Surgery is the usual treatment for primary hyperparathyroidism. However, some patients with high surgical risks are not suitable for surgery. For such patients, we propose, as an alternative treatment, ultrasonically guided percutaneous ethanol injection into parathyroid adenomas, in order to induce necrosis of the tumor. We report, here, the results of ultrasonically guided percutaneous ethanol injection into parathyroid adenomas, during a prolonged follow-up period up to 49 months, in a group of 13 patients (median age 79 years) with primary hyperparathyroidism and contraindications for surgery. In seven patients, complete normalization of plasma calcium, phosphorus and parathyroid hormone (PTH) levels was achieved after ethanol injections, with no recurrence of hypercalcemia during a median follow-up period of 28 months (total success). In these seven patients, plasma calcium, phosphorus and PTH levels were normalized 48 h after the successful ethanol injection. In four patients, a partial success was obtained with clinical improvement and normalization of plasma calcium levels but without complete normalization of plasma PTH levels. This partial success is due to incomplete necrosis of the adenoma, as has been confirmed in one patient by histopathological examination. The ethanol injection treatment failed in only two patients. This treatment was always well tolerated and no major side-effects were observed. In conclusion, our results give evidence that ultrasonically guided percutaneous ethanol injection into parathyroid adenomas can be a very useful alternative therapy in patients not suitable for surgery.

gramme. This is in keeping with the tremor of other body parts, for example the wingbeating arm tremor of Wilson's disease and task-specific tremors such as writing and other occupational tremors.3 We have examined clinically, three other patients with clear dystonic head tremor in whom head tremor was altered by the position of the head in the anterior-posterior plane. In none of the others could we demonstrate a vestibular (otolith) mechanism. Despite these negative observations for a clear otolith influence upon head tremor electrophysiological measurements have shown that otolith spinal reflexes may be modulated by both head and body position.6 Thus there still remains the possibility that a change in head or body position may in itself modify vestibular influences upon body movement. S MOSSMAN L CLEEVES L FINDLEY MRC Human Movement and Balance Unit, Section of Neuro-otology, National Hospital for Neurology and Neurosurgery, London, UK

The finding of endocrine gland lesions at pathological examination in AIDS and reports of several cases of endocrine disease in patients with this syndrome have prompted us to study endocrine functions in 63 patients (51 men, 12 women) with HIV-1 infection. According to the Center for Disease Control (CDC) classification system, 13 of these patients were stage CDC II, 27 stage CDC III and 23 stage CDC IV. We explored the adrenocortical function (ACTH, immediate tetracosactrin test) and the thyroid function (free T3 and T4 levels, TRH on TSH test) in all 63 patients. The hypothalamic-pituitary-gonadal axis (testosterone levels, LHRH test) and prolactin secretion (THR test) were explored in the 51 men. The results obtained showed early peripheral testicular insufficiency at stage CDC II and early pituitary gland abnormalities with hypersecretion of ACTH and prolactin also at stage CDC II. On the other hand, adrenocortical and pituitary abnormalities were not frequently found. The physiopathology of the endocrine abnormalities observed in HIV-1-infected patients remains unclear, but one may suspect that it involves interleukin-1 since this protein factor has recently been shown to stimulate the corticotropin-releasing hormone secretion and to act directly on the glycoprotein capsule of the virus (gp 120) whose structure is similar to that of some neurohormones.

The finding of endocrine gland lesions at pathological examination in AIDS and reports of several cases of endocrine disease in patients with this syndrome have prompted us to study endocrine functions in 63 patients (51 men, 12 women) with HIV-1 infection. According to the Center for Disease Control (CDC) classification system, 13 of these patients were stage CDC II, 27 stage CDC III and 23 stage CDC IV. We explored the adrenocortical function (ACTH, immediate tetracosactrin test) and the thyroid function (free T3 and T4 levels, TRH on TSH test) in all 63 patients. The hypothalamic-pituitary-gonadal axis (testosterone levels, LHRH test) and prolactin secretion (THR test) were explored in the 51 men. The results obtained showed early peripheral testicular insufficiency at stage CDC II and early pituitary gland abnormalities with hypersecretion of ACTH and prolactin also at stage CDC II. On the other hand, adrenocortical and pituitary abnormalities were not frequently found. The physiopathology of the endocrine abnormalities observed in HIV-1-infected patients remains unclear, but one may suspect that it involves interleukin-1 since this protein factor has recently been shown to stimulate the corticotropin-releasing hormone secretion and to act directly on the glycoprotein capsule of the virus (gp 120) whose structure is similar to that of some neurohormones.

UNLABELLED:Since anatomopathological lesions of the adrenal gland have been frequently observed at autopsy in AIDS, we investigated the glucocorticoid function in 63 patients (51 men, 12 women) infected by the human immunodeficiency virus (HIV) in order to determine the incidence and the nature of any adrenocortical abnormalities at various stages of HIV infection. The patients were classified according to the Centers for Disease Control (CDC) recommendations into group II (asymptomatic; N = 13), group III (lymphadenopathy; N = 27) and group IV (clinical manifestations; N = 23). Plasma ACTH and cortisol before and after an exogenous ACTH stimulation test were measured in patients as in 30 age-matched controls. Plasma renin activity and plasma aldosterone before and after ACTH stimulation were also measured in 31 patients (group II: 12; group III: 10; group IV: 9). Compared with controls patients from group II-III had higher levels of ACTH (39.11 +/- 17.01 vs 29.73 +/- 8.53 ng/l; p = 0.003) and basal cortisol (232 +/- 91.2 vs 184.3 +/- 30.9 micrograms/l; p = 0.03). No significant differences were noted between group IV patients and controls as to ACTH and basal and stimulated cortisol levels. Among the 63 patients, only one from group IV had a blunted cortisol response after ACTH stimulation test. Plasma renin activity, and basal and stimulated aldosterone levels in the 3 groups of patients were not different from control values.IN CONCLUSION:1. Adrenal insufficiency does not seem very frequent in group IV patients and is likely to be a late complication in AIDS. 2. The increased ACTH and basal cortisol levels found in group II and group III patients argue for an early dysregulation of the adrenocortical axis in HIV infection. The exact physiopathological mechanism is not yet known, but an enhanced CRH production by interleukin 1 and/or a direct role of the HIV envelope glycoprotein (gp 120) may explain the high ACTH level in HIV patients.

Bien que rare l'association d'une maladie de Basedow et d'un purpura thrombopénique auto-immun est plus souvent retrouvée que ne le voudrait une simple coïncidence. Un désordre immunologique commun responsable de la maladie de Basedow et du purpura thrombopénique auto-immun et/ou la responsabilité directe de l'hyperthyroïdie dans la genèse des perturbations immunologiques à l'origine du purpura thrombopénique auto-immun ont été proposés pour tenter d'expliquer l'association de ces deux pathologies auto-immunes. Nous rapportons deux observations au cours desquelles l'auto-immunité anti-plaquettes évolue de façon indépendante de l'état fonctionnel thyroïdien, rendant peu vraisemblable un rôle direct de l'hyperthyroïdie dans la survenue des troubles immunologiques responsables du purpura thrombopénique auto-immun. La physiopathologie réglant l'association maladie de Basedow et purpura thrombopénique auto-immun demeure mal connue. L'existence d'un dénominateur pathogénique, de nature immunologique, commun aux deux affections, apparaît vraisemblable, possiblement par l'intermédiaire d'un déterminant antigénique commun aux cellules thryoïdiennes et aux plaquettes.

The association between Graves' disease and autoimmune thrombocytopenic purpura is rare and yet more frequent than would be expected from a mere coincidence. The existence of an immunological disorder common to Graves' disease and autoimmune thrombocytopenic purpura and/or a direct responsibility of hyperthyroidism in the genesis of immunological disturbances resulting in autoimmune thrombocytopenic purpura are hypotheses put forward to try and explain why these two pathologies are associated. We report two cases in which the antiplatelet autoimmunity developed independently of the thyroid functional disorder, making it unlikely that hyperthyroidism played a direct role in the occurrence of the immunological disorders responsible for the autoimmune thrombocytopenic purpura. The physiopathology responsible for the Graves' disease-autoimmune thrombocytopenic purpura association remains imperfectly known. The existence of an immunological pathogenetic mechanism underlying both diseases seems to be likely; it probably acts through an antigenic determinant that is common to thyroid cells and platelets.

Because of vomiting, a 15 years old girl inserted one metoclopramide suppository. Her mother has Huntington's chorea. She had a transient choreiform syndrome. Could latent Huntington's chorea be revealed by this drug?

22 cases of hyperthyroidism occurring during or following treatment with amiodarone are reported and compared with more than 15 cases in the literature. The specific clinical features of these cases of hyperthyroidism are presented and the problems in interpretation of the laboratory thyroid function tests are discussed. A study of the course of these cases reveals a number of prognostic factors. Finally, the authors describe the practical management of this form of hyperthyroidism.