Endocrine Dysfunction in A Patient with Phace Syndrome,Including Port-Wine Stain of the Right Periorbital Area

ObjectiveTo report a case of PHACE syndrome— Posterior fossa brain abnormalities, Hemangioma (usually facial), Arterial anomalies, Coarctation of the aorta along with cardiac defects, and Eye abnormalities—in a 16-yearold female patient with a port-wine stain of the right periorbital area present since birth in conjunction with hypoplasia of the contralateral internal carotid artery.MethodsThyroid-stimulating hormone, free thyroxine, and growth hormone (GH) levels were measured, and insulin-induced hypoglycemia and arginine infusion tests were done. Radiologic investigations included sagittal enhanced T1-weighted magnetic resonance imaging of the brain and the pituitary gland as well as computed tomography and magnetic resonance angiography of the head and neck.ResultsThe patient had a normal karyotype. Her height and weight were below the 5th percentile for her chronologic age, and she had amenorrhea. Laboratory investigations revealed both thyroid and GH deficiencies and confirmed the diagnosis of hypogonadotropic hypogonadism. The imaging studies showed a right intraorbital hemangioma as well as an enhancing mass in the right internal auditory canal at the cerebellopontine angle, consistent with a posterior fossa hemangioma. Initiation of both thyroid and GH replacement therapy improved her growth rate and yielded a good clinical outcome.ConclusionIn patients with facial or neck hemangiomas, PHACE syndrome should be suspected, and brain imaging and cardiac, ophthalmologic, and endocrinologic evaluations are recommended to screen for other potential PHACE abnormalities. (Endocr Pract. 2010;16:255-259)     

Endocrine actions of opioids

The widespread occurrence of opioid peptides and their receptors in brain and periphery correlates with a variety of actions elicited by opioid agonists and antagonists on hormone secretion. Opioid actions on pituitary and pancreatic peptides are summarized in Table 1. In rats opioids stimulate ACTH and corticosterone secretion while an inhibition of ACTH and cortisol levels was observed in man. In both species, naloxone, an opiate antagonist, stimulates the release of ACTH suggesting a tonic suppression by endogenous opioids. In rats, a different stimulatory pathway must be assumed through which opiates can stimulate secretion of ACTH. Both types of action are probably mediated within the hypothalamus. LH is decreased by opioid agonists in many adult species while opiate antagonists elicit stimulatory effects, both apparently by modulating LHRH release. A tonic, and in females, a cyclic opioid control appears to participate in the regulation of gonadotropin secretion. Exogenous opiates potently stimulate PRL and GH secretion in many species. Opiate antagonists did not affect PRL or GH levels indicating absence of opioid control under basal conditions, while a decrease of both hormones by antagonists was seen after stimulation in particular situations. In rats, opiate antagonists decreased basal and stress-induced secretion of PRL. Data regarding TSH are quite contradictory. Both inhibitory and stimulatory effects have been described. Oxytocin and vasopressin release were inhibited by opioids at the posterior pituitary level. There is good evidence for an opioid inhibition of suckling-induced oxytocin release. Opioids also seem to play a role in the regulation of vasopressin under some conditions of water balance. The pancreatic hormones insulin and glucagon are elevated by opioids apparently by an action at the islet cells. Somatostatin, on the contrary, was inhibited. An effect of naloxone on pancreatic hormone release was observed after meals which contain opiate active substance. Whether opioids play a physiologic role in glucose homeostasis remains to be elucidated.     

New Horizons in Skeletal Physiology and Pathophysiology

ObjectiveTo review new discoveries that revisit our current thinking on the genesis of osteoporosis using hypogonadal and thyrotoxic bone loss as examples.MethodsWe focus on cell biologic, mouse genetic, and human studies that have established a direct action of the interior pituitary hormones follicle-stimulating hormone and thyrotropin on the skeleton and discuss emerging clinical evidence for a novel pituitary-bone axis in humans that bypasses master endocrine organs, namely the ovaries and thyroid gland.ResultsThe cataloguing of human mutations, the use of genetically modified mice that recapitulate human disease, and the rapid growth of genomic sciences have together had a profound impact on how basic research is translated into clinical practice. The skeleton has become a paradigm for the application of such advances to an extent that hitherto unrecognized physiologic and pathophysiologic findings have emerged. We propose that hypogonadal and thyrotoxic bone loss are not solely due to changes in the level of master hormones, but instead also arise from the direct action of anterior pituitary hormones on the skeleton.ConclusionsWe predict a pituitary-bone axis in which pituitary hormones bypass traditional endocrine targets to affect the skeleton directly with remarkable sensitivity. New therapeutic targets thus become a likely possibility. (Endocr Pract. 2010;16:874-881)     

Pituitary Evaluation in Patients with Low Prostate-Specific Antigen

Objective: To evaluate pituitary function in men with a low screening prostate-specific antigen (PSA) of ≤0.1 ng/mL and test the hypothesis that low PSA is associated with hypogonadism alone or other hormone deficiency.Methods: This was a case-control study evaluating the rates of hypogonadism and low insulin-like growth factor (IGF)-1 in a cohort of men with low or normal screening PSA level. Sixty-four men >40 years old without known prostate disease were divided into a low-PSA group (PSA ≤0.1 ng/mL) and normal-PSA group (PSA 1 to 4 ng/mL). Hormonal evaluation included total testosterone, prolactin, luteinizing hormone, follicle-stimulating hormone, IGF-1, growth hormone, thyroid-stimulating hormone, free thyroxine, morning cortisol, and adrenocorticotropic hormone. The difference between each patient's observed IGF-1 and the IGF-1 age-specific lower limit was calculated. The odds ratios (ORs) for having hypogonadism and associated 95% confidence intervals (CIs) were calculated using the Cochran-Mantel-Haenszel test.Results: The rate of hypogonadism was significantly higher in the low-PSA group (n = 44) compared with the normal-PSA control group (n = 20) (45.5% vs. 15.0%; OR, 4.7; 95% CI, 1.2 to 18.4; P = .027). The total testosterone in the low-PSA group was significantly lower compared with the control group (181.7 ng/dL vs. 263.7 ng/dL; P = .008). IGF-1 values were below their lower bound in 18.6% of subjects in the low-PSA group, compared with 0% in the control group.Conclusion: Men with low PSA have significantly higher rates of hypogonadism and low IGF-1 compared with those with normal PSA. In such men, we recommend hormonal evaluation to exclude associated pituitary dysfunction.Abbreviations: BMI = body mass index; GH = growth hormone; IGF-1 = insulin-like growth factor 1; MRI = magnetic resonance imaging; PSA = prostate-specific antigen; T2DM = type 2 diabetes mellitus; VA-NWIHCS = VA-Nebraska Western Iowa Health Care System     

Endocrine Involvement in Systemic Amyloidosis

ObjectiveTo present an overview of the published data on endocrine involvement and endocrine dysfunction in patients with systemic amyloidosis.MethodsWe conducted a review of the medical literature using MEDLINE data sources, including clinical trials, in vitro studies, and case reports on pituitary, thyroid, parathyroid, pancreatic, adrenal, and gonadal involvement in systemic amyloidosis.ResultsReports of endocrine involvement in systemic amyloidosis seem to consist primarily of small-samplesize clinical trials or case reports, probably because of the rarity of the disease itself. Systemic amyloidosis mainly involves and causes functional impairment in the thyroid and testes in the endocrine system. Evaluation of adrenal function necessitates special consideration because amyloid infiltration of the adrenal glands resulting in failure may be a life-threatening condition. Amyloid deposition commonly seen in the pituitary gland and the pancreas of patients with Alzheimer disease and type 2 diabetes mellitus, respectively, is generally classified as local amyloidosis and should not be confused with systemic involvement. Additionally, detection of amyloid deposition in the thyroid and testes may have a diagnostic role in patients with suspected systemic or renal amyloidosis.ConclusionPublished data suggest that systemic amyloidosis frequently involves the endocrine system, and endocrine dysfunction seems to be not as rare as previously thought. A rapidly growing goiter or symptoms and signs of adrenal or gonadal dysfunction should raise suspicion of amyloid infiltration. Involvement of pituitary, parathyroid, and pancreatic sites in systemic amyloidosis still remains to be clarified. Further studies with larger sample sizes are needed for complete characterization of the effect of systemic amyloidosis on the endocrine system. (Endocr Pract. 2010;16:1056-1063)     

Invasive Breast Cancer After Initiation of Testosterone Replacement Therapy in A Man—A Warning To Endocrinologists

ObjectiveTo alert fellow endocrinologists of a rare side effect of testosterone therapy, for which men with hypogonadism must receive appropriate counseling and monitoring.MethodsWe present clinical features, laboratory data, and histopathologic findings in a man with hypogonadism who received testosterone replacement therapy.ResultsA 61-year-old man was referred to an endocrinologist after presenting to his general practitioner with erectile dysfunction and low libido. He had no history of hypothalamic, pituitary, or testicular disorders. There were no other illnesses or medications to account for low testosterone levels. Physical examination was unremarkable. There was no family history of malignant disease. Biochemical investigations confirmed the presence of primary hypogonadism, for which no cause (including Klinefelter syndrome) was identified. Testosterone therapy was initiated to improve sexual function and preserve bone density. Five weeks later, the patient returned to his general practitioner, complaining of a gradually enlarging lump in his right breast. When biopsy showed breast cancer, testosterone therapy was discontinued. Right mastectomy and axillary node clearance were performed. Further histologic examination revealed estrogen receptor-positive, invasive carcinoma, without nodal involvement. The patient remains on tamoxifen therapy and is undergoing follow-up in the breast clinic. After 6 months of treatment, estradiol levels were undetectable, and testosterone levels remained low.ConclusionAlthough breast cancer has been described in men with hypogonadism receiving long-term testosterone replacement therapy, to our knowledge this is the first report of breast cancer becoming clinically manifest after a short duration (5 weeks) of testosterone treatment. This case should remind clinicians that men receiving testosterone therapy should be warned of the risk of not only prostate cancer but also breast cancer. Patient self-monitoring and breast examinations by the attending physician are recommended. (Endocr Pract. 2008;14: 201-203)     

Unusual Case of Metastatic Neuroendocrine Tumor

ObjectiveTo report a rare case of metastatic growth hormone (GH)-secreting pituitary carcinoma causing acromegaly.MethodsWe present a case report and review the available literature on this topic.ResultsA 68-year-old woman presented with persistent acromegaly after treatment for a GH-secreting pituitary adenoma. Evaluation of long-standing cervical adenopathy revealed findings consistent with a metastatic neuroendocrine tumor. Further work-up revealed additional thyroid, parathyroid, and cervical masses. After operative treatment including total thyroidectomy, subtotal parathyroidectomy, partial thymectomy, and right modified radical neck dissection, the patient’s symptoms diminished, and her GH levels approached the normal range. Surgical pathology findings were consistent with a GH-secreting pituitary carcinoma metastatic to the cervical lymph nodes, multinodular thyroid hyperplasia with a focus of papillary microcarcinoma, and parathyroid hyperplasia.ConclusionOverall, pituitary carcinomas are extremely rare. To date, about 100 cases have been reported in the world’s literature, and of these, only 19 cases originated from GH-secreting cells. Our examination of the symptoms, signs, diagnosis, and treatment of our patient, in comparison with the previously reported cases, should enhance awareness of this unusual disease process. (Endocr Pract. 2007;13:72-76)     

Insulin hypoglycemia test and releasing hormone (corticotropin-releasing hormone and growth hormone-releasing hormone) stimulation in patients with pituitary failure of different origin

To investigate the efficacy of endocrine evaluation in diagnosing and localizing the cause of anterior pituitary failure, 17 patients with suprasellar space-occupying lesions, 4 patients with intrasellar tumors, 8 patients with no detectable anatomical lesion, 1 patient with posttraumatic failure and 1 patient with septooptical dysplasia were investigated. Endocrine evaluation consisted of measuring adrenocorticotropic hormone (ACTH), cortisol, and growth hormone (GH) levels during insulin hypoglycemia test (IHT) and after administration of corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GRH). In addition, basal prolactin levels, gonadal and thyroid function were evaluated. The results showed that 4 of 17 patients with suprasellar tumors had normal ACTH and GH responses during IHT and after releasing hormone (RH) administration. Five of these patients had a normal ACTH or cortisol rise but no GH response during IHT. All 5 had a normal ACTH and 3 had normal GH rise after RH. Seven patients with suprasellar tumors had no ACTH or GH response during IHT, but all had an ACTH response to CRH. Only 3 of this group had a GH response to GRH. There was one exception of a patient who showed a GH and ACTH rise during IHT but only a blunted ACTH and no GH rise after RH administration. Four patients with pituitary failure and no demonstrable lesion had an ACTH rise after CRH but no GH rise after GRH, whereas in 3 patients with isolated ACTH deficiency no ACTH rise after CRH was seen. In 4 patients with nonsecreting pituitary tumors normal ACTH responses to IHT and CRH were seen, whereas GH rose during IHT only in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Unexpected Clinical Course During Treatment of a TSH-Secreting Pituitary Adenoma

ObjectiveTo report the rare occurrence of a patient with thyrotropinoma that transitioned into a secretory thyro-somatotroph adenoma during medical treatment with somatostatin analogue.MethodsWe report the case of a patient with a thyrotroph pituitary adenoma who developed de novo evidence of growth hormone cosecretion following one year of successful medical treatment.ResultsA 78-year-old woman was diagnosed with a thyroid stimulating hormone (TSH) secreting pituitary macroadenoma (TSHoma) based on classical clinical and biochemical features. There was no clinical or biochemical evidence of growth hormone (GH) cosecretion. She declined surgical resection and was treated with primary medical therapy, octreotide long acting repeatable (LAR), to which she had an antitumor and antisecretory response; however, following 12 months of successful medical treatment she developed de novo hypersecretion of growth hormone despite involution of the tumor mass. TSH-secreting pituitary adenomas may rarely become plurihormonal during apparently successful medical treatment. This may represent an unusual form of secondary resistance to somatostatin analogue or the rarer phenomenon of tumor transformation into a secretory thyro-somatotroph adenoma.ConclusionThe unexpected clinical course of this case highlights the need for careful long-term surveillance in patients with TSH secreting pituitary adenomas. (Endocr. Pract. 2013;19:e88-e91)     

Does Testosterone Therapy Increase the Risk of Prostate Cancer?

ObjectiveTo review factors affecting use of testosterone therapy for hypogonadism including the persistent controversial link between testosterone therapy and prostate cancer.MethodsWe reviewed studies investigating the relationship between testosterone therapy and prostate cancer progression and summarized strategies for hypogonadism management and prostate monitoring.ResultsTrials of up to 36 months in length and longitudinal studies consistently fail to demonstrate an increased prostate cancer risk associated with increased testosterone levels. No evidence of an associated relationship between exogenous testosterone therapy and prostate cancer has emerged from clinical trials or adverse event reports. It does not appear that exogenous testosterone accumulates in the prostate or provokes major biologic change in the prostate gland. In addition, preliminary evidence indicates that low endogenous testosterone may confer an increased risk of prostate cancer.ConclusionsMounting evidence demonstrates that there is a lack of association between testosterone therapy and prostate cancer progression. Testosterone therapy may be prescribed for men for whom it was once not considered. Careful monitoring of patients with hypogonadism who are receiving testosterone therapy is imperative. Well-designed, large-scale prospective clinical trials are necessary to adequately address prostate safety in hypogonadal men receiving testosterone therapy. (Endocr Pract. 2008;14:904-911)     

The Effect and Potential Mechanism Analysis of Growth Hormone–Secreting Pituitary Adenomas on Thyroid Function

ObjectiveCurrent studies on the effect of high growth hormone (GH)/insulin-like growth factor (IGF)-1 on thyroid function are inconsistent. The aim was to explore the effect and potential mechanism of high GH/IGF-1 on thyroid function by analyzing the changes of thyroid function in patients with growth hormone–secreting pituitary adenoma (GHPA).MethodsThis was a retrospective cross-sectional study. Demographic and clinical data of 351 patients with GHPA who were first admitted to Beijing Tiantan Hospital, Capital Medical University, from 2015 to 2022 were collected to analyze the relationship between high GH/IGF-1 levels and thyroid function.ResultsGH was negatively correlated with total thyroxine (TT4), free thyroxine (FT4), and thyroid-stimulating hormone (TSH). IGF-1 was positively correlated with total triiodothyronine (TT3), free triiodothyronine (FT3), and FT4 and negatively correlated with TSH. Insulin-like growth factor–binding protein (IGFBP)-3 was positively correlated with TT3, FT3, and FT3:FT4 ratio. The FT3, TT3, TSH, and FT3:FT4 ratio of patients with GHPA and diabetes mellitus (DM) were significantly lower than those with GHPA but without DM. With the increase of tumor volume, thyroid function gradually decreased. GH and IGF-1 were correlated negatively with age in patients with GHPA.ConclusionThe study emphasized the complex interaction between the GH and the thyroid axes in patients with GHPA and highlighted the potential effect of glycemic status and tumor volume on thyroid function.     

Endocrine Complications in Patients with Gvhd

Objective: Graft-versus-host disease (GVHD) is an immune phenomenon that occurs in 30 to 70% of patients after allogeneic hematopoietic stem cell transplantation (HST). Chronic GVHD is a state of immune dysregulation wherein, depending on the severity and organ involved, patients may require prolonged treatment with additional or higher corticosteroids and other immunosuppressive agents. The objective of this study was to review the endocrine manifestations following HST that can arise as a consequence of the primary disease or its treatment, including chemotherapeutic agents, corticosteroids, radiation, or GVHD.Methods: We performed a narrative review of GVHD after HST. An English-language search for relevant studies was conducted on PubMed from inception to August 1, 2018, using the following search terms: “endocrine complications,” “bone marrow transplantation,” “graft-versus-host disease,” and “GVHD.” The reference lists of relevant studies were also reviewed.Results: Chronic GVHD may be associated with considerable pediatric growth impairment and may also contribute to thyroid gland dysfunction and thyroid cancer. These patients may also be at increased risk for low bone mineral density, reduced fertility, metabolic syndrome, and suppression of the pituitary-adrenal axis with adrenal insufficiency.Conclusion: This review indicates the importance of monitoring, diagnosing, and properly treating the endocrine complications in this population. More studies are needed to investigate the independent impact of GVHD on the endocrine system and treatment for complications.Abbreviations: BMD = bone mineral density; GH = growth hormone; GVHD = graft-versus-host disease; HST = hematopoietic stem cell transplantation; IGF-1 = insulin-like growth factor 1     

Endocrine disorders in pediatric - onset Langerhans Cell Histiocytosis.

Langerhans Cell Histiocytosis (LCH) is a rare disorder with a great variety of clinical manifestations. The purpose of this retrospective study was to evaluate the pattern and the long-term course of clinical, laboratorial and radiological findings in pediatric-onset LCH. We reviewed 46 children with histological diagnosis of LCH. Ten children (22%) showed endocrine disorders. Central diabetes insipidus (DI) was observed in all ten patients; GH deficiency was confirmed in four and hypogonadism in two children. There were no adrenal, prolactin or thyroid axis abnormalities. Obesity was observed in three patients. Eight patients showed soft tissue infiltration and five bone involvement. The MRI showed a lack of posterior pituitary bright spot in all DI patients; infundibular infiltration (II) associated or not with sellar or supra-sellar mass was observed in 4 patients. We conclude that the investigation of LCH, a multi-systemic disease, should include central nervous system images. The presence of II and/or DI should raise the diagnosis of LCH. Complete endocrine evaluation, allowing an early hormone therapy, is required to obtain a better quality of life in children with LCH.     

Differential Regulation of 11β-Hydroxysteroid Dehydrogenase Type 1 Activity in Patients with Differing Etiologies of Hypopituitarism

Objective: Pituitary patients with different etiologies of hypopituitarism exhibit differing phenotypes, despite similar replacement therapy strategies. We hypothesized that differential regulation of the isoenzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), which mediates the net autocrine conversion of cortisone to cortisol in adipose tissues and liver, may play a role.Methods: We studied 11β-HSD1 activity (using urine cortisol/cortisone metabolites ratio) in 36 hypopituitary patients with treated craniopharyngiomas, treated remitted Cushing disease, and treated nonfunctioning pituitary adenomas + prolactinomas on and off growth hormone (GH) replacement.Results: 11β-HSD1 activity was higher in subjects with craniopharyngioma both on and off GH, as evidenced by increased tetrahydrocortisol to tetrahydrocortisone metabolite ratios compared to other diagnostic groups, but there was no difference in body mass index, insulin levels, serum hormone measurements, or hydrocortisone dose between groups.Conclusion: Craniopharyngiomas are associated with enhanced 11β-HSD1 activity compared to other diagnostic hypopituitary groups, and this may contribute to the adverse phenotypic and metabolic features seen in this condition.Abbreviations: BMI = body mass index; Em = cortisone metabolites; Fm = cortisol metabolites; GH = growth hormone; 11β-HSD1 = 11β-hydroxysteroid dehydrogenase type 1; IGF-1 = insulin-like growth factor 1; NFPA = nonfunctioning pituitary adenoma; THE = tetrahydrocortisone; THF = tetrahydrocortisol     

American Association of Clinical Endocrinologists and American College of Endocrinology Disease State Clinical Review: A Neuroendocrine Approach to Patients With Traumatic Brain Injury

Objective: Traumatic brain injury (TBI) is now recognized as a major public health concern in the United States and is associated with substantial morbidity and mortality in both children and adults. Several lines of evidence indicate that TBI-induced hypopituitarism is not infrequent in TBI survivors and may contribute to the burden of illness in this population. The goal of this article is to review the published data and propose an approach for the neuroendocrine evaluation and management of these patients.Methods: To identify pertinent articles, electronic literature searches were conducted using the following keywords: “traumatic brain injury,” “pituitary,” “hypopituitarism,” “growth hormone deficiency,” “hypogonadism,” “hypoadrenalism,” and “hypothyroidism.” Relevant articles were identified and considered for inclusion in the present article.Results: TBI-induced hypopituitarism appears to be more common in patients with severe TBI. However, patients with mild TBI or those with repeated, sports-, or blast-related TBI are also at risk for hypopituitarism. Deficiencies of growth hormone and gonadotropins appear to be most common and have been associated with increased morbidity in this population. A systematic approach is advised in order to establish the presence of pituitary hormone deficiencies and implement appropriate replacement therapies.Conclusion: The presence of traumatic hypopituitarism should be considered during the acute phase as well as during the rehabilitation phase of patients with TBI. All patients with moderate to severe TBI require evaluation of pituitary function. In addition, symptomatic patients with mild TBI and impaired quality of life are at risk for hypopituitarism and should be offered neuroendocrine testing.Abbreviations: CBG = corticosteroid-binding globulin DI = diabetes insipidus GH = growth hormone IGF-1 = insulin-like growth factor 1 SIADH = syndrome of inappropriate antidiuretic hormone T₄ = thyroxine TBI = traumatic brain injury TSH = thyroid-stimulating hormone     

Daily endocrine profiles in parr and smolt Atlantic salmon

To elucidate possible mechanisms behind the endocrine control of parr–smolt transformation, the daily plasma profiles in thyroid hormones (TH; free thyroxine (FT₄), total thyroxine (TT₄), and total 3,5,3′-triiodothyronine (TT₃)), growth hormone (GH) and cortisol were studied in Atlantic salmon parr and smolts under simulated-natural winter (8 L:16D) and spring (16.5 L:7.5D) photoperiods, respectively. Overall, TT₄, TT₃ and GH levels were higher in smolts than in parr, whereas FT₄ levels fluctuated within the same range in parr and smolts. Significant diurnal changes in plasma TH were present in parr. Both FT₄ and TT₄ levels increased during the photophase and decreased during the scotophase, while TT₃ levels followed an inverse pattern. Growth hormone showed no significant changes in parr. Changes in FT₄, TT₄, GH, and cortisol, but not TT₃, levels, were observed in smolts with peak levels during both the photophase and scotophase for FT₄, TT₄ and GH. Plasma cortisol was not assayed in parr but in smolts the peaks were associated with dusk and dawn. In addition to the general increases in TH, GH and cortisol, the distinct endocrine differences in nighttime levels between parr in the winter and smolts in the spring suggest different interactions between TH, GH, cortisol and melatonin at these different time points. These spring scotophase endocrine profiles may represent synergistic hormone interactions that promote smolt development, similar to the synergistic endocrine interactions shown to accelerate anuran metamorphosis. The variations in these diurnal rhythms between parr and smolts may represent part of the endocrine mechanism for the translation of seasonal information during salmon smoltification.     

Evaluation of Secondary Causes of Bone Loss in a Primary Care Setting

ObjectiveTo evaluate the clinical and laboratory work-up for secondary causes of bone loss in a primary care setting.MethodsWe conducted a retrospective review of medical records of 100 patients with either osteoporosis or osteopenia, who presented to a university-based primary care clinic. Patients with chronic kidney disease or a history of organ transplantation were excluded, as were premenopausal women.ResultsAge at menopause was ascertained in 43% of female patients. Only 2% of patients were asked specifically about symptoms of malabsorption, whereas a history of malignant disease or its treatment was elicited from 24%. Of the overall study group, 50% were asked about a history of thyroid disease and 18% about a history of liver disease. Testicular examination was documented in 40% of male patients. Serum calcium and creatinine, complete blood cell count, and thyroid function tests were evaluated in 100% of patients. Vitamin D status was assessed in only 1 patient; no study patient had a 24-hour urine collection for determination of calcium excretion. Serum parathyroid hormone was measured in 7% and serum phosphorus in 10% of patients. Sixty percent of male patients had their testosterone levels assessed. Although the serum creatinine level was determined in all patients, only 1% had a formal estimation of the creatinine clearance or glomerular filtration rate.ConclusionThe evaluation of secondary causes of bone loss was notably inadequate in our study population. Because most patients with osteoporosis or osteopenia are managed in the primary care setting, a distinct need exists for consensus guidelines and recommendations from professional endocrine organizations to advise primary care physicians in the appropriate diagnostic evaluation for secondary causes of bone loss in such patients. (Endocr Pract. 2009;15:410-414)     

Development of Thyroid Storm After Surgical Resection of A Thyrotropin-Secreting Pituitary Adenoma

ObjectiveTo describe a patient with a thyrotropinsecreting pituitary adenoma in whom postoperative thyroid storm developed.MethodsWe present a case report with details of the initial presentation, laboratory evaluation, surgical and pathologic findings, and subsequent course in a patient with a thyrotropin (thyroid-stimulating hormone or TSH)- secreting adenoma and postoperative thyroid storm.ResultsAn 18-year-old male patient presented with severe headaches and was found to have a large suprasellar tumor and a mildly elevated level of TSH. Thyroid storm developed immediately after surgical resection of the pituitary mass. Results of laboratory evaluation undertaken preoperatively became available after the patient had undergone the surgical procedure and revealed thyroid hormone levels 2 to 3 times the upper limit of normal. Propylthiouracil and β-adrenergic blocking agents controlled the postoperative thyrotoxicosis and were subsequently discontinued as his TSH and thyroid hormone levels normalized.ConclusionThis case demonstrates the rare case of a TSH-secreting adenoma in a young patient, which was complicated by the development of postoperative thyroid storm. In addition, this case emphasizes the importance of preoperative pituitary hormonal evaluation and treatment of hormonal abnormalities in all patients presenting with sellar or suprasellar tumors. (Endocr Pract. 2008;14:732- 737)     

Diurnal rhythms of plasma growth hormone,somatostatin, thyroid hormones,cortisol and glucose concentrations in rainbow trout,Oncorhynchus mykiss,during progressive food deprivation

Abstract

The diurnal patterns of changes in plasma cortisol, growth hormone (GH), somatostatin‐14 (SRIF), thyroid hormones (L‐thyroxine, T₄ and triiodo‐L‐thyronine, T₃) and glucose were investigated in rainbow trout, Oncorhynchus mykiss, both during single meal‐feeding and during a progressive fast of 13 weeks. All measured variables exhibited a diurnal pattern in fed rainbow trout, most of which appeared to be correlated with the time of feeding (30–60 min after the onset of light), while additional changes, associated with the scotophase were also found for cortisol. Although fasting had no affect on mean daily plasma cortisol or SRIF concentrations, there was a progressive increase in mean daily plasma GH concentrations and a progressive decrease in mean daily plasma thyroid hormone and glucose concentrations associated with fasting. However, for GH, significant changes were not evident until week 10 of the fast. In addition, fasting appeared to phase‐shift the diurnal patterns of plasma GH, cortisol and glucose concentrations; the consequence of such a shift is that conclusions as to the effects of fasting, if based on a single time of sampling, may be flawed.     

Andropause or Male Menopause? Rationale for Testosterone Replacement Therapy in Older Men with Low Testosterone Levels

ObjectiveTo provide rationale for testosterone replacement therapy (TRT) in older men with low testosterone levels and symptoms consistent with testosterone deficiency.MethodsThe relevant literature was reviewed using PubMedResultsCross-sectional and longitudinal population-based studies indicate that total and free testosterone levels fall with aging, and they may be accompanied by symptoms consistent with androgen deficiency. Testosterone treatment of younger men with very low testosterone levels and hypothalamic, pituitary, or testicular disease is associated with improvements in symptoms, body composition, bone density, and hematocrit/hemoglobin. Studies evaluating testosterone treatment of older men with low testosterone levels are limited, but they suggest some increase in fat free mass, some decrease in fat mass, and some increase in bone density of the lumbar spine and femoral neck.ConclusionThe Testosterone Trial should provide definitive information regarding the potential benefits of TRT in men ≥ years of age. If efficacy is confirmed, we will still need more information regarding the risks of TRT in older men. (Endocr Pract. 2013;19:847-852)