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Biomedical subjects

J Timsit

Publications and source records attributed to J Timsit.

At least 127 records · Page 7Linked to original sources
PubMed1989

The effect of somatostatin analogue on chiasmal dysfunction from pituitary macroadenomas.

The long-acting somatostatin analogue SMS 201-995 has been shown to be efficient in the treatment of somatotropic and thyrotropic adenomas. In some cases, it can suppress adenoma secretion and lead to tumor shrinkage. Pituitary macroadenomas are often associated with a vision-threatening chiasmal syndrome. In this series, SMS 201-995 was administered subcutaneously to eight patients with pituitary macroadenomas of various types responsible for severe long-lasting visual defects. An obvious improvement of both visual fields and acuity occurred in six patients, in two of these during the first 4 to 6 hours of treatment; in two patients, gonadotropic adenomas were unresponsive. Maximal improvement (normalization of visual fields in three cases) occurred within 6 to 45 days and was sustained during the 1- to 12-month follow-up period. This effect seems independent of the type of adenoma since the adenomas secreting growth hormone (GH) and thyroid-stimulating hormone and silent corticotropic-secreting adenomas responded as well as did two of the non-functioning adenomas. In one acromegalic patient visual improvement was obtained while the abnormal GH secretion remained unaltered. In all cases but one, no tumor shrinkage could be demonstrated. These data demonstrate that SMS 201-995 can rapidly improve the chiasmal syndrome due to pituitary macroadenoma, and suggest that this effect might be independent of a reduction in tumor volume.

Adenoma↗
PubMed1988

Hashimoto's thyroiditis with a monoclonal antithyroglobulin autoantibody: disappearance of the monoclonal antibody after thyroidectomy.

A 46-yr-old man had typical Hashimoto's thyroiditis (HT) and a serum monoclonal immunoglobulin (MIgG kappa). There was no evidence of disseminated lymphoid malignancy. Because of rapid enlargement of the goiter with pressure symptoms, a total thyroidectomy was performed. The surgery was followed by the complete disappearance of the MIgG kappa paralleled by the disappearance of serum antithyroglobulin autoantibodies. Thyroid sections demonstrated HT. Direct immunofluorescence assay showed diffuse infiltration by lymphocytes and plasma cells that were mainly IgG kappa positive. Moreover, the serum MIgG kappa had antithyroglobulin activity, as demonstrated by two different methods, namely labeling of focused serum proteins with radioiodinated human thyroglobulin and immunoadsorption of the monoclonal IgG on a human thyroglobulin affinity column. These results demonstrate that a monoclonal antithyroglobulin autoantibody was produced within the thyroid in a patient with HT. As the production of a MIg is regarded as the last stage preceding the malignant transformation of normal B lymphocytes, this report strongly suggests that a B lymphoma can directly emerge from the intrathyroidal lymphocytes involved in the pathogenesis of Hashimoto's thyroiditis.

Antibodies, Monoclonal↗
PubMed1988

Cell-mediated immunity to pancreatic islet cells in the non-obese diabetic (NOD) mouse: in vitro characterization and time course study.

The non-obese diabetic (NOD) mouse is an animal model of insulin-dependent diabetes mellitus (IDDM), in which 80% of the females become diabetic after the age of 12 weeks. Using an in vitro assay we investigated the capacity of spleen lymphocytes from NOD mice to inhibit the insulin secretion of normal islet cells after stimulation by theophylline plus arginine. Spleen cells from diabetic NOD mice inhibited the insulin release of DBA/2 islet cells. Depletion experiments using monoclonal antibodies demonstrated that inhibitory cells belonged to the Lyt2 positive T lymphocyte subset. The phenomenon was not restricted by the MHC class I K region, shared by NOD and DBA/2 mice, since lymphocytes from diabetic NOD mice also inhibited the insulin secretion of normal Wistar rat islet cells. Inhibitory T cells were detected in overtly diabetic mice but also in non-diabetic females aged 5-11 weeks indicating that they are not secondary to metabolic disturbances and might contribute to their onset. Conversely they were not found in male NOD mice although some of these mice show insulitis. The presence of these inhibitory T cells might thus represent an early and sensitive marker of anti-islet cell-mediated autoimmunity.

Aging↗
PubMed1987

The effect of subcutaneous infusion versus subcutaneous injections of a somatostatin analogue (SMS 201-995) on the diurnal GH profile in acromegaly.

Multiple sc injections of a long-acting somatostatin analogue (SMS 201-995) are currently used in the treatment of acromegaly. However, plasma GH concentration often reaches a pathological level (less than 5 micrograms/l) between two injections. In seven patients with active acromegaly we compared, in a short-term trial, the effect of SMS 201-995 administered by continuous sc infusion (50 micrograms and 100 micrograms a day) and by three sc injections (100 micrograms each). In six patients, plasma GH levels were significantly reduced regardless of the mode and dose of treatment (P less than 0.05). However, comparing diurnal profiles, 100 micrograms continuous sc infusion was more effective than discontinuous administration in reducing the number of GH levels above 5 micrograms/l (P less than 0.01). In two patients, continuous infusion was the only way to decrease all plasma GH values below 5 micrograms/l during the diurnal profile determination. Moreover, even when, in a long-term study, the dose of multiple injections was progressively increased to 500 micrograms three times a day, GH levels remained consistently elevated in one of these patients. Thus, in some acromegalic patients continuous sc injection seems currently the most efficient way of treatment with SMS 201-995.

Acromegaly↗
PubMed1986

[Hyperthyroidism induced by amiodarone].

The incidence of amiodarone-induced thyrotoxicosis remains unclear, partly due to the difficulties encountered in making a firm diagnosis based on thyroid hormone levels. Amiodarone is known to inhibit thyroxine (T4) metabolism, thus bringing plasma T4 concentrations up to levels that may simulate T4 toxicosis. On the other hand, the iodine overload due to the drug itself may create true hyperthyroidism. The purpose of this paper is to suggest practical means of detecting thyrotoxicosis in patients on amiodarone and to discuss the treatment of this side-effect.

Amiodarone↗
PubMed1986

[Hashimoto's thyroiditis with intra-thyroid production of a monoclonal antithyroglobulin autoantibody].

A 46-year old man had an Hashimoto's thyroiditis. The disease was particular by the voluminous goiter, associated with pressure symptoms and by the presence of a monoclonal Ig.G Kappa. Because of a possibly associated lymphoma of the thyroid, a total thyroidectomy was performed. Post-operative course showed a rapid and total disappearance of monoclonal Ig.G and antithyroglobulin autoantibodies. There was no pathological feature of thyroid malignancy. We could show that the monoclonal Ig.G bore an antithyroglobulin activity and that this monoclonal antithyroglobulin autoantibody was produced with in the thyroid. This case demonstrate that a monoclonal proliferation can arise from autoreactive B lymphocytes infiltrating the thyroid during Hashimoto's thyroiditis. Such a mechanism could explain, in some cases, the well-known association between lymphomas of the thyroid and Hashimoto's thyroiditis.

Antibodies, Monoclonal↗