ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Osteoporosis is a major public health problem that is increasing in magnitude as the average age of the population rises. Effective treatment of osteoporosis is confined largely to the women at increased risk at an early age so that preventative treatment can be instituted. Because osteoporosis always implies bone breakdown in excess of bone formation, biochemical indices of these processes have been an important research initiative in the study of osteoporosis. This short review will examine the currently available biochemical markers for bone remodeling and examine the clinical utility of each. In addition, new measurements of bone turnover will be described and an attempt made to evaluate their potential role in the evaluation of osteoporosis. Finally, categories of bone turnover, “fast” versus “normal,” will be described, and the clinical implications of this classification will be reviewed in terms of diagnosis and treatment.

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

In the United States, diabetic nephropathy is now the leading cause of end-stage renal disease (ESRD) leading to kidney transplant. In insulin-dependent diabetes mellitus (IDDM), the evolution of renal disease follows five characteristic stages: glomerular hyperfiltration and nephromegaly are observed at the time of diagnosis (stage 1). This is followed by a clinically silent phase of developing structural injury (stage 2). “Incipient” diabetic nephropathy follows with microalbuminuria (stage 3). Overt nephropathy (stage 4) leads to ESRD (stage 5). Much less is known about renal disease in patients with non-insulin-dependent diabetes mellitus. Recent studies, however, indicate that the process is functionally and structurally analogous to that in IDDM. Experimental and clinical studies have improved our understanding of the pathophysiology of diabetic renal disease. The most promising interventions appear to be optimal glycemic control, dietary protein restriction, and antihypertensive therapy. Efficacy varies with stage of disease. Current evidence suggests that during stages 1 and 2 the rate of progression of microalbuminuria and the decline in glomerular filtration rate can be reduced by maintaining near-normoglycemia and, possibly, with angiotensin-converting enzyme inhibitor (CEI) administration. Following the appearance of persistent protein-uria, progression to ESRD can be delayed by aggressive antihypertensive therapy and restriction of dietary protein intake. Recent studies suggest that CEI may be better than other antihypertensive agents. Therapies have been identified that can slow the progression of diabetic renal disease and delay the appearance of ESRD.

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

In the majority of patients with delayed puberty, the history and physical examination will provide a reliable indicator of the diagnosis. Statistics alone dictate strong consideration of gonadal dysgenesis and its variants in a phenotypic female and constitutional delay in the male. In this regard, the importance of childhood growth patterns, careful inspection for stigmata of Turner's syndrome, and accurate measurements of testicular size is apparent. Under any circumstance, every effort must be made to rule out the rare CNS tumor. The “perfect” test for determining the cause of hypogonadotropism in 13 or 14-year-old patients does not exist and doubt will remain in many cases. In such instances, patients should not be subjected to prolonged sexual infantilism. Short-term treatment with sex steroids should be utilized after due consideration, but not reluctantly. Long-term replacement therapy requires a firm understanding of the normal components of growth and physical change during puberty.

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

It was postulated from experiments done in para-biotic rats in the 1930s that a water-soluble factor of testicular origin played an important role in regulating pituitary FSH secretion. That factor was termed “inhibin.” Years of intense effort to isolate and characterize inhibin proved fruitless until a molecule with the ability to suppress FSH secretion from dispersed pituicytes was isolated from bovine follicular fluid in 1985. The molecule is a hetero-dimer composed of an “alpha” and a “beta” subunit and has a molecular weight of about 31 kD. Dimers of the beta subunit yield a different class of molecules that stimulate FSH secretion and are termed “activins.” Development of a radioimmunoassay for inhibin has revealed that the major source of inhibin in the male is the seminiferous tubule and in the female the granulosa cell. Contrary to expectation, inhibin measurements fail to distinguish the various causes of male infertility one from the other. The possible reasons underlying this and an overview of inhibin physiology, including its recent application as a tumor marker for ovarian cancer, are discussed in the following paper.

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Interest in and research on the mechanisms and the clinical significance of the relationship between insulin resistance and ovarian hyperandrogenism have both increased rapidly over the past 10 years. This article will review all of the clinical syndromes of insulin resistance and ovarian hyperandrogenism but will focus primarily on the polycystic ovary syndrome (PCOS), the most common disorder in which these abnormalities occur together. It will also discuss the mechanisms of insulin action and the pathogenesis of insulin resistance in these disorders, as well as potential reasons for the association of insulin resistance and hyperandrogenism.

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Generalized resistance to thyroid hormone (GRTH) is an inherited syndrome characterized by reduced responsiveness of target tissues to thyroid hormone (TH). The clinical presentation is variable. At one extreme, affected subjects are euthyroid, the partial hormone resistance being compensated by elevated TH levels. At the other extreme, there is severe growth or mental retardation and, in some infants, cretinism. More than 250 patients with this syndrome have been identified. The mode of inheritance is autosomal dominant in the majority of families. Examples of recessive transmission have also been found. It has long been speculated that this defect is caused by an abnormal TH receptor (TR). This hypothesis could not be tested directly until the recent isolation of two TR genes, TRα and TRβ, located in chromosomes 17 and 3, respectively. Mutations in the TRβ gene have been identified in 31 families with GRTH. All are located in the T3-binding domain straddling the putative dimerization region. All exhibit various degrees of hormone-binding impairment. This finding, and the fact that heterozygous subjects with complete TR deletion are not affected while those with point mutations are, indicates that interactions of a mutant TR with the normal TRs or with other factors through dimer formation are responsible for the dominant inheritance of GRTH. Elucidation of the etiology of GRTH has added a new dimension to the early diagnosis of the syndrome and provided new insights into the mechanism of thyroid hormone action.

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1992

数据来源: OVID