Endocrine function in 98 HIV-infected patients: a prospective study.

Endocrine function was prospectively evaluated in 98 patients (73 men and 25 women) infected by HIV in various stages of illness: Centers for Disease Control groups II (19), III (20), IVA and IVC2 (27), IVC1 and IVD (32). Testing included baseline and post-stimulation evaluation of gonadal, thyroidal, and adrenal axes. Although adrenal function was within normal values in most cases, with no differences between patient groups, nine out of 98 patients had either a low baseline or post-stimulation serum cortisol, cytomegalovirus adrenalitis being suspected in two cases. Mineralocorticoid response was normal in all individuals. The main abnormalities were sick euthyroid syndrome with low tri-idothyronine and/or thyroxine in 16% of patients and hypotestosteronemia in 29% of men with AIDS. These abnormalities, related to a functional deficiency of the hypothalamic-pituitary axis, were highly correlated with the degree of illness, i.e. weight loss and low CD4+ cell count. It was concluded that endocrine dysfunction in HIV-infected patients is rarely of clinical significance, that it is related more to cachexia and advanced disease than to HIV or opportunistic infections, and that it could serve as a prognostic marker.

Hypotensive anesthesia with isoflurane and enflurane during total hip replacement: a comparative study of catecholamine and renin angiotensin responses.

Catecholamine and renin-angiotensin responses to enflurane- or isoflurane-hypotensive anesthesia were compared in a randomized study. Two groups of 10 patients undergoing total hip arthroplasty were premedicated with morphine hydrochloride (0.1 mg/kg). Anesthesia was induced with thiopental and the trachea intubated after pancuronium. Equal concentrations of each volatile agent (1.3 MAC) were administered until mean arterial blood pressure decreased to 50-60 mm Hg. Hemodynamic data and blood samples for measurements of plasma renin activity (PRA) and plasma epinephrine (E) and norepinephrine (NE) concentrations were collected 1) after induction and intubation but before the start of isoflurane or enflurane; 2) 15 min (T15) after the start of isoflurane or enflurane administration; and 3) 45 min (T45) after the start of isoflurane or enflurane administration. The desired level of hypotension was achieved at T15 with isoflurane and at T45 with both anesthetics. When hypotension was achieved, cardiac index and stroke index were significantly lower in the enflurane group while systemic vascular resistance index was lower in the isoflurane group. Increases in E and NE levels above baseline levels were significantly greater in the isoflurane group than in the enflurane group. Use of isoflurane to induce hypotension is associated with more rapid induction of hypotension, less depression of cardiac output, and better preservation of homeostatic responses than is use of enflurane.

Additive effects of dihydralazine during enflurane or isoflurane hypotensive anaesthesia for spinal fusion.

Sixteen patients (13-38 yr) undergoing spinal fusion for scoliosis under controlled hypotension were studied to determine the haemodynamic and neuroendocrine responses to IV dihydralazine (1.0 mg.kg-1) followed by 0.5 and 1 MAC of enflurane or isoflurane. Twenty minutes after dihydralazine administration mean arterial pressure (-20 per cent) and systemic vascular resistance (-50 per cent) decreased, and cardiac index (+57 per cent), heart rate (+37 per cent) and intrapulmonary shunt increased. Plasma renin activity and aldosterone and norepinephrine levels increased. Further decreases in mean arterial pressure and in systemic vascular resistance were observed when 0.5 MAC enflurane or isoflurane were added. With 1 MAC anaesthetic levels a further decrease in mean arterial pressure was observed in both groups, but pressure fell to a lower level with isoflurane than with enflurane (p less than 0.01). The reduction of arterial blood pressure to a level of 50-60 mmHg for three to four hours was easy to control and was free of complications. The preliminary IV administration of dihydralazine allowed a reduced volatile agent concentration which attenuated undesirable haemodynamic effects, in spite of renin and norepinephrine release, and permitted a rapid intraoperative awakening.

Impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension.

It has been suggested that stimulation of adrenoreceptors could be responsible for some of the haemodynamic effects of isoflurane. But there are no solid data demonstrating the role of sympatho-adrenal stimulation induced by pain during isoflurane administration. The impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension has been investigated in 28 patients (47-76 years), scheduled for total hip arthroplasty. After premedication with morphine hydrochloride (0.1 mg/kg), patients were randomly assigned to receive either no fentanyl (control group) or fentanyl (5 micrograms/kg before tracheal intubation, 5 micrograms/kg before skin incision, and 2 micrograms/kg each 15 min during the 1st hour). Isoflurane was given to maintain mean arterial blood pressure in the range 6.7-8 kPa in both groups. Haemodynamic data and blood samples for determination of plasma renin activity (PRA) and epinephrine (E) and norepinephrine (NE) levels were collected before and during hypotension. The fentanyl group and the control group differed significantly during hypotension: heart rate, cardiac index, oxygen consumption and E, NE and PRA were lower (P less than 0.01) in the fentanyl group than in control group. Fentanyl lowered the required concentration of isoflurane to achieve the same degree of hypotension (end-tidal concentration: 0.8 +/- 0.2% in the fentanyl group and 1.4 +/- 0.15% in the control group; P less than 0.001). Our results demonstrate that the cardiovascular effects of higher isoflurane concentrations in the absence of narcotic analgesia are counterbalanced by adrenergic stress stimulation of released epinephrine and norepinephrine. Among the likely reasons for catecholamine release during isoflurane administration, inadequate analgesia may be considered.

[Use of cyclosporin A after antilymphocyte serum in renal transplantation]. / Utilisation de la cyclosporine A en relais du sérum antilymphocytaire en transplantation rénale.

For the past 18 months, cyclosporin A has been used in our renal transplantation center, according to a randomized protocole in which the drug is introduced late (3rd month), following a standard treatment with prednisone, azathioprine and antilymphocyte serum, in a low dosage (4-6 mg/mg/day) and alone. This protocol has been designed to preserve the full benefits of the antilymphocyte serum given immediately after transplantation, to reduce the risk of cyclosporine nephrotoxicity and to allow the withdrawal of corticosteroids. When compared with 27 patients under standard treatment, the 31 patients who received cyclosporin A have an actuarial graft survival rate of 94% at 12 and 18 months, against 68% in the other group. At least one rejection episode was observed in 43% and 51% of patients under respectively cyclosporin A and standard treatment. Renal function remained stable after cyclosporin A was introduced and 1 year post-grafting mean serum creatinine values were similar in both groups. Acute and chronic nephrotoxicity has been the major complication of cyclosporin A. Excellent results (94% graft survival rate at 18 months) can be obtained using the sequential association of antilymphocyte serum and cyclosporin A, without the impairement in renal function that has been observed in other studies where cyclosporin A is given on the day of transplantation.

[Should the assay of serum free thyroxine and triiodothyronine replace the other methods of evaluating thyroid function?]. / Le dosage de la thyroxine et de la tri-iodothyronine libres sériques doit-il supplanter les autres méthodes d'évaluation de la fonction thyroïdienne?

Total T4, total T3, free T4 and free T3 were measured at the same time in 633 subjects. These subjects were classified according to the clinic state and the hormonal results in 426 euthyroid, 145 hyperthyroid and 62 hypothyroid cases. The results permitted to define the sensitivity, specificity and predictive value of the different tests. When each measure was considered alone, free T4 was the most useful test for all the hormonal states. In association, FT4 + FT3 is more useful than T3T + T4T for all the diagnostic parameters and for all the clinical situations. To measure FT4 with an adequate kit appears to be in 1985 the key method for evaluating the thyroïd function. To associate FT3 is useful in some difficult cases.

[Alcoholic neuroacropathy. Recent diagnostic and pathogenic attainments]. / La neuroacropathie éthylique. Acquisitions diagnostiques et pathogéniques récentes.

The authors report the results of a prospective study of 28 patients with alcoholic neuroacropathy or the Bureau and Barrière syndrome. The investigations included biochemical analysis of the alcoholism, electrophysiological studies and, in 4 cases, electron microscopy of the musculocutaneous nerve biopsy. Bone scintigraphy with foot and hand scans was carried out in all cases for a more exact and above all, earlier diagnosis of the neurological osteoarthropathy. The clinical syndrome was attributed to a polyneuropathy with a large sensory component of the alcoholic "dying back" variety in all cases. High VGM levels associated with high serum IgA levels appears to be a biochemical diagnostic criteria of this condition. The latter parameter was not closely related to the hepatocytic status of the patient but suggests a direct or indirect effect of the neuropathy on humoral immunity. All cases had characteristic bone scans with high uptake at points of mechanical stress of the anterior part of the foot (first metatarsophalangeal joint). This finding, which is also observed in alcoholic sensory neuropathy without trophic disturbances prompts the authors to define a preacropathic state and an evolutive and pathogenic outline of the disease.

[Hormone and metabolic profile in diabetic hyperosomolar coma. Plasma insulin response to intravenous tolbutamide (author's transl)]. / Profil hormonal et métabolique du coma hyperosmolaire diabétique. Réponse insulinique au tolbutamide intra-veineux.

Fifteen patients with non-ketotic hyperosmolar diabetic coma were investigated and compared with ketoacidotic patients. Basal plasma insulin levels were low in all patients (14.8 +/- 1.0 micronU/ml in hyperosmolar coma, 11.0 +/- 1.3 in keto-acidosis), but insulin level increased after intravenous tolbutamide (between 30 and 105 micronU/ml) in eight hyperosmolar comas. Insulin showed no increase in seven hyperosmolar comas and in none of the ketoacidotic patients. In hyperosmolar coma plasma free fatty acids (1710 +/- 197 micronEq/1), triglycerides (3,4 +/- 0,4 g/1) and cortisol levels (49,7 +/- 9,0 microgram/100 ml) were increased, must as in keto-acidosis. Growth hormone (1,7 +/- 0,1 ng/ml) was normal, unlike the case in keto-acidosis. Plasma lactate concentrations were elevated and account for the frequent mild acidosis found in hyperosmolar coma. In spite of the low peripheral "insulin/glycemia ratio", the positive response to tolbutamide in half of the hyperosmolar cases suggests a less complete pancreatic deficiency than in keto-acidosis. The plasma high free fatty acid and triglyceride levels suggest that the lack of ketosis is not due to inhibition of lipolysis but could be a consequence of inhibition of hepatic ketogenesis.