ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

A 63-year-old man was referred to the endocrine service when he was found to have a 3-cm incidental pituitary macroadenoma. He reported decreased sexual drive, erectile dysfunction, fatigue, and cold intolerance. Biochemical studies revealed markedly increased serum prolactin and adrenocorticotropic hormone (ACTH) levels. However, he had no symptoms or signs of Cushing syndrome. A 24-hour, urinary-free cortisol level was normal. His plasma cortisol level responded appropriately to cosyntropin stimulation test and low-dose over-night dexamethasone suppression test. He was treated medically with dopamine agonist and thyroid hormone replacement. He declined testosterone replacement. After an initial improvement of fatigue and cold intolerance, he reported dizziness, fatigue, and poor overall sense of well being. These symptoms paralleled a steady decrease in ACTH levels. Adrenal insufficiency was confirmed by a suboptimal cortisol response to cosyntropin administration and by a blunted plasma 11-deoxycortisol response and a subnormal ACTH response after an overnight, single-dose metyrapone test. Symptoms improved after adrenal cortical hormone replacement.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

A normotensive 38-year-old woman had severe hypokalemia and metabolic alkalosis in her 16th week of pregnancy. She also had hypomagnesemia and hypocalciuria and evidence of activation of the renin/aldosterone system. DNA analysis revealed a mutation in the sodium chloride co-transporter gene, NCCT, located in the distal renal tubule. Gitelman syndrome was diagnosed, and she required massive potassium and magnesium supplements during pregnancy. She delivered, uneventfully, a healthy baby girl. We review the molecular pathophysiology of Gitelman syndrome and related tubular disorders and discuss management in pregnancy.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

The definition of error is imprecise. To learn from error, a precise definition and process for determining error must be established. Rush University’s Department of Medicine convened a Patient Safety Committee and charged this committee to develop a model for determining error. A description showing how we evaluated a case involving a patient using steroids daily for rheumatoid arthritis and who had an adverse event after being transferred to the intensive care unit with a small bowel obstruction. Four physicians independently reviewed the case to determine if an error occurred. The four physicians completely disagreed about which event was the error. To resolve the disagreement, we constructed a temporal chain of events, decisions, and processes of care, leading from the first decision made during care to the adverse outcome. Then, we used the principles of evidence-based medicine to examine each decision for benefit in excess of risk, and we used the concepts of constraint theory to examine each process for failed delivery. Error was defined as the failed decision or process that sufficiently caused the chain of events leading to the adverse event. Through group discussion and the use of explicit criteria we were able to agree finally on the event that was an error. Adverse events and errors are different events. Chart review and interviews with providers followed by a group discussion of the clinical issues is needed to fully examine the decisions and the processes of care for each adverse event. An explicit process to identify error may be necessary to assure a standard, sharable definition before embarking on changes to reduce error.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

There is a growing interest in preventing bone loss through medical treatment of patients with primary hyperparathyroidism who have mild asymptomatic disease or who are not candidates for surgical parathyroidectomy. Bisphosphonates are inhibitors of bone resorption and could be useful to improve the bone resorption of hyperparathyroidism. Therefore, we conducted a controlled trial of alendronate therapy in patients with primary hyperparathyroidism. Participants were 45 asymptomatic patients with primary hyperparathyroidism who either had mild disease or a coexistent disease making surgical therapy hazardous or who refused parathyroidectomy. Their femoral bone mineral density (BMD) was in the osteoporotic or osteopenic range. Eight assigned to alendronate therapy had complete biochemical studies performed prospectively before therapy, then after 1 month, and every 2 months for 1 year. Another 37 patients were assigned as: 11 to the alendronate group and 26 to the nonalendronate or control group; all of them had regular follow-up with their endocrinologists. All the patients administered the alendronate therapy were administered 10 mg/d of alendronate for 1 year. Bone mineral density was measured by dual-energy x-ray absorptiometry at the lumbar spine and proximal femur initially and at 12 months in all patients. Eight patients had measurement of BMD of the radius and a complete biochemical profile. By 12 months, patients using alendronate had a significant increase in BMD at the lumbar spine by 3.38% and at the femoral neck by 3.05%. In contrast, the control group had losses of 1.41% at the lumbar spine and 0.80% at the femoral neck. The markers of bone turnover (urine pyridinoline and deoxypyridinoline) decreased in the eight patients using alendronate at 1 to 4 months. The serum total alkaline phosphatase level decreased significantly at 6 months and remained decreased at 12 months. Serum calcium, phosphorus, intact parathyroid hormone, 1,25-dihydroxyvitamin D3, and 25-hydroxyvitamin D levels did not change significantly, but there was a small increase in ionized calcium at 6 months. We conclude that in patients with hyperparathyroidism, alendronate prevents bone loss and significantly improves BMD at the lumbar spine and femoral neck.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Angiogenesis has been shown to be related to tumor behavior in many different types of neoplasms. Pituitary tumors, although usually benign, exhibit a wide variation in behavior from complete latency to aggressive infiltration and distant metastasis. Pituitary tumors are less vascular than the normal anterior pituitary gland, and vascular endothelial growth factor (VEGF) expression is lower in tumors than in normal gland. However, angiogenesis is directly related to tumor size in prolactinomas, to tumor invasiveness in macroprolactinomas, and to carcinoma development. Although the proangiogenic growth factor VEGF and inhibitory factors such as the 16-kDa fragment of prolactin are present in the pituitary, the mechanism of control of the balance of angiogenesis and the source of the blood supply to tumors are still unclear. Whether differences in angiogenesis may play a role in determining different aspects of pituitary tumor behavior and the potential mechanisms involved are reviewed.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

The somatomedin hypothesis, formulated in 1972, states that circulating somatomedin C, synthesis of which in the liver is stimulated by growth hormone (GH), is the effector of GH activity on body tissues. Somatomedin C was found to have an equivalent identity to nonsuppressible insulin-like activity, and subsequently, both were referred to as insulin-like growth factors (IGF-I and II). The evidence summarized in this review, which casts doubt on the hypothesis, is extensive. First, the experiments performed in 1957, showing that GH did not stimulate mucopolysaccharide incorporation into cartilage in vitro, have recently been repeated by one of the original investigators who found that incorporation was indeed stimulated by GH, provided the appropriate media were used. Second, GH receptors have been found in a variety of tissues involved in the growth process; this suggests that the hormone is capable of interaction directly with those tissues without the need for a second messenger mediator. Third, two groups of investigators have found that elimination of hepatic-derived IGF-I in mice does not impair their growth despite a 75% reduction in circulating concentrations of IGF-I. Fourth, there is a considerable body of evidence that administration of IGF-I to humans produces effects that are the opposite of those produced by GH administration, i.e., lipogenesis and insulin resistance.Thus, although IGF-I concentrations in the circulation may be a reflection of GH activity in some clinical conditions, such acromegaly, it fails to account for the effects of IGF produced locally in tissues with or without the influence of GH. It should be discarded.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

With diabetes in the United States reaching alarming proportions, reduction of cardiovascular (CV) risk has become a unique challenge to health care providers. Recent studies suggest that the magnitude of the atherosclerotic burden in diabetic patients is much greater than previously appreciated. Modern diagnostic techniques indicate that most patients with type 2 diabetes mellitus (T2DM) have clinical or “subclinical” macrovascular disease. Cardiovascular disease (CVD) continues to be the leading cause of morbidity and mortality among patients with T2DM, despite the availability of newer and more effective CV interventions. These facts highlight the need for more aggressive prevention strategies. There is growing consensus that given these patients’ high risk for CV, all interventions in those with T2DM should be considered secondary prevention, even in diabetic subjects apparently free of CVD. This review focuses on recent randomized, clinical trials on the effect of controlling hyperglycemia, dyslipidemia, and hypertension in patients with T2DM. Taken together, they indicate that even modest improvements of risk factors have a great impact on CVD, in particular, treatment of lipids and blood pressure. The time has come for clinicians to adopt an aggressive strategy of risk factor reduction in subjects with T2DM.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Cortisol regulates adipose tissue differentiation, function, and distribution. In excess, cortisol causes visceral obesity. Visceral obesity is one of the key components of the metabolic syndrome. During the past decade, there has been an increasing interest in the role of stress in the pathogenesis of the metabolic syndrome, but in the absence of definitive data, the mechanisms have not been disclosed. With use of new methods for the assessment of cortisol, it has now been shown that inadequate cortisol secretion is associated with abnormalities in glucose, insulin, and lipid metabolism, including hypertension, bringing the importance of the hypothalamic-pituitary-adrenal (HPA) axis in the control of human health to the forefront. In this overview, we briefly summarize the currently available information on physiological alterations in the HPA axis in the metabolic syndrome.

ISSN:1051-2144    

出版商:OVID    

年代:2001

数据来源: OVID