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IN BRIEF This study was conducted to ascertain the opinions of endocrinologists about diabetes care as it relates to the health care provider workforce. A survey was administered to endocrinologists in the Planning Research in Inpatient Diabetes and Planning Research in Outpatient Diabetes (PRIDE/PROUD) group and given to attendees of the American Diabetes Association (ADA) Scientific Sessions special interest group whose focus was primary care. The majority of respondents agreed that there is a need for more providers to be trained to take care of patients with diabetes and that more trained providers are needed, and almost half agreed that primary care providers (PCPs) with advanced training in diabetes should be part of the workforce for managing the diabetes pandemic. Expanding diabetes fellowship programs for PCPs remains an important potential solution for addressing workforce development needs in diabetes care.

Inpatient hyperglycemia, hypoglycemia, and glucose variability are associated with increased mortality. The use of an electronic glucose management system (eGMS) to guide intravenous (IV) insulin infusion has been found to significantly improve blood glucose (BG) control. This retrospective observational study evaluated the 7-year (January 2009-December 2015) impact of the EndoToolPatients assigned to eGMS had indications for IV insulin infusion, including uncontrolled diabetes, stress hyperglycemia, and/or postoperative BG levels140 mg/dL. This study evaluated time required to achieve BG control (180 mg/dL;140 mg/dL for cardiovascular surgery patients); hypoglycemia incidence (70 and40 mg/dL); glucose variability (assessed by SD and coefficient of variation percentage [CV%]); excursions (BG levels180 mg/dL after control attained); and the impact of eGMS on hospital-acquired condition (HAC)-8 rates.Data were available for all treated patients (492,078 BG readings from 16,850 patients). With eGMS, BG levels were brought to target within 1.5 to 2.3 hours (4.5 to 4.8 hours for cardiovascular patients). Minimal hypoglycemia was observed (BG values70 mg/dL, 0.93%;40 mg/dL, 0.03%), and analysis of variance of BG values70 mg/dL showed significant reductions over time in hypoglycemia frequency, from 1.04% in 2009 to 0.46% in 2015 (P.0001). The CV% per patient visit was 26.5 (±12.9)%, and 4% of patients experienced glucose excursions (defined as BG levels180 mg/dL once control was attained). HAC-8 rates were reduced from 0.083 per 1,000 patients (2008) to 0.032 per 1,000 patients (2011).The use of eGMS resulted in rapid, effective control of inpatient BG levels, including significantly reduced hypoglycemia rates.BG = blood glucose CMS = Centers for Medicare and Medicaid Services CV = coefficient of variation CV% = coefficient of variation percentage eGMS = electronic glucose management system GV = glycemic variability HAC = Hospital-Acquired Condition ICU = intensive care unit IU = intermediate unit IV = intravenous LOS = length of stay VMC = Vidant Medical Center.

Oral meal consumption increases glucagon-like peptide 1 (GLP-1) release which maintains euglycemia by increasing insulin secretion. This effect is exaggerated during short-term follow-up of Roux-en-y gastric bypass (RYGB). We examined the durability of this effect in patient with type 2 diabetes (T2DM)10 years after RYGB.GLP-1 response to a mixed meal in the 10-year post-RYGB group (n = 5) was compared to lean (n = 9), obese (n = 6), and type 2 diabetic (n = 10) controls using a cross-sectional study design. Analysis of variance (ANOVA) was used to evaluate GLP-1 response to mixed meal consumption from 0 to 300 min, 0-20 min, 20-60 min, and 60-300 min, respectively. Weight, insulin resistance, and T2DM were also assessed.GLP-1 response 0-300 min in the 10-year post-RYGB showed a statistically significant overall difference (p = 0.01) compared to controls. Furthermore, GLP-1 response 0-20 min in the 10-year post-RYGB group showed a very rapid statistically significant rise (p = 0.035) to a peak of 40 pM. GLP-1 response between 20 and 60 min showed a rapid statistically significant (p = 0.041) decline in GLP-1 response from ~40 pM to 10 pM. GLP-1 response in the 10-year post-RYGB group from 60 to 300 min showed no statistically significant difference from controls. BMI, HOMA, and fasting serum glucose before and10 years after RYGB changed from 59.9 → 40.4, 8.7 → 0.88, and 155.2 → 87.6 mg/dl, respectively, and were statistically significant (p0.05).An exaggerated GLP-1 response was noted 10 years after RYGB, strongly suggesting a durability of this effect. This phenomenon may play a key role in maintaining type 2 diabetes remission and weight loss after RYGB.

To report a case that substantiates the presence of hypoglycemia at the time of death of a young man with type 1 diabetes, who was found unresponsive in his undisturbed bed in the morning.We describe a 23-year-old man with a history of type 1 diabetes treated with an insulin pump, who had recurrent severe hypoglycemia. In an effort to understand these episodes better and attempt to eliminate them, a retrospective (non-real-time) continuous subcutaneous glucose monitoring system (CGMS) was attached to the patient. He was found dead in his undisturbed bed 20 hours later. The insulin pump and CGMS were both downloaded for postmortem study.Postmortem download of the data in the CGMS demonstrated glucose levels below 30 mg/dL around the time of his death, with only a minimal counter-regulatory response. This finding corresponded to a postmortem vitreous humor glucose of 25 mg/dL. An autopsy showed no major anatomic abnormalities that could have contributed to his death.To our knowledge, this is the first documentation of hypoglycemia at the time of death in a patient with the "dead-in-bed" syndrome. This report should raise the awareness of physicians to the potentially lethal effects of hypoglycemia and provide justification for efforts directed at avoiding nocturnal hypoglycemia.

Background: To address the need of caring for the growing number of patients with diabetes, East Carolina University implemented a 1-year fellowship in diabetes. Most of the region has been designated as Health Professional Shortage Areas. Description: The objective of the fellowship is to educate primary care physicians to serve as regional specialists in diabetes. The program is administered by physicians, educators, and representatives of the university's affiliated teaching hospital. The curriculum includes clinical, didactic, and experiential learning strategies in outpatient and inpatient settings. Adult and pediatric endocrinologists, obstetricians, and generalists mentor and evaluate the fellows. Evaluation: This innovative training program has improved the availability of high-quality diabetes care for underserved patients in the region. Mean glycemic control in fellows' patients improved and other clinical endpoints were also met. Conclusions: A 1-year diabetes fellowship is a replicable solutio...

Objective To address the likelihood of thyroid malignancy for each cytologic interpretation, highly cellular and benign vs. follicular carcinoma, with particular attention to the indeterminate cytologic result, follicular neoplasm. Study Design We retrospectively reviewed thyroid nodule cytologic and histologic interpretations from 1994 to 2002 in a tertiary medical center setting. Patients were referred for evaluation of thyroid nodules found incidentally or on physical examination. Results A total of 886 thyroid nodules were aspirated in 802 patients (500 benign, 195 indeterminate, 129 inadequate, 62 malignant). Of 195 indeterminate lesions, 180 were classified as follicular neoplasm or "cannot rule out/possible " follicular neoplasm, with 144 of these ultimately removed and with malignant histologic findings in 28. Any mention of follicular neoplasm in the cytology report conferred a 19.4% risk of malignancy in patients who went on to surgery (including an unexpected 18.2% rate of malignancy in the subcategory in which a possible follicular neoplasm was a secondary listing in an otherwise-benign cytologic differential diagnosis). Conclusion There was no difference in the likelihood of histologic malignancy between the cytologic subcategories of "definite" follicular neoplasm and "cannot rule out/possible" follicular neoplasm. We recommend that cytologic reports on fine needle aspiration of thyroid nodules with a diagnosis of follicular neoplasm reflect this fact.

Objective To describe a rare case of acute myocardial infarction in a patient with neurofibromatosis 1 and pheochromocytoma and to review the literature on the coexistence of these 2 diseases, the causes of myocardial injury in patients with pheochromocytoma, and the utility of genetic testing and pheochromocytoma screening for those patients and their families. Methods We present a case report, including the detailed clinical, laboratory, and radiographic data, results of adrenal mass pathology, and results of coronary angiography. We also survey other relevant reports available in the literature. Results A 43-year-old woman with a history of longstanding hypertension, neurofibromatosis 1, headaches, sweating, and palpitations presented to the hospital with chest pain and shortness of breath. She was found to have an acute myocardial infarction and pulmonary edema, as well as a right adrenal mass. A pheochromocytoma was suspected, and phenoxybenzamine was added to her treatment regimen. Cardiac catheterization showed nonobstructive coronary disease. The levels of plasma catecholamine metabolites were extremely high. The patient underwent uncomplicated laparoscopic right adrenalectomy 2 weeks after this admission. Surgical pathology confirmed the diagnosis of pheochromocytoma. Conclusion Adrenergic crisis attributable to pheochromocytoma can result in acute myocardial infarction even in the absence of obstructive coronary disease. Inclusion of pheochromocytoma in the differential diagnosis of hypertension in patients with neurofibromatosis is very important and helps avoid mistakes in the management of such patients. (Endocr Pract. 2007;13:269-273)

Papillary thyroid carcinoma (PTC) commonly metastasizes to cervical lymph nodes. Distant metastases are unusual with the lungs most frequently involved. Well-differentiated thyroid carcinoma very rarely presents with metastases to the spleen. This is the case of a 25-year-old man with a history of PTC (1.4 cm primary; no capsular invasion and negative lymph node metastases). One year after initial surgery, recurrent disease was found in multiple neck nodes by central neck dissection. Whole body scan (WBS) following a therapeutic ablation dose of 150 mCi I(131) revealed mediastinal metastases. Computerized axial tomography (CT) of the chest one year later showed no gross mediastinal or pulmonary disease. However, multiple large splenic lesions were incidentally noted. Evaluation by ultrasound (US) showed lesions to be solid echogenic masses without remarkable Doppler characteristics to suggest vascular tumors. US-guided percutaneous fine-needle aspiration biopsy (FNAB) of one lesion was nondiagnostic. After withdrawal from Levothyroxine, serum TSH was >100 mU/L with a thyroglobulin of 9.4 ng/mL and negative anti-thyroglobulin antibodies. Diagnostic WBS revealed faint splenic uptake but was otherwise unremarkable. Following treatment with 192 mCi I(131), WBS demonstrated increased activity in the mediastinum as well as in the spleen suggesting mediastinal and splenic metastases. Contrast CT of the abdomen showed multiple low-attenuated heterogeneously enhancing splenic masses, normal liver and no intra-abdominal lymphadenopathy. The largest mass (4.5 x 3.5 cm) was exophytic and in close proximity to the splenic capsule. Despite the serum thyroglobulin of only 9.4 ng/mL, the finding of I(131) accumulation within solid splenic masses led to a preoperative diagnosis of thyroid carcinoma metastases. To establish the diagnosis and to remove the risk for splenic rupture, a laparoscopic splenectomy was performed. Histopathologic analysis showed large littoral cell angiomas (LCA). False-positive radioiodine scintigraphy in the setting of PTC involving a vertebral hemangioma has been reported. To our knowledge, this is the first case that describes multiple angiomas mimicking metastatic thyroid carcinoma to the spleen. In one-third of all cases reported, LCA co-exists with various visceral organ cancers or malignant lymphoma. This is the first report of an association between LCA and thyroid carcinoma.

One hundred sixty-four (164) healthy, young Caucasian women enrolled as midshipmen at the United States Naval Academy with no known disease or bone injury were followed for 3.6 years. Change in bone mineral density (BMD) of the hip, lumbar spine and distal tibia, and total body bone mineral content (TBMC) was measured by dual energy X-ray absorptiometry (DXA). Bone mineral density and TBMC of these women were measured within 2 months (60 +/- 4 days) of entering the Academy and annually. Over the study period, hip BMD increased 2.26% (P < 0.001), lumbar spine BMD increased 3.27% (P < 0.001) and distal tibia BMD increased 5.2% (P < 0.001). Total body bone mineral content showed a 5.25% (P < 0.001) increase during the study period. In this group of young women, gain in BMD and TBMC continued until age 22. These results suggest that bone mass may accrue in certain groups of women beyond age 22. The significance of this increase in bone mass during early adulthood on risk for osteoporotic fractures in later life and its impact on exercise-related bone injuries are unknown and warrant further examination.

Objective To compare the clinical and biochemical features, bone densitometry data, and results of diagnostic imaging to localize parathyroid tumors in patients with radiation-associated hyperparathyroidism (R-HPT) and patients with HPT who had no history of radiation exposure (NR-HPT). Methods We performed a retrospective analysis of 34 patients with HPT who underwent evaluation and subsequent neck exploration between 1990 and 1995. We recorded and compared the symptoms, biochemical findings, bone densitometry data, results of diagnostic imaging, and pathologic findings in R-HPT and NR-HPT groups. Results The R-HPT group (8 men and 4 women) generally was older than the NR-HPT group (14 men and 8 women), but the age difference was not statistically significant. Patients in the R-HPT group had received radiotherapy (6.9 to 21.7 Gy) between 2 and 9 years of age for various diagnoses. Eight patients (67%) in the R-HPT group and 13 (59%) in the NR-HPT group had no symptoms of HPT. The rest of the patients in both groups had nonspecific symptoms, such as fatigue and dyspepsia. Four patients (18%) in the NR-HPT group had nephrolithiasis, and 3 (14%) had skeletal manifestations at initial assessment. Serum calcium, phosphorus, and parathyroid hormone levels and 24-hour urine calcium excretion were similar in both groups. Mean lumbar spine bone mineral density was lower in women in the R-HPT group than in those in the NR-HPT group, but the prevalence of osteoporosis did not differ significantly in the two study groups. Sestamibi scintigraphy accurately localized adenomas in both groups equally well (sensitivity > 90%). In the R-HPT group, 11 patients had a single parathyroid adenoma and 1 had hyperplasia of all four parathyroid glands. In the NR-HPT group, 21 patients had a single parathyroid adenoma and 1 had parathyroid hyperplasia. In nine patients in the R-HPT group, ultrasonography showed thyroid nodules > 1 cm. Pathologic examination of surgical specimens in the R-HPT group confirmed thyroid carcinoma in 11 patients (10 papillary and 1 follicular cancer); no patient in the NR-HPT group had thyroid cancer. Six weeks after thyroidectomy, patients with thyroid cancer received 131I (mean dose, 145 mCi), five of whom needed additional 131I treatments. Conclusion Patients with a history of childhood neck irradiation who have HPT have a high likelihood of coexisting thyroid cancer. This observation may justify surgical exploration rather than vigilant follow-up in asymptomatic patients with primary HPT and coexisting thyroid nodules who have a history of radiation exposure. (Endocr Pract. 2003;9:353-362)

Usual causes of intolerance to thyroxine sodium include coronary artery disease, advanced age, untreated adrenal insufficiency, and severe hypothyroidism. We describe 4 patients with iron deficiency anemia and primary hypothyroidism. After treatment with thyroxine sodium, these patients developed palpitations and feelings of restlessness, which necessitated discontinuation of the thyroid hormone. After the anemia was treated with ferrous sulfate for 4 to 7 weeks, they were able to tolerate thyroxine sodium therapy. Iron deficiency anemia coexisting with primary hypothyroidism results in a hyperadrenergic state. In such patients, we postulate that thyroid hormone administration causes palpitations, nervousness, and feelings of restlessness. Correction of any existing pronounced anemia in hypothyroid patients who are intolerant to thyroxine sodium therapy may result in tolerance to this agent.

To assess the efficacy of alendronate therapy on bone mineral density (BMD) at the lumbar spine and hip in men with osteoporosis.Medical records of male patients with osteoporosis, who had undergone follow-up in the Endocrinology Clinic at the National Naval Medical Center, were reviewed, and nine patients treated with alendronate for at least 1 year were identified. Patients were excluded from analysis if they had evidence of osteomalacia or if baseline and follow-up BMD results on the same dual-energy x-ray absorptiometry (DEXA) densitometer, at least 10 months apart, were not available. DEXA BMD results at the lumbar spine and hip, before and after at least 10 months of alendronate treatment, were analyzed for significant differences. Patients were also receiving calcium supplementation (1,000 to 1,500 mg/day), and all but one patient received vitamin D (400 to 800 U/day).Lumbar spine BMD increased by 6.4 +/- 1.8% per year with alendronate treatment (P = 0.008). A mean absolute gain of 0.052 +/- 0.010 g/cm 2 (P = 0.005) in lumbar spine BMD was noted for the entire study group (N = 9), after a mean duration of treatment of 14 +/- 1 months. The mean lumbar spine BMD Z score improved by 0.40 +/- 0.09 (P = 0.002) with alendronate therapy. The femoral neck BMD also increased by 4.5 +/- 1.4% per year with alendronate treatment (P = 0.013). The mean absolute gain in femoral neck BMD was 0.028 +/- 0.009 g/cm 2 (P = 0.013) for the study group (N = 9) after 14 +/- 1 months of therapy. The mean femoral neck BMD Z score improved 0.30 +/- 0.08 (P = 0.005) with treatment. BMD gains at the greater trochanter of 3.2 +/- 1.5% per year (P = 0.067) and at Ward's triangle of 9.1 +/- 4.2% per year (P = 0.061) were not statistically significant. Two patients discontinued alendronate treatment after 1 year because of epigastric or retrosternal pain.Oral alendronate treatment, given in combination with calcium supplementation and physiologic doses of vitamin D, resulted in significant improvements in lumbar spine and femoral neck BMD after a 14-month period in this small group of men with osteoporosis. Although controlled, prospective trials involving larger numbers of male patients with fracture incidence data are needed before definitive conclusions can be made, alendronate treatment seems to be effective in improving BMD in men with osteoporosis, similar to its efficacy in women.

In recent years, incretin-based therapies such as glucagon-like peptide-1 agonists (GLP-1) and dipeptidyl peptidase-IV inhibitors (DPP-IV) have become important therapeutic options for treatment of type 2 diabetes. Although these agents are considered safe, long-term safety outcome studies are lacking. Theoretically, the combination of these two classes of agents could increase efficacy, but there is no strong supporting clinical evidence. While both GLP-1 and DPP-IV agents are approved for use as monotherapy and with other diabetes drugs, the combined use of these drugs classes has not been approved by the U.S. Food and Drug Administration (FDA). In a recent case report, Patel et al. (1) noted an improvement in glycemic control in a patient with type 2 diabetes on a combination of …

Objective To characterize a disorder of episodes of flushing and increased levels of 5-hydroxy-indoleacetic acid (5-HIAA) in men with secondary hypogonadism who respond to testosterone therapy. Material and Methods We present detailed case reports of three male patients who had flushing, secondary hypogonadism, and increased urinary 5-HIAA levels and describe their clinical and laboratory features before and after treatment with testosterone. In addition, six male patients with hypogonadism (three with primary and three with secondary hypogonadism) without flushing were assessed. Results The three patients with flushing and secondary hypogonadism (serum total testosterone 5.45 ± 0.63 nmol/L, free testosterone 89.3 ± 7.0 pmol/L, follicle-stimulating hormone 3.85 ± 0.58 IU/L, and luteinizing hormone 4.41 ± 0.98 IU/L) had increased urinary 5-HIAA levels (98.5 ± 12.2 (imol/24 h) but normal blood serotonin levels (9.66 + 1.58 (imoI/L). During a pentagastrin-calcium stimulation test, serum calcitonin and blood serotonin values were normal in patients with secondary hypogonadism and flushing. Detailed investigation showed no evidence of a carcinoid tumor. Urinary 5-HIAA levels became normal (16.6 ± 1.73 umol/24 h) after treatment with testosterone. When testosterone therapy was discontinued in two patients, flushing and increased urinary 5-HIAA levels recurred. Furthermore, flushing and the elevated urinary 5-HIAA values resolved when testosterone treatment was reinitiated. The six patients with hypogonadism without flushing had normal urinary 5-HIAA levels (14.9 ±3.31 umol/24 h). Conclusion Male patients with flushing and increased urinary 5-HIAA levels should undergo assessment for hypogonadism after screening for carcinoid tumor. If hypogonadism is diagnosed, resolution of flushing and normalization of 5-HIAA may be achieved with testosterone treatment. We suggest that pseudocarcinoid syndrome associated with hypogonadism be the descriptive label used for this combination of clinical features.

To report the first postmarketing case of necrotizing pancreatitis in a patient on combination therapy of sitagliptin and exenatide.We describe the patient's clinical presentation, laboratory test results, imaging, and autopsy findings.A 76-year-old woman with a history of type 2 diabetes mellitus presented with severe abdominal pain, vomiting, and fever requiring hospital admission. She had been treated with exenatide for 3 years to manage her diabetes mellitus. A few weeks before presentation, sitagliptin was added, presumably to further optimize her glycemic control. Acute pancreatitis was diagnosed during hospital admission. At initial presentation, her serum amylase concentration was 1136 U/L (reference range, 10-130 U/L) and her lipase concentration was greater than 3500 U/L (reference range, 0-75 U/L). In addition, computed tomography of the abdomen and pelvis demonstrated extensive previous cholecystectomy, reported no alcohol consumption, and had a normal lipid profile. Although she had a long-standing history of diabetes mellitus, she had no history of pancreatitis or other risk factors that would have caused her to develop the underlying condition. After initial brief improvement, her symptoms worsened, and despite aggressive care, her clinical state deteriorated and she died. Autopsy findings demonstrated acute necrotizing pancreatitis with complete digestion of the pancreas.Considering the temporal relationship of her symptoms to the addition of sitagliptin to her existing exenatide regimen, this case strongly suggests a possible causal link between exenatide or sitagliptin (or the combination of the 2 drugs) and the etiology of pancreatitis in this patient.

Objective. To report a case of diabetic muscle infarction (DMI), a rare complication of long-standing poorly controlled diabetes mellitus.Methods. We describe a case of a 45-year-old male with an approximately 8-year history of poorly controlled type 2 diabetes mellitus with multiple microvascular complications who presented with the sudden onset of left thigh pain and swelling. He had a swollen left thigh and a CK of 1670 U/L. He was initially treated with intravenous antibiotics for a presumptive diagnosis of pyomyositis or necrotizing fasciitis with no improvement. A diagnosis of diabetic muscle infarction was considered.Results. An MRI of the thigh demonstrated diffuse edema in the anterior compartment. A muscle biopsy demonstrated coagulation necrosis in skeletal muscle and inflammation and infarction in the walls of small blood vessels. These studies confirmed the final diagnosis of DMI. He was treated with supportive care and gradually improved.Conclusion. DMI is a rare complication of diabetes that is often mistaken for infections such as pyomyositis and necrotizing fasciitis or thrombophlebitis. Treatment is supportive. Although the short-term prognosis is good in these patients, the long-term prognosis is poor.

To address the likelihood of thyroid malignancy for each cytologic interpretation, highly cellular and benign vs. follicular carcinoma, with particular attention to the indeterminate cytologic result, follicular neoplasm.We retrospectively reviewed thyroid nodule cytologic and histologic interpretations from 1994 to 2002 in a tertiary medical center setting. Patients were referred for evaluation of thyroid nodules found incidentally or on physical examination.A total of 886 thyroid nodules were aspirated in 802 patients (500 benign, 195 indeterminate, 129 inadequate, 62 malignant). Of 195 indeterminate lesions, 180 were classified as follicular neoplasm or "cannot rule out/possible" follicular neoplasm, with 144 of these ultimately removed and with malignant histologic findings in 28. Any mention of follicular neoplasm in the cytology report conferred a 19.4% risk of malignancy in patients who went on to surgery (including an unexpected 18.2% rate of malignancy in the subcategory in which a possible follicular neoplasm was a secondary listing in an otherwise-benign cytologic differential diagnosis).There was no difference in the likelihood of histologic malignancy between the cytologic subcategories of "definite "follicular neoplasm and "cannot rule out/possible" follicular neoplasm. We recommend that cytologic reports on fine needle aspiration of thyroid nodules with a diagnosis of follicular neoplasm reflect this fact.

Objective To evaluate the effects of nicotinic acid on serum thyroid hormone levels in the absence of systemic illness or hepatic dysfunction. Design We determined the effect of treatment with nicotinic acid on serum thyroid hormone levels in one female and four male patients (mean age, 44.4 years) with hyperlipidemia. Material and Methods In the five study patients, we measured serum lipids in conjunction with serum thyroxine (T 4 ), triiodothyronine (T 3 ) resin uptake, T 3 , free T 4 , thyroid-stimulating hormone (TSH), and thyroxine-binding globulin before, during, and after treatment with nicotinic acid. Results Serum lipid levels responded appropriately to nicotinic acid treatment. Thyroid function studies done a mean of 1.3 years (range, 0.5 to 3.5) after initiation of nicotinic acid therapy (mean daily dose, 2.6 ± 0.7 g) revealed significant decreases in serum levels of total T 4 (21 %), free T 4 index (16%), T 3 (13 %), and thyroxine-binding globulin (23 %) ( P 4 , T 3 resin uptake, and TSH levels. During the course of treatment, the patients, who were carefully questioned, had no symptoms of hypothyroidism. Hypothyroidism was further excluded in three patients who had a normal serum TSH response to administration of thyrotropin-releasing hormone. In two patients, measurements of thyroid function returned to pretreatment levels after discontinuation of nicotinic acid therapy. No patient had significant abnormalities in liver-associated enzymes or evidence of systemic illness during the course of treatment. Conclusion These results suggest that nicotinic acid decreases serum thyroid hormone concentrations while maintaining a euthyroid state. This effect may be mediated through reduction in thyroxine-binding globulin, but other mechanisms may also be involved.

A 43 year old female presented with chest pain and shortness of breath and was determined to have hypertensive crisis, pulmonary edema, and acute non-ST elevation myocardial infarction (MI). She had a history of neurofibromatosis 1 (NF1), poorly controlled hypertension (HTN) and spells of headaches, palpitations and sweating. On transthoracic echocardiogram she had a hyperdynamic left ventricular function with ejection fraction of 75% and inferior and inferoseptal wall motion abnormality. Cardiac catheterization revealed a nonobstructive coronary artery disease. Given her NF1, HTN and the presence of the “classic triad” of pheochromocytoma, she was screened for this tumor. Plasma catecholamine metabolites levels drawn on the third day post acute MI with the patient pain free and stable evidenced a 10-fold increase of free normetanephrine and 4.5-fold increase of free metanephrine. MRI of adrenal glands revealed a 4.5 × 3.3 cm right adrenal mass. The patient was diagnosed with pheochromocytoma and started on labetalol. The patient underwent uncomplicated laparoscopic adrenal pheochromocytoma excision two weeks after the first admission. Pathology has confirmed the diagnosis of pheochromocytoma. Conclusion Adrenergic crisis secondary to pheochromocytoma can result in acute MI even in the absence of the obstructive coronary artery disease. Consider pheochromocytoma early in the management of unexplained hypertension and MI in patients with NF1.