ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

&NA;Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. However, with improved screening methodologies, it appears that primary aldosteronism is the most common form of secondary hypertension. Patients with hypertension and hypokalemia and most patients with treatment‐resistant hypertension should undergo screening for primary aldosteronism. A ratio of plasma aldosterone concentration (PAC; in ng/dL) to plasma renin activity (PRA; in ng/mL per hour) of >20 (with a PAC >15 ng/dL) is a positive screen for primary aldosteronism. An elevated PAC/PRA ratio is not diagnostic and primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion. The two major subtypes of primary aldosteronism are unilateral aldosterone‐producing adenoma (APA) and bilateral idiopathic hyperaldosteronism (IHA). Patients with APA are usually treated with unilateral adrenalectomy, and patients with IHA are treated medically. The subtype evaluation may require one or more tests, of which the first is imaging the adrenals with computed tomography (CT). When a solitary unilateral macroadenoma (>1 cm) and normal contralateral adrenal morphology are found on CT in a patient with primary aldosteronism, unilateral laparoscopic adrenalectomy is a reasonable therapeutic option. However, in many cases, CT imaging may reveal normal‐appearing adrenals or ambiguous findings. Adrenal venous sampling helps solve these clinical dilemmas.

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

&NA;Is there anything new about the etiology of Pagest's disease of bone (PD)? Decidedly yes! Since its description in 1877, numerous reviews have been written about this fascinating bone disease. As greater insight develops, new hypotheses as well as revisions of familiar theories about the etiology of the disease are being proposed. The subjects of this update will include comments about recent analyses of the familial aggregation of P*D, newly discovered genetic linkages, chromosomal translocations involving the centrosome, new illustrations of the ultrastructure associating a virus with osteoclasts, results from the use of PD models for research, the proposed mechanism of the paramyxovirus effect on the immune system, the expression of cytokines in PD, and inferences drawn from the effect of therapeutic agents.

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

&NA;Central hypothyroidism has been considered to be a rare condition. Using the nocturnal TSH surge, a sensitive diagnostic test, we have accurately identified central hypothyroidism in children and adults. Development of the nocturnal TSH surge test has been based on the physiologic circadian pattern of TSH secretion. An abnormally low rise in TSH concentrations at night confirms central hypothyroidism in patients with known hypothalamic‐pituitary disorder or in children otherwise thought to have id iopathic short stature. The nocturnal TSH surge is more sensitive than the thyrotropin‐releasing hormone test in diagnosing central hypothyroidism. Children with apparent idiopathic short stature and with free T4 (FT4) levels in the lowest third of the normal range have a 32% incidence of central hypothyroidism. Their growth velocities were improved significantly during thyroid hormone supplementation. Mild central hypothyroidism (FT4 within normal range) does not in itself significantly alter growth hormone (GH) secretion, and does not confound the interpretation of GH stimulation testing. We conclude that central hypothyroidism occurs more frequently than recognized in the past, and the nocturnal TSH surge test is the most sensitive test for diagnosing central hypothyroidism.

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

&NA;After the cessation of longitudinal growth, growth hormone (GH) continues to subserve an important role in the regulation of body metabolism to optimize body composition and function. Adults who are deficient in GH exhibit a number of abnormal features including increased adiposity and reduced lean body mass associated with reduced physical fitness. These features are reversible with GH therapy and suggest the need for long‐term GH replacement in GH‐deficient adults. Accurate diagnosis of GH deficiency is important because GH replacement is an expensive, life‐long treatment. Although GH deficiency causes recognizable physical changes, the clinical features are not sufficiently distinct to permit accurate bedside diagnosis. GH status is traditionally assessed by undertaking stimulation tests, by measuring spontaneous secretion, or by measuring markers of GH action such as insulin‐like growth factor‐1 (IGF‐1) and IGF binding protein‐3 (IGFBP‐3). In an evaluation of the relative merits of these three diagnostic testing modalities (specifically the insulin tolerance test [ITT], mean 24 hour GH levels, IGF‐1, and IGFBP‐3), the ITT was found to be the most accurate test. The ITT correctly identified all patients with GH deficiency with a GH response clearly below that of healthy subjects. The use of other stimulation tests should not be extrapolated from the ITT and needs to be independently evaluated.

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

&NA;Preeclampsia, a hypertensive disorder of human pregnancy, is one of the most significant causes of fetal growth retardation, premature delivery, and maternal and fetal morbidity and mortality. The major clinical symptoms of preeclampsia include hypertension and proteinuria with edema. The major pathophysiologic characteristics of this disorder include an increase in vascular resistance leading to maternal hypertension and decreased uteroplacental blood flow and coagulation abnormalities resulting in increased platelet aggregation, thrombin generation, and thrombus formation. In women with preeclampsia, there are several disturbances in the levels of hormones, cytokines, and paracrine and autocrine compounds that relate to the clinical symptoms of the disorder. These disturbances include increased levels of thromboxane, decreased levels of prostacyclin, decreased levels of renin, angiotensin II, and aldosterone but enhanced pressure responsiveness to angiotensin II, increased levels of atrial natriuretic peptide, increased levels of serotonin, increased levels of lipid peroxides, decreased levels of antioxidants, and increased activation of neutrophils with the generation of tumor necrosis factor and IL‐6. Reports on the levels of nitric oxide and endothelin are inconsistent as to whether these vasoactive compounds are increased, decreased, or unchanged. Although the cause of preeclampsia is not known, the placenta may be a key organ in the pathogenesis. Increased production and secretion of lipid peroxides by the placenta could be responsible for neutrophil activation and increased levels of lipid peroxides in the maternal circulation. Increased levels of lipid peroxides would contribute to coagulation abnormalities, neutrophil activation, endothelial cell dysfunction, and increased thromboxane and decreased prostacyclin.

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

&NA;Iodine excess usually is well tolerated by healthy individuals because of escape from its acute inhibitory effects on thyroid hormone synthesis (acute Wolff‐Chaikoff effect) and only subtle, physiological changes in thyroid function occur. In contrast, excess iodine administration to patients with a wide variety of underlying thyroid disorders can induce hypothyroidism or hyperthyroidism, the latter more common in areas of iodine deficiency. Although less common, iodine‐induced thyroid dysfunction also can occur in patients without recognized underlying thyroid disease. This review hopefully will provide the reader with an understanding of the pathophysiology of the effects of excess iodine on thyroid function and the diagnosis and therapy of these disorders, including a brief section on the adverse effects of the iodinerich drug amiodarone.

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:1051-2144    

出版商:OVID    

年代:1997

数据来源: OVID