ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Hypoaldosteronism has a spectrum of presentations, from asymptomatic hyperkalemia to life-threatening volume depletion. The clinical pictures can result from problems with renin production and release, conversion of angiotensin I to angiotensin II, aldosterone synthesis and secretion, or impaired renal tubular responsiveness to aldosterone. Both endogenous and iatrogenic causes have been identified. Careful attention to the clinical presentation and selective laboratorytestingshouldmakeitpossibleto elucidate the problem in the individual patient and to provide appropriate therapy.

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Transplantation of either pancreas or islet tissue is the only available therapy for type I diabetes that establishes normoglycemia and restores physiologic insulin secretion. This restoration of eu-glycemia may, in turn, be associated with beneficial effects on secondary diabetic complications.Despite increasing success rates and the obvious benefits for carbohydrate metabolism and diabetic complications, pancreas and islet transplantation are not yet considered standard therapy for patients with diabetes. The limitations of pancreas and islet transplantation include the morbidity and mortality associated with the surgery, the need for lifelong immunosuppressive therapy, and the significant financial costs of the procedure. In contrast to these limitations, successful pancreas transplantation establishes sustained normoglycemia without the need for exogenous insulin, restores glucose-responsive insulin secretion and glucagon response to hypoglycemia, and improves quality of life.For pancreas transplantation to achieve the clinical acceptability of other forms of transplantation, clear advantages over exogenous insulin therapy must be demonstrated. This can only happen with the completion of well-controlled comparative studies that permit a clearer understanding of the benefits and risks of pancreas transplantation in the treatment of type I diabetic patients.

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The insulin-like growth factors (IGFs) are potent mitogenic agents involved in the regulation of somatic growth and cellular proliferation. Recently, the complex milieu in which they operate has begun to be unraveled. Endocrine and autocrine patterns of IGF secretion have been identified and specific cell surface receptors that bind IGFs and mediate their biological actions have been characterized. The IGF binding proteins (IGFBPs), a family of six peptides that bind IGFs with high affinity (thus regulating IGF availability to its receptors), have been recognized as a new class of growth modulators. The IGFBPs can inhibit IGF actions, enhance the mitogenic effects of IGFs, or function as independent cell regulatory factors, possibly by interacting with their own receptors on the cell membrane. The IGFBPs, in turn, are regulated by the IGFBP proteases, a group of proteolytic enzymes that are capable of cleaving IGFBPs into smaller fragments with lower affinity for the IGFs, thus enhancing IGF action.The six IGFBPs, while similar, have unique biological properties and appear to have specific patterns of expression and function. Radioimmunoassays for IGFBP-1, −2, and −3 are currently commercially available and information is accumulating on their diagnostic usefulness. This includes several clinical situations, such as growth disorders, where serum IGFBP-3 is a highly specific screening tool for growth hormone deficiency, various malignancies in which serum IGFBP-2 levels are elevated, and disorders of carbohydrate metabolism that display an inverse relationship between serum IGFBP-1 and insulin secretion. Current clinical practice may include the judicious use of these tests for the diagnosis and for monitoring the therapeutic response of such disorders.

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

This brief review will outline the discovery of the somatostatin receptor subtypes, comment on their tissue specific distribution and function, especially in relationship to the pituitary and speculate on future therapeutic potential of subtype specific somatostatin receptor analogues.

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Approximately 25% of reproductive-age women have clinically recognizable uterine leiomyomas. These hormone-sensitive benign neoplasms may cause symptoms due to an enlarged pelvic mass; excessive menstrual flow; and, less commonly, reproductive dysfunction. Women with moderate to severe symptoms traditionally undergo surgery: hysterectomy or myomectomy. A greater understanding of the hormone sensitivity of these tumors and the development of a new class of drugs, the gonadotropin-releasing hormone agonists (GnRH-a), have recently led to medical treatment options. Both estrogens and progestins modulate the growth of uterine tissue. GnRH agonist administration results in a biphasic endocrine response, with transient increases in serum levels of gonadotropins and gonadal steroids followed by sustained suppression of these hormones. The resultant hypogonadotropic/hypogonadal milieu leads to decreases in uterine volume of 40%-50% by the third month of treatment and to menstrual suppression, often with significant increases in hemoglobin concentrations. The changes induced by GnRH agonists often reduce or eliminate leiomyoma-related symptoms but last only until treatment is discontinued, after which ovarian steroidogenesis resumes, leading to uterine and tumoral regrowth and a return to pretreatment menstrual patterns. Because of the adverse sequelae of chronic hypoestrogenemia, therapy with GnRH agonists alone is usually limited to 3–6 months. Use of GnRH agonists preoperatively may provide certain benefits, such as an increase in hemoglobin concentration and a reduction in uterine and tumoral size. These changes may reduce the extent and complexity of the surgical treatment required and/or may decrease surgical morbidity. One recently developed long-term strategy is to combine GnRH agonists with small doses of steroids (e.g., estrogen, progestin), so-called “add-back” therapy, to diminish or eliminate adverse sequelae of prolonged hypoestrogenemia. The differential sensitivities of tissues to these steroids in some cases allow sustained uterine shrinkage and menstrual suppression without accelerated bone loss or vasomotor flushes. GnRH agonist/steroid add-back therapy provides both another treatment option for leiomyomas and a model for studies of their steroid sensitivity.

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The genetic etiology of thyroid hormone resistance syndromes is now well-established. Two clinical variants, generalized resistance to thyroid hormone (GRTH) and selective pituitary resistance to thyroid hormone (PRTH), are, in most cases, caused by heterozygous mutations in the ligand-binding domain of the c-erbAβ thyroid hormone receptor gene. No mutations have been found in the other related receptor gene, c-erbAα, associated with these syndromes. In resistant patients, the mutant β receptors act as dominant negative proteins and inhibit function of the normal β receptor (expressed from one allele) and the normal α receptor (expressed from two alleles). Patients homozygous for a dominant negative allele (the Refetoff patient) and without any β receptor (the Refetoff patient) have been described. GRTH and PRTH are both diagnosed by elevated serum free thyroid hormones and inappropriately normal TSH, but in the former case patients are clinically euthyroid whereas in the latter case patients have symptoms and signs of hyperthyroidism. Interestingly, there are examples of different patients who have been classified as having GRTH and PRTH who harbor identical β mutations. Various mechanisms can explain the clinical heterogeneity seen in thyroid hormone resistance syndromes: overexpression of the mutant β receptor allele, additional contributory genes, and variable perturbations of the dimerization domain of the receptor that in turn affect DNA-binding affinity. These factors may modulate the magnitude of tissue resistance resulting in variable levels of circulating thyroid hormone and other differences in phenotype such as stature.

ISSN:1051-2144    

出版商:OVID    

年代:1995

数据来源: OVID