{"title":"Hemodynamic changes as early markers of diabetic retinopathy","authors":"J. Grunwald, S. Bursell","doi":"10.1097/00060793-199608000-00004","DOIUrl":"https://doi.org/10.1097/00060793-199608000-00004","url":null,"abstract":"Abnormalities of retinal blood flow and its ability to respond to metabolic and environmental changes have been described in patients with long-standing diabetic retinopathy. In order to assess the role of these abnormalities in the pathophysiology of diabetic retinopathy, it is important to investigate how early in the disease these derangements occur. Measurements of the effect of new treatment modalities on these hemodynamic abnormalities may help in the assessment of their therapeutic potential.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"298–306"},"PeriodicalIF":0.0,"publicationDate":"1996-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199608000-00004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61608987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of oxidative stress in diabetic complications","authors":"J. Baynes, S. Thorpe","doi":"10.1097/00060793-199608000-00001","DOIUrl":"https://doi.org/10.1097/00060793-199608000-00001","url":null,"abstract":"Diabetes eventually affects the function of most, if not all, tissues in the body. Thus, it is reasonable to consider a basic mechanism, such as oxidative stress, as a possible common cause of the diverse complications of diabetes. This review discusses current methods for assessing the status of oxidative stress in diabetes, the convincing evidence that oxidative stress mediates neuropathy and vasculopathy in animal models of diabetes, and the developing evidence that increased oxidative stress may have a role in the pathogenesis of the long-term complications of human diabetes. Because oxidative stress impairs vascular function, the treatment of diabetic complications should include multidrug therapies aimed at limiting oxidative stress and improving vascular tone.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"277–284"},"PeriodicalIF":0.0,"publicationDate":"1996-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199608000-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61608945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Modern approach to corticosteroid replacement therapy","authors":"F. Czerwiec, G. Cutler","doi":"10.1097/00060793-199606000-00008","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00008","url":null,"abstract":"The therapeutic index of corticosteroids for adrenal insufficiency is narrowing with recognition of the adverse consequences from even minor overtreatment. As in endogenous Cushing syndrome, chronically excessive glucocorticoid dosage can produce weight gain, hypertension, hypercholesterolemia, glucose intolerance, and bone demineralization. By contrast, deficient replacement leads to the constitutional and other symptoms of adrenal insufficiency and can induce lifethreatening shock, particularly during major stress. Optimum therapy depends on the cause of adrenal insufficiency. Primary and secondary adrenal insufficiency, congenital adrenal hyperplasia, and Nelson syndrome each present unique problems that require specific approaches to treatment. The clinician's major challenge is to adjust mineralocorticoid and glucocorticoid doses so as to meet physiologic requirements without inducing corticosteroid excess. Herein, we review the patho-physiology of adrenal insufficiency, outline a stepwise approach to adrenal hormone replacement, and discuss literature relevant to current issues of corticosteroid replacement therapy.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"239–246"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Angiotensin II receptors","authors":"O. Holland","doi":"10.1097/00060793-199606000-00011","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00011","url":null,"abstract":"In addition to blood pressure and volume regulation, the renin-angiotensin system is now believed to play a role in diverse areas. In recent years, new information conceming angiotensin receptors has improved dramatically our understanding of cellular and molecular mechanisms by which the renin-angiotensin system exerts its actions. Two major distinct classes of angiotensin II receptors, type 1 and type 2, have been noted. The vast majority of currently recognized actions of angiotensin II are mediated by angiotensin II type 1 receptors. Significant progress has been made in elucidating multiple signal transduction mechanisms for angiotensin II type 1 receptors. Angiotensin II type 2 receptors are noted in a variety of tissues, and functions mediated by these receptors are just beginning to be defined. Interactions among subtypes of angiotensin II receptors are increasingly recognized as having considerable potential medical importance with respect to the pathogenesis of cardiovascular and renal disease and to physiologic functions in a variety of organ systems.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"258–264"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Corticotropin‐dependent synthesis of mitochondrial proteins involved in the acute regulation of steroidogenesis","authors":"D. Stocco, B. Clark","doi":"10.1097/00060793-199606000-00002","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00002","url":null,"abstract":"","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"37 1","pages":"195–201"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Glucocorticoids and growth","authors":"R. Gaillard, W. Wehrenberg","doi":"10.1097/00060793-199606000-00006","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00006","url":null,"abstract":"Glucocorticoids play a critical role in the regulation of the hypothalamic-somatotropic-insulin-like growth factor axis. These steroids enhance growth hormone gene transcription and increase growth hormone-releasing hormone receptor synthesis. However, glucocorticoid excess inhibits somatic growth. Evidence to date suggests that this is in part due to impaired growth hormone secretion observed during hypercortisolism as well as impaired actions of growth hormone at the peripheral level. This includes impaired spontaneous growth hormone secretion, suppressed growth hormone responses to a number of stimuli, including growth hormone-releasing hormone, and increased insulin-like growth factor inhibitors and binding proteins. The inhibitory effect of the glucocorticoids appears to be due to increased hypothalamic somatostatin tone and inhibition of insulin-like growth factor bioactivity.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"227–232"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advances in understanding the regulation and biologic actions of dehydroepiandrosterone","authors":"J. Nestler","doi":"10.1097/00060793-199606000-00003","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00003","url":null,"abstract":"Dehydroepiandrosterone and its ester, dehydroepiandrosterone sulfate, are adrenal steroids that demonstrate a unique age-related decline in humans, and may possess beneficial biologic properties. This review focuses on recent advances in our understanding of the regulation and biologic actions of dehydroepiandrosterone in human beings.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"202–211"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Genetic disorders affecting aldosterone synthesis and action","authors":"P. White","doi":"10.1097/00060793-199606000-00005","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00005","url":null,"abstract":"Genetic defects in aldosterone biosynthesis and action affect blood pressure and electrolyte homeostasis. Aldosterone synthase deficiency, salt-wasting forms of congenital adrenal hyperplasia, and adrenal hypoplasia congenita cause aldosterone deficiency, signs of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma renin activity, and sometimes shock. End-organ unresponsiveness to aldosterone (pseudohypoaldosteronism) has a similar phenotype. Conversely, the inappropriate regulation of aldosterone synthesis seen in glucocorticoid-suppressible hyperaldosteronism may cause hypokalemia, suppressed plasma renin activity, and hypertension. Similar problems occur when the normal ligand specificity of the aldosterone receptor is lost, as occurs in the syndrome of apparent mineralocorticoid excess due to 11 β-hydroxysteroid dehydrogenase deficiency. With the exception of pseudohypoaldosteronism, all of the genes involved in these disorders have recently been cloned and mutations causing each disease have been identified.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"220–226"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Glucocorticoid‐remediable aldosteronism","authors":"W. Litchfield, R. Dluhy","doi":"10.1097/00060793-199606000-00012","DOIUrl":"https://doi.org/10.1097/00060793-199606000-00012","url":null,"abstract":"Glucocorticoid-remediable aldosteronism, an uncommon form of primary aldosteronism that is inherited in an autosomal dominant pattern, is characterized by early onset of moderate-to-severe hypertension and suppressed plasma renin activity. The family history is generally positive. However, the clinical and biochemical features that define mineralocorticoid excess states are not consistently present in glucocorticoid-remediable aldosteronism. As a result, recognition of this syndrome can be difficult. A high index of suspicion in individuals based on their clinical presentation and a diagnostic approach based on direct genetic testing of all at-risk individuals offers the best chance for early diagnosis. Therapy with aldosterone antagonists and potassium-sparing diuretics can provide adequate medical therapy for most patients, and yet avoid the toxicity of exogenous glucocorticoids.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"3 1","pages":"265–270"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00060793-199606000-00012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61609424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}