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Biomedical subjects

R Doumith

Publications and source records attributed to R Doumith.

At least 19 recordsLinked to original sources
PubMed1993

[Antiphospholipid syndrome. A new cause of bilateral hemorrhage of the adrenal glands. 4 cases].

Four cases of adrenal insufficiency due to bilateral adrenal haemorrhage in patients with antiphospholipid syndrome are reported. The 1st patient had repeated episodes of thrombosis on a background of altered general condition; he was examined by computed tomography (CT) which showed enlarged and presumably tumoral adrenal glands; adrenal insufficiency was present and improved under hormone replacement therapy; the thrombotic episodes were attributed to the antiphospholipid antibodies; after a 5-year follow-up the antiphospholipid syndrome remained alone, and further examinations showed progressive adrenal atrophy. The 2nd patient had systemic lupus erythematosus with thrombocytopenia; because of abdominal pain CT was performed, showing bilateral adrenal enlargement; treatment with intravenous pulses of cyclophosphamide and high-dose immunoglobulins combined with corticosteroids failed, and splenectomy was performed disclosing an old adrenal haematoma which was evacuated. The 3rd patient had bilateral and asymmetrical adrenal hypertrophy at CT; subsequently, systemic lupus erythematosus was diagnosed with anti-prothrombinase and anticardiolipin accounting for the initial findings; follow-up examinations showed the formation of pseudocysts in the adrenals; following myocardial infarction the patient died of cerebral haemorrhage, and autopsy confirmed the presence of old, bilateral adrenal haematomas. The 4th patient had recurrent vein thrombosis associated with distal ischaemia, which prompted CT in search of a neoplasia; this examination revealed 2 large adrenal haematomas while anticardiolipin antibodies were found. In patients with antiphospholipid syndrome any functional or morphological abnormality of the adrenals should prompt a search for bilateral adrenal haemorrhage. Conversely, in all cases of adrenal insufficiency a search for antiphospholipid antibodies should be part of all aetiological investigations, and this search should be carried out prior to withdrawing corticosteroids in cases of systemic lupus erythematosus with antiphospholipid antibodies.

Adrenal Gland Diseases↗
PubMed1993

[Acquired corticotropin insufficiency in adults. 2 new cases].

We report two new cases of isolated corticotropin deficiency, associated with TSH deficiency in one of the two patient. The diagnostic was made difficult because the symptoms were mainly psychiatric. Low plasmatic cortisol and ACTH level were found, with low T3, T4 and TSH in the second patient. The TSH did not respond to the stimulation by TRH. The cerebral tomodensitometry and magnetic resonance imaging focused on the sella turcica were normal, eliminated a tumor and showed an empty sella turcica. The patients have to be followed-up because an isolated deficiency may further complete to panhypopituitarism.

Adrenocorticotropic Hormone↗
PubMed1990

Spectroscopic MRI: a tool for the evaluation of systemic lipid storage disease.

Spectroscopic MR imaging allows to measure the lipid content of a region inside the human body. This technique has been applied to the case of a woman with a severe multisystemic triglyceride storage disease. Lipid contents of liver, pancreas, kidneys, left ventricle, skeletal muscles (calves, thighs, arms) were measured by using the Dixon spectroscopic imaging sequence. In some heterogeneous muscles, localized proton spectra were recorded. Results agreed with clinical findings (muscle weakness, normal renal and cardiac function, diabetes). These techniques could help to quantify the severity of the disease and to follow up its evolution under therapy.

Adult↗
PubMed1987

Complete iodide trapping defect in two cases with congenital hypothyroidism: adaptation of thyroid to huge iodide supplementation.

Two cases of congenital defect in iodide trapping mechanism are related. The absence of thyroid and gastric concentration of 99mTcO4 led to the diagnosis. The study of saliva and gastric:serum concentration ratios confirmed the complete defect. The kinetics of radioiodine studied by external detection showed an early simultaneous decay in the thyroid, the stomach and the left ventricle. Thyroid accumulation of 131I, demonstrated by camera imaging, was estimated to be 0.1% at 48 h. It probably originated from simple diffusion. Iodide supplementation was progressively increased to 4.5 g and 10 g day-1 respectively. It resulted in a normalization of all parameters. Huge doses of iodide did not result in any evidence of hyperthyroidism as TSH rose normally after TRH. Intermittent iodide supplementation in one case could not maintain euthyroidism longer than a few weeks. Daily treatment, therefore, seems necessary.

Adolescent↗
PubMed1984

[Value of hormonal markers in the detection and therapeutic surveillance of malignant adrenal cortical carcinoma].

The value of hormonal markers in the diagnosis and early and late surveillance of adrenocortical carcinoma was assessed in a series of 10 cases and from a review of the literature. Although hormonal investigation with measurement of precursors, performed whenever there is the least clinical suspicion of ACC, is of certain diagnostic value, the possibilities of postoperative controls have not yet been fully exploited: the results are difficult to interpret because of possible interference due to the secretion of the controlateral adrenal; plasma renin activity is rarely assessed in the late postoperative period. A general strategy of investigation and surveillance is proposed.

Adrenal Cortex Hormones↗
PubMed1983

[Hypertension in malignant tumors of the adrenal cortex. A review of clinical, biological and hormonal features].

Hypertension may be a prominent and sometimes the dominant expression of tumours of the adrenal cortex as demonstrated in a personal series of 9 cases and in comparable series in the literature. It is therefore important, despite their relatively low incidence, to recognise adrenal cortical tumours as the cause of hypertension. The present study was undertaken to show that this diagnosis is relatively easy. The simplest indicators are:--the change in body electrolytes with hypokalaemia and hyper-kaliuria is practically constant and should prompt a hormonal investigation to demonstrate increases adrenal secretion of mineralocorticoids;--there is also a high incidence, despite the variable profiles of plasma and urinary corticosteroids, of paradoxical lowering of plasma aldosterone in parallel with normal or low PRA which does not react to orthostatism. These two preliminary investigations are the prelude and invitation to the measurement of other mineralocorticoids, especially desoxycorticosterone secondary to a relative block of 11-betahydroxylation from what other in vivo and in vitro studies have shown. Repeated monitoring of the preceding investigations is important for the post-operative follow-up and diagnosis of recurrences or metastases.

Adrenal Cortex Neoplasms↗
PubMed1983

[Progressive external ophthalmoplegia and Hashimoto's thyroiditis].

Signs of moderately increased metabolism in a patient with progressive external ophthalmoplegia and mitochondrial anomalies on muscle biopsy revealed the presence of Hashimoto's thyroiditis. The relations between ophthalmoplegia plus and thyroid dysfunction are discussed.

Adult↗
PubMed1982

Exaggerated prolactin response of thyrotropin-releasing hormone in women with anovulatory cycles: possible role of endogenous estrogens and effect of bromocriptine.

Twenty-one women 18 to 36 years old, presenting with chronic anovulation, were compared with 10 normally cycling women. The patients were characterized by low progesterone (P) levels (0.93 +/- 0.14 ng/ml versus 15.5 +/- 1.4 in controls), whereas 17 beta-estradiol (E2) was moderately decreased (110.2 +/- 8.3 pg/ml versus 162.8 +/- 14.5 in controls) realizing a relative hyperestrogenism. Basal prolactin (PRL) levels were not elevated (12.1 +/- 0.97 ng/ml versus 9.2 +/- 0.7 in controls), but after thyrotropin-releasing hormone (TRH) stimulation an exaggerated response was observed (114.5 +/- 7 ng/ml versus 55.8 +/- 9 in controls). Patients were treated with bromocriptine (1.25 mg 2 times a day) for 3 months. Fifteen responded with ovulatory cycles, and five became pregnant. Progesterone increased significantly (10.2 +/- 1.3 ng/ml), whereas in patients who did not ovulate P increased only slightly (1.56 +/- 0.18 ng/ml). The particular endocrine profile of these patients (P/E2 imbalance) realizing relative hyperestrogenism may be responsible for the exaggerated PRL response to TRH. Bromocriptine, in reducing this transient, or masked, hyperprolactinemia, allows in many patients the return to ovulatory cycles. This mechanism may be one of the possible pathways leading to chronic functional or organic hyperprolactinemia.

Adolescent↗
PubMed1982

Pituitary prolactinoma, adrenal aldosterone-producing adenomas, gastric schwannoma and colonic polyadenomas: a possible variant of multiple endocrine neoplasia (MEN) type I.

A large pituitary prolactinoma was found in a mentally deficient 45 year old woman presenting with amenorrhoea, galactorrhoea, headache, anaemia and hypertension, and removed surgically. She was subsequently found to have multiple adrenal aldosterone-producing adenomas, a gastric schwannoma and colonic polyadenomas. All these tumors were also removed surgically. Despite the absence of parathyroid and islet-cell hyperplasia, this case seems to be a variant of multiple endocrine neoplasia (MEN) type I.

Adenoma↗
PubMed1981

[Inappropriate thyrotropin secretion. Part 2: non tumoral (author's transl)].

Some patients are clinically euthyroid despite high thyroid hormones levels associated with detectable but not elevated serum TSH. These patients are considered as being resistant to thyroid hormones. The resistance may be severe or partial and in most cases seems to be autosomal dominant; it affects some tissues more than others, thus giving rise to a variety of clinical symptoms. In a few patients with high TSH levels extensive studies have failed to provide evidence of pituitary tumour of resistance to thyroid hormones; the cause of TSH hypersecretion in such cases remains uncertain. Several factors (non specific serum proteins, cross-reactivity circulating antibodies) may result in falsely high T3, T4 and TSH values on radioimmune assays and must be carefully investigated in the presence of unexpectedly high serum TSH levels.

Child↗
PubMed1981

[Inappropriate thyrotropin secretion. Part 1: tumoral (author's transl)].

Release of thyroxine and triiodothyronine from the thyroid gland is stimulated by the pituitary hormone thyrotropin, or thyroid-stimulating hormone (TSH). TSH secretion in turn is regulated by control mechanisms, which include a negative feedback effect of the thyroid hormones themselves and the actions of the hypothalamic peptide TRH and of several central neurotransmitters. Hyperthyroidism secondary to excessive TSH secretion is a rare entity. In most cases TSH hypersecretion results from an adenoma of the pituitary gland and may then be associated with increased prolactin or growth hormone production. It should be emphasized that most patients with pituitary adenoma have high serum levels of alpha TSH subunit and undetectable beta TSH subunit.

Adenoma↗
PubMed1981

[Lingual necrosis from Horton's disease (author's transl)].

A patient with necrosis of the tongue was found to have Horton's disease. The other typical manifestations of this disease, though present, were overshadowed by the lingual necrosis. Recovery occurred after relatively high doses of corticoids.

Aged↗