[An aortic insufficiency diagnosed under cabergoline]. / Une insuffisance aortique diagnostiquée sous cabergoline.

We report the case of a restrictive aortic insufficiency diagnosed on a 53-year old woman while being treated by low dose of cabergoline for hyperprolactinemia. Such valves involvements had already been described with cabergoline and other dopamine agonists, drugs the patient was previously exposed to. However, chronology of events leads us to suspect cabergoline, although such effects had only been described with much higher doses. This case may recommend to perform echocardiograms upon patients treated by cabergoline, and probably such a caution may be enforced in patients previously exposed to other dopamine agonists. On another hand, the diagnostic of a restrictive valvulopathy may lead to suspect a iatrogenic origin including dopamine agonists.

[Aortic insufficiency under weak doses of cabergoline for non-tumoral hyperprolactinemia]. / Insuffisance aortique sous faibles doses de cabergoline pour hyperprolactinémie non tumorale.

Used in its neurological indication, cabergoline is known to induce cardiac valve regurgitations, essentially mitral and aortic valvular diseases, by its action on the 5HT2b receptors. Until now, it was assumed that the dose and the duration of exposure were the major factors of appearance. We describe a case of aortic insufficiency which developed in a patient given low doses of cabergoline (0.5 mg weekly) for non-tumoral hyperprolactinemia. Because of previous use of appetite suppressants and of bromocriptine, the exclusive responsibility of cabergoline remained uncertain. The potential gravity of these valvular heart diseases emphasizes the importance of careful cardiologic examination before and during treatment.

Demonstration of defective glucose uptake and storage in erythrocytes from non-insulin dependent diabetic patients and effects of metformin.

1. Red blood cells can store glucose and may thus participate in blood glucose homeostasis. We investigated if a defect in this process exists in non-insulin dependent diabetes (NIDD). 2. Blood was obtained in fasting conditions from 10 normal and 10 newly diagnosed NIDD patients (before and after 4 weeks Metformin therapy). Washed erythrocytes were resuspended in media containing various glucose concentrations (4.4, 6.6, 8.8 and 13.2 mmol/L). Total glucose uptake was calculated as the sum of the measurements of lactate as well as free glucose, the latter being determined before and after addition of amyloglucosidase to the pellet. 3. Cells from diabetics showed a pronounced reduction in glucose uptake, particularly in their capacity to store glucose as glycogen (reactive to amyloglucosidase). Metformin treatment almost normalized glycogen levels, whereas lactate declined concomitantly in the pellet. 4. Our data demonstrate that a defect in glucose uptake exists in erythrocytes from NIDD patients, affecting both free and stored glucose, and that this defect is reversed by Metformin treatment, indicating that this drug can increase glycogen levels even in insulin-insensitive cells. 5. Thus, in view of their total mass, erythrocytes may be important in the impaired glucose homeostasis in NIDD, in particular in marked hyperglycaemia such as after a meal.

[Influence of acute hyperinsulinism on arterial pressure of diabetics. Reproducibility of the hypotensive effect]. / Influence de l'hyperinsulinisme aigu sur la tension artérielle de diabétiques. Reproductibilité de l'effet hypotenseur.

We have observed effects of acute hyperinsulinaemia on arterial pressure of five diabetics and tested the reproducibility of this action. Systolic (TAS) and diastolic (TAD) arterial pressure were studied during two hyperinsulinaemic-euglycaemic clamps effected with Artificial Pancreas (Biostator CGIIS, Miles) at one month of interval. During the first clamp, between the beginning of insulin infusion and the end of 4th stage, we have observed a fall of TAS (115 +/- 4, VS 137 +/- 6 mmHg; moy +/- SEM; p less than 0.05) and in less degree of TAD (76 +/- 2, VS 86 +/- 4 mmHg; NS). These modifications of arterial pressure were associated with no changes of heart rate and urinary sodium flow. On the other hand, we have observed a fall of serum levels of sodium (139 +/- 1, VS 141 +/- 1 mEq/l; p less than 0.05), urea (0.20 +/- 0.01, VS 0.32 +/- 0.02 g/l; p less than 0.001) whereas, balance-sheet of water was positive (+445 +/- 338 ml) at the end of clamp. During the second clamp, the fall of pressure has been reproducible, relating to the TAS (123 +/- 5, VS 145 +/- 4 mmHg; p less than 0.01) and non significantly to the TAD (78 +/- 2, VS 88 +/- 5 mmHg; NS). During the two tests, the mean of tension fall was identical (22 +/- 6 mmHg during first clamp, 22 +/- 4 mmHg during second one). So, acute hyperinsulinaemia induces a fall of arterial pressure, probably in bringing an influence on arterial vasodilatation since heart rate and urinary sodium excretion are unchanged and water balance-sheet is positive.(ABSTRACT TRUNCATED AT 250 WORDS)