scholarly journals SUN-492 Treatment of Uncontrolled Graves’ Disease Reveals Underlying Thyroiditis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nicole Sheung ◽  
Ligia Maria Belalcazar
Keyword(s):  
Beta Blockers ◽  
Ventricular Rate ◽  
Graves Disease ◽  
Dramatic Improvement ◽  
Free T4 ◽  
Hormone Synthesis ◽  
Increased Risk ◽  
Threatening Condition ◽  
Potassium Iodine ◽  
History Of

Abstract Thyrotoxicosis is a life-threatening condition that may result from poor adherence to medical therapy. We describe the case of a patient with Graves’ disease and a history of medication non-compliance who presented with tachyarrhythmia and heart failure (HF). His protracted course after weeks of inpatient treatment with thionamides, iodine, resin and beta-blockers, was followed by a dramatic improvement within days of adding steroids, suggesting the presence of concurrent untreated thyroiditis. Case Description: A 38-year-old man with an 18-month history of known Graves’ disease presented to the endocrinology clinic requesting thyroidectomy. He complained of 3 weeks of worsening palpitations, shortness of breath, bilateral lower extremity edema, and frequent loose stools. History revealed frequent interruption of thionamide and recent discontinuation of propranolol due to patient’s perceived lack of improvement. Physical exam showed a thin male with a large goiter. He was in moderate distress due to tachypnea. He had atrial fibrillation with rapid ventricular rate (A Fib with RVR) but was not in pulmonary edema. Laboratories showed a suppressed TSH (<0.02 mIU/L [0.45 - 4.70 mIU/L]), a free T4 above the level of detection (>6.99 ng/dL [0.78 - 2.20 ng/dL], and a total T3 level of above 781 pg/mL (97.0 - 170.0 ng/dL). Methimazole 30 mg BID and propranolol 40 mg TID were started, followed within a few hours with potassium iodine (SSKI) 3 drops TID. Although the patient’s HF improved and there was down-trending of free T4, he continued to have A fib with RVR. SSKI and propranolol were increased; diltiazem 90 mg QID and cholestyramine 2g BID were later added. Despite aggressive treatment, the patient continued to have intermittent tachyarrhythmia, postponing his planned thyroidectomy for weeks. Dexamethasone 2mg Q8H was then started aiming to further decrease T4 to T3 conversion. Interestingly, within 48 hours of the start of steroid therapy, his free T4 level markedly decreased and was well within the normal range several days later when he underwent a successful thyroidectomy, with no further tachyarrhythmia recurrence. Discussion: Thyrotoxicosis is aggressively treated given its high mortality rate. Treatment algorithms guide physicians to categorize hyperthyroidism either as the type associated with increased hormone synthesis and secretion or that which results from increased hormone release due to gland destruction. This thought process may lead, as in our case, to a delay in appropriate therapy and an increased risk of disease complications. Furthermore, providers should not assume that the lack of treatment response in a patient with Graves’ disease is the result of medication non-adherence. The possibility of coexisting thyroiditis and the absence of a treatment regimen that effectively addresses both underlying processes may be the actual cause for the lack of clinical improvement.

scholarly journals Call for Emergency Room Guidelines to Identify Hyperthyroid Patients Prior to Contrast Imaging

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A922-A923
Author(s):  
Sandhya Bassin ◽  
Louis F Amorosa
Keyword(s):  
Atrial Fibrillation ◽  
Emergency Room ◽  
Definitive Treatment ◽  
Graves Disease ◽  
Contrast Imaging ◽  
Iodinated Contrast ◽  
Increased Risk ◽  
History Of ◽  
The Impact ◽  
Hyperthyroid Patients

Abstract Background: Thyrotoxicosis can be mistaken for conditions such as atrial fibrillation and pulmonary embolism (PE) given the nonspecific symptoms of fatigue, palpitations, and dyspnea. Patients often undergo further imaging on presentation to the emergency room (ER), many of which use iodine for contrast. This can put patients at increased risk for iodine induced hyperthyroidism and delay definitive treatment in patients with Graves’ disease, the most common cause of hyperthyroidism. Clinical Case: A 53-year-old male with history of hyperthyroidism, atrial fibrillation, and prior PE presented with palpitations to the ER. He developed worsening dyspnea on exertion and palpitations over the last three days. He was unable to afford his medications, including methimazole, for the last nine months. In the ER he was in atrial fibrillation with rapid ventricular response. Due to concern for PE, he underwent a CTA with contrast, which was negative. His physical exam was notable for a diffusely enlarged goiter. His labs showed low TSH <0.01 (norm 0.35-5.50mIU/L) and high free T4 >7.77 (norm 0.9-1.8ng/dL). TSH stimulating antibodies were elevated at 1.9 (norm <1.3 TSI index), consistent with Graves’ hyperthyroidism. Endocrinology was then consulted for severe thyrotoxicosis, initially treating the patient with PTU and propranolol. The patient was transitioned to methimazole and continued propranolol on discharge. Since he was given contrast, plan was for repeat thyroid uptake scan and iodine ablation in 3 months. However, patient was not compliant with medications, resulting in readmission for thyrotoxicosis 3 months later. Conclusion: This case highlights the impact of increased use of contrast in imaging in hyperthyroid patients. Hyperthyroid patients are at an increased risk for emboli. However, iodine can cause contrast-induced hyperthyroidism and delay definitive treatment of Graves’ disease. As almost half of thyrotoxic patients receive iodinated contrast prior to an endocrine consultation, endocrinologists should work with emergency physicians to develop a set of guidelines to identify at risk populations for hyperthyroidism (1). We advocate for urgent thyroid testing in patients with new onset atrial fibrillation, a history of Graves’ disease, specific symptoms of Graves’, or those taking thyrotoxic-inducing medications. This will assist in determining if patients should receive a prophylactic dose of anti-thyroid medication prior to iodinated contrast imaging. These guidelines can help prevent contrast induced hyperthyroidism and disruptions in treatment of Graves’ while still imaging patients for other diagnoses on the differential. Reference: (1) Giacomini A, et al. Urgent thyroid-stimulating hormone testing in emergency medicine: A useful tool? J Emerg Med. 2015;49(4):481-487.

P1588Beta-blocker therapy and risk of dementia: a population-based prospective study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Holm ◽  
F Ricci ◽  
G Di Martino ◽  
E Bachus ◽  
E D Nilsson ◽  
...  
Keyword(s):  
Vascular Dementia ◽  
Beta Blocker ◽  
Beta Blockers ◽  
Population Based ◽  
Mixed Dementia ◽  
Propensity Score Matching Analysis ◽  
Increased Risk ◽  
History Of ◽  
Coronary Events ◽  
Study Participants

Abstract Introduction Cerebral side effects have long been recognized as complications to beta-blocker treatment. However, evidence of a longitudinal relationship between the use of beta-blockers and incident dementiais still controversial. Objective To evaluate the longitudinal relationship between use of beta-blockers, as a class, and incident risk of all-cause dementia, vascular dementia, Alzheimer and mixed dementia. Methods From the prospective, population-based, Malmö Preventive Project, 18,063 individuals (mean age 68.2, males 63.4%) were included at baseline and followed for 84,506 person-years. Patients with prevalent cerebrovascular disease and dementia were excluded. In order to weight the risk of incident dementia associated with beta-blocker consumption, we performed propensity score matching analysis, resulting in 3,720 matched pairs of beta-blocker users and non-users at baseline, and multivariable Cox proportional-hazardsregression. Results Overall, 122 study participants (1.6%) were diagnosed with dementia over the course of follow-up. Use of beta-blockers was independently associated with increased risk of developing vascular dementia, regardless of confounding factors (HR: 1.72, 95% CI 1.01–3.78; p=0.048). Conversely, treatment with BB was not associated with increased risk of all-cause, Alzheimer and mixed dementia (HR: 1.15; 95% CI 0.80–1.66; p=0.44; HR: 0.85; 95% CI 0.48–1.54; P=0.59 and HR: 1.35; 95% CI 0.56–3.27; p=0.50, respectively). Conclusions and relevance We observed that use of beta-blockers, as a class, is associated with increased longitudinal risk of vascular dementia in the general elderly population, regardless of cardiovascular risk factors, prevalent or incident history of atrial fibrillation, stroke, coronary events and heart failure. Further studies are needed to confirm our findings in the general population and to explore the mechanisms underlying the relationship between use of beta-blockers and increased risk of vascular dementia.

Graves’ Hyperthyroidism-Induced Psychosis Treated With Aripiprazole—A Case Report

2012 ◽  
Vol 26 (1) ◽  
pp. 59-61 ◽  
Author(s):  
Livia R. Macedo ◽  
Jehan Marino ◽  
Brady Bradshaw ◽  
Joseph Henry
Keyword(s):  
Atrial Fibrillation ◽  
Psychiatric Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Long Term Effects ◽  
Free T4 ◽  
History Of ◽  
Antithyroid Peroxidase Antibody ◽  
First Time

Graves’ disease is an autoimmune syndrome with symptoms such as tachycardia, atrial fibrillation, and psychiatric symptoms. Limited evidence exists for the treatment of Graves’ hyperthyroidism-induced psychosis with atypical antipsychotics. A 47-year-old female with a psychiatric history of bipolar disorder presented for the first time to the psychiatric hospital. She was agitated and grossly psychotic with delusions. Electrocardiogram showed atrial fibrillation and tachycardia. Drug screen urinalysis was negative. Endocrine workup resulted in a diagnosis of Graves’ disease (thyroid-stimulating hormone [TSH]: 0.005 μIU/mL, triiodothyronine [T3]: 537 ng/dL, thyroxine [T4]: 24 mcg/dL, free T4: 4.5 ng/dL, positive antithyroid peroxidase antibody, and antinuclear antibody). Aripiprazole 10 mg daily was initiated and titrated to 15 mg daily on day 4. On day 16, her suspicious behavior, judgment, and insight improved. Other medications given included aspirin 325 mg daily, metoprolol 25 mg twice daily, titrated to 12.5 mg twice daily, and methimazole 30 mg daily, titrated to 20 mg twice daily, and discontinued on day 29. The patient received radioiodine I-131 treatment 1 week later. We report the first known case on the use of aripriprazole to treat Graves’ hyperthyroidism-induced psychosis. Further studies examining the long-term effects and appropriate dose and duration of aripiprazole in this patient population are needed.

Graves' disease, endocrine ophthalmopathy and smoking

1993 ◽  
Vol 128 (2) ◽  
pp. 156-160 ◽  
Author(s):  
Brita Winsa ◽  
Agneta Mandahl ◽  
F Anders Karlsson
Keyword(s):  
Confidence Interval ◽  
Odds Ratio ◽  
Eye Disease ◽  
Graves Disease ◽  
Retrospective Survey ◽  
Eye Problems ◽  
Increased Risk ◽  
Endocrine Ophthalmopathy ◽  
History Of ◽  
Receptor Antibodies

We have evaluated the association between smoking, Graves' disease and endocrine ophthalmopathy in a case-control study of 208 patients with newly diagnosed Graves' disease and carried out a retrospective survey of 72 patients treated for Graves' disease and admitted to our ward because of endocrine ophthalmopathy. In the prospective study, patients with Graves' disease smoked significantly more than their healthy controls (41% vs 30%, p<0.01 for current smokers, odds ratio 1.6, 95% confidence interval 1.1-2.3, and p<0.05 for patients with a history of smoking, odds ratio: 1.4, 95% confidence interval 1.0-1.9). Among the patients with endocrine ophthalmopathy at diagnosis, there were slightly more patients with a history of smoking (p <0.05, odds ratio 2.1, 95% confidence interval 1.1-3.9), but not more current smokers when compared with the remaining group. The patients with eye problems tended to have a more active disease with higher levels of thyroxine and TSH-receptor antibodies, but no difference was seen in thyrogastric autoantibodies. No effect of smoking on thyroid hormone and autoantibody levels could be detected. In the retrospective survey we found 64%, 71% and 87% smokers among patients with moderate, severe and malignant eye disease, respectively. In summary, the results show that smoking is associated with an increased risk of contracting Graves' disease and that it enhances the severity of the eye disease in cases that develop endocrine ophthalmopathy during the course of treatment.

scholarly journals SUN-524 Patient with Pseudohypoparathyroidism Type 1B, Graves Disease, and False Positive HIV Screen- a Rare Presentation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Viraj V Desai ◽  
Pratima V Kumar
Keyword(s):  
Western Blot ◽  
Autoimmune Diseases ◽  
False Positive ◽  
Thyroid Stimulating Hormone ◽  
Laboratory Evaluation ◽  
Graves Disease ◽  
Free T4 ◽  
Rare Presentation ◽  
Elisa Testing ◽  
History Of

Abstract Background: Pseudohypoparathyroidism 1B (PHP1B) is a disorder that can lead to thyroid stimulating hormone (TSH) resistance and hypothyroidism, although it is rarely associated with thyrotoxicosis. Clinical Case: A 25-year-old female with a history of PHP1B, seizures due to hypocalcemia, and family history of PHP1B in her three sisters and brother presented to our emergency room with a fever of 1030F and generalized malaise. Two months prior, she was seen at an outside hospital with palpitations and bulging of the left eye. There, she was diagnosed with hyperthyroidism, started on methimazole, and asked to continue levetiracetam and calcitriol upon discharge. On our exam, she had tachycardia of 120 beats per minute, left eye proptosis, positive Chvostek sign, and a large goiter with bruit. Reflexes were 3+. Laboratory evaluation revealed corrected serum calcium of 6.1 (8.5-10.5 mg/dL), TSH &lt; 0.01 (0.34-5.60 mU/L), free T4 2.81 (0.60-1.60 ng/dL), free T3 13.0 (2.4-4.2 ng/dL), and iPTH 131 (12-88 pg/mL). ELISA testing for screening of HIV was positive. She was treated with IV calcium gluconate, methimazole, propranolol, and hydrocortisone. Her home doses of calcitriol and calcium were resumed. She was referred for total thyroidectomy as an outpatient once she became euthyroid. The confirmatory Western blot test for HIV was negative. It was determined that presence of thyroid stimulating immunoglobulin resulted in the false positive ELISA test. Discussion: Hyperthyroidism with Graves disease seen in PHP has only very rarely been reported. (1) It has been postulated that abnormal electrolytes and elevated parathyroid hormone from PHP may lead to stimulation of the thyroid gland and perpetuate Graves disease symptoms. (2) Furthermore, the presentation of thyrotoxicosis despite TSH resistance in PHP indicates that there may be other mechanisms for TSH receptor antibodies to take effect in these patients which have not yet been determined. (3) Lastly, autoimmune diseases, including Graves disease, can cause a false-positive HIV ELISA as seen in our patient. Conclusion: Although rare, thyrotoxicosis may present in patients with PHP1B. Additionally, it should be kept in mind that autoimmune diseases such as Graves disease can cause a false positive HIV ELISA, and follow-up Western blot testing should therefore be performed. References: (1) Gerhardt A, Hackenberg K. 2002. Pseudohypoparathyroidism and Graves’ disease: a rare combination of two endocrinological diseases. Exp Clin Endocrinol Diabetes. 110:245-247 (2) Morón-Díaz et al. 2019. A rare case of Graves’ disease in a patient with type 1B pseudohypoparathyroidism and associated TSH resistance. Endocrine Abstracts. 63:96 (3) Richard Prokesch. 2010. Navigating False Positive Testing. HIV Specialist (AAHIVS). 2:27

scholarly journals Thyroid Storm Treated With Nonconventional Therapy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A962-A962
Author(s):  
Caroline Tashdjian ◽  
Paul Shiu ◽  
Tarandeep Kaur
Keyword(s):  
Atrial Fibrillation ◽  
Critically Ill ◽  
Liver Enzymes ◽  
Normal Liver ◽  
Ventricular Rate ◽  
Thyroid Storm ◽  
Free T4 ◽  
History Of ◽  
Chest X Ray ◽  
Iodine Treatment

Abstract Background: Thyroid storm is a rare sequela of thyrotoxicosis with mortality rate of 10-30%. Management of thyroid storm is heavily dependent on thionamides. Cholestyramine and potassium iodide (SSKI) are used as adjunctive therapy and not as the sole treatment for storm. We present a case of thyroid storm treated with cholestyramine and SSKI. Clinical Case: A 45 year old male with past medical history of atrial fibrillation, congestive heart failure, hypertension, substance abuse and grave’s disease presented to the emergency department (ED) for diarrhea. During the course of ED, patient went into atrial fibrillation with rapid ventricular rate. Chest X-ray showed pulmonary edema. Labs were: TSH &lt;0.0025 mIU/L (0.35-4.94 mIU/L) and free T4 3.52 ng/dl (0.7-1.40 ng/dl). Patient was noncompliant with methimazole. Upon admit, ACLS was initiated due to hypoxia and transferred to ICU for ventilator and pressor support. Wartofsky score was 60, suggestive of thyroid storm. Management included methimazole 20mg every 4hours, hydrocortisone 100mg every 8 hours, cholestyramine 4mg every 6 hours, and SSKI 250mg every 6 hours for thyrotoxicosis and amiodarone infusion for afib. Despite normal liver enzymes on admit, day 3 AST increased to 2740 U/L (5-34) and ALT 2684 U/L (0-55). Methimazole was stopped due to potential hepatotoxicity. Day 3 free T4 remained high at 4.16 ng/dl and patient remained critically ill. Plasmapheresis was offered as methimazole was stopped and patient was hemodynamically unstable to undergo surgery. However, family declined this intervention; SSKI and cholestyramine were continued. Free T4 was monitored over the course of treatment; by day 5 free T4 trended down to 1.93 ng/dl. SSKI was eventually stopped on day 8 of treatment as free T4 had normalized and cholestyramine reduced to 4mg twice daily. By day 15, free T4 was 0.8 ng/dl, so cholestyramine was stopped. Due to clinical improvement, patient was weaned off the ventilator and pressor support along with hydrocortisone. Liver enzymes normalized by Day 17. Patient was restarted on methimazole 5mg daily before discharge. Discussion: Thyroid storm is associated with varying degree of liver dysfunction, which can pose a challenge to treatment. In our case, acute fulminant liver failure was multifactorial in the setting of shock, thyroid storm and potential drug toxicity. Thus, thionamides were contraindicated. Radioactive iodine treatment was contraindicated due to use of amiodarone. Plasmapheresis and emergent thyroidectomy could not be done. Thus, nonconventional therapy was used and patient responded well to treatment. This case emphasizes the use of cholestyramine along with SSKI as an effective treatment in patients who are critically ill the setting of a thyroid storm, especially when thionamides are contraindicated and other avenues of treatment are limited.

scholarly journals THYROID ACROPACHY: A RARE MANIFESTATION OF GRAVES DISEASE IN JOINTS

2019 ◽  
Vol 5 (6) ◽  
pp. e369-e371 ◽  
Author(s):  
Nicolas Perini ◽  
Roberto Bernardo Santos ◽  
João Hamilton Romaldini ◽  
Danilo Villagelin
Keyword(s):  
Elevated Serum ◽  
Clinical Signs ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Tissue Edema ◽  
Rare Manifestation ◽  
Small Joint ◽  
History Of ◽  
Hands And Feet

Objective: The objective of this report was to describe a patient with Graves acropachy, a rare manifestation of Graves disease (GD) that is clinically defined by skin tightness, digital clubbing, small-joint pain, and soft tissue edema progressing over months or years with gradual curving and enlargement of the fingers. Methods: The patient was evaluated regarding thyroid function (serum free T4 [FT4] and thyroid-stimulating hormone [TSH] quantifications) and autoimmunity biomarkers (thyroid receptor antibody [TRAb]) as well as radiographic investigation of the extremities. Results: A 52-year-old man presented with a history of thyrotoxicosis and clinical signs of Graves orbitopathy. Laboratory tests showed suppressed TSH (0.01 UI/L; normal, 0.4 to 4.5 UI/L) and elevated serum FT4 (7.77 ng/dL; normal, 0.93 to 1.7 ng/dL), with high TRAb levels (40 UI/L; normal, <1.75 UI/L). A diagnosis of thyrotoxicosis due to GD was made and the patient was treated with methimazole. After the patient complained of swelling in hands and feet, X-ray evaluation was conducted and established the thyroid acropachy. Conclusion: We present a case of a patient with GD associated with worsening extrathyroid manifestations during orbitopathy, dermopathy, and developed acropachy in hands and feet.

scholarly journals Graves disease-induced thrombotic thrombocytopenic purpura: a case report

2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Saira Chaughtai ◽  
Ijaz Khan ◽  
Varsha Gupta ◽  
Zeeshan Chaughtai ◽  
Raquel Ong ◽  
...  
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
African American Woman ◽  
Case Reports ◽  
American Woman ◽  
Pulseless Electrical Activity ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Thrombocytopenic Purpura ◽  
History Of

Abstract Background Thrombotic thrombocytopenic purpura is an autoimmune disease that carries a high mortality. Very few case reports in the literature have described a relationship between Graves disease and thrombotic thrombocytopenic purpura. We present a case of a patient with Graves disease who was found to be biochemically and clinically hyperthyroid with concurrent thrombotic thrombocytopenic purpura. Case presentation Our patient was a 30-year-old African American woman with a history of hypertension and a family history of Graves disease who had recently been diagnosed with hyperthyroidism and placed on methimazole. She presented to our hospital with the complaints of progressive shortness of breath and dizziness. Her vital signs were stable. On further evaluation, she was diagnosed with thrombotic thrombocytopenic purpura, depending on clinical and laboratory results, and also was found to have highly elevated free T4 and suppressed thyroid-stimulating hormone. She received multiple sessions of plasmapheresis and ultimately had a total thyroidectomy. The patient’s hospital course was complicated by pneumonia and acute respiratory distress syndrome. Her platelets stabilized at approximately 50,000/μl, and her ADAMTS13 activity normalized despite multiple complications. The patient ultimately had a cardiac arrest with pulseless electrical activity and died despite multiple attempts at cardiopulmonary resuscitation. Conclusion Graves disease is an uncommon trigger for the development of thrombotic thrombocytopenic purpura, and very few cases have been reported thus far. Therefore, clinicians should be aware of this association in the appropriate clinical context to comprehensively monitor hyperthyroid patients during treatment.

scholarly journals SUN-513 Severe Hyperthyroidism in a Complete Molar Pregnancy

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nikoletta Proudan ◽  
Kersthine Andre
Keyword(s):  
Perioperative Complications ◽  
Hydatidiform Mole ◽  
Gestational Trophoblastic Disease ◽  
Thyroid Storm ◽  
Molar Pregnancy ◽  
Free T4 ◽  
Trophoblastic Disease ◽  
Increased Risk ◽  
History Of

Abstract Hydatidiform mole (HM), a type of gestational trophoblastic disease (GTD), is a rare cause of clinical hyperthyroidism. The development of hyperthyroidism requires an elevation of HCG &gt;100,000 mlU/mL for several weeks. Complete mole has a marked HCG elevation compared to partial mole thus presents with a higher incidence of thyrotoxicosis. Surgical uterine evacuation is the treatment of choice for HM. However, untreated hyperthyroidism can pose a risk for the development of thyroid storm and high-output cardiac failure in the perioperative period. To our knowledge, there are no specific guidelines for management at this time. We present a case of hyperthyroidism secondary to complete molar pregnancy successfully treated with propylthiouracil (PTU), potassium iodide (SSKI), and atenolol in the preoperative period. A 42-year-old female with history of migraines presented to her gynecologist with a 3-week history of lower abdominal cramping, vomiting, loss of appetite, and abnormal vaginal bleeding. She also endorsed a 6-pound weight loss, intermittent tachycardia, exertional dyspnea, and increased anxiety. Pregnancy test was positive, and ultrasound was concerning for GTD. Laboratory work up was significant for HCG 797,747 mIU/mL (&lt; 5mlU/mL), TSH &lt;0.005 mIU/mL (0.4-4.0 mlU/mL), Free T4 3.09 ng/dL (0.9-1.9 ng/dL), and Free T3 11.48 pg/dL (1.76-3.78 pg/dL). The patient was admitted to the hospital and started on PTU 100 mg Q6H, SSKI 200 mg TID following the first dose of PTU, and atenolol 25 mg daily. She underwent an uncomplicated D & C the next day. On post-op day 1, HCG decreased to 195,338 mIU/mL and Free T4 to 2.39 ng/dL. The patient was discharged on the aforementioned doses of PTU and atenolol. One-week follow-up labs showed HCG 8,917 mIU/mL and Free T4 1.22 ng/dL. Surgical pathology confirmed a complete hydatidiform mole. PTU was decreased to 50 mg TID. On post-op day 14, HCG had risen to 15,395 mIU/mL with onset of nausea and vomiting. Repeat Free T4 remained within reference range. Patient was taken back to surgery for a laparoscopic total hysterectomy with bilateral salpingectomy. Pathology confirmed an invasive hydatidiform mole. Two-week follow-up lab work showed HCG 155 mIU/mL, TSH 1.5 mIU/mL, and Free T4 1.19 ng/dL. PTU and atenolol were then discontinued. The development of hyperthyroidism in molar pregnancy is largely influenced by the level of HCG and usually resolves with treatment of GTD (1). However, it’s crucial to control thyrotoxicosis to avoid perioperative complications. This case also highlights the importance of monitoring HCG levels following a complete molar pregnancy due to an increased risk for invasive neoplasm. 1. Walkington, L et al. “Hyperthyroidism and human chorionic gonadotrophin production in gestational trophoblastic disease.” British journal of cancer vol. 104,11 (2011): 1665-9. doi:10.1038/bjc.2011.139

Severe hypercalcaemia secondary to relapsed Graves’ disease

2021 ◽  
Vol 14 (1) ◽  
pp. e238898
Author(s):  
Haris Khan ◽  
Maimoona Nawaz ◽  
Jonathan Schofield ◽  
Handrean Soran
Keyword(s):  
Vitamin D ◽  
Thyroid Stimulating Hormone ◽  
Bisphosphonate Therapy ◽  
Graves Disease ◽  
Oral Vitamin ◽  
Free T4 ◽  
History Of ◽  
Severe Hypercalcaemia ◽  
Intravenous Bisphosphonate ◽  
Learning Points

A 21-year-old woman presented to hospital with abdominal pain and nausea. She had a history of Graves’ disease which had been effectively treated with carbimazole for 15 months. Investigations revealed a serum adjusted calcium level of 3.69 mmol/L with a suppressed parathyroid hormone, thyroid stimulating hormone <0.01 mu/L (0.2–5.0) and free T4 of 76.1 pmol/L (9-24). She was treated as a relapsed case of Graves’ disease and started on propylthiouracil. Calcium levels continued to increase over the next 3 days despite adequate fluid resuscitation. A decision was taken to administer intravenous bisphosphonate (pamidronate) which resulted in a lowering of calcium levels. She became mildly hypocalcaemic following treatment with pamidronate which was presumed secondary to low vitamin D and oral vitamin D replacement was commenced. This case was unique as this is to our knowledge the most significant hypercalcaemia observed in a patient with hyperthyroidism. All other causes of hypercalcaemia were excluded. The learning points were recognising hypercalcaemia as a complication of thyrotoxicosis and the risk of hypocalcaemia following bisphosphonate therapy with low vitamin D stores.

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