ResearchPad - thyroid-disorders-case-reports-i Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[SUN-516 Unplanned Pregnancy Post Thyroid RAI Ablation]]> A patient’s pregnancy and fetus are at an increased risk for complications secondary to history of recent RAI ablation and maternal secondary hypothyroidism.

A 31 year old female with a recent history of miscarriage presented with abnormal thyroid function tests and was history of low dose levothyroxine use. She complained of a 3 month history of extreme fatigue, palpitations and 18 pound weight loss at the time of presentation. Her thyroid stimulating immunoglobulin was 9.21 IU/L (0-0.55), free thyroxine 6.2ng/dL (0.9-1.8), free triiodothyronine 20.04 pg/mL (1.8-4.6) with a suppressed TSH 0.01 uIU/ml (0.27 - 4.2). She was started on methimazole. Her 24 hour radioactive iodine uptake was 60% and she subsequently underwent radioactive iodine-131 ablation in capsule form. She failed the ablation after 7 months and remained on methimazole during that duration. Her second radioactive iodine uptake was 58% and she underwent a second RAI ablation. Her TSH was 50 uIU/ml and her free thyroxine was 0.1 ng/dl. She was started on levothyroxine for replacement. Patient unexpectedly became pregnant approximately six weeks after her radioactive iodine treatment.

Studies have shown that with the exception of miscarriages, there is no evidence that exposure to radioiodine affects the outcome of subsequent pregnancies and offspring. Although the number of children born of mothers exposed to radioiodine is relatively small, the present data indicates that there is no reason for patients exposed to radioiodine to avoid pregnancy. The only adverse effect observed in the study series is an increased incidence of miscarriages in women exposed to therapeutic radioiodine during the year which preceded conception. The fetus would be at risk due to maternal hypothyroidism.

Discussion: Radioactive iodine exposure does not appear to be associated with an increased risk of miscarriage or abnormal subsequent pregnancies.

Conclusion: Pregnancies achieved after exposure to radioactive iodine treatment do not appear to be at increased risk for negative outcomes. Nevertheless, it is recommended that pregnancy be avoided for 1 year following radioactive iodine therapy to allow reproductive function to normalize.

<![CDATA[SUN-509 Plasmapheresis Treatment of Thyrotoxicosis in Pregnancy for Preparation of Thyroidectomy]]> Introduction: Thyrotoxicosis in pregnancy presents the challenge of maintaining a normal level of maternal free thyroid hormone, while minimizing adverse drug effects, obstetric complications, and the risk fetal hypothyroidism.

Propylthiouracil is used for treatment in the first trimester with thyroidectomy typically performed in the second trimester if PTU/ MTZ are intolerable or if thyrotoxicosis persists. When thyroidectomy is indicated, thyroid hormone levels must be normalized prior to the operation, as there is risk of thyroid storm that can occur during and up to several hours postoperatively. In such cases, preoperative plasmapheresis may be considered.

Case Presentation: We present a 24 year old G2P0101 Hispanic female who reported to the ED with throat pain, chills, tachycardia, and shortness of breath who was found to have a TSH less than 0.005, free T4 3.15, elevated alkaline phosphatase, and an incidentally discovered early pregnancy approximately 4 - 6 weeks gestation. Medical history includes hyperthyroidism with over ten hospitalizations for thyrotoxicosis within the last three years and preterm delivery during her first pregnancy. A recent thyroid biopsy in 2017 showed a benign multinodular goiter. She had been taking methimazole and current CT of the neck demonstrated marked thyroid goiter with mild tracheal narrowing and mild tonsillitis. She was discharged on propylthiouracil 100 mg TID, metoprolol 25 mg TID, and augmentin 875 mg BID with the goal of decreasing her free T4 and T3 in preparation for thyroidectomy. Four days later, the patient returned to the ED with similar symptoms. Labs revealed TSH 0.001, free T4 3.70, FreeT3 15.1 WBC 3.1, platelets 103, and elevated total bilirubin, transaminases, and alkaline phosphatase. EKG demonstrated sinus tachycardia with minimal diffuse ST depression. Ultrasound showed a 0.34 cm round hypoechoic focus in the endometrial cavity without a fetal pole or cardiac activity. Chest X-ray demonstrated minor bibasilar atelectasis. The patient was admitted and PTU was discontinued due to leukopenia and elevated transaminases. Dexamethasone was started and metoprolol was continued.

Total thyroidectomy was planned for when free T4 less 2.0 The patient received two treatments of plasmapheresis, which decreased free T4 to 2.11 and then to 1.40. The thrombocytopenia and transaminitis resolved

A total thyroidectomy was performed and well tolerated. patient had full term pregnancy, uneventful delivery while on thyroid hormone replacement.

Conclusion: Preoperative plasmapheresis can be considered for the normalization of free T4 if thionamides fail or cannot be tolerated. This case demonstrates the successful management of thyrotoxicosis with plasmapheresis in the first trimester of Our knowledge Plasmapheresis was not used before in Pregnancy in preparation for thyroidectomy.

<![CDATA[SUN-493 A “Curve Ball” in the Management of an Infertile Hyperthyroid Patient]]> Introduction: We present the case of a young female patient referred for hyperthyroidism with persistently detectable TSH despite elevated free thyroxine (FT4) levels which, interestingly, failed to normalize following anti-thyroidal treatment. Further testing elucidated the underlying causation for detectable TSH in presence of hyperthyroxinemia to be due to interfering substances in the thyroid function assays.

Case: A 35-year-old female is evaluated for hyperthyroidism discovered in preparation for embryo transfer. History includes transient hyperthyroidism two years ago while undergoing in vitro fertilization. Prior workup included negative antibodies and nuclear uptake scan revealing a right-sided autonomously functioning thyroid nodule with 24-hour uptake of 40.7%. She was briefly treated with PTU in first trimester and lost to follow-up. While once again undergoing fertility treatment with clomiphene, the patient developed tremor and heat intolerance. She was found to have TSH 0.3 (0.45-4.12 mU/L) and analog FT4 of 6.4 (0.8-1.8 ng/dL). She denied use of OTC supplements. PTU 50 mg twice daily was initiated with minimal improvement with TSH 0.7 mU/L, FT4 3.7 ng/dL. On evaluation, slight tremor and mild thyroid enlargement were noted. Our differential expanded to include TSH-secreting pituitary adenoma, thyroid hormone resistance (no family history), and assay interference. Both MRI pituitary and an alpha-subunit level (0.36) were normal. Symptoms improved gradually with repeat TSH 1.79 mU/L, FT4 2.4 ng/DL by standard analog methods. We suspected ‘assay interference’ for which FT4 via direct equilibrium dialysis was obtained and was indeed normal at 0.76 ng/dL. Further lab testing verified interference in both in the standard TSH and FT4 assays presumed secondary to heterophile antibodies.

Discussion: Interpretation of thyroid studies discordant with the clinical picture or incongruent with each other requires understanding of thyroid physiology and the intricacies of commonly utilized assays. The differential of elevated thyroxine levels with detectable/normal TSH rests between thyroid hormone resistance syndromes, TSH secreting pituitary tumors and interfering substances in the assay. Most commercially available TSH assays are based on a ‘sandwich’ assay which is notoriously interfered with by heterophile antibodies and excess biotin. Determination of FT4 is also challenging as the assay must detect very low concentrations of free hormone relative to excess of protein-bound analyte. When in question, it is important consider utilization of laboratory expertise and retesting by alternative assays.

<![CDATA[SUN-502 Graves’Disease and Autoimmune Hepatitis: Management Challenges]]> Graves’ disease (GD) is the most common etiology of hyperthyroidism and may be associated with other autoimmune disorders. Case report: A.J.M.N., 27 years old, previously healthy, presented with abdominal discomfort, nausea and headache. She used paracetamol 750mg t.i.d for seven days. After that, she noticed jaundice and sought medical care. On admission, patient was icteric, oriented, afebrile, without signs of heart failure or alterations in the intestinal habit. Admission laboratory tests: AST 1287 U/L (RR<46), ALT 1090 U/L (RR < 50), total bilirubin (TB) 45.66mg/dL (RR<1.3), direct bilirubin 42.22mg/dL (RR<0.8), TSH 0.04 mcUI/ml, FT4 > 6.99 ng/dL (RR< 2.19). Serology for infectious diseases (A, B and C viral hepatitis; cytomegalovirus; Epstein-Bar Virus, syphilis; Dengue virus) were negative. Available antibodies for autoimmune hepatitis (anti-LKM1, anti-mitochondria, anti-smooth muscle, anti-SSB, anti-SSA, anti-Rnp / Sm, anti-DNA) were non-reactive. Ceruloplasmin and serum copper were normal. TRAB 3 IU/L (RR<1.75 IU /L); Thyroid scintigraphy showed homogeneous distribution of parenchymal contrast and regular contours of the gland; 15-minute uptake was 9.19% (RR: 1%-6%). Propranolol (40mg q.i.d) was prescribed. Burch and Wartofsky score was 30 (possible previous infection episode as precipitation factor = 10 points and unexplained jaundice = 20 points). Since the patient did not have diagnostic criteria for thyroid storm and since liver function was greatly altered, we opted to treat the thyroid disease with 12mCi of radioiodine, instead of antithyroid drugs (ATD). Differential diagnosis of the liver disease, whether due to autoimmunity or due to hyperthyroidism itself or both, were considered. Corticosteroid therapy (prednisone 40mg) was added due to the possibility of the coexistence of GD and autoimmune hepatitis previously reported as been 1.8% of the autoimmune hepatitis cases. Liver biopsy was performed 4 days later, and the findings were compatible with this condition. Ten days after prednisone and 20 days after radioiodine, we noticed a drop in TB (45 to 20mg/dL) and liver enzymes (AST= 69 and ALT 106) and she was discharged with normal FT4. Autoimmune hepatitis and GD presents a management challenge because sometimes it is not possible to confirm the etiology before treatment. The abnormalities could have been due to hyperthyroidism itself, since all autoantibodies to autoimmune hepatitis have been ruled out, but liver biopsy was very suggestive of the autoimmune cause. Initiating ATD for rapid improvement of hyperthyroidism could represent a risk due to hepatotoxicity of these drugs. On the other hand, withholding the treatment in cases of hepatic insufficiency due to hyperthyroidism, can have disastrous consequences. The option with beta-blocker, radioiodine and corticosteroid was successful and might be considered in similar cases.

<![CDATA[SUN-523 Thyroid Storm: A Rare Presentation of HCG Producing Metastatic Choriocarcinoma]]> Background: The beta subunit of human Chorionic Gonadotropin (hCG) and TSH are very similar and hCG is known to weakly bind the TSH receptor. hCG induced hyperthyroidism has been previously reported as a rare paraneoplastic syndrome in non-seminomatous germ-cell tumors and usually presents with subclinical thyrotoxicosis. We present a noteworthy case of thyroid storm in a patient with hCG producing testicular Choriocarcinoma.

Clinical case: A 19-year-old Hispanic man presented to an outside emergency department (ED) with one day of abdominal pain, nausea, recurrent emesis and subjective fever. He had presented to the same ED 9 days prior with similar symptoms which prompted contrasted CT Abdomen/Pelvis demonstrating hepatic masses and a large right testicular mass, suspicious for primary testicular malignancy. On return evaluation, he was noted to have tachycardia with HR 165, mild scleral icterus, tenderness to palpation of right upper quadrant, abdominal pain and a right scrotal mass (5x5 cm). CBC revealed; WBC 12.0 k/uL (n: 4-10.8), AST: 428 u/L (n: 3-34); ALT: 176 u/L (n: 15-41); total bilirubin: 6.3 mg/dL (n: 0.2-1.3), TSH <0.005 uIU/mL (n: 0.4-4.0) and FT4 5.02 ng/dL (n: 0.7-1.4). Clinical scenario was consistent with thyrotoxicosis concerning for thyroid storm (Burch-Wartofsky Point Scale: 50) requiring intensive care for which he was transferred to our institution. Thyroid US revealed increased thyroid vascularity without nodularity. Laboratory workup revealed negative TG Ab, Anti-TPO Ab, TRAb, and TSIG. Conversely, TBG was elevated at 31.2 mcg/ml (n: 13-30). Initial hCG level was obtained as 6,074. After re-testing with dilution was specifically requested, initial hCG was corrected to 6,760,713. Oncologic workup confirmed diagnosis of hCG producing testicular choriocarcinoma with liver and lung metastases. On admission, he was started on oral methimazole and propranolol as well as intravenous steroids which led to marked symptomatic improvement and normalization of FT4 to 1.37 allowing for discontinuation of antithyroid medication on 7th day of hospitalization. He completed 1 cycle of cisplatin/etoposide and experienced marked reduction of his hCG level to 951,460 which correlated with improvement of his TFTs and resolution of his hyperthyroid symptoms.


A low threshold of suspicion should be maintained for the possibility of hyperthyroidism in patients with suspected testicular choriocarcinoma, particularly in the context of recent iodinated contrast imaging. If the clinical picture does not support a primary etiology of hyperthyroidism and hCG is not concordantly elevated, re-assessment of hCG by dilution should be considered as hCG assay is also subject to prozone (hook) effect. Hyperthyroidism should be actively managed and closely monitored as response to treatment can be rapid.

<![CDATA[SUN-505 Total Thyroidectomy in Severe Hyperthyroidism]]> Introduction: Patients with hyperthyroidism may be treated with ATDs, RAI therapy or thyroidectomy; in some cases like thyroid storm, plasmapheresis can be used to remove excess hormones prior to surgery. In some cases, such as those with complications derived from ATDs (agranulocytosis, hepatotoxicity), or those with large goiters with l symptomatic compression of surrounding organs within the neck, surgical treatment is considered. Clinical cases: Seven patients were treated with total thyroidectomy for the definitive control of the hyperthyroidism. Six were female, 4 used thionamides, 1 lithium and 2 discontinued treatment. All diffuse goiter (60-160 gr), 2 with autoimmune ophthalmopathy and, 4 had thyroid storm. The thyroid ultrasonography of thyroid evidenced hypoechogenicity and hypervascularity and in 4 cases tracheal compression. All patients had suppressed TSH and free T4 within 2,6-7,76 ng /dl (N: 0.7-1.7). Previous to surgery, six received glucocorticoids and beta-adrenergic blockade, five lugol solution, four thionamides (30-90mg/d), four lithium (3 with agranulocytosis) and two calcium with vitamin D. One patient received plasmapheresis which had a poorly response for thyroid storm treatment.After surgery 2presented hungry bone syndrome, two transient hypoparathyroidism and two permanent hypoparathyroidism. One patient was re-admitted for surgery. Pathological examination reported autoimmunity characteristics (cylindrical thyrocytes, vacuolated colloid, papillae formation and / or lymphocytic infiltrate) in 4 cases. In 3 cases, nodules were found without malignancy signs. Conclusions: Thyroidectomy is a definitive therapeutic option in severe hyperthyroidism with difficult management, particularly in those cases with contraindication to the use of thionamides, large goiters compromising the upper airway, because it leads to faster control of the hyperthyroid state. Hypocalcemia is a frequent postoperative complication that can be attenuated with the pre-operative vitamin D and calcium supplements.

<![CDATA[SUN-510 Prolonged RAIA Induced Thyroiditis After 131 I Therapy for Graves’ Hyperthyroidism]]> Radioactive iodine ablation (RAI) has been used for the treatment of Graves’ hyperthyroidism since 1946 and it is the primary recommended modality for Graves’ disease treatment in many countries. Acute painful radiation thyroiditis after radioiodine treatment for hyperthyroidism of Graves’ disease is considered uncommon. The prevalence is 1-5% in patients treated with 131I therapy for hyperthyroidism. Dose of RAI and thyroid volume can be precipitating factors for post radiation thyroiditis. The higher RAI dose increases the chance of RAI thyroiditis while the larger goiter size decreases the absorbed radiation dose in the thyroid gland. We present a 25-year-old Emirati male previously healthy, who was referred to our service for hyperthyroidism management. He presented with thyrotoxicosis in absence of goiter. All investigations revealed that graves’ disease is the primary cause of his hyperthyroidism. He was treated with RAI ablation 18.3 mCi. Day four after RAI, he presented with severe pain in the anterior neck associated with fatigue, tremor, palpitation and weight loss. Symptoms lasted for 6 weeks post RAI. There was laboratory evidence of thyrotoxicosis presented with further suppression of TSH and higher fT4 than the baseline. Acute radiation thyroiditis was diagnosed and has been commenced on propranolol 10mg BID. Symptoms completely resolved after 6 weeks of treatment and thyroid function returned to normal level. The patient has remained asymptomatic on continued follow up care till eventually became hypothyroid clinically and biochemically. Our case reflects that radioiodine thyroiditis can last for longer period and occur after larger doses of 131I treatment in absence of goiter. Our patient has RAIA induced thyroiditis lasted for 6 weeks post 18.3mCi of 131I, and has no goiter, which were both contributing factors for RAIA induced thyroiditis

<![CDATA[SUN-517 Methimazole-Induced Neutropenia in Premature Twins with Graves’ Disease]]> Introduction: Neonatal Graves’ disease (NGD) occurs in approximately 1-5% of infants born to women with Graves’ disease. It is caused by trans-placental crossing of thyroid stimulating immunoglobulin (TSI) antibodies during third trimester. Hyperthyroidism during pregnancy can lead to craniosynostosis, goiter, premature bone maturation, developmental delay or even heart failure in the neonate. Neonatal Hyperthyroidism is usually transient and resolves in few weeks. Treatment consists of beta blockers and Methimazole. Studies in adults recommend discontinuing of Methimazole if patients develop neutropenia. However due to lack of alternatives, we present a case of continued use of Methimazole with neutropenia in newborn twins.

Case Report:

33 weeks gestational age mono-chorionic/di-amniotic twins born to a 34-year-old woman with poorly controlled hyperthyroidism. Mother diagnosed with Graves’ disease during 2nd trimester with poor control throughout pregnancy. At the time of delivery, maternal TSH was <0.005uIU/mL(0.358-3.74uIU/mL) and FT4 2.18ng/dL(0.76-1.46ng/dL). Antenatal ultrasound at 32 weeks showed homogeneous enlargement of fetal thyroid glands with increased vascularity in both twins. Babies found to have diffuse goiter and exophthalmos at birth. Thyroid tests remained normal for first 3 days of life. By day 3, babies labs showed TSH <0.005uIU/mL, FT4 -8 ug/dL and TSI >700%. Baseline CBC showed ANC of 4.95K/mm3. Babies were started on Methimazole 0.5mg/kg/day and Propranolol 2mg/kg/day. TFTs fluctuated throughout their stay in NICU and they developed neutropenia with ANC 1.23K/mm3 on day 20 of life. Methimazole was initially discontinued then restarted at 0.25 mg/kg/day 3 days later. There is no recommended protocol for restarting Methimazole. Further follow up showed persistent neutropenia despite multiple dose adjustments in Methimazole, including dosing every other day. ANC was maintained around 800-1100K/mm3. At age 2 months, Methimazole was discontinued completely after TSI antibodies decreased to 400%. ANC remained low until 6 months of life, even after discontinuing Methimazole. Both babies ultimately developed central hypothyroidism and were started on l-thyroxine.


NGD can range anywhere from transient hyperthyroidism to persistent central hypothyroidism. Early diagnosis and treatment is crucial to prevent significant morbidity and mortality. Methimazole is the only approved treatment at this age, and management of Methimazole-induced neutropenia has not been established. Adult studies recommend discontinuing Methimazole in context of neutropenia; we took an approach of decreasing dose gradually. Further studies are needed to establish step-wise approach in managing Methimazole-induced neutropenia.

<![CDATA[SUN-500 Viral-Induced Autoimmune Hyperthyroidism in an Adult Patient Without Established Thyroid Disease]]> Introduction: Subacute thyroiditis is a self-limited inflammation of the thyroid associated with recent upper respiratory tract viral infection. Graves’ disease has also been associated with viral illness.

Clinical Case:A 55-year-old female presented to the emergency department complaining of sore throat, cough, and shortness of breath. She also had fatigue, dyspnea on exertion, palpitations, and a family member who recently had bronchitis. She denied chest pain, weight changes, temperature intolerance, constipation, or diarrhea. She had never had similar symptoms before.

On initial evaluation, the patient was febrile at 101.2 °F, tachycardic at 156 beats per minute (bpm), and tachypneic at 33 breaths per minute. She was thin and her thyroid gland was tender upon palpation. She had eyelid lag, her skin was warm, and she was diaphoretic. Chest x-ray showed increased interstitial lung markings bilaterally. CBC showed anemia with hemoglobin of 9.7 g/dL (n<12 g/dL). Lactic acid was elevated to 2.00 mmol/L (n<1.9 mmol/L). D-dimer was 3020 ng/mL (n<230 ng/mL) and BNP was 961 pg/mL (n<100 pg/mL). An electrocardiogram showed sinus tachycardia at 140 bpm. Blood, sputum, and urine cultures were drawn, as were studies for viral respiratory pathogens. CT angiography of the chest and bilateral lower extremity venous ultrasound were ordered to rule out thromboembolism.

A point-of-care echocardiogram showed reduced ejection fraction of 20%. Thyroid function tests revealed TSH < 0.03 mIU/mL (range 0.5-5.0 mIU/L), free T4 of 4.5 ng/dL (n<2.15 ng/dL), and T3 251 ng/dL (n<200 ng/dL). Patient was started on an esmolol drip for heart rate control. CT angiogram of the chest was negative for thromboembolism but revealed a bilaterally enlarged thyroid gland with multiple small nodules. RNA for Respiratory Syncytial Virus (RSV) type A was detected by PCR. A thyroid ultrasound was done and revealed heterogenous echotexture with increased blast flow.

Thyroid antibody studies revealed thyrotropin receptor antibody of 26.5 IU/L (n<1.75 IU/L), thyroid-stimulating immunoglobulin 19.40 IU/L (n<0.55 IU/L), thyroglobulin antibody 235.6 IU/mL (n<0.9 IU/mL), and thyroid peroxidase antibody 11 IU/mL (range 0-34 IU/mL). Patient was started on methimazole 30 mg daily. A formal echocardiogram showed preserved ejection fraction of 50-55%. She was transitioned to oral propranolol. Patient’s shortness of breath and cough resolved, and she was discharged on methimazole 10 mg daily.

Conclusion:This case emphasizes the importance of measuring thyrotropin receptor antibodies in confirming Graves’ disease in a patient presenting with upper respiratory viral illness and supports the idea of viral-induced autoimmune thyroid disease.

<![CDATA[SUN-520 Graves Disease and T3 Thyrotoxicosis: A Case Report]]> Introduction: Hyperthyroidism is one of the common problems in the world of endocrinology. Identifying the type of thyrotoxicosis is crucial before starting treatment. We present a case of a 37-year-old woman presented with hyperthyroidism and was started on methimazole. Her symptoms persisted and further workup showed T3 thyrotoxicosis. Her symptoms improved after switching her to PTU. She eventually underwent thyroidectomy.

Case description: Thirty-seven-year old African American woman presented to her primary care physician(PCP) with symptoms suggestive of hyperthyroidism for three months. Her past medical history is significant for recent delivery one year ago. Her Physical exam is pertinent for hypertension of 160/80 with a heart rate of 120. Her neck is diffusely enlarged with bilateral bruits. Bilateral lid retraction with lid lag was noted along with left lid proptosis. There were no tremors or leg swelling noted. Her Initial workup showed sinus tachycardia in the electrocardiogram. Her TSH level was <0.010 and a free T4 level of 3.48. Ultrasound showed diffuse enlargement of the thyroid gland with no focal nodule. She was started on methimazole 10mg twice daily and metoprolol 25mg twice daily.

Three months later, she presented to the emergency room(ER) with tachycardia of 130 and hypertension of 170/85. Work up showed a TSH level of <0.010 and a free T4 level of 3.94. She was compliant with medications. When free T3 levels were checked it turned out to be >30. She was diagnosed with T3 Thyrotoxicosis and was started on propylthiouracil 150mg every 8 hours. Her metoprolol was increased to 50mg every 12 hours. Her symptoms improved and she finally underwent surgery for thyroidectomy.

Discussion: Hyperthyroidism is seen in about 1 in 5000 with a strong female predominance. Graves disease, the most common cause of hyperthyroidism is due to excess production of TSH receptor stimulating antibodies. Hyperthyroid patients with graves disease sometimes have a disproportionate increase in serum T3 levels when compared to serum T4. This is thought to be due to increased T3 production or extrathyroidal conversion of T4 to T3. It is very crucial to identify the free hormone levels in a new patient with hyperthyroidism because of the difference in management. Antithyroid drugs are traditionally the first-line treatment option along with beta-blockers prior to definitive therapy like radioactive iodine or thyroidectomy. The main drugs used are methimazole and propylthiouracil(PTU). Methimazole is more commonly used than PTU because of its rapid efficacy, longer duration of action and less adverse effects. For patients with T3 thyrotoxicosis, PTU is preferred as it is known to reduce the peripheral conversion of T4 to T3. Our patient medication was changed from methimazole to PTU, after which she started to notice improvement. She eventually underwent definitive treatment with thyroidectomy.

<![CDATA[SUN-512 Graves’ Disease Induced Renal Tubular Acidosis]]> Thyroid gland can affect kidney function in different ways. Thyroxine as a master hormone of metabolism and growth works in many cellular levels include the renal tubules.

We present a 34-year-old Emirati gentleman who presented with multiple episodes of hypokalemic periodic paralysis. Blood test revealed thyrotoxic state, with highly positive serology for thyroid peroxidase, anti-thyroglobulin and thyrotropin receptor antibodies. Thyroid uptake scan confirmed homogenous diffuse uptake consistent with toxic diffuse goitre [Graves’ disease]. In view of recent fracture, bone profile and DXA scan were done. Investigations revealed vitamin D deficiency and below expected for age bone mass density.

The patient was started on symptomatic treatment with propranolol, IV and oral potassium along with IVF hydration. Routine blood work during admission showed a persistent normal anion Gap metabolic acidosis, serum bicarb 15 mmol/l. 24 hours urine electrolytes revealed normal potassium, sodium, high magnesium, low calcium and PH levels. Biochemical lab results suggested type 1 renal tubular acidosis. As the patient had hypokalaemia, high urine magnesium and low urine calcium and limbs weakness, Gitleman Syndrome was considered in the differential diagnosis. Whole Exome Sequencing (CentoXome GOLD®) was sent which came back negative. The following gene panels were studied: Renal tubular acidosis panel: ATP6V0A4, ATP6V1B1, CA2, EHHADH, HNF4A, SLC34A1, SLC4A1, SLC4A4. Bartter Syndrome panel: ATP6V1B1, BSND, CA2, CASR, CLCNKA, CLCNKB, CLDN16, CLDN19, FXYD2, HSD11B2,KCNJ1, KCNJ10, KLHL3, NR3C2, SCNN1A, SCNN1B, SCNN1G, SLC12A1, SLC12A2, SLC12A3, SLC4A1, SLC4A4, WNK1. Gene related to Gitelman syndrome: SLC12A3

Renal tubular acidosis was treated with KCL 600mg PO TID, Na bicarb 1200mg PO BID and spironolactone 25 mg PO OD. The patient received radioactive iodine (RAI) as the ultimate treatment for Graves’ disease. He developed hypothyroidism post RAI ablation and commenced on levothyroxine. Improvement of the metabolic acidosis was noticed in line with improvement of thyroid function. Na bicarb and spironolactone tablets were stopped eventually as the patient was euthyroid clinically and biochemically.

Overt hyperthyroidism is associated with accelerated bone remodelling, leading to hypercalciuria, which can predispose to nephrocalcinosis and renal tubular damage, and therefore causes type 1 renal tubular acidosis. Once the patient becomes euthyroid, bone remodelling and urine calcium return to normal levels and that would correct the renal acidosis.

This case report serves to highlight the effect of Graves’ disease on renal tubules which may result in type 1 renal tubular acidosis. This effect could be reversible with normalization of thyroid function.

<![CDATA[SUN-507 Fueling the Fire: A Case of Hypokalemic Periodic Paralysis Associated with Type I Renal Tubular Acidosis and Thyrotoxicosis in Pregnancy]]> Background: Hypokalemic periodic paralysis (HPP) related to thyrotoxicosis, though rare, is more often seen in Asian males. Type 1 renal tubular acidosis (T1 RTA), which can also cause HPP, is typically managed with alkali therapy and potassium supplementation, though there are no well-established guidelines for management in pregnancy.

Clinical Case: A 27-year-old Puerto Rican woman, at 32 weeks gestation, presented to the hospital with sudden onset muscle weakness, and was found to have 1/5 muscle strength in her lower extremities. She had no personal or family history of similar illness. Laboratory analysis revealed hypokalemia (potassium 2.0 mmol/L, range: 3.5 – 5); non-gap metabolic acidosis (sodium 137mmol/L, range 136 – 145; chloride 113 mmol/L, range 98- 107; and bicarbonate 8 mmol/L, range 22 – 29); and an arterial pH of 7.09. Urine studies demonstrated a urine pH of 6.5 and a urine sodium of 32 mmol/L which was diagnostic of T1 RTA in the context of her metabolic derangements. She was treated emergently with potassium and bicarbonate infusions, with improvement in her symptoms. Subsequent thyroid function testing revealed: a low TSH of 0.01 uIU/ml, normal free T4 of 1.66 (range: 0.9 - 1.7) ng/dl, normal free of T3 3.7 (range: 2.0 -4.4) pg/ml and elevated total T4 of 16.5 (range: 4.5 - 11.7) ug/dl. Renal ultrasound demonstrated medullary nephrocalcinosis. She was discharged on potassium and sodium citrate tablets. At 37 weeks, the patient was readmitted for induction of labor due to pre-eclampsia, and delivered a healthy male baby. Several months later, she presented to the Endocrinology clinic with symptoms of increased frequency bowel movements, palpitations and heat intolerance, which had been ongoing since pregnancy. On review, a metabolic panel prior to pregnancy had demonstrated non-gap acidosis and mild hypokalemia. Further testing demonstrated the following: TSH < 0.01 uIU/ml, Free T4 1.71 ng/dl, Free T3 4.8 pg/ml, TSI 280%, and a thyroid uptake scan with homogenous radiotracer uptake, with a 24-hour uptake of 40%. She was started on methimazole therapy, and continued on potassium and sodium citrate tablets with clinical and biochemical improvement.

Conclusion: Thyrotoxicosis can augment hypokalemia in T1 RTA, and can increase the risk of HPP. Our patient had biochemical evidence of RTA prior to pregnancy, though without episodes of HPP, and we believe that her hyperthyroidism, triggered by pregnancy, may have been the additional insult that precipitated her paralysis. This is the first reported case of HPP related to co-existing thyrotoxicosis and T1 RTA in a pregnant individual.

Reference:1. Tu ML, Fang YW, Leu JG, Tsai MH. An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report. BMC Nephrol. 2018;19(1):160. Published 2018 Jul 4. doi:10.1186/s12882-018-0971-9

<![CDATA[SUN-495 Rapid Resolution of Hyperthyroidism Induced Hepatic Dysfunction with Methimazole]]>



Hepatic dysfunction in the setting of hyperthyroidism is difficult to diagnose and poses a challenge in therapy, since the classic medications used are potentially hepatotoxic.

Clinical case:

A 51-year-old female patient presented with fatigue, palpitations and tremors. BP 146/65 mmHg, HR 111 bpm and Temp 97.8 F. She was severely thyrotoxic with 3 + DTRs, tremors, enlarged thyroid gland with bruit on auscultation, clear lungs and no lower extremities edema. Blood tests showed TSH <0.003 IU/ml (0.450-5.330 IU/ml), Free T4 5.33 ng/dL (0.45-1.80 ng/dL), Free T3 > 30.0 pg/mL (2.3-4.2 pg/mL). Liver enzymes showed elevation in transaminases with ALT 319 IU/L (7-40 IU/L), AST 330 IU/L (7-40 IU/L) normal total Bilirubin 0.7 mg/dL (0.1-1.5 mg/dL) and Alkaline phosphatase 65 IU/L (40-200 IU/L). Transaminases were also elevated 3 weeks prior to presentation and this was extensively worked up with no identifiable etiology to explain the liver dysfunction. She was started on beta blocker therapy and admitted to the ICU. She had no clinical or echocardiographic evidence of cardiac dysfunction and remained hemodynamically stable. She was started on Methimazole 45 mg daily. The patient improved clinically and a pronounced decline in transaminase levels was documented in the first 72 hours. She was discharged home on day 3 of admission. On follow up visit her transaminases were found to have completely normalized within 14 days.


The diagnosis of elevated transaminases in hyperthyroidism is a challenge. This is due to the possibility of multiple etiologies including decreased cardiac output and/or liver congestion, concomitant primary liver disease or more specifically autoimmune hepatic disease such as primary biliary cirrhosis. (1-2). Incidentally Methimazole has been associated with transient asymptomatic transaminitis typically during the first three months of therapy (3). Our case indicates, that methimazole can be used in patients with a presumed diagnosis of hyperthyroidism induced hepatotoxicity after all possible etiologies are ruled out. Hyperthyroidism as the cause of liver dysfunction can only be entertained after all those etiologies are ruled out and upon resolution of transaminase elevation in conjunction with improvement in the hyperthyroid state itself, as was demonstrated in this case.


Methimazole can be safely used in patients with severe hyperthyroidism and elevated liver enzymes when all other etiologies of liver dysfunction have been ruled out.


1. Khemichian S, Fong TL. Hepatic dysfunction in hyperthyroidism. Gastroenterol Hepatol (N Y).

2. Elias RM, Dean DS, Barsness GW. Hepatic dysfunction in hospitalized patients with acute thyrotoxicosis: a decade of experience.

3. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Bethesda (MD): Methimazole

<![CDATA[SUN-496 A Challenging Diagnosis of Thyrotoxic Periodic Paralysis]]>


Thyrotoxic Periodic Paralysis (TPP) is a rare but potentially lethal manifestation of hyperthyroidism which is characterized by muscular weakness due to intracellular shift of potassium and subsequent hypokalemia. The muscular weakness may range from mild weakness to complete flaccid paralysis. It is predominantly seen in Asian young men. Graves’ disease has been described as the most common cause of TPP. Other rare causes of hypokalemic periodic paralysis include inherited disorders and acquired cases due to drug abuse, specifically cocaine. It is important to recognize and diagnose TPP to provide appropriate treatment and prevent serious cardiopulmonary complications.

A 26 year old Hispanic male with past medical history of cocaine abuse presented to the emergency department with profound lower extremity weakness since that morning. Laboratory studies on initial evaluation revealed hypokalemia. He was admitted to the intensive care unit (ICU) for IV potassium replacement and cardiac monitoring. Upon obtaining further history, the patient had suffered a similar episode of weakness and hypokalemia two months prior. At the time, he had a positive urine toxicology for cocaine. He was treated with IV potassium with resolution of his weakness and was told the reason for the episode was cocaine induced periodic paralysis. No further work up was done due to patient leaving Against Medical Advice. The patient stopped recreational drug abuse after this diagnosis.

During current hospitalization, further laboratory studies revealed hyperthyroidism. TSI and TPO antibodies were elevated and thus patient was diagnosed with Graves’ disease. On questioning, patient was asymptomatic and clinically euthyroid. He was treated with IV potassium, methimazole and propranolol with quick resolution of weakness. He has been followed in an out-patient basis and he has had no further exacerbations.

In this case, we present a case of TPP that was initially diagnosed as cocaine induced periodic paralysis which is an extremely rare disorder with only a couple of described cases in the literature. Diagnosis was initially missed as the patient was clinically euthyroid and had history of recreational drug abuse. Restoration of euthyroidism eliminates attacks of TPP. It is important to recognize and diagnose these patient to prevent further attacks.

<![CDATA[SUN-501 Grave’s Disease Concealing the Diagnosis of Pancreatic Carcinoma]]> 900 IU/ml, TSI 358(n=<140%). He was diagnosed with Grave’s disease and was started with Methimazole and Propranolol, which were titrated to an optimal range over the next few months. However, the patient was lost to follow up, and presented one year later to the ED with complaints of abdominal pain, jaundice for one-week, greasy diarrhea for 6 months, also reporting noncompliance with thyroid medications during this time. On examination, he was icteric and jaundiced with hepatomegaly, trace pedal edema. Although LFT’s were previously normal, the labs now showed alkaline phosphatase=533, (n=40-129 IU/L); AST=107 units (n= 0-32 IU/L), ALT=213units (n= 0-40 IU/L), total bilirubin 11.4 (n= 0-1.0 mg/dl), TSH=0.01, FT4=0.6, FT3=3.2. Ultrasound showed gallbladder sludge, CT abdomen-dilatation of the pancreatic duct in neck and body of pancreas, MRCP- marked pancreatic ductal dilatation and soft tissue fullness within the pancreatic head. CA 19-9= 64.8, he underwent ERCP, and was later diagnosed with adenocarcinoma of the Pancreatic head. He was discharged with referrals to GI and Oncology for further treatment. Discussion:Although weight loss and diarrhea are nonspecific, and can often result from hyperthyroidism, this case highlights the importance of further investigation for other causes and avoiding attribution to a single diagnosis. Other diagnoses were only looked into when the patient presented with painless jaundice and hepatomegaly several months later. The effects of autoimmune hyperthyroidism on the pancreas function remain unclear. However, patients with Grave’s hyperthyroidism have a higher number of islet cell antibodies, as compared to controls. Further studies are required in this regard. We also emphasize the importance of patient education and compliance which can lead to earlier diagnosis, and overall better outcomes. ]]> <![CDATA[SUN-498 A Case of Thyroid Storm with Systemic Thromboembolism]]> <![CDATA[SUN-511 Thyroid Storm Caused by Subacute Thyroiditis in a Patient with Methicillin-Resistant Staphylococcus Aureus Septicemia]]> 6.99 ng/dL). Burch-Wartofsky score was 75, highly suggestive of thyroid storm. In addition to treating her sepsis, the patient was started on a beta blocker, high dose hydrocortisone, and methimazole. Thyroid ultrasound showed a diffusely enlarged heterogeneous thyroid gland with decreased flow on color Doppler. Upon improvement, the patient admitted to symptoms of anterior neck pain, heat intolerance, palpitations, excessive sweating, and anxiety for two days prior to presentation. Blood cultures later grew MRSA. Methimazole was discontinued when the thyrotropin-receptor antibody result came back negative. The patient continued to improve clinically. Her thyroid tenderness improved, and her free T4 and T3 decreased over a 3-week period. Steroids were tapered off.Discussion:SAT usually causes mild to moderate thyrotoxicosis. It is unusual for SAT to cause thyroid storm. Identifying such a diagnosis in a patient with sepsis is complex. In a septic patient, it is crucial to obtain detailed history, perform a comprehensive physical exam (including neck exam), and have a high level of clinical suspicion for thyroid storm in order to reach the diagnosis early and institute appropriate interventions. Establishing the underlying etiology of the thyrotoxicosis would have long term implications regarding prognosis and treatment.References:Salih AM, Kakamad FH, Rawezh QS, et al. Subacute thyroiditis causing thyrotoxic crisis; a case report with literature review. Int J Surg Case Rep. 2017;33:112-114.Swinburne JL, Kreisman SH. A rare case of subacute thyroiditis causing thyroid storm. Thyroid. 2007;17(1):73-6.Sherman SI, Simonson L, Ladenson PW. Clinical and socioeconomic predispositions to complicated thyrotoxicosis: a predictable and preventable syndrome?. Am J Med. 1996;101(2):192-8. ]]> <![CDATA[SUN-525 Successful Surgical Management of Graves’ Disease in Pregnancy]]> 100/min and diffusely enlarged goiter with a bruit. Thyroid Ultrasound showed a right lobe of 6.5 x 2.8 x 2.7 cm and left lobe 5.3 x 2.6 x 2.4 cm. Free thyroxine (FT4) was 42.3 pmol/L (12–22), free triiodothyronine (FT3) 9.09 nmol/L (1.3–3.1), and TSH < 0.01 mIU/L (0.27–4.2). TRAB titer was >40 IU/L (0.0–1.75). She was advised to switch to propylthiouracil (PTU) and labetalol to minimize fetal adverse outcomes. She reported that she was unable to afford PTU and requested a switch back to CBZ.During her course of therapy, she had recurrent admissions with thyrotoxicosis, tachycardia, panic attacks and difficulty in swallowing. A decision was made to manage her with total thyroidectomy in the second trimester. She was treated with Lugol’s iodine, beta blockers and CBZ 2 weeks prior to her surgery and there were no immediate post-operative adverse events. Histology was consistent with GD. Her post-op TRAB titer remained >40 IU/L until present.She delivered at 28 weeks of gestation due to threatened premature labor a baby boy who had neonatal thyrotoxicosis, required admission to the neonatal ICU and therapy with flecanide and CBZ. His TSH was 0.09 mIU/L, (FT4) 68.7 pmol/L and TRAB 19.4 IU/L. He is currently 18 months old, well and not on any medications. Conclusion: Poor control of thyrotoxicosis is associated with pregnancy loss, prematurity, stillbirth, thyroid storm, and maternal congestive heart failure. Therefore, pre-pregnancy counseling is crucial to establish Euthyroid state for the safety of mother and fetus. Reference: (1) Davis LE, Lucas MJ, Hankins GD, Roark ML, Cunningham FG. Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol. 1989;160:63–70. doi: 10.1016/0002-9378(89)90088-4. (2) Vini L, Hyer S, Pratt B, et al. Management of differentiated thyroid cancer diagnosed during pregnancy. Eur J Endocrinol. 1999;140:404–406. ]]> <![CDATA[SUN-497 Life-Saving Management of Thyrotoxicosis with a Single Session of Plasmapheresis]]> <![CDATA[SUN-524 Patient with Pseudohypoparathyroidism Type 1B, Graves Disease, and False Positive HIV Screen- a Rare Presentation]]>