[Results of pan-retinal argon laser coagulation in proliferative diabetic retinopathy]. / Ergebnisse nach panretinaler Argonlaserkoagulation bei proliferativer diabetischer Retinopathie.

To minimize the risk of visual loss and to stop the progression of diabetic retinopathy argon laser treatment is the therapy of choice in proliferative diabetic retinopathy (PDR). The results after panretinal argon laser coagulation (ALC) were studied retrospectively considering visual outcome and frequencies of diabetic ocular complications. In all 95 patients were included in whom laser treatment had been performed due to clinically and angiographically diagnosed proliferative diabetic retinopathy at the Department of Ophthalmology between 1990 and 1994 with a follow-up of at least 1 year. The most frequent diabetic complications observed were vitreous haemorrhage in 9 (or 9.5%) and iris neovascularization in 10 cases (or 10.5%). Rare complications were neovascular glaucoma in 3 patients (or 3.2%) and tractional retinal detachment in 4 patients (or 4.2%). Nearly 70% of the patients maintained or improved visual acuity after laser treatment. The frequency of diabetic complications of PDR after ALC was significantly associated with older age, diabetes type II, longer duration of diabetes and elevated blood pressure.

Pharmacodynamics of insulin Lispro in 2 patients with type II diabetes mellitus.

We studied the effects of the new rapid acting human insulin analogue (Lys(B28), Pro(B29) insulin), insulin Lispro (Lispro) on metabolic control and insulin receptor binding in type II diabetes mellitus. We investigated 2 patients: Patient 1 was obese, clearly insulin-resistant, injected high doses of insulin (3-4 IU/kg body weight), and had insufficient diabetes control. Patient 2 was of normal body weight, injected normal insulin doses (0.7-0.8 IU/kg body weight), and had good diabetes control. Patient 1 showed a considerable improvement of insulin binding after receiving Lispro (26,700 vs. 5,600 receptors/monocyte; Kd 560 vs. 1,500 pM). Concommitantly, a decrease of serum glucose and insulin dose was observed, reflecting a higher insulin sensitivity during Lispro treatment. In patient 2 injected with Lispro the time course of serum glucose, serum insulin, and insulin binding after an oral meal was comparable to values obtained in healthy controls. We conclude that the quick and pulsatile pharmacokinetic profile of the insulin analogue Lispro may improve glycemia, insulin receptor binding, and insulin resistance in type II diabetes.

[Behçet disease with primary involvement of the cerebral vessels]. / Morbus Behçet mit primärem Befall zerebraler Gefässe.

HISTORY AND CLINICAL FINDINGS: Two months after the onset of mainly frontal headaches a 25-year-old man of Turkish descent additionally developed double vision. Fundoscopy revealed bilateral choked discs and right trochlear paralysis. Computed tomography and digital subtraction angiography demonstrated thrombosis of the superior sagittal sinus. On admission to hospital the patient was fully conscious but had marked meningism, bilaterally positive Lasègue's sign (painful straight leg raising) at a 50 degree angle, and multiple oral aphthous ulcers. The sinus thrombosis suggested a chronic inflammatory process, while the oral ulcers pointed to Behçet's syndrome. INVESTIGATIONS: Inflammatory parameters (erythrocyte sedimentation rate, C-reactive protein and white blood cell count) were increased and the HLA-B27 test was positive. Other laboratory tests, cerebrospinal fluid, chest radiogram and ECG were unremarkable. TREATMENT AND COURSE: Despite intravenous administration of heparin nad cefuroxim for one week the sagittal sinus thrombosis spread to the straight sinus. In the third week scrotal ulcerations were noted and taken to confirm Behçet's syndrome. Immunosuppressive treatment with methylprednisolone (initially 80 mg daily) and 2 weeks later together with chlorambucil (0.1 mg/kg daily) was started. Four weeks later the patient was free of symptoms and discharged. CONCLUSION: Neurological signs are not adequately stressed by the International Study Group for Behçet's Disease among its listed diagnostic criteria.

Stimulated thyrotropin and prolactin secretion in lactating and non-lactating women.

During the postpartum period, lactation is initiated by a massive release of prolactin which, in turn, reflects reduced dopaminergic inhibition of the pituitary lactotrophs. This postpartum prolactin rise can be prevented by administration of dopamine agonists. The release of thyrotropin (TSH) is also controlled by dopaminergic inputs and, therefore, TSH secretion may also be affected by postpartum alterations in dopaminergic activity. To gain further insight into the regulation of TSH and prolactin secretion during the postpartum period, we compared the basal and stimulated TSH and prolactin levels of postpartum lactating (n = 10) and non-lactating women (treated with 5 mg bromocriptine daily, n = 9) with those of normal cycling women (n = 9). Frequent blood samples were obtained on postpartum day 5 or in the early follicular phase before and after administration of thyrotropin-releasing hormone (TRH) for serial determination of TSH and prolactin by immunoradiometric assay (IRMA). Based serum prolactin levels were high (p < 0.001) in lactating women and low in both non-lactating and normal cycling women. When these differences in the basal prolactin concentrations were taken into account, the stimulated prolactin release (relative prolactin increase and area under the prolactin curve) was found to be highest (p < 0.05) in non-lactating women and lowest in lactating women. Basal TSH secretion was not significantly different between the groups of women (p > 0.2). Yet, both the relative TSH increases and the response curves following TRH stimulations were high (p < 0.05) in normal cycling women and low in both lactating and non-lactating postpartum women. These observations confirm a difference in the basal and stimulated prolactin release between lactating and non-lactating women. They also indicate that the TRH-stimulated TSH release is greatly affected by the postpartum state, irrespective of lactation or therapeutic weaning. The observation of a decreased sensitivity of pituitary thyrotrophs in concert with unchanged basal TSH secretion is suggestive of changes in hypothalamic TRH secretion and/or in the TSH metabolic half-life during the postpartum period.