Pharmacokinetic profiles of biphasic insulin aspart 30/70 and 70/30 in patients with Type 1 diabetes: a randomized double-blinded crossover study.

AIMS: To compare pharmacokinetic characteristics of two biphasic insulin aspart (BIAsp) formulations: BIAsp30 and BIAsp70 (30% and 70%, respectively, of fast-acting insulin aspart) during 15 days of multiple dosing (thrice daily). METHODS: A total of 22 patients with Type 1 diabetes (nine women, 13 men) aged 41.4 +/- 9.9 years (mean +/- sd) with a diabetes duration of 18.9 (2.3-40.3) years (median and range) completed the randomized, double-blinded, two-period crossover study. On day 1 and day 15 of each treatment period, 24-h serum insulin and glucose profiles were evaluated. Total area under the insulin aspart concentration-time curve (AUC(0-24 h)), AUC after dinner administration stratified into early (AUCdinner(0-6 h)) and intermediate-phase (AUCdinner(6-14 h)), maximum insulin concentration (Cmax), time to maximum insulin concentration (Tmax) after each meal were recorded. RESULTS: On day 15 BIAsp70 was associated with a shorter Tmax, and more than 40% elevated Cmax. Comparing with BIAsp30, AUC(0-24 h) and AUCdinner(0-6 h) were increased by 25% and 28%, respectively, but AUCdinner (6-14 h) was markedly lower for BIAsp70 [BIAsp30/BIAsp70: 1.9; 95% CI (1.42, 2.55)]. Similar findings were also observed on day 1. The fasting or pre-meal serum insulin levels on day 15 tended to be higher with BIAsp30, but the differences were not statistically significant. CONCLUSIONS The pharmacokinetic properties of BIAsp30 and 70 remain constant during 2 weeks of daily administration in patients with Type 1 diabetes. In comparison with BIAsp30, the administration of BIAsp70 results in a shorter time to and larger maximum insulin aspart concentration. Furthermore, total and early post-dinner insulin AUC were greater, whereas late-phase insulin exposure was lower with BIAsp70.

[Large parathyroid adenoma in a 38-year old woman with primary hyperparathyroidism]. / Meget stort parathyreoideaadenom hos en 38-årig kvinde med primaer hyperparatyroidisme.

We report a case of severe primary hyperparathyroidism in a 38 year-old female reporting only vague symptoms. Serum PTH at the time of diagnosis was 201 pmol/l. A palpable, encapsulated chief cell adenoma weighing 25.5 grams was removed and the hyperparathyroidism resolved.

Systemic treatment in the rat with epidermal growth factor causes polycystic growth of the ovaries.

BACKGROUND: It has previously been suggested that epidermal growth factor (EGF) plays a role in the function of the ovary. We administered systemic EGF to assess the influence of EGF receptor stimulation on the morphology of the ovaries. METHODS: Forty-eight female Wistar rats were allocated to five groups receiving EGF treatment (150 microgram/kg/day) for 0 (controls), 1, 2, 3 and 4 weeks. All rats were exactly 8 weeks at the start of the experiment and 12 weeks at sacrifice. The EGF was administered in the weeks prior to sacrifice. At sacrifice, the perfusion-fixed ovaries were removed and weighed, and the volumes of tissue components were quantified using stereology. RESULTS: EGF administration increased the total weight of the ovaries from 129 +/- 18 mg in the controls to 158 +/- 29 mg (p<0.05) after one week. In subsequent weeks the total weight increased to 230 +/- 73 mg (p<0.001). The weight gain after one week of treatment was exclusively due to a fourfold increase in follicular cyst volume (p<0.01). In subsequent weeks the cyst volume was increased up to eightfold. After 2, 3 and 4 weeks of treatment the quantity of luteinizing cells was likewise increased by 70% (p<0.01). CONCLUSION: EGF administration causes the follicular cells to produce cysts and increases the quantity of luteinizing cells.

[Postulosis palmoplantaris caused by angiotensin-converting enzyme inhibitors]. / Pustulosis palmoplantaris udløst af angiotensinkonverterende enzymhaemmere.

Angiotensin-converting enzyme (ACE) is identical to kinase II, which inactivates bradykinin. Inhibition of bradykinin degradation by ACE inhibitors alters the kinin-kallikrein arachidonic acid system leading to increased concentrations of inflammatory metabolites. It has previously been demonstrated that the arachidonic acid system may play a role in the pathogenesis of psoriasis/volar pustulosis. Our patient was treated with Captopril and developed a rash identical to volar pustulosis within six weeks. Captopril was substituted with Perindopril, and the eruptions had almost disappeared five months later after a short systemic treatment with steroids. One month later the patient developed the same rash. Perindopril was withdrawn and the eruptions had disappeared two months later.