult↗
PubMed1978

Somatostatin inhibits the pentagastrin-induced release of serum calcitonin in medullary carcinoma of the thyroid.

The effect of somatostatin on the secretion of calcitonin was studied in four patients with medullary carcinoma of the thyroid (MCT). The basal serum calcitonin level was markedly elevated in all cases. A bolus injection (100 microgram) of somatostatin followed by an intravenous infusion (5 microgram/min) for 60 min suppressed the basal calcitonin level in three of the four patients by 24-42%, while it had no inhibitory effect in one case. In another experiment, the pentagastrin-stimulated (6 microgram/kg s.c.) calcitonin release was partially blocked by a simultaneous i.v. injection of somatostatin (200 microgram) in all four patients studied. These experiments add human calcitonin to the list of hormones whose release in inhibited by somatostatin.

Adult↗