Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244222.91280.71
A. Goldfine, E. Mun, M. Patti
Purpose of reviewTo examine the recently recognized association between bariatric surgery-induced weight loss and postprandial hyperinsulinemic hypoglycemia. Recent findingsPostprandial hypoglycemia following gastric bypass for obesity is generally considered a late manifestation of the dumping syndrome and can usually be managed with dietary modification. A rare syndrome characterized by more severe postprandial hypoglycemia and hyperinsulinemia, accompanied by diffuse pancreatic islet hyperplasia and expansion of beta-cell mass, however, has recently been identified. In our experience, the therapeutic approach to these patients is guided by the severity and frequency of hypoglycemia, and includes nutritional modification to reduce postprandial glycemic excursion and stepped medical management, including acarbose, octreotide and diazoxide. Other therapeutic agents previously used to inhibit insulin secretion or action, including calcium channel blockade, β-blockers and anticholinergics, have been minimally effective. For life-threatening hypoglycemia refractory to medical management, partial pancreatectomy may be necessary, but hypoglycemia has recurred in some patients. These findings suggest that gastric bypass-induced weight loss may unmask an underlying beta-cell defect or contribute to pathologic islet hyperplasia. SummarySevere postprandial hyperinsulinemic hypoglycemia may be regarded as a rare, late complication of bariatric surgery. Management of these patients may require nutritional, pharmacological and, on occasion, surgical intervention. The pathophysiology remains incompletely understood.
{"title":"Hyperinsulinemic hypoglycemia following gastric bypass surgery for obesity","authors":"A. Goldfine, E. Mun, M. Patti","doi":"10.1097/01.med.0000244222.91280.71","DOIUrl":"https://doi.org/10.1097/01.med.0000244222.91280.71","url":null,"abstract":"Purpose of reviewTo examine the recently recognized association between bariatric surgery-induced weight loss and postprandial hyperinsulinemic hypoglycemia. Recent findingsPostprandial hypoglycemia following gastric bypass for obesity is generally considered a late manifestation of the dumping syndrome and can usually be managed with dietary modification. A rare syndrome characterized by more severe postprandial hypoglycemia and hyperinsulinemia, accompanied by diffuse pancreatic islet hyperplasia and expansion of beta-cell mass, however, has recently been identified. In our experience, the therapeutic approach to these patients is guided by the severity and frequency of hypoglycemia, and includes nutritional modification to reduce postprandial glycemic excursion and stepped medical management, including acarbose, octreotide and diazoxide. Other therapeutic agents previously used to inhibit insulin secretion or action, including calcium channel blockade, β-blockers and anticholinergics, have been minimally effective. For life-threatening hypoglycemia refractory to medical management, partial pancreatectomy may be necessary, but hypoglycemia has recurred in some patients. These findings suggest that gastric bypass-induced weight loss may unmask an underlying beta-cell defect or contribute to pathologic islet hyperplasia. SummarySevere postprandial hyperinsulinemic hypoglycemia may be regarded as a rare, late complication of bariatric surgery. Management of these patients may require nutritional, pharmacological and, on occasion, surgical intervention. The pathophysiology remains incompletely understood.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"13 1","pages":"419–424"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244222.91280.71","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61655675","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}
Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244223.98904.84
R. Tamler, J. Mechanick
Purpose of reviewThe use of dietary supplements or nutraceuticals in clinical endocrinology has been growing steadily despite controversy regarding the appropriateness of such therapies. This review provides an evidence-based survey of some popular dietary supplements or nutraceuticals targeting a variety of endocrine disorders. Recent findingsThe use of thyroid extracts or other natural remedies for thyroid disease is not evidence-based and is not superior to synthetic preparations. Insufficient data support the use of dehydroepiandrosterone or ginkgo biloba for hormonal disorders. Black cohosh and isoflavones may alleviate menopausal symptoms. Weak clinical data support the well tolerated use of several dietary supplements or nutraceuticals in diabetology, including a variety of botanicals and chromium. Carnitine and α-lipoic acid may alleviate diabetic neuropathy. Vitamin E is not a cardiovascular protectant. N-3 polyunsaturated fatty acids improve certain dyslipidemias. Data regarding conjugated linoleic acid and obesity are inconclusive. Isoflavones and vitamin K1 are promising but still unproven agents in osteoporosis, whereas the use of calcium and vitamin D alone has recently been challenged. SummaryPatients and physicans must evaluate dietary supplements or nutraceuticals in terms of the – qualitatively variable – supporting clinical evidence and relative risk–benefit profiles. Otherwise, the use of unproven therapies can be dangerous.
{"title":"Dietary supplements and nutraceuticals in the management of endocrine disorders","authors":"R. Tamler, J. Mechanick","doi":"10.1097/01.med.0000244223.98904.84","DOIUrl":"https://doi.org/10.1097/01.med.0000244223.98904.84","url":null,"abstract":"Purpose of reviewThe use of dietary supplements or nutraceuticals in clinical endocrinology has been growing steadily despite controversy regarding the appropriateness of such therapies. This review provides an evidence-based survey of some popular dietary supplements or nutraceuticals targeting a variety of endocrine disorders. Recent findingsThe use of thyroid extracts or other natural remedies for thyroid disease is not evidence-based and is not superior to synthetic preparations. Insufficient data support the use of dehydroepiandrosterone or ginkgo biloba for hormonal disorders. Black cohosh and isoflavones may alleviate menopausal symptoms. Weak clinical data support the well tolerated use of several dietary supplements or nutraceuticals in diabetology, including a variety of botanicals and chromium. Carnitine and α-lipoic acid may alleviate diabetic neuropathy. Vitamin E is not a cardiovascular protectant. N-3 polyunsaturated fatty acids improve certain dyslipidemias. Data regarding conjugated linoleic acid and obesity are inconclusive. Isoflavones and vitamin K1 are promising but still unproven agents in osteoporosis, whereas the use of calcium and vitamin D alone has recently been challenged. SummaryPatients and physicans must evaluate dietary supplements or nutraceuticals in terms of the – qualitatively variable – supporting clinical evidence and relative risk–benefit profiles. Otherwise, the use of unproven therapies can be dangerous.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"13 1","pages":"425–430"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244223.98904.84","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61655688","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}
Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244227.21776.70
A. Boelen, W. Wiersinga, J. Koehrle
Purpose of reviewNonthyroidal illness is characterized by changes in thyroid hormone metabolism, such as decreased serum T3, increased serum rT3 and, during severe illness, diminished serum T4. Thyroid stimulating hormone remains unchanged or even decreases. Several mechanisms at various levels are involved in the observed changes in thyroid hormone metabolism although the pathogenesis is still incompletely understood. Nonthyroidal illness has been proposed as a useful adaptation mechanism of the body during illness and is viewed as part of the acute phase response. Cytokines are involved in the acute phase response and have the capacity to interfere with a variety of thyroid functions and to alter thyroid hormone metabolism in vitro and in vivo. Recent findingsSeveral inflammatory stimuli have proven to be suitable experimental models to study the pathogenesis of nonthyroidal illness. Inflammation leads to increased cytokine expression in organs involved in the regulation of the hypothalamus–pituitary–thyroid axis and the inflammatory response precedes changes in thyroid hormone metabolism. Both inhibiting and stimulating effects have been described in different organs and are probably mediated by cytokine-induced signal transduction pathways. SummaryThe differential effects of cytokines on thyroid functions suggest that cell-specific factors determine the final outcome of inflammatory stimuli on thyroid hormone metabolism.
{"title":"Contributions of cytokines to nonthyroidal illness","authors":"A. Boelen, W. Wiersinga, J. Koehrle","doi":"10.1097/01.med.0000244227.21776.70","DOIUrl":"https://doi.org/10.1097/01.med.0000244227.21776.70","url":null,"abstract":"Purpose of reviewNonthyroidal illness is characterized by changes in thyroid hormone metabolism, such as decreased serum T3, increased serum rT3 and, during severe illness, diminished serum T4. Thyroid stimulating hormone remains unchanged or even decreases. Several mechanisms at various levels are involved in the observed changes in thyroid hormone metabolism although the pathogenesis is still incompletely understood. Nonthyroidal illness has been proposed as a useful adaptation mechanism of the body during illness and is viewed as part of the acute phase response. Cytokines are involved in the acute phase response and have the capacity to interfere with a variety of thyroid functions and to alter thyroid hormone metabolism in vitro and in vivo. Recent findingsSeveral inflammatory stimuli have proven to be suitable experimental models to study the pathogenesis of nonthyroidal illness. Inflammation leads to increased cytokine expression in organs involved in the regulation of the hypothalamus–pituitary–thyroid axis and the inflammatory response precedes changes in thyroid hormone metabolism. Both inhibiting and stimulating effects have been described in different organs and are probably mediated by cytokine-induced signal transduction pathways. SummaryThe differential effects of cytokines on thyroid functions suggest that cell-specific factors determine the final outcome of inflammatory stimuli on thyroid hormone metabolism.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"13 1","pages":"444–450"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244227.21776.70","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61656291","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}
Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244229.29399.83
Michael Mingzhao Xing
Purpose of reviewExtensive recent research on BRAF mutation in thyroid cancer has advanced understanding of its role in thyroid carcinogenesis and its clinical implications. The purpose of this review is to summarize the recent advances in this exciting area of thyroid cancer medicine. Recent findingsSince the initial discovery of the oncogenic T1799A BRAF mutation in papillary thyroid cancer 3 years ago, numerous studies continue to show a high prevalence and specificity of this mutation in papillary thyroid cancer. Recent studies have focused on the role of this mutation, through activation of the Ras → Raf → MEK → MAP kinase pathway, in papillary thyroid cancer carcinogenesis. This role of BRAF mutation is now strongly supported by clinicopathological, in-vitro cell line, and in-vivo animal studies that showed BRAF mutation as an initiator, as well as a promoter of aggressiveness, of papillary thyroid cancer. SummaryBRAF mutation represents one of the most important molecular discoveries in thyroid cancer in recent years. Its role in papillary thyroid cancer carcinogenesis and potential as a novel prognostic molecular marker, as well as therapeutic target for papillary thyroid cancer, have been recognized. The recent work on BRAF mutation may have an important impact on thyroid cancer medicine.
{"title":"BRAF mutation in thyroid carcinogenesis and its clinical implications","authors":"Michael Mingzhao Xing","doi":"10.1097/01.med.0000244229.29399.83","DOIUrl":"https://doi.org/10.1097/01.med.0000244229.29399.83","url":null,"abstract":"Purpose of reviewExtensive recent research on BRAF mutation in thyroid cancer has advanced understanding of its role in thyroid carcinogenesis and its clinical implications. The purpose of this review is to summarize the recent advances in this exciting area of thyroid cancer medicine. Recent findingsSince the initial discovery of the oncogenic T1799A BRAF mutation in papillary thyroid cancer 3 years ago, numerous studies continue to show a high prevalence and specificity of this mutation in papillary thyroid cancer. Recent studies have focused on the role of this mutation, through activation of the Ras → Raf → MEK → MAP kinase pathway, in papillary thyroid cancer carcinogenesis. This role of BRAF mutation is now strongly supported by clinicopathological, in-vitro cell line, and in-vivo animal studies that showed BRAF mutation as an initiator, as well as a promoter of aggressiveness, of papillary thyroid cancer. SummaryBRAF mutation represents one of the most important molecular discoveries in thyroid cancer in recent years. Its role in papillary thyroid cancer carcinogenesis and potential as a novel prognostic molecular marker, as well as therapeutic target for papillary thyroid cancer, have been recognized. The recent work on BRAF mutation may have an important impact on thyroid cancer medicine.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"70 1","pages":"455–459"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244229.29399.83","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61656361","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}
Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244220.53163.85
R. Kushner
Purpose of reviewBariatric surgery is associated with the development of several micronutrient deficiencies that are predictable, preventable and treatable based on the surgically altered anatomy and imposed dietary changes. With an increasing number of severely obese patients undergoing bariatric surgery, clinicians need to become familiar with the surgical procedures and associated nutritional deficiencies. This article will review the pathophysiology, clinical presentation, screening tests, and treatment for selected micronutrient deficiencies. Recent findingsThe three restrictive malabsorptive procedures – Roux-en-Y gastric bypass, biliopancreatic diversion and biliopancreatic diversion with duodenal switch – pose a greater risk for micronutrient malabsorption and deficiency than the purely restrictive laparoscopic adjustable silicone gastric banding. Although other micronutrients have been reported, the metabolic and clinical deficiencies of two minerals (iron and calcium) and four vitamins (thiamine, folate, vitamin B12 and vitamin D) have been most frequently described in the literature. Subclinical and clinical presentation of deficiencies can occur from weeks to years following the surgical procedures. Metabolic bone disease is the most concerning long-term nutritional complication. SummaryAll patients undergoing restrictive–malabsorptive procedures must be evaluated for development of micronutrient deficiencies. With careful monitoring and adequate supplementation, these deficiencies are largely avoidable and treatable.
{"title":"Micronutrient deficiencies and bariatric surgery","authors":"R. Kushner","doi":"10.1097/01.med.0000244220.53163.85","DOIUrl":"https://doi.org/10.1097/01.med.0000244220.53163.85","url":null,"abstract":"Purpose of reviewBariatric surgery is associated with the development of several micronutrient deficiencies that are predictable, preventable and treatable based on the surgically altered anatomy and imposed dietary changes. With an increasing number of severely obese patients undergoing bariatric surgery, clinicians need to become familiar with the surgical procedures and associated nutritional deficiencies. This article will review the pathophysiology, clinical presentation, screening tests, and treatment for selected micronutrient deficiencies. Recent findingsThe three restrictive malabsorptive procedures – Roux-en-Y gastric bypass, biliopancreatic diversion and biliopancreatic diversion with duodenal switch – pose a greater risk for micronutrient malabsorption and deficiency than the purely restrictive laparoscopic adjustable silicone gastric banding. Although other micronutrients have been reported, the metabolic and clinical deficiencies of two minerals (iron and calcium) and four vitamins (thiamine, folate, vitamin B12 and vitamin D) have been most frequently described in the literature. Subclinical and clinical presentation of deficiencies can occur from weeks to years following the surgical procedures. Metabolic bone disease is the most concerning long-term nutritional complication. SummaryAll patients undergoing restrictive–malabsorptive procedures must be evaluated for development of micronutrient deficiencies. With careful monitoring and adequate supplementation, these deficiencies are largely avoidable and treatable.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"13 1","pages":"405–411"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244220.53163.85","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61655616","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}
Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244221.53163.cc
M. Holick
Purpose of reviewAs obese adults often have normal bone mineral density, vitamin D deficiency is not considered to be a major health issue for them. It is. Recent findingsVitamin D deficiency, common in obese children and adults, has been linked to decrease in outdoor activities, avoiding vitamin D fortified foods and the irreversible sequestration of vitamin D by the large pool of body fat. Vitamin D deficiency is associated with muscle weakness and aches and pains in the skeleton, and may alter insulin secretion and sensitivity. SummaryObese children and adults are often less active and suffer from muscle weakness and bone aches and pains which further decrease their activity and increase their potential for being more obese. Vitamin D sufficiency has been linked to insulin secretion and insulin sensitivity, and, thus, vitamin D deficiency may exacerbate type II diabetes. Monitoring for serum 25-hydroxyvitamin D and treatment with pharmacologic doses of vitamin D typically 50 000 IU of vitamin D2, once a week for 8 weeks followed by every other week will often correct vitamin D deficiency and maintain a normal vitamin D status. Patients with a body mass index of over 30 may require higher doses or more frequent dosing with vitamin D.
{"title":"Vitamin D deficiency in obesity and health consequences","authors":"M. Holick","doi":"10.1097/01.med.0000244221.53163.cc","DOIUrl":"https://doi.org/10.1097/01.med.0000244221.53163.cc","url":null,"abstract":"Purpose of reviewAs obese adults often have normal bone mineral density, vitamin D deficiency is not considered to be a major health issue for them. It is. Recent findingsVitamin D deficiency, common in obese children and adults, has been linked to decrease in outdoor activities, avoiding vitamin D fortified foods and the irreversible sequestration of vitamin D by the large pool of body fat. Vitamin D deficiency is associated with muscle weakness and aches and pains in the skeleton, and may alter insulin secretion and sensitivity. SummaryObese children and adults are often less active and suffer from muscle weakness and bone aches and pains which further decrease their activity and increase their potential for being more obese. Vitamin D sufficiency has been linked to insulin secretion and insulin sensitivity, and, thus, vitamin D deficiency may exacerbate type II diabetes. Monitoring for serum 25-hydroxyvitamin D and treatment with pharmacologic doses of vitamin D typically 50 000 IU of vitamin D2, once a week for 8 weeks followed by every other week will often correct vitamin D deficiency and maintain a normal vitamin D status. Patients with a body mass index of over 30 may require higher doses or more frequent dosing with vitamin D.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"26 1","pages":"412–418"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244221.53163.cc","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61655632","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}
Pub Date : 2006-10-01DOI: 10.1097/01.med.0000244226.83657.39
Xia Cao, H. Seo
Purpose of reviewA nongenomic action that does not directly and initially influence gene expression but rather causes a rapid effect such as activation of signaling cascades, has been recently described. The involvement of a thyroid hormone receptor, however, is not clear. In this review, we focus on the recent advances made in our understanding of the mechanism concerning a thyroid hormone receptor-mediated nongenomic action of thyroid hormone. Recent findingsIt was recently reported that thyroid hormone induces the activation of phosphatidylinositol 3OH-kinase which generates phosphatidylinositol 3,4,5-triphosphate, leading to the activation of the downstream signaling molecules such as protein kinase B. This nongenomic action of thyroid hormone requires binding with the thyroid hormone receptor. Moreover, the interaction between the thyroid hormone receptor and the regulatory subunit of phosphatidylinositol 3OH-kinase, p85α, was demonstrated in human skin fibroblasts, thyroid tissue extracts and a rat pituitary cell line GH4C1. SummaryThe phosphatidylinositol 3OH-kinase pathway plays critical roles in cell survival and differentiation through regulating enormous downstream molecules. Understanding of the thyroid hormone action on this pathway will provide a new insight into the physiological and pathological roles played by thyroid hormone.
{"title":"Nongenomic activation of phosphatidylinositol 3-kinase by thyroid hormone","authors":"Xia Cao, H. Seo","doi":"10.1097/01.med.0000244226.83657.39","DOIUrl":"https://doi.org/10.1097/01.med.0000244226.83657.39","url":null,"abstract":"Purpose of reviewA nongenomic action that does not directly and initially influence gene expression but rather causes a rapid effect such as activation of signaling cascades, has been recently described. The involvement of a thyroid hormone receptor, however, is not clear. In this review, we focus on the recent advances made in our understanding of the mechanism concerning a thyroid hormone receptor-mediated nongenomic action of thyroid hormone. Recent findingsIt was recently reported that thyroid hormone induces the activation of phosphatidylinositol 3OH-kinase which generates phosphatidylinositol 3,4,5-triphosphate, leading to the activation of the downstream signaling molecules such as protein kinase B. This nongenomic action of thyroid hormone requires binding with the thyroid hormone receptor. Moreover, the interaction between the thyroid hormone receptor and the regulatory subunit of phosphatidylinositol 3OH-kinase, p85α, was demonstrated in human skin fibroblasts, thyroid tissue extracts and a rat pituitary cell line GH4C1. SummaryThe phosphatidylinositol 3OH-kinase pathway plays critical roles in cell survival and differentiation through regulating enormous downstream molecules. Understanding of the thyroid hormone action on this pathway will provide a new insight into the physiological and pathological roles played by thyroid hormone.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"13 1","pages":"439–443"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000244226.83657.39","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61656239","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}
Pub Date : 2006-08-01DOI: 10.1097/01.med.0000235328.77282.29
L. Nachtigall, B. Biller
Purpose of reviewMany neuroendocrine tumors express a variety of somatostatin receptor subtypes and somatostatin analogues are used in medical treatment. The development of pasireotide (SOM230), a novel somatostatin analogue with multiligand properties, may offer a new potential therapy for these tumors. This review considers in-vitro, animal and early human clinical studies of pasireotide (SOM230). Recent findingsSomatostatin analogues, such as lanreotide and octreotide, are effective in many patients, but biochemical control is not achieved in over one third of patients with acromegaly, and in carcinoid, symptoms may become refractory after chronic use. Pasireotide, with high affinity binding to four of the five subtypes of somatostatin receptors (1, 2, 3, and 5) may control hormone oversecretion or tumor proliferation. Somatostatin receptor-5 appears to be important in regulating adrenocorticotropic hormone secretion, suggesting the possible use of pasireotide in Cushing's disease. Preliminary results from phase II studies of pasireotide in acromegaly, Cushing's, and carcinoid are presented. SummaryShort-term, small clinical studies using pasireotide for acromegaly and pituitary Cushing's and for symptomatic relief in refractory carcinoid are promising. Further investigation will determine whether pasireotide will be effective and safe for treating hormone excess, clinical symptoms or tumor proliferation in neuroendocrine disorders.
{"title":"The potential role of the investigational somatostatin analog pasireotide (SOM230) in the treatment of neuroendocrine disorders","authors":"L. Nachtigall, B. Biller","doi":"10.1097/01.med.0000235328.77282.29","DOIUrl":"https://doi.org/10.1097/01.med.0000235328.77282.29","url":null,"abstract":"Purpose of reviewMany neuroendocrine tumors express a variety of somatostatin receptor subtypes and somatostatin analogues are used in medical treatment. The development of pasireotide (SOM230), a novel somatostatin analogue with multiligand properties, may offer a new potential therapy for these tumors. This review considers in-vitro, animal and early human clinical studies of pasireotide (SOM230). Recent findingsSomatostatin analogues, such as lanreotide and octreotide, are effective in many patients, but biochemical control is not achieved in over one third of patients with acromegaly, and in carcinoid, symptoms may become refractory after chronic use. Pasireotide, with high affinity binding to four of the five subtypes of somatostatin receptors (1, 2, 3, and 5) may control hormone oversecretion or tumor proliferation. Somatostatin receptor-5 appears to be important in regulating adrenocorticotropic hormone secretion, suggesting the possible use of pasireotide in Cushing's disease. Preliminary results from phase II studies of pasireotide in acromegaly, Cushing's, and carcinoid are presented. SummaryShort-term, small clinical studies using pasireotide for acromegaly and pituitary Cushing's and for symptomatic relief in refractory carcinoid are promising. Further investigation will determine whether pasireotide will be effective and safe for treating hormone excess, clinical symptoms or tumor proliferation in neuroendocrine disorders.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"60 1","pages":"369–376"},"PeriodicalIF":0.0,"publicationDate":"2006-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000235328.77282.29","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61655604","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}
Pub Date : 2006-08-01DOI: 10.1097/01.med.0000235324.46788.47
P. Crock, S. Bensing, C. Smith, C. Burns, P. Robinson
Purpose of reviewThe aim of this article is to review recent advancements in pituitary autoantibody assays. Recent findingsThe newest assay is based on the in-vitro transcription and translation of pituitary specific proteins followed by immunoprecipitation with patient sera. The two proteins, PGSF1a and PGSF2, were identified as pituitary specific from a human pituitary gland cDNA library. Autoantibodies were found in one patient with biopsy proven lymphocytic hypophysitis and seven with suspected hypophysitis, including idiopathic hypopituitarism. Patients with rheumatoid arthritis, especially if rheumatoid factor negative, also had autoantibodies to PGSF1a. An immunoblotting method identified the autoantigen enolase (both α and neuron-specific), as a marker of neuroendocrine autoimmunity but an in-vitro transcription and translation assay has shown that enolase autoantibodies are nonspecific. Enolase autoantibodies have also been found in Sheehan's syndrome. Immunoblotting identified a novel 36 kDa pituitary cytosolic autoantigen in adrenocorticotropin (ACTH) deficiency and pituitary membrane proteins of 68, 49 and 43 kDa in patients with lymphocytic hypophysitis. Indirect immunofluorescence using baboon pituitary has been revisited and somatotroph autoantibodies found in patients with idiopathic growth hormone (GH) deficiency. High titre antibodies were thought to be clinically significant. Enyme-linked immunosorbent assays using human pituitary adenoma cells or rat tissue have identified antibodies in patients with type 1 diabetes, Hashimoto's thyroiditis and various pituitary disorders but not hypophysitis. SummaryThe search for reliable and specific pituitary autoantibody markers continues.
{"title":"Pituitary autoantibodies","authors":"P. Crock, S. Bensing, C. Smith, C. Burns, P. Robinson","doi":"10.1097/01.med.0000235324.46788.47","DOIUrl":"https://doi.org/10.1097/01.med.0000235324.46788.47","url":null,"abstract":"Purpose of reviewThe aim of this article is to review recent advancements in pituitary autoantibody assays. Recent findingsThe newest assay is based on the in-vitro transcription and translation of pituitary specific proteins followed by immunoprecipitation with patient sera. The two proteins, PGSF1a and PGSF2, were identified as pituitary specific from a human pituitary gland cDNA library. Autoantibodies were found in one patient with biopsy proven lymphocytic hypophysitis and seven with suspected hypophysitis, including idiopathic hypopituitarism. Patients with rheumatoid arthritis, especially if rheumatoid factor negative, also had autoantibodies to PGSF1a. An immunoblotting method identified the autoantigen enolase (both α and neuron-specific), as a marker of neuroendocrine autoimmunity but an in-vitro transcription and translation assay has shown that enolase autoantibodies are nonspecific. Enolase autoantibodies have also been found in Sheehan's syndrome. Immunoblotting identified a novel 36 kDa pituitary cytosolic autoantigen in adrenocorticotropin (ACTH) deficiency and pituitary membrane proteins of 68, 49 and 43 kDa in patients with lymphocytic hypophysitis. Indirect immunofluorescence using baboon pituitary has been revisited and somatotroph autoantibodies found in patients with idiopathic growth hormone (GH) deficiency. High titre antibodies were thought to be clinically significant. Enyme-linked immunosorbent assays using human pituitary adenoma cells or rat tissue have identified antibodies in patients with type 1 diabetes, Hashimoto's thyroiditis and various pituitary disorders but not hypophysitis. SummaryThe search for reliable and specific pituitary autoantibody markers continues.","PeriodicalId":88857,"journal":{"name":"Current opinion in endocrinology & diabetes","volume":"13 1","pages":"344–350"},"PeriodicalIF":0.0,"publicationDate":"2006-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.med.0000235324.46788.47","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61655500","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}
Pub Date : 2006-08-01DOI: 10.1097/01.med.0000235322.01047.86
F. Kaufman
Purpose of reviewMultiple aspects of the obesity and type 2 diabetes epidemics, how to distinguish type 2 from type 1 diabetes in youth, and how to manage type 2 diabetes are reviewed. Recent findingsSixteen percent of youth were overweight in the US in 1999–2000; in 2003–2004 this increased to 17.1%. This has resulted in a marked increase in the incidence of metabolic syndrome and type 2 diabetes in pediatric subjects. Risk factors that predispose to insulin resistance and limited β cell reserve include race/ethnicity, obesity, sedentary behavior, family history of type 2 diabetes, puberty, low birth weight and female gender. There appears to be a rapid progression from impaired glucose tolerance to type 2 diabetes in severely obese youth. Tests should be performed to differentiate type 1 from type 2 diabetes. Treatment algorithms are aimed to avoid poor long-term outcomes for youth with type 2 diabetes. SummaryClinically relevant information is given in this review to understand risk factors for type 2 diabetes, including how obesity causes insulin resistance, and to promote the appropriate work-up and management of type 2 diabetes in the pediatric population.
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