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Biomedical subjects

J Quichaud

Publications and source records attributed to J Quichaud.

At least 37 records · Page 2Linked to original sources
PubMed1985

[Intrasellar carotid aneurysm simulating prolactin adenoma].

A 52-year-old woman with secondary amenorrhea presented with ophthalmoplegia, subarachnoidal bleeding. Pituitary function tests showed mild hyperprolactinemia and deficiencies of other functions of adenohypophysis. X-ray films of the skull showed enlarged sella turcica, and CT scan was interpreted as demonstrating pituitary tumour. Carotid arteriography led to diagnosis of intrasellar aneurysm of the right internal carotid, without any pituitary tumour. After embolisation of the aneurysm, followed, by a temporo-sylvian anastomosis, endocrine functions did not improve. The mechanism of hyperprolactinemia is discussed, probably due to pituitary ischemia. This case provides evidence of interest of further investigations before a transsphenoidal surgery in pituitary tumours, in particular if subarachnoidal bleeding occurs.

Adenoma↗
PubMed1985

[Insulinoma: critical study of methods of localization and strategy].

In patients with proven hyperinsulinism, localization of the underlying insulinoma may be difficult. The localization diagnosis may be performed preoperatively using different procedures, such as ultrasonography, computed tomography, selective arteriography of the pancreatic vessels and percutaneous transhepatic blood sampling in the portal venous system. At operation, insulinomas may be detected by inspection and bidigital palpation, pancreatico-sonography and rapid determination of insulin concentration after sampling of blood in pancreatic veins. By discussing the advantages and disadvantages of each localization procedure, the authors propose a strategy fort the detection of pancreatic insulinomas.

Adenoma, Islet Cell↗
PubMed1985

[Pathogenesis of diabetic neuropathies].

There are two types of diabetic neuropathy: on the one hand, mononeuritis and, on the other hand, the symmetric polyneuropathy with a glove and stocking distribution and autonomic polyneuropathy. Mononeuritis (or mononeuritis multiplex) seems to be the result of ischaemia due to intrinsic or extrinsic (altered coagulability) vascular disease. Polyneuropathy is probably due to metabolic factors related to chronic hyperglycaemia: abnormal nerve energy metabolism, impaired axonal transport, increased activity of the sorbitol pathway, non-enzymatic nerve protein glucosylation and abnormal myo-inositol metabolism. The respective roles of these different factors in the pathogenesis of polyneuropathy are discussed.

Animals↗
PubMed1985

[Primary empty sella turcica. Analysis of 14 cases and review of the literature].

14 patients (13 women, 1 man) presenting with primary empty sella had endocrinologic and radiological investigations. 8 women are obese, 5 multiparous. Initially, headaches have needed a radiological study of sella turcica in 8 cases (57%). Pneumoencephalography and/or CT scan have led to diagnosis; but in 3 cases, a suspected associated pituitary adenoma justified a surgical exploration. In one case, a GH-secreting microadenoma was found, in both other cases histologic studies revealed fibrous or normal pituitary. Endocrine findings were normal, regarding to gonadotrophs, corticotrophs and thyreotrophs. GH was blunted in four cases, below 5 ng/ml during insulin tolerance test. In 9 cases, GH rose to 19,51 +/- 10,03 ng/ml (mean +/- S.D.). In 13 patients, serum prolactin was normal: 7,1 +/- 3,9 ng/ml (normal values 2 -20 ng/ml), elevated in the last case: 112,5 ng/ml. One year later, two patients did not show any modification on clinical, radiological or endocrine data. Physiopathology of intrasellar arachnoidocele is discussed: intrasellar extension of subarachnoid space may be due to diaphragm insufficiency and disturbances of dynamics of cerebrospinal fluid, flattening the otherwise normal pituitary gland.

Adult↗
PubMed1977

[The sympathetic nervous system inhibition in the antihypertensive effect of beta-blockers (author's transl)].

The decrease of sympathetic activity by the beta-blocking drug, as demonstrated by the decreased electric activity of the splanchnic nerve and by the decreased urinary catecholamine reponse to tilt as well as by the decreased levels of plasma dopamine beta-hydroxylase exists not only in hypertension with elevated PRA but also in hypertension with normal or low PRA. In these latter cases the antihypertensive effect is better explained by the decrease in the sympathetic nervous system activity than by the decrease of PRA. This effect seems to be indirect and probably, as suggested by Lewis, as a result of damping sensory input to the central nervous system from the heart, whose capacity to respond to exercice and stress is blunted by beta-adreno-receptor blockade.

Adrenergic beta-Antagonists↗
PubMed1977

[Systemic arterial hypertension: pathogentic role of the sympathetic nervous system].

Role of the clinical and experimental data suggesting the role of the sympathetic nervous system in some essential hypertension are reviewed: increase in heart rate and diastolic blood pressure during orthostatism, increase in cardiac output resulting from increase in cardiopulmonary blood volume and/or in myocardial contractility, increase in peripheral resistances, elevated plasma catecholamines and dopamine-bêta-hydroxylase, disturbances in arterial baroreceptor sensitivity and in vascular response to adrenergic stimuli, elevated plasma renin activity. It appears that the role of a sympathetic overactivity is mainly important in labile hypertension with hyperkinetic syndrome and elevated plasma renin activity.

Animals↗