Retroperitoneal fibrosis caused by pergolide in a patient with Parkinson's disease.

Retroperitoneal fibrosis (RPF) is an uncommon disorder that may cause ureteric obstruction with renal damage. Pergolide, a dopaminergic agonist used in the treatment of Parkinson's disease, has rarely been related to the development of RPF. We report on a 78-year-old woman with Parkinson's disease who presented with hydroureteronephrosis and developed RPF and serosal fibrosis during treatment with pergolide. Following discontinuation of pergolide therapy and placement of a double-J stent, her renal function improved. Inflammatory markers returned to normal limits within two months and the retroperitoneal fibrotic mass became smaller.

The modulation of glucocorticoid receptor content by 3-O-methyl-D-glucose transport in human mononuclear leukocyte in obesity.

Glucocorticoid receptors (GR) and 3-O-methyl-D glucose (3-O-MG) transport were determined in mononuclear leukocytes (MNL) from 11 abdominal obese subjects, 10 pituitary-dependent Cushing's syndrome (Cushing's disease) and 10 healthy controls. Using a whole-cell competitive binding assay and 3H-dexamethasone as tracer, MNL of abdominal obese subjects were found to have 4855 +/- 1389 sites/cell which was significantly lower (p < 0.05) than controls (6234 +/- 1568 sites/cell), although no significant difference was found in the mean serum cortisol level. Their mean Kd (affinity) was also significantly lower than that found in the healthy controls (obese Kd:2.92 +/- 0.84 nmol/l, control Kd: 4.55 +/- 0.67 nM, p < 0.05). On the other hand, the receptor characteristics in Cushing's disease patients were within the normal range. At the same time, 3-O-MG transport was determined in the same subjects. In Cushing's disease, 3-O-MG transport was within the normal range, whereas in abdominal obesity this value was significantly lower than the healthy controls (abdominal obese: 31.90 +/- 8.20; control: 46.26 +/- 12.91 fmol/10(6) cell, min, p < 0.05). We also found a positive correlation between 3-O-MG transport and GR binding capacity in abdominal subjects (r = 0.89, p < 0.001), however we did not find such a correlation in Cushing's disease (r = 0.60, p > 0.05). These results indicated that, in abdominal obesity, the GR binding capacity in MNL is influenced by the changes in glucose transport.

[Intracerebral solitary plasmacytoma. Apropos of a case possibly induced by head injury]. / Plasmocytome solitaire intracérébral. A propos d'un cas peut-être induit par un trauma crânien.

We report a rare occurrence of an intraparenchymal plasmocytoma. On the past history of a severe head injury twenty years ago and the presence of a porencephalic area on the computerized tomography scan and magnetic resonance imaging we suspected a possible trauma-tumor relation. Accuracy of the histological diagnosis of plasmocytoma was confirmed. The treatment was a surgical excision only, and after a 4.5 years follow-up period, no clinical nor radiographic recurrence was noted.

The effect of metformin on insulin receptors and lipid peroxidation in alloxan and streptozotocin induced diabetes.

Biguanides are used for the treatment of non-insulin dependent diabetes mellitus but there is no evidence for an improving action of biguanide on the enhancement of peripheral glucose disposal in type 1 diabetes. It is known that biguanide agents reduce the oxidation of free fatty acids. Using alloxan and streptozotocin (STZ) induced diabetic rats as a model for type 1 diabetes mellitus, we measured insulin binding capacity and plasma lipid peroxidation levels before and after metformin induction. There was a significant increase in insulin binding capacity and lipid peroxidation levels in alloxan and STZ diabetes compared to controls. We examined the effect of metformin on alloxan and STZ-induced diabetic rats. In alloxan-induced diabetes metformin (Met) treatment led to an increase in insulin receptor number in liver plasma membranes (before Met: 46.50 +/- 2.69, after Met: 76.00 +/- 3.39 fmol/mg, p < 0.001) and a decrease in plasma lipid peroxidation levels compared to the non-treated group (before Met: 1.85 +/- 0.53, after Met: 1.10 +/- 0.09 nmol MDA/ml, p < 0.05). In STZ-induced diabetic rats metformin treatment did not change the lipid peroxidation levels (before Met: 1.26 +/- 0.31, after Met: 1.38 +/- 0.44 nmol MDA/ml, p > 0.05) whereas it did increase the receptor numbers (before Met: 41.60 +/- 4.33, after Met: 63.40 +/- 8.64 fmol/mg, p < 0.002).