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We performed a study in 92 diabetic patients (76 Type 1 and 16 Type 2) without retinopathy to determine the relation between diabetic dyschromatopsia and neuropathy, which has been evoked in previous studies. Color vision was explored with Lanthony's desaturated D 15 panel. Peripheral nervous function was explored with an electrophysiological score which has been beforehand validated. Moreover evoked visual potentials were performed in 38 diabetic subjects in order to determine whether dyschromatopsia was related to an impairment of central optic pathways. Fifty-one among the 92 diabetic subjects had a blue-yellow dyschromatopsia. Among the recorded parameters, only peripheral nervous impairment was significantly more frequent in the group with dyschromatopsia than in the group without. Ten among 38 diabetics had impairment of the evoked visual potentials. Frequency of alteration of evoked visual potentials was not different between the group with and the group without dyschromatopsia. Our results confirm the relationship between dyschromatopsia and the alteration of the nervous function in diabetic subjects. In return, lack of significant modification of evoked visual potentials among diabetic patients with dyschromatopsia and the blue-yellow axis of dyschromatopsia are in opposition with a direct neurological origin of dyschromatopsia. We therefore evoke a common process in the beginning of the diabetic dyschromatopsia and of peripheral neuropathy.

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This study was a 6-month open trial of the effects of naftidrofuryl fumarate (600 mg/day orally) on the clinical and electrophysiological signs of diabetic polyneuropathy in 15 patients. A scored clinical evaluation and an indexed electrophysiological examination were done at inclusion, and after 3 and 6 months. Mean clinical score and electrophysiological index was improved after 3 months of therapy, the improvement persisting at 6 months, with no change in control of diabetes. These results could be related to the vasodilating properties of the drug, causing an increase in nerve temperature, or to a specific neurotropic action, as recently demonstrated in rats. Controlled studies are necessary to confirm these results, and explore the mechanism of this improvement.

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Diabetic dyschromatopsia is frequent and is a true complication of diabetes mellitus. Causative factors other than retinopathy have been suggested, but they remain unclear. We have explored the color vision of 100 diabetics aged 16 to 65 (88 insulin-dependent, 12 non-insulin dependent) with Lanthony's D15 desatured panel. Degenerative complications were looked for, especially by fundoscopy and electrophysiological exploration of peripheral nerves using specific scoring. 73% of the diabetics had dyschromatopsia. Dyschromatopsia was significatively more frequent when retinopathy was present (26 out of 30 diabetics with retinopathy versus 47/70 without). We explain the absence of a strict parallelism between dyschromatopsia and retinopathy by the intervention of other factors. Whereas the equilibration of the diabetes was not different between the groups with or without dyschromatopsia, patient age, microalbuminuria, blood pressure and alcohol intake were higher in patients with dyschromatopsia. The greater prevalence of peripheral neuropathy in patients with dyschromatopsia, confirmed by electrophysiology, and independently from the existence of retinopathy, is an indicator of the existence of neuronal disease, whose level remains to be determined. Our results are the indispensible preliminary step to a study of the respective importance of these pathogenic factors.

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This study examined the relationship between uteroplacental blood flow and fetal hypotrophy in streptozocin-induced diabetic rats (40 mg/kg body wt i.v.). Our results showed that, in diabetic rats, fetal hypotrophy was associated with a significant reduction in arterial blood velocity in the uterine artery (P less than 0.001), placenta (P less than 0.01), umbilical artery (P less than 0.01), and fetal aorta (P less than 0.05). This was not observed when diabetic rats were treated with insulin. Treatment of rats with the alpha 1-blocking vasodilator nicergoline restored fetal growth and arterial blood velocity to control values without affecting the degree of hyperglycemia. Nicergoline in control rats did not change fetal weight and caused only minor hemodynamic changes on presumably already maximally vasodilated arteries. We concluded that the uteroplacental hemodynamic disturbances observed in diabetic rats play a major role in the establishment of fetal growth retardation.

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The aim of this study was to determine if placental prostanoids could mediate the vasodilating action of an alpha-1-adrenoceptor antagonist, nicergoline (400 micrograms/kg i.p.), during late pregnancy in streptozotocin-induced diabetic rats (40 mg/kg i.v.). Placental prostanoid concentrations were evaluated by radioimmunoassay. Prostaglandin E2 levels showed a highly significant increase in diabetic and nondiabetic rats treated with nicergoline (p less than 0.001). 6-Keto-PGF1 alpha concentrations were slightly increased in diabetic rats compared to controls, and this increase was reversed by both nicergoline and insulin treatments. In all groups studied thromboxane B2 levels were comparable. It is concluded that prostaglandin E2 could mediate the vasodilating action of nicergoline on the placental irrigation and, therefore, improved the hemodynamic state of this organ in diabetic rats.

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The electrophysiological diagnosis of peripheral neuropathy in diabetics becomes increasingly difficult with the increase in number of parameters measured. We have examined 102 subjects: 60 diabetics, 32 control subjects and 10 with impaired glucose tolerance. From the 37 recorded parameters during 8 examinations, a linear discriminant analysis allowed us to separate the 19 diabetics with clinical neuropathy and the control subjects with only 5 parameters, with a good concordance (96%): the motor conduction velocities (MCV) of the peroneal and median nerves, the amplitude of the action potential (AP) of the sural nerve, the Hmax/Mmax ratio and the M latency of the Hoffman reflex. These parameters, weighted with a coefficient, constitute a score of discrimination. This score has been tested by the Jackknife method on the same sample (94% of well-classified patients), then validated on the other patients. Thus we propose a method to aid the diagnosis of diabetic peripheral neuropathy, without the arbitrary character of the classical single parameter method, and allowing easy repetition.

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This experiment was conducted to determine the effect of diabetes on uterine prostanoids production in near-term rats. The incidence of an insulin therapy was also studied. On the 21st day of pregnancy, uterine PGE2, PGF2 alpha and PGI2 levels showed a significant increase (respectively p less than 0.05, p less than 0.01 and p less than 0.05) in diabetic rats compared to controls whereas TxA2 production remained unchanged. The insulin therapy restored PGE2 levels, the most potent stimulatory factor of the myometrial fiber at control values, whereas it enhanced significantly PGI2 concentrations (p less than 0.05) and had no effect on PGF2 alpha production; TxA2 levels remaining always unchanged. It is suggested that the increase in uterine protanolds production during diabetes could induce a myometrial hypertonicity and play a role in the disturbances of the fetal development. The maintenance of PGE2 levels to control values by the insulin therapy might contribute to a normal delivery.

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A case of carbimazole-induced cholestatic hepatitis is presented. A woman received carbimazole for hyperthyroidism for 3 months. Five months later, she had prompt recurrence of cholestasis parameters after rechallenge (2 days of treatment). Histologic examination showed predominantly centrilobular cholestasis. Only 5 other cases have been published in the literature. An idiosyncratic mechanism seems likely.

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The effects of bilateral ovariectomy on uterine motility and levels of progesterone, oestradiol, cAMP, adrenaline and PGF2 alpha were studied in the rat at midpregnancy. Animals were randomly divided into two groups, at least 15 rats in each, sham-operated serving as controls and ovariectomized. The spontaneous uterine mechanical activity of Wistar rats was recorded isometrically and the electrical activities were recorded simultaneously by two bipolar electrodes. Within 30 minutes of ovariectomy a significant increase of the amplitude of uterine contractions was observed and the simultaneity of electrical activity was significantly improved; these effects became more pronounced at 1h post-ovariectomy (p less than 0.005). Plasma progesterone levels decreased by 20% (p less than 0.01) at 30 min and by 50% (p less than 0.001) 1h after ovariectomy, whereas oestrogen levels remained unchanged. Levels of adrenaline, cAMP and PGF2 alpha in the uterine tissue 1h following ovariectomy were affected as follows: adrenaline (p less than 0.05) and cAMP (p less than 0.001) were reduced and PGF2 alpha augmented (p less than 0.05). It appears that variation of the ratio oestrogens/progesterone induces precociously the activation of uterine mobility and exerts an effect on some factors involved in the regulation of the rat myometrium at midpregnancy.

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Forty-two patients with prolactin-secreting pituitary adenoma (prolactinoma) demonstrated by a radiologically abnormal sella turcica and hyperprolactinaemia were treated with bromocriptine. Baseline serum prolactin levels, which before treatment correlated with the size of the adenoma, returned to normal under bromocriptine in 30 out of 36 cases; in 6 female patients, however, they were lowered but remained moderately high. The dose of bromocriptine and the time required for normalization of prolactinaemia correlated with the size of the tumour. In 11 patients with macroadenoma bromocriptine dosage and prolactinaemia were inversely correlated; in 8 of these the adenoma was reduced in size. In 12 cases where the long-term treatment was interrupted, prolactinaemia rose again, suggesting that the medical treatment alone has no lasting curative effect.

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The effects of two adrenoceptor antagonists, nicergoline (alpha 1) and acebutolol (beta 1), on the contraction of myometrium in the proestrous rat were compared to those of noradrenaline and phentolamine. The spontaneous myometrial contractions of Wistar rats on the day of proestrus were recorded isometrically and the data were analysed using Wilcoxon non-parametric statistics. All drugs were administered i.v. and the doses are expressed as microgram/kg body weight. Noradrenaline (1200 micrograms/kg per h) induced a 32.5% reduction (P less than 0.001) of the uterine contraction amplitude. Nicergoline did not alter uterine motility significantly when administered alone at doses ranging from 400 to 1600 micrograms/kg. However, successive injections of nicergoline in the same range given during noradrenaline infusion at 600 micrograms/kg per h potentiated the relaxing action of the latter (38%, P less than 0.01). Phentolamine (120 micrograms/kg) reduced myometrial activity by 25% (P less than 0.05). This inhibitory response rose to 65% (P less than 0.001) when the dose of phentolamine was increased to 960 micrograms/kg. When a single injection of nicergoline (400 micrograms/kg) was followed by the administration of increasing doses of acebutolol (120, 1200, 2400 micrograms/kg) the slight inhibitory effect on uterine motility observed after administration of each of the two agents separately became more pronounced (P less than 0.05). It appears from these results that combining noradrenaline with nicergoline and nicergoline with acebutolol leads to potentiation of their relaxing effects. Furthermore the results confirm that nicergoline is a partial alpha-blocker.

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