Uncontrolled Hypothyroidism Research Articles

Knowledge, Attitudes, Beliefs, and Treatment Burden Related to the Use of Levothyroxine in Hypothyroid Pregnant Women in the United States.

Background: The use of prescribed medications during pregnancy is a challenge and an underestimated source of treatment burden. Levothyroxine (LT4) for the treatment of overt and subclinical hypothyroidism is extensively prescribed during pregnancy. To this end, we aimed to explore the patients' perceived benefits and risks, knowledge, beliefs, attitudes, and related burden of LT4 therapy during pregnancy. Methods: In this cross-sectional study, we surveyed pregnant women who were treated with LT4 during pregnancy from January 1, 2019, to December 31, 2019, in a tertiary academic medical center of the United States. The anonymous online survey included questions to gather demographic data and multiple-choice questions regarding the benefits and risks, knowledge, beliefs, attitudes, and burden related to LT4 use during pregnancy. Results: Sixty-four pregnant women (mean age 31.5 years) completed the study survey (response rate: 96%): 62% were diagnosed with hypothyroidism more than 12 months before pregnancy, 16% less than or about 12 months before pregnancy, and 22% during pregnancy. We found that one-third of pregnant women using LT4 had a feeling of uneasiness/anxiety due to their hypothyroidism diagnosis. About half of the respondents (45%) reported that they did not receive an explanation by their clinician regarding the maternal/fetal risks of uncontrolled hypothyroidism or the benefits of adequate control. Finally, two in three patients expressed various concerns of LT4-related treatment burden. Conclusions: Our findings support the need for increased effective communication and tailored counseling to address fears, anxiety, and uncertainties about the benefits and risks of LT4 use in pregnancy. For patients with clear benefits from LT4 treatment in pregnancy, it could help to overcome their concerns, promote adherence, and decrease adverse maternal/fetal outcomes. For patients with no clear benefits established, clinicians need to be aware of LT4-related treatment burden in pregnancy and implement patient-centered approaches in their clinical practices.

SUN-281 Pituitary Hyperplasia Secondary to Uncontrolled Primary Hypothyroidism

Background: There are several recognized causes of hyperplasia of the pituitary gland. These may present as sellar masses and be misdiagnosed as pituitary adenomas. Pituitary hyperplasia can occur in the presence of long standing primary hypothyroidism due to the loss of negative feedback caused by decreased secretion of thyroxine (T4) and triiodothyronine (T3) by the thyroid gland, leading to excessive thyrotropin releasing hormone (TRH) production by the hypothalamus causing Thyrotroph pituitary hyperplasia Clinical case: 51 y/o female with a past medical history that includes anxiety & depression, obesity, pre-diabetes and uncontrolled hypothyroidism due to Hashimoto’s, presented to the Endocrinology clinic for recent diagnosis of pituitary macroadenoma. Patient reported tiredness, decrease energy, myalgias, weight gain, abnormal menstrual periods and frontal headaches. On physical exam, she had a body mass index of 37.39kg/m2, blood pressure of 130/85mmHg, heart rate of 91 bpm. There was no thyromegaly noted on exam. No abdominal striae was noted. Overall, exam was unremarkable. Her neurological exam was normal and there were no obvious visual field deficits. Initial laboratory tests revealed a thyroid stimulating hormone (TSH) >150 uIU/mL (0.46–4.7 uIU/mL), free T4 0.3 ng/dL (0.7–1.3 ng/dL) and positive TPO antibodies. Other endocrine work up including ACTH, cortisol, prolactin, FSH, LH and IGF-1, were normal. An MRI of the pituitary revealed a heterogeneous enhancing mass replacing the pituitary gland in the sella that measured 16 x 17 x 11 mm. She was evaluated by Neurosurgery, for presumed diagnosis of pituitary macroadenoma. However, prompt recognition of uncontrolled primary hypothyroidism causing pituitary hyperplasia lead to medical management, first. She was started on weight based (1.6mcg/kg/day) levothyroxine at 175 mcg per day. Six weeks after thyroid replacement therapy laboratory evaluation showed improvement in thyroid function test with a TSH of 0.8mIU/mL, free T4 2.8ng/dL and total T3 307ng/dL. A repeat MRI of the pituitary showed decrease in size of the pituitary gland measuring 15 x 4 x 10 mm. Conclusion: This case illustrates the importance of early recognition of uncontrolled primary hypothyroidism during the evaluation of a pituitary mass. Complete regression of this pituitary gland abnormality can be achieved with thyroid hormone replacement avoiding the irreversible consequences of inappropriate pituitary surgery.

SAT-480 Myxedema Madness: A Rare Case of Severe Hypothyroidism Presenting as Psychosis

IntroductionMyxedema coma is a rare, life-threatening medical emergency resulting from uncontrolled hypothyroidism. Myxedema coma refers to the neurological sequelae of severe hypothyroidism, which classically manifests as depressed mental status. Rarely, myxedema coma can present with a hyperactive mental state and psychosis. We present an unusual case of a drug overdose secondary to myxedema coma-induced psychosis.Clinical CaseA 48 year old woman with a history of seizure disorder and hypothyroidism presented to the hospital after lamotrigine overdose. The patient’s spouse witnessed her ingest forty-five tablets of lamotrigine after an argument. The patient had no previous psychiatric diagnoses or suicide attempts. On examination, the patient was hemodynamically stable but was agitated, disoriented, and uncooperative. She had a normal neurologic exam and no peripheral edema. Her lamotrigine level was 25.4 ug/ml (2.5-15.0 ug/ml). The patient’s mental status did not improve with lamotrigine cessation. Psychiatry determined that the patient’s psychosis was not consistent with lamotrigine overdose. Given these recommendations, alternative causes of psychosis were considered. The patient’s husband stated she had not taken levothyroxine for over one year. Thyroid function tests revealed a thyroid stimulating hormone (TSH) of 299 mcIU/ml (0.35-5.50 mcIU/ml) with a free thyroxine (T4) level of 0.27 ng/dl (0.89-1.76 ng/gl). The patient was started on levothyroxine intravenously. After five doses of intravenous levothyroxine, her mental status improved to baseline and she was transitioned to oral levothyroxine. She denied that the lamotrigine ingestion was a suicide attempt. Based on the patient’s presentation and clinical course, we concluded that her overdose was due to severe hypothyroidism leading to myxedema madness.ConclusionSevere hypothyroidism with myxedema coma often presents with depressed mental status, which can manifest as progressive confusion, lethargy, and eventually coma. However, in the case of our patient, severe hypothyroidism presented as psychosis, a rare manifestation. Remarkably, the patient had no other obvious physical manifestations of severe hypothyroidism. Psychosis, though rare, has been seen in cases typically after thyroidectomy or in patients with previously undiagnosed Hashimoto’s thyroiditis. In this patient’s case, it is likely that her myxedema madness was precipitated by long-term nonadherence with her thyroid replacement therapy, as the patient had no prior psychiatric history. Additionally, her rapid reversal of symptoms after the administration of levothyroxine supports the diagnosis of hypothyroid-induced myxedema madness.

SAT-479 Atypical Presentation of Recurrent Cardiac Tamponade Following Pericardial Window in the Setting of Uncontrolled Hypothyroidism

INTRODUCTION:Classically, cardiac tamponade presents with hypotension, distant heart sounds and tachycardia (Beck’s triad). Pericardial window is considered effective treatment. Pericardial effusions are relatively common in hypothyroidism (3-6%) (1). Cardiac tamponade, however, is rarely seen in patients with hypothyroidism secondary to pericardial distensibility and the slow accumulation of fluid, allowing significant fluid accumulation without hemodynamic compromise (2).CLINICAL CASE:A 84 year-old female with history of post-surgical hypothyroidism (on levothyroxine 150 mcg) following total thyroidectomy for thyroid cancer, cardiac tamponade requiring pericardial window formation two years prior, presented for dyspnea on exertion and pedal edema for several days. She was tachypneic to 22/min with heart rate 47/min and blood pressure 92/62. Distant heart sounds were noted on exam.EKG demonstrated sinus bradycardia, low voltage QRS and T wave flattening. Further workup revealed TSH elevated to 44 uIU/mL (N:0.27–4.2 uIU/mL), free T4 0.17 ng/dl (N:0.93-1.7 ng/dl) and undetectable T3 (N: 80-100 ng/dl). Echocardiogram unexpectedly demonstrated a large circumferential pericardial effusion with diastolic collapse of the right atrial, right ventricular free wall, significant respiratory variations and interventricular dependence. These findings were consistent with cardiac tamponade physiology. She underwent a video assisted left thoracotomy pericardial window formation along with drainage of 400cc of yellow pericardial fluid. Fluid cytology and tissue histopathology were negative for malignancy. Her uncontrolled hypothyroidism was considered the cause for recurrence of cardiac tamponade and her levothyroxine dose was increased to 175 mcg. At two week follow up, she reported symptomatic improvement on the higher levothyroxine dose. Echocardiogram did not show reaccumulation of fluid.CONCLUSIONS:Sinus tachycardia is found in most patients with cardiac tamponade, except in hypothyroid patients (2). A high degree of suspicion is needed to diagnose cardiac tamponade in hypothyroidism, even in patients who have undergone presumed definitive therapy with a pericardial window in the past. The recent onset of pedal edema and low blood pressure were important indicators of impending cardiac compromise in our patient.Hypothyroid patients may be at higher risk of pericardial window failure compared to patients with cardiac tamponade of other etiologies, especially if thyroid replacement therapy is inadequate. The scientific literature is lacking in this regard and warrants further investigation.

SAT-467 A Case of Pituitary Hyperplasia Secondary to Uncontrolled Primary Hypothyroidism

17 year old female presented for evaluation of galactorrhea of 3 months duration. Patient was diagnosed with papillary thyroid cancer and underwent total thyroidectomy in 2011. She was prescribed Synthroid 175 mcg but was not compliant with taking her medicine. In April 2019 she developed bilateral galactorrhea for which she was evaluated at an outside facility and was found to have a prolactin 143.7ng/mL (n 7.2-63) and TSH 996 mIU/L (n 0.5 -4.0). Pituitary MRI revealed pituitary macroadenoma measuring 1.5 x 1.4 x 1.2 cm with slight elevation of the optic chiasm and infundibulum. She was advised to restart Synthroid and was referred for the neurosurgery team at our facility for surgical resection of pituitary macroadenoma. Over the same period of time, she gained 25 lbs, developed headaches, excessive fatigue, constipation, hair loss, lower extremity swelling, and puffiness of her face. Her menstrual cycles were regular but this was only after she was placed on norelgestromin/ ethinyl estradiol transdermal patch. She denied visual changes. By the time she was seen at our clinic in June 2019, she was taking Synthroid daily for 1 month. TSH decreased to 1.0 mIU/L and prolactin improved to 68 ng/mL. IGF-1 was low at 98 ng/mL (n 149-509). ACTH, morning cortisol, and 24 hour urine free cortisol were within reference range. Visual field testing showed no visual defects. We advised patient to continue taking Synthroid and to follow up in 1 month. On the follow up visit in July 2019, TSH was 0.2 mIU/L, prolactin was 52 ng/mL and IGF-1 was 105 ng/mL. Pituitary MRI showed pituitary hyperplasia that has decreased compared to previous MRI, now measuring around 1 cm at the largest dimension without contact with the optic chiasm and the Infundibulum was at midline. Galactorrhea and headaches resolved and fatigue significantly improved.

SAT-520 Unusual Case of Hypothyroidism Possibly Due to Dialysis Leading to Van Wyk Grumbach Syndrome (VWGS)

BACKGROUND: Van Wyk Grumbach Syndrome (VWGS) is characterized by precocious central puberty in the setting of juvenile chronic primary hypothyroidism with symptom regression following thyroxine replacement. Clinical Case: A 2 year old girl with dysplastic kidneys and chronic renal disease had been treated by her nephrologist with growth hormone for poor growth. She was referred to Endocrinology for evaluation of bloody dialysate thought to be retrograde menstrual flow. Pelvic US showed bilateral large cystic adnexae possibly ovarian cysts versus septated collections of dialysate fluid. Hormone measurements showed pubertal levels of LH 0.4mIU/mL and FSH 5.4mIU/mL, with a relatively low Estradiol 5.3pg/mL. Brain MRI showed impressive pituitary enlargement measuring 1.3cm craniocaudally. Additional laboratory testing was notable for a low normal free T4 fT4 0.9ng/dL and markedly elevated TSH>1000uIU/mL and Prolactin 835ng/mL. Thyroid US showed thyroid enlargement, and echogenic and hyper vascular gland. Anti-thyroid antibodies titers were normal, AM cortisol and IGF1 were also normal for age. We speculate that this case of profound hypothyroidism was due to dialysis, as thyroid function improved after the child underwent renal transplantation. Levothyroxine was discontinued 5 months after renal transplantation. Elevated TSH may induce a form of pseudopuberty as the TSH alpha subunit is similar to that of LH and binds to the LH receptor to stimulate the ovaries with cyst formation. Conclusion: In VWGS, primary hypothyroidism with elevated TSH induces central precocious puberty. This child’s bloody diasylate was likely the result of transient central precocious puberty associated with uncontrolled primary hypothyroidism with elevated TSH and prolactin. Although the literature on dialysis suggests minimal thyroid hormone losses, this case shows the importance of monitoring thyroid hormones in dialysis patients. Early recognition of VWGS and initiation of thyroid hormone replacement can lead to resolution of symptoms.

SUN-290 Pituitary Hyperplasia Due to Uncontrolled Primary Hypothyroidism: Case Series and Literature Review

Background: Pituitary hyperplasia secondary to primary hypothyroidism results from the loss of thyroxine feedback inhibition and the subsequent overproduction of TSH. Case 1: A 18-year-old female presented with a chronic history of spontaneous galactorrhea, headache and malaise. Autoimmune primary hypothyroidism was diagnosed, with elevated TSH of 490 mIU/L (0.3-5) and low fT4 of 0.33 ng/dL (0.63-1.34). Pituitary MRI showed an enlarged pituitary with compression of the optic chiasm. Hormonal replacement with levothyroxine 75 mcg qd was started. Five months later she was asymptomatic, and normal TSH (1.64 mIU/L) and fT4 (0.9 ng/dL) levels. A new MRI revealed normal size of pituitary gland, with no compression of the optic chiasm and an intact infundibulum. Case 2: A 24-year-old female with type 1 diabetes and autoimmune primary hypothyroidism, presented with a five-year history of galactorrhea and oligomenorrhea. She was treated with insulin glargine 20U qd, and levothyroxine 200 mcg/day. However, patient’s adherence was bad. She consulted a primary health physician who suspected a prolactinoma after high prolactin levels (77.65, normal 2.64-13.13 ng/mL). Cabergoline was started without any clinical improvement. She then was referred to our service for follow-up. TSH results showed 500 mIU/L, with low fT4 (0.08 ng/dL). Prolactin levels was normal. Pituitary MRI revealed diffuse enlargement of the gland, with compression of infundibulum and optic chiasm. Treatment was modified to levothyroxine/liothyronine 100/20mcg 1 ½ tablet qd. After 7 months, we confirmed normal TSH (0.76 mIU/L) and fT4 (1.23 ng/dL), and the patient was asymptomatic. After 17 months, new MRI showed normal pituitary gland without any compression. Case 3: A 23-year-old female with a history of Addison′s disease and hypothyroidism diagnosed at age 17 presented with a 6-month history of somnolence, fatigue, headache and amenorrhea. She was previously treated with hydrocortisone 25mg/day, fludrocortisone 0.1mg/day, and levothyroxine 200mcg/day. Patient’s adherence was bad, and multiple hospitalizations because of adrenal crises were reported. Her initial hormonal evaluation revealed high TSH of 460 mIU/L and low fT4 of 0.25 ng/dL, mild hyperprolactinemia (32.16 ng/mL), and very high ACTH levels (2,700 pg/mL, normal 10-100). Pituitary MRI revealed an enlarged pituitary with mild compression of the optic chiasm. Hormonal replacement was modified to fasting levothyroxine alternating 200mcg and 300mcg qd. Her last follow-up showed normal TSH (0.53 mIU/L) and fT4 (1.18 ng/dL) levels. New MRI showed normal pituitary size Conclusion: We presented three young women, with autoimmune hypothyroidism, who developed pituitary hyperplasia and responded to proper hormonal replacement normalizing pituitary size. Reference: Endocrinol Diabetes Metab Case Rep. 2015; 2015: 150056.

Management of Hypothyroidism in Patients with Acute Myocardial Infarction.

Background and Objectives: Thyroid hormones (TH) affect cardiac function through effects on cardiac contractility and systemic vascular resistance. While TH replacement for patients with hypothyroidism might be necessary for restoration of cardiac output after an acute myocardial infarction (AMI), it could theoretically lead to excessively rapid restoration of the metabolic rate. The appropriate management of hypothyroidism in patients with AMI is unknown. We describe the practice patterns in the management of hypothyroidism in the setting of AMI as well as patients’ clinical outcomes. Material and Methods: Retrospective study of patients that were admitted to a tertiary care hospital with AMI and newly diagnosed or uncontrolled hypothyroidism (TSH ≥ 10 mIU/L) between 2011–2018. Eligible patients were identified using diagnosis codes for AMI and laboratory values, followed by medical record review. We categorized patients according to treatment status with TH and by degree of hypothyroidism. Clinical outcomes included: 30-day mortality/readmission, bleeding, stroke, arrhythmia, sudden cardiac death, and new or worsening heart failure. Summary statistics and group comparisons are presented. Results: Sixty-four patients were included, their median age was 64 years and 61% (n = 39) were women. Most of the patients (59%) had a documented history of hypothyroidism. Of these, all were restarted on levothyroxine (LT4) during the index admission when compared to patients without a history of hypothyroidism, of which 54% received LT4 treatment (p = 0.001). The median TSH in those treated with LT4 was higher (25 mIU/L) when compared to those who were not (12 mIU/L), (p = 0.007). Patients who received intravenous LT4 had higher TSH levels and other variables suggesting worse clinical presentation, but these differences were not statistically significant. No statistically significant differences were noted on clinical outcomes according to LT4 treatment status. Conclusion: A history of hypothyroidism and the degree of TSH elevation seem to guide the management of hypothyroidism in patients with AMI. The clinical effect of correcting hypothyroidism in this setting requires further evaluation.

A Novel Conception Towards Effect of Preconception Hypothyroidism and First Diagnosed Hypothyroidism During Pregnancy on Offspring's Neurocognitive Function: Evidence from a Prospective, Cohort Study in China

Background: Hypothyroidism during pregnancy is associated with offspring’s neurodevelopment. Current prenatal screening is not effective, and hypothyroidism screening before conception is expected to be beneficial for improving offspring’s neurocognitive development. This study was to evaluate offspring’s neurocognitive development and pregnancy outcomes among women with hypothyroidism before conception and firstly diagnosed in early pregnancy. Method: In this prospective cohort study, women with hypothyroidism before 14 gestational week were recruited in Obstetrics and Gynecology Hospital of Fudan University. They were assigned into preconception controlled hypothyroidism, preconception uncontrolled hypothyroidism and hypothyroidism firstly diagnosed in early pregnancy based on their history of hypothyroidism before pregnancy and thyroid stimulating hormone (TSH) at first antenatal visit. Their general characteristics and pregnancy outcome were recorded. Gesell development diagnosis scale (GDDS) was applied for the evaluation of offspring’s neurocognitive function at six-month and one-year old. Results: During January 2012-December 2013, 295 women were firstly diagnosed during pregnancy (TSH≥3.61mIU/L), and 78 women with hypothyroidism controlled (TSH<2.5mIU/L) and 107 with uncontrolled thyroid function (TSH≥2.5mIU/L). Full-scale quotation of Gesell scale in clinical hypothyroidism group was of no statistical difference compared to that of subclinical hypothyroidism (P=0.309). In offspring’s Gesell assessment at six-month old, children in controlled hypothyroidism group performed a better adaptive ability compared to those firstly diagnosed during pregnancy (104.45±13.93 vs 99.38±17.71, P=0.022). At one-year old, children in preconception uncontrolled group performed inferior to those those firstly diagnosed during pregnancy, in the GDDS full-scale DQ (100.61±5.96 vs 105.14±7.40, P=0.001), and fine motor, adaptability, language and social emotional response category. Conclusions: Maternal hypothyroidism before conception and during pregnancy possibly shares different effect on offspring’s neurodevelopment. Impaired offspring’s neurocognitive function suggested the necessity of preconception hypothyroidism screening and close follow up of offspring’s neurodevelopment in early infancy. Trial Registration: The registered ClinicalTrials ID was NCT01744743. Funding Statement: This study was funded by the grants from Health industry special funds for Public Benefit Research Foundation from the Ministry of Health, People's Republic of China (201002013), the National Science Fund of China (81270712), National Science Foundation for Young Scholars of China (81200449), National Science Foundation for Young Scholars of China (81300506), National Key Basic Research Plan of China (973 Plan) (2010CB529500), National Science Foundation for Young Scholars of Shanghai (13ZR1452000), the Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, and the Key Specialty Project of the Ministry of Health, People's Republic of China. Declaration of Interests: The authors report no conflict of interest. Ethics Approval Statement: The study was reviewed and approved by the Ethics and Research Committee of Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China. All the women have signed the consent.

1631 A Rare Case of Myxedema Ascites and Ischemic Colitis

INTRODUCTION: Myxedema is a severe form of hypothyroidism with various signs and symptoms. We present a rare case of myxedema ascites complicated with ischemic colitis (IC). CASE DESCRIPTION/METHODS: A 71-year-old female with a history of coronary artery disease and congestive heart failure (Ejective fraction 40%) presented with abdominal distention. Pertinent vitals included blood pressure of 100/54 mmHg and heart rate 38 beats/min. Pertinent labs included hematocrit of 28.2 %, albumin 3.1 g/dL, transaminases mildly elevated, alkaline phosphatase (ALP) 382 IU/L, thyroid stimulating hormone (TSH) 141 IU/mL, free triiodothyronine (T3) 1.26 pg/ml, total T3 45.30 ng/dL. Rest of the electrolytes, blood counts, including coagulation parameters, were normal. Electrocardiogram showed sinus bradycardia. She was started on levothyroxine for severe hypothyroidism. Abdominal ultrasound showed a large volume of ascites and normal liver contour. Paracentesis showed total nucleated cells of 2242, total protein 3.6 g/dL, lactate dehydrogenase 229, albumin 1.8 g/dL, serum ascites albumin gradient (SAAG) &lt; 1.1, and glucose 86 mg/dL. Ascitic fluid cultures were negative. Hence, the patient was diagnosed with neutrocytic ascites and treated with empiric antibiotics. Ascitic fluid was negative for malignancy and tuberculosis. She was managed with diuretics (furosemide and spironolactone) and therapeutic paracentesis. She later developed bloody diarrhea, and flexible sigmoidoscopy showed mild to moderate IC of the rectosigmoid colon. She was treated conservatively. Her transaminases normalized, but ALP remained elevated. She was discharged after a two-week hospital stay and six weeks follow up showed significant improvement in ascites and TSH of 10 IU/mL. DISCUSSION: Myxedema ascites is seen in only 4% of the patients with uncontrolled hypothyroidism. There are no case reports on IC in the setting of myxedema ascites thus far. It is a rare complication of myxedema megacolon; however, our patient had no signs of megacolon on repeated imaging. Therefore, our case is unique as it highlights a rare (ascites) and uncommon (IC) complication of severe hypothyroidism. Ascites with SAAG &lt; 1.1 should prompt physicians to consider hypothyroidism in the differential diagnosis for ascites especially when total ascitic fluid protein is &gt; 2.5 g/dL and other causes such as portal hypertension, malignancy, and infections are ruled out. It is easy to treat, can lead to complete resolution of ascites and decrease morbidity.

CARDIAC TAMPONADE: A RARE MANIFESTATION OF MYXEDEMA COMA

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Myedema coma is a medical emergency requiring prompt recognition and appropriate treatment. This condition often results from uncontrolled long-standing hypothyroidism or triggered by an acute event such as a myocardial infarction, infection, or a variety of systemic illnesses. Symptomology can affect a broad range of systems, including but not limited to hypotension, hypothermia, hypoglycemia, altered mental status, and hyponatremia. In this case report we discuss a case of an unstable patient with myxedema coma presenting with paranoid delusions and cardiac tamponade. CASE PRESENTATION: 66 year old Ethiopian female with hypothyroidism and chronic lymphedema, noncompliant with levothyroxine, presented to the hospital via EMS, due to altered mental status, paranoid outbursts, and a subacute history of visual and auditory hallucinations. Review of symptoms were unable to be obtained due to paranoid delusions and nonsensical speech. Physical exam revealed a temperature of 90.5 degrees Fahrenheit, blood pressure of 64/43mmhg, heart rate of 56 bpm, and she was on three liters nasal canula oxygen. A thyroid goiter, distal heart sounds and pretibial myxedema were present on exam. TSH was 20.26 and free T4 was undetectable. WBC count was 2.5, sodium 135mmol/L, blood glucose 80, with normal renal function. Urine drug screen was negative. Chest x-ray showed an enlarged cardiac silhouette, and an echocardiogram revealed cardiac tamponade. She underwent an emergent pericardiocentesis with removal of more than 1300mL of transudative fluid. She was diagnosed with myxedema coma and treated with IV levothyroxine, liothyronine and hydrocortisone. TSH normalized and the patient was transitioned into oral levothyroxine. Mental status, hemodynamics, and metabolic derangements resolved, and the patient was subsequently discharged with close outpatient follow up. DISCUSSION: The thyroid gland is intimately involved in the regulation of metabolic and physiologic demands of the living organism. An imbalance could potentially lead to catastrophic multisystem collapse. Myxedema coma is a rare manifestation of hypothyroidism with only 0.1% prevalence (1). Patients present with neuropsychiatric manifestations, hypothermia, cardiovascular collapse and multiorgan failure (1,2). The severity of hypothermia is proportionally related to the risk of mortality. CONCLUSIONS: Cardiac tamponade is a rare cardiac manifestation of hypothyroidism, however prompt recognition, urgent pericardiocentesis, and thyroid hormone replacement therapy are critical in preventing pericardial fluid accumulation and reduction in mortality (2-4). Reference #1: Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, Mukhopadhyay S, Chowdhury S. Myxedema coma: a new look into an old crisis. J Thyroid Res. 2011;2011:493462. Reference #2: Kabadi UM, Kumar SP. Pericardial effusion in primary hypothyroidism. Am Heart J. 1990;120(6 Pt 1):1393–1395 Reference #3: Patil VC, Patil HV, Agrawal V, Patil S. Cardiac tamponade in a patient with primary hypothyroidism. Indian J Endocrinol Metab. 2011;15(Suppl 2):S144–S146. DISCLOSURES: No relevant relationships by Shoheb Ali, source=Web Response No relevant relationships by Rupesh Dave, source=Web Response No relevant relationships by Joshua Lovelock, source=Web Response No relevant relationships by Arish Maknojia, source=Web Response No relevant relationships by mustaf shariff, source=Web Response

OR19-3 Utility of the Levothyroxine Absorption Test: The Mayo Clinic Experience

Introduction: While hormone replacement with levothyroxine (LT4) is the most effective management for hypothyroidism, there is a subset of patients who remain hypothyroid despite high doses of LT4. These patients warrant evaluation for conditions that may contribute to poor LT4 absorption. Several case reports have documented a condition known as LT4 pseudomalabsorption, a factitious disorder in which overt hypothyroidism persists despite endorsed medication adherence and absent evidence for gastrointestinal malabsorption. LT4 absorption testing (LT4AT) is a non-invasive method for effectively distinguishing malabsorption from pseudomalabsorption. Given the lack of standardization of this test and the morbidity associated with uncontrolled hypothyroidism, we reviewed our institution’s experience with LT4AT and investigated the impact of this test on long-term management in patients with primary refractory hypothyroidism. Methods: We conducted chart reviews between 2015 to 2018 for patients who had undergone LT4AT at our institution for primary refractory hypothyroidism. Pertinent information collected included medications known to interfere with LT4 absorption or metabolism, adherence and timing of ingestion in relation to food intake, and comorbidities including celiac disease, heart failure, nephrotic syndrome, cirrhosis, gastritis, or short bowel syndrome. Our LT4AT protocol involves observed administration of LT4 dosed according to age and BMI (600mcg, 1000mcg, or 1500mcg). Total thyroxine is measured at baseline, 1 hour, 2 hours, 3 hours, 4 hours, and 6 hours. TSH is measured at baseline and at 6 hours. Percent LT4 absorption is calculated using the following formula: [[Increment TT4 (mcg/dL) x 10] / total administered LT4 (mcg)]] x Vd (L) x100. Absorption of >60% is considered normal. Results: Fifteen patients completed LT4AT during the search period, and 14 demonstrated normal absorption. One patient had virtually no LT4 absorption and was diagnosed with atrophic gastritis. Ten patients had follow up ranging from 2 months to 2 years. Three achieved normal TSH values within one year, 5 demonstrated improvement, but had yet to achieve TSH normalization, and 2 remained poorly controlled. Direct observation of LT4 administration was performed in 2 patients, both of whom achieved a normal TSH at 3 and 7 months, respectively. Conclusions: Our review confirms the utility of LT4AT for differentiating pseudomalabsorption from gastrointestinal malabsorption. Most of our patients had improvement in thyroid function during follow up, contending that performance of this test may enhance compliance by establishing an objective framework from which both clinicians and patients can work to develop effective, long-term management strategies.

Abstract #648 Uncontrolled Hypothyroidism Presenting as Myxedema Ascitesa Case Report

Abstract #648 Uncontrolled Hypothyroidism Presenting as Myxedema Ascitesa Case Report

Vitamin D Status in Primary Hypothyroid Subjects Attending a Specialized Endocrine Center of Bangladesh

Background: Association between vitamin D deficiency and hypothyroidism has been reported by many authors though the study results are mixed. Objective: The study was conducted to observe vitamin D status among primary hypothyroid subjects. Materials/Methods: In this single-center cross-sectional study, 356 subjects with primary hypothyroidism (either new or previously diagnosed) were evaluated for serum thyroid stimulating hormone (TSH) and 25(OH) vitamin D levels. 25(OH)D levels were classified as normal (≥30 ng/ml), insufficient (>20 to 29.9 ng/ml), and deficient (≤20 ng/ml). Results: The mean age of the study subjects was 36.33 (±12.44) years; majority of them were female (89.9%), homemaker (79.8%), residing in urban or suburban areas (64%), and literate (85.7%); almost half (48%) of them were obese. Their median TSH was 6.17 μIU/ml and mean 25(OH)D was 25.16 (±12.18) ng/ml. The frequencies of vitamin D deficiency and insufficiency were 39.6% and 34.3% respectively. No statistical differences were observed in 25(OH)D levels between males and females, obese and non-obese, new cases and previously diagnosed cases, new cases with subclinical and overt hypothyroidism, the previously diagnosed cases with controlled and uncontrolled hypothyroidism, and among subjects living in urban, suburban and rural areas. Serum 25(OH) vitamin D level showed no correlations with age, body mass index (BMI) and TSH levels of the study subjects. Conclusion: The observed frequency of hypovitaminosis D (deficiency and insufficiency) was high (73.9%) in primary hypothyroid subjects from Bangladesh.

Elevated triglycerides: A matter of the heart and pancreas

Mild-to-moderate hypertriglyceridaemia (triglyceride (TG) &gt;1.7 - 10.0 mmol/L) is an independent cardiovascular risk factor, while severe hypertriglyceridaemia (TG &gt;10.0 mmol/L) can cause acute pancreatitis. Hypertriglyceridaemia is polygenic in most patients, and secondary factors, such as uncontrolled diabetes, hypothyroidism, alcohol, renal disease and medication (e.g. corticosteroids, retinoids, oestrogen), often play an important role in precipitating or exacerbating the condition. Patients with mild-to-moderate hypertriglyceridaemia require cardiovascular risk assessment and are in the first instance treated with statins if their cardiovascular risk is high. Control of secondary factors and lifestyle modifications are important in managing residual hypertriglyceridaemia in patients treated with statins. Multiple trials are ongoing to determine whether there is further cardiovascular outcome benefit from adding drugs such as fibrates or omega-3 supplements to the regimen of patients who are receiving statins. Severe hypertriglyceridaemia is managed by removing or controlling secondary factors, following a very low-fat diet and prescribing a fibrate.

Elevated triglycerides: A matter of the heart and pancreas

Mild-to-moderate hypertriglyceridaemia (triglyceride (TG) >1.7 - 10.0 mmol/L) is an independent cardiovascular risk factor, while severe hypertriglyceridaemia (TG >10.0 mmol/L) can cause acute pancreatitis. Hypertriglyceridaemia is polygenic in most patients, and secondary factors, such as uncontrolled diabetes, hypothyroidism, alcohol, renal disease and medication (e.g. corticosteroids, retinoids, oestrogen), often play an important role in precipitating or exacerbating the condition. Patients with mild-to-moderate hypertriglyceridaemia require cardiovascular risk assessment and are in the first instance treated with statins if their cardiovascular risk is high. Control of secondary factors and lifestyle modifications are important in managing residual hypertriglyceridaemia in patients treated with statins. Multiple trials are ongoing to determine whether there is further cardiovascular outcome benefit from adding drugs such as fibrates or omega-3 supplements to the regimen of patients who are receiving statins. Severe hypertriglyceridaemia is managed by removing or controlling secondary factors, following a very low-fat diet and prescribing a fibrate.

An Unusual Cause of Completely Reversed Complete Heart Block “Uncontrolled Hypothyroidism”

An Unusual Cause of Completely Reversed Complete Heart Block “Uncontrolled Hypothyroidism”

Developmental milestones at one year for the offspring of mothers with congenital hypothyroidism: a population-based study

Maternal thyroid dysfunction during pregnancy is associated with neurodevelopmental impairment in the offspring. No data are currently available for the offspring of patients treated early for congenital hypothyroidism (CH). The aim of this study was to investigate motor and language milestones at one year of age in a population-based registry of children born to young women with CH. We assessed 110 children born to mothers with CH, and 1367 children from the EDEN French population-based birth cohort study prospectively, at the age of one year, with identical questionnaires. Outcomes were assessed in terms of scores for childhood developmental milestones relating to mobility, motor coordination, communication, motricity and language skills. After adjustment for confounding factors, children born to mothers with CH were found to have a higher risk of poor motor coordination than those of the EDEN cohort (OR: 4.18, 95% CI: 2.52-6.93). No differences were identified for the other four domains investigated. Children born to mothers with gestational diabetes have a higher risk of low motor coordination score than their peers (OR: 2.10, 95% CI: 1.21-3.66). Children born to mothers with TSH ≥ 10 IU/L during the first six months of pregnancy were more likely to have low motricity or communication skills scores than those born to mothers with lower TSH concentrations (56% vs 21% for each score, P < 0.04). Maternal CH may have slight adverse effects on some developmental milestones in the child at one year of age, particularly for children born to mothers with uncontrolled hypothyroidism. However, it remains unclear whether these adverse effects modify subsequent neurodevelopment.

Rhabdomyolysis in a patient with chronic uncontrolled diabetes mellitus and hypothyroidism

Rhabdomyolysis is a syndrome characterised by muscle necrosis and dispersing its intracellular content in the circulation. Clinical symptoms are usually presented by muscle pain and muscle weakness. Rhabdomyolysis could be produced, among other causes, by diabetic ketoacidosis and hypothyroidism. We report a case of a 36 years old female patient who was admitted to the medical intensive care unit (MICU) because of rhabdomyolysis. At her admission we found compensated diabetic ketoacidosis with normal serum osmolarity and mild hypothyroidism. The patient was treated by rehydration, urine alkalinisation, forced augmentation of diuresis, correction of blood glucose levels, and levothyroxine substitution therapy. After 17 days, she was completely recovered and discharged home. We believe that rhabdomyolysis in our patient developed as a summary of two important factors, uncontrolled diabetes mellitus and hypothyroidism. Hypothyroidism, possibly fueled by bad regulate diabetes, may amplify the symptoms. Each considered factor separately may not be cause a muscle breakdown, but their combination can lead to serious and severe clinical symptoms associated with high levels of creatine kinase (CK) enzyme.

Prevalence of Metabolic Syndrome among Patients with Hypothyroidism

Background: hypothyroidism is of concern in our society; it has an effect on metabolic parameters. Objective: this study aimed to predict the prevalence of metabolic syndrome (MetS) among patients with hypothyroidism in Jeddah, Saudi Arabia and to determine the effect of treating hypothyroidism on MetS. Methods: we conducted this cross-sectional study, in which MetS was defined by presence of at least three of the five AHA/NHLBI criteria. We included patients with hypothyroidism that were managed in an outpatient department or admitted in King Abdulaziz University Hospital from 1 March to 30 April 2016. We measured lipid parameters, blood pressure (BP), waist circumference (WC) and serum fasting blood glucose (FBG). Results: in total 57 patients were included in our study, of which 47 (82%) were females. the majority of patients were greater than 50 years of age (n=35, 60%). We found that 36.8% of patients uncontrolled for hypothyroidism had high levels of TSH (serum level of TSH >5 mlu/L) , while 64.9% of patients who were controlled for hypothyroidism had normal levels of TSH (serum level of TSH 0.5 - 5 mlu/L). Overall, 71.9% (n=41) of hypothyroidism patients had MetS. However, we found that 51.8% (n=21) uncontrolled hypothyroidism patients suffered from MetS and 48.2% (n= 20) patients controlled for hypothyroidism suffered from MetS. However, 70.68 %, 31.03%, 34.48%, 79.31% and 70.6% of participants had abnormal waist circumference (WC), hypertriglyceridemia, abnormal high-density lipoprotein (HDL), hypertension and elevated serum levels of fasting blood sugar, respectively Conclusion: hypothyroidism plays an important role in MetS. Future advanced studies including larger numbers of patients are needed to test the effect of treating hypothyroidism on MetS. Routine screening for cardiovascular risk factors in patients with hypothyroidism may unmask MetS.