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2.
Endocr Pract ; 28(11): 1159-1165, 2022 Nov.
Article in English | MEDLINE | ID: mdl-35985561

ABSTRACT

CONTEXT: The Accreditation Council for Graduate Medical Education has instituted common program requirements related to diversity, equity, and inclusion (DEI) for postgraduate trainees in the United States; however, the extent to which DEI training is being incorporated across endocrinology fellowship programs is unknown. OBJECTIVES: To describe the sociodemographic representation and DEI training experiences within endocrinology fellowship programs. DESIGN, SETTING, AND PARTICIPANTS: National cross-sectional survey study of fellows and fellowship program leaders in the United States whose fellowships were members of the Association of Program Directors in Endocrinology and Metabolism. MAIN OUTCOME MEASURES: (1) Demographics of fellows and program leaders and (2) programs' experience, confidence, and interest in formal DEI training. RESULTS: A total of 108 and 106 fellow and faculty responded to the survey, respectively. The majority of fellows and faculty are female. Less than 3% of fellows and 3.7% of faculty identify as Black. More than 90% of fellows/faculty are heterosexual and no respondents identified as transgender/nonbinary; however, 5% and 2% of all respondents preferred not to disclose their sexual orientation and gender identity, respectively. While 85% of faculty received institutional diversity and inclusion training, 67.6% of fellows did. Fellows are more likely to have received training in health equity than program leaders. Both fellows and program leaders express a high interest in health equity curriculum. CONCLUSIONS: Within the diversity of endocrinology training programs, Black physicians are underrepresented in medicine, which persists in endocrinology fellowships. Fellowship programs express enthusiasm for national diversity and health equity curricula, with the majority of programs reporting institutional DEI training.


Subject(s)
Fellowships and Scholarships , Health Equity , Female , United States , Humans , Male , Cross-Sectional Studies , Gender Identity , Education, Medical, Graduate , Curriculum , Surveys and Questionnaires
4.
BMJ Case Rep ; 20172017 Feb 27.
Article in English | MEDLINE | ID: mdl-28242803

ABSTRACT

Antithyroid arthritis syndrome is a constellation of symptoms of myalgia, arthralgia, arthritis, fever and rash associated with the use of antithyroid medications. We report a case of a patient with severe hyperthyroidism likely secondary to Graves' disease who presented with the abovementioned symptoms after being treated with methimazole (antithyroid medication). Our aim is to increase awareness regarding this uncommon but disabilitating and life-threatening adverse effect of antithyroid medications among clinicians. We also discuss the proposed pathophysiology for this immunological reaction as well as management options in these patients.


Subject(s)
Antithyroid Agents/adverse effects , Arthralgia/etiology , Arthritis/etiology , Drug Eruptions/etiology , Fever/etiology , Methimazole/adverse effects , Female , Humans , Hyperthyroidism/drug therapy , Middle Aged , Syndrome
5.
Am J Emerg Med ; 35(6): 937.e5-937.e6, 2017 Jun.
Article in English | MEDLINE | ID: mdl-28043728

ABSTRACT

Acute compartment syndrome is increased tissue pressure exceeding perfusion pressure in a closed compartment resulting in nerve and muscle ischemia. Common precipitating causes are crush injuries, burns, substance abuse, osseous or vascular limb trauma. This is a case of 42year old female with history of hypothyroidism who presented to emergency room with acute onset of severe pain and swelling in right lower extremity. Physical examination was concerning for acute compartment syndrome of right leg which was confirmed by demonstration of elevated compartmental pressures. No precipitating causes were readily identified. Further laboratory testing revealed uncontrolled hypothyroidism. Management included emergent fasciotomy and initiating thyroid hormone replacement. This case represents a rare association between acute compartment syndrome and uncontrolled hypothyroidism. We also discuss the pathogenesis of compartment syndrome in hypothyroid patients and emphasize the importance of evaluating for less common causes, particularly in setting of non-traumatic compartment syndrome.


Subject(s)
Compartment Syndromes/etiology , Hypothyroidism/complications , Lower Extremity/physiopathology , Acute Disease , Adult , Female , Humans , Pain , Physical Examination
6.
Curr Diabetes Rev ; 13(3): 315-321, 2017.
Article in English | MEDLINE | ID: mdl-27097605

ABSTRACT

INTRODUCTION: Diabetic ketoacidosis (DKA) is one of the most serious complications of diabetes. It is characterised by the triad of hyperglycemia (blood sugar >250 mg/dl), metabolic acidosis (arterial pH <7.3 and serum bicarbonate <18 mEq/L) and ketosis. Rarely these patients can present with blood glucose (BG) levels of less than 200 mg/dl, which is defined as euglycemic DKA. The possible etiology of euglycemic DKA includes the recent use of insulin, decreased caloric intake, heavy alcohol consumption, chronic liver disease and glycogen storage disorders. DKA in pregnancy has also been reported to present with euglycemia. The recent use of sodium glucose cotransporter 2 (SGLT2) inhibitors has shed light on another possible mechanism of euglycemic DKA. Clinicians may also be misled by the presence of pseudonormoglycemia. CONCLUSION: Euglycemic DKA thus poses a challenge to physicians, as patients presenting with normal BG levels in ketoacidosis may be overlooked, leading to a delay in appropriate management strategies. In this article, we review all the possible etiologies and the associated pathophysiology of patients presenting with euglycemic DKA. We also discuss the approach to diagnosis and management of such patients. Despite euglycemia, ketoacidosis in diabetic patients remains a medical emergency and must be treated in a quick and appropriate manner.


Subject(s)
Blood Glucose , Diabetic Ketoacidosis/etiology , Alcohol Drinking/adverse effects , Diabetic Ketoacidosis/blood , Diabetic Ketoacidosis/therapy , Female , Humans , Pregnancy , Pregnancy Complications/blood , Sodium-Glucose Transporter 2 , Sodium-Glucose Transporter 2 Inhibitors , Starvation/blood
7.
Endocr Pract ; 22(5): 555-60, 2016 May.
Article in English | MEDLINE | ID: mdl-26720252

ABSTRACT

OBJECTIVE: The standard treatment for primary hypothyroidism is replacement with levothyroxine to achieve a thyroid-stimulating hormone (TSH) level within the normal range, (0.45-4.5 mIU/L), which is known to prevent complications including weight gain. While the normal TSH range includes the 95% confidence intervals, it is not known if there is an association between weight and TSH within this interval in treated hypothyroid patients. METHODS: We conducted a retrospective analysis of patients treated within the Cooper Health System from January 1 to August 31, 2014. A sample of 245 treated hypothyroid patients and 162 euthyroid controls were studied. Data collected included age, sex, race/ethnicity, height, weight, levothyroxine dose, and diabetes and smoking history. RESULTS: Hypothyroid and control groups were similar in height, weight, body mass index (BMI), and the number of patients with diabetes. There were more females, Caucasians, and nonsmokers in the hypothyroid group. The average TSH was slightly higher in the treated hypothyroid patients versus nonhypothyroid controls (median 1.87 vs. 1.55, P<.01). There was no significant relationship between TSH and BMI in the treated hypothyroid patients or the euthyroid controls. CONCLUSION: Since no significant relationship was found between BMI and TSH in treated hypothyroidism, there may be no weight reduction benefit gained by adjusting TSH to the lower end of normal range. Patients should be counseled that properly treated hypothyroidism is unlikely to contribute to weight gain. Other treatments such as nutrition and exercise counseling should be offered instead.


Subject(s)
Body Mass Index , Hypothyroidism/blood , Hypothyroidism/therapy , Thyrotropin/blood , Adult , Female , Healthy Volunteers , Humans , Male , Middle Aged , Reference Values , Retrospective Studies , Thyroid Function Tests/standards , Young Adult
8.
Pharmacotherapy ; 33(3): 319-29, 2013 Mar.
Article in English | MEDLINE | ID: mdl-23436494

ABSTRACT

Cushing's syndrome is a debilitating endocrine disorder caused by elevated circulating glucocorticoid levels. Although uncommon, Cushing's syndrome is associated with significant morbidity necessitating rapid reversal of hypercortisolemia. Primary therapy for most patients with Cushing's syndrome is surgical, but many patients will require additional treatments with radiation or drugs. Although several options for drug therapy exist, few are readily available and all have dose-limiting adverse effects. Mifepristone (RU 486), a first-in-class glucocorticoid receptor antagonist, was approved by the United States Food and Drug Administration in 2012 for use in Cushing's syndrome to control hyperglycemia in patients who are not surgical candidates or have not achieved remission from surgery. The drug is approved for oral once-daily administration. In its pivotal trial, 60% of patients responded to mifepristone with significant improvements in glycemic control and 38% had a reduction in diastolic blood pressure. The most common adverse events were nausea, fatigue, headache, endometrial hyperplasia, and hypokalemia. Adrenal insufficiency occurred in fewer than 5% of patients. The recommended starting dosage of mifepristone is 300 mg/day. The dosage may be increased every 2-4 weeks up to a maximum of 1200 mg/day, although it should not exceed 20 mg/kg/day. Significant drug-drug interactions exist due to mifepristone's effects on a number of cytochrome P450 enzymes. Despite its limitations, mifepristone is a welcome addition and an appropriate alternative to the available drug therapy for Cushing's syndrome.


Subject(s)
Cushing Syndrome/drug therapy , Hormone Antagonists/therapeutic use , Mifepristone/therapeutic use , Cushing Syndrome/metabolism , Dose-Response Relationship, Drug , Drug Interactions , Hormone Antagonists/administration & dosage , Hormone Antagonists/adverse effects , Hormone Antagonists/pharmacokinetics , Humans , Mifepristone/administration & dosage , Mifepristone/adverse effects , Mifepristone/pharmacokinetics , Receptors, Glucocorticoid/antagonists & inhibitors
9.
Expert Rev Endocrinol Metab ; 8(2): 183-193, 2013 Mar.
Article in English | MEDLINE | ID: mdl-30736178

ABSTRACT

Cushing's syndrome is a debilitating endocrine disorder which results from hypercortisolemia. While endogenous Cushing's syndrome can be caused by an adrenocorticotrophic hormone (ACTH)-dependent or ACTH-independent mechanism, it is most often a result of excess secretion of ACTH by a corticotroph adenoma (Cushing's disease). Untreated hypercortisolemia causes significant morbidity and increased mortality due to its metabolic effects including hypertension, osteoporosis, obesity, dyslipidemia, osteoporosis and glucose intolerance. Although primary therapy is surgical, a substantial portion of patients will go on to require second-line therapies including repeat surgery, radiotherapy or drug therapy. While medical therapy for Cushing's syndrome has been limited, several new agents are being investigated. This aim of this review is to analyze and present the available options for medical management of Cushing's syndrome as well as review potential new therapies and their role in the treatment of this disorder.

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