Impact of a phone follow-up program on persistence with teriparatide or PTH(1-84) treatment.

A follow-up program to help patients suffering from severe osteoporosis during their therapy with teriparatide or PTH(1-84) has been designed and performed. The objective of this study was to evaluate the 18-month persistence on these therapies in patients participating in the program. We enrolled 382 patients who started teriparatide or PTH(1-84) following this program and compared them with a historical cohort of 398 patients treated with the same therapies but who did not participate in any follow-up program.

Alendronate reduces osteoclast precursors in osteoporosis.

Unlabelled: This study evaluates the effect of alendronate on osteoclastogenesis, cytokine production, and bone resorption in postmenopausal women. We suggest that it acts on mature bone resorbing osteoclasts after 3 months of treatment, whereas, after 1 year, it diminishes their formation by reducing their precursors and serum RANKL.

Introduction: Osteoclasts are the target cells of bisphosphonates, though the most drug-sensitive steps of their formation and activity have not been determined.

Hypoparathyroidism and co-existing celiac disease.

A 62-yr-old woman with idiopathic hypoparathyroidism was admitted to our hospital for severe anemia (Hb 5.6 gr/dl) and hypoalbuminemia (3.2 gr/dl).

Intracellular protein glycation in cultured retinal capillary pericytes and endothelial cells exposed to high-glucose concentration.

There is now increasing evidence suggesting that non-enzymatic glycation (NEG) of proteins is involved in the pathogenesis of chronic diabetic complication. In this study we demonstrate that chronic exposure to high-glucose concentration leads to intracellular protein glycation in cultured bovine retinal capillary pericytes and endothelial cells. The level of intracellular protein glycation, as measured using a competitive enzyme-linked immunoabsorbant assay (ELISA), was found to increase in both pericytes and endothelial cells as function of time.

Dehydroepiandrosterone protects bovine retinal capillary pericytes against glucose toxicity.

Pericyte loss is an early feature of diabetic retinopathy and represents a key step in the progression of this disease. This study aimed to evaluate the effect of dehydroepiandro-sterone (DHEA) on glucose toxicity in retinal capillary pericytes. Bovine retinal pericytes (BRP) were cultured in a high glucose concentration, with or without DHEA.

Toxic action of advanced glycation end products on cultured retinal capillary pericytes and endothelial cells: relevance to diabetic retinopathy.

The toxic effects of advanced glycation end products (AGEs) on bovine retinal capillary pericytes (BRP) and endothelial cells (BREC) were studied. AGE-modified bovine serum albumin (AGE-BSA) was toxic to BRP. At a concentration of 500 micrograms/ml it reduced the BRP number to 48 +/- 3% (p < 0.

Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions.

This study aimed at verifying whether thiamine, a co-enzyme which decreases intracellular glycolysis metabolites by allowing pyruvate and glyceraldheyde 3-phosphate to enter the Krebs cycle and the pentose-phosphate shunt, respectively, corrects delayed replication caused by high glucose concentrations in cultured human umbilical vein (HUVEC) and bovine retinal endothelial cells (BREC). After incubation in physiological (5.6 mmol/l) or high (28.

Levels of vascular endothelial growth factor are elevated in the vitreous of patients with subretinal neovascularisation.

Background: Vascular endothelial growth factor (VEGF) has been shown to play a major role in intraocular neovascularisation in ischaemic retinal diseases. Subretinal neovascularisation is an important cause of central visual loss, but little is known about the role of this growth factor in its pathogenesis. The aim of this study was to investigate the possible role of VEGF in the development of subretinal neovascularisation.

The effect of aminoguanidine and tolrestat on glucose toxicity in bovine retinal capillary pericytes.

Cultured bovine retinal capillary pericytes (BRP) were used to investigate the effect of an aldose reductase inhibitor, tolrestat, and an inhibitor of advanced glycation end products (AGE) formation, aminoguanidine, on glucose toxicity. Glucose at high concentration reduced the replicative activity of pericytes in a dose-dependent manner. Tolrestat completely inhibited the production of sorbitol in cells exposed to a high concentration of glucose but failed to protect the cells from glucose toxicity.

Growth of bovine retinal pericytes and endothelial cells in high hexose concentrations.

Selective loss of capillary pericytes occurs early in diabetic and galactosemic retinopathies, at a stage when endothelial cells are still spared. To ascertain whether such loss is directly related to high hexose concentrations, the replication of bovine retinal pericytes and endothelial cells was studied by culturing them in media containing 5.6 mmol/l glucose alone and enriched with extra glucose, mannitol or galactose to achieve final concentrations of 16.

A study of the effects of human blood derivatives and individual growth factors on [3H]thymidine uptake in bovine retinal pericytes and endothelial cells.

Pericytes disappear early, selectively and specifically from retinal capillaries in diabetic microangiopathy, but little is known of their growth and turnover in health and disease. We have studied the effects of human blood derivatives and of a panel of individual growth factors on [3H]thymidine incorporation in bovine retinal pericytes and endothelial cells. Human serum and platelet-rich plasma stimulated incorporation of the nucleotide in a dose-dependent manner in both cell types, and did so more potently than platelet-free plasma.

Delayed replication of human umbilical vein endothelial cells in high glucose is corrected by L-tyrosine.

Human umbilical vein endothelial cells (HUVEC) cultured in high glucose exhibit delayed replication and colchicine-resistant microtubules. Tubulin dysfunction and stabilization, brought about by acetylation of the NH2-terminal residues, loss of the C-terminal tyrosine and binding of microtubular-associated proteins (MAPs) may be involved in the above phenomenon. The effects of L-tyrosine on HUVEC replication in high glucose were tested and the hypothesis that non-enzymatic glycosylation might impair tubulin depolymerization was also checked by growing the cells in the presence of L-glucose, which binds to intracellular proteins but remains metabolically inactive.

von Willebrand factor and endothelial abnormalities in diabetic microangiopathy.

We briefly summarize current knowledge on 1) the abnormalities of von Willebrand factor (vWF) as an indicator of endothelial cell (EC) dysfunction in diabetes and 2) the modifications induced in the growth of cultured ECs by high glucose in the incubation media. A MEDLINE search (1986 through Sept. 1989) was performed to update previous relevant references on vWF and ECs in healthy and diabetic subjects.

Cytokine stimulated endothelin release from endothelial cells.

Endothelin release from bovine endothelial cells of the aorta, pulmonary artery, and retinal microvessels was measured in response to various cytokines. Transforming growth factor beta (0.05-5 ng/ml) was found to be a potent stimulator (3-4 fold increase) of endothelin secretion in all three cell types.

Gynaecomastia and azoospermia as sole presenting symptoms of feminizing adrenal tumor.

Adrenal feminizing tumours are rare but frequently malignant. A case of adrenal feminizing tumour in a 35-year-old man, which presented with gynaecomastia and infertility due to azoospermia, without loss of libido and sexual potency is reported in this paper. Our patient represents a relatively unusual case.

[Endothelium and its morphofunctional changes in the pathogenesis of diabetic microangiopathy].

Recent advances in our knowledge of endothelial function in health and in the presence of generalized microvascular damage, such as found in diabetic microangiopathy, are discussed in this review article. In microangiopathy there are no typical morphological signs of endothelial stress, apart from ubiquitous thickening of the basement membrane and the finding of both hyper- and acellular capillaries, whereas important derangements of endothelial function may occur in the early stages of the disease, like accelerated turnover, intracellular accumulation of potentially toxic intermediate metabolites, hyperpermeability of the vessel wall, altered synthesis of some haemostatic factors, expression of angiogenetic potentialities in inappropriate situations. The possible pathogenetic mechanisms underlying such alterations are reviewed, with special emphasis on the shortcomings of the experimental models available for laboratory investigation and on the in vivo situation.

Growth hormone responses to pyridostigmine in normal adults and in normal and short children.

There is evidence indicating that the cholinergic system positively modulates GH release probably by inhibiting somatostatinergic tone. In the present study, the effects of cholinergic enhancement by pyridostigmine, (PD), a cholinesterases inhibitor, on GH release in normal adults (n = 14) (NA) and in both normal (n = 5) (NC) and short children (n = 19) (SC) with familial short stature (n = 7) or constitutional growth delay (n = 12) were studied. In SC the insulin hypoglycaemia (IH)-induced GH increase was also studied.

Potentiation of cholinergic tone by pyridostigmine bromide re-instates and potentiates the growth hormone responsiveness to intermittent administration of growth hormone-releasing factor in man.

It is known that in normal subjects repeated administration of the growth hormone-releasing factor (GRF) induces a state of partial refractoriness of the somatotropes to GRF. Studies were conducted to verify whether the cholinergic system plays a role in the mechanism(s) underlying the reduced GH responsiveness to the neuropeptide. In five healthy men, the GH response to three consecutive injections of GRF (50 micrograms iv), administered at 2 h intervals, was considerably blunted after the second and third GRF bolus.

Metastasis to pituitary adenoma.

Neoplasm to neoplasm metastasis is a medical curiosity. We report two cases of adenocarcinoma metastatic to pituitary adenoma. In both, abrupt progression of symptoms referable to the sellar region was noted and followed by the death of the patient.