In iodine-induced thyrotoxicosis, steroid therapy today could keep the surgical knife at bay

2018 ◽  
Vol 31 (5) ◽  
pp. 585-588 ◽  
Author(s):  
Rohan K. Henry ◽  
Monika Chaudhari

Abstract Background: Amiodarone-induced thyrotoxicosis (AIT) type 2, characterized as a destructive thyroiditis, is well described in the medical literature; however, iodine-induced thyrotoxicosis (IIT) is not, though the latter has similar features and can be managed similarly. Case presentation: We present a 17-year-old female who presented with a history of an intermittent goiter with thyroid function tests (TFTs): thyroid-stimulating hormone (TSH)<0.015 (0.4–4 μU/mL), free thyroxine (T4)≥6 (0.7–2.1 ng/dL) and total triiodothyronine (T3) 651 (50–200 mg/dL). Thyroid antibodies were all negative. Despite methimazole therapy for 6 weeks, hyperthyroidism proved refractory to medical management. 123I scan uptake was suppressed. With hyperthyroidism being recalcitrant to therapy, a nutritional history revealed consumption of an iodine supplement containing at least 7 times the recommended daily allowance (RDA) for 5 years, contributing to the Jod-Basedow phenomenon. Urinary spot and 24-hour urinary iodine were both elevated. Though a surgical consult was obtained, surgery was cancelled once TFTs improved and then normalized with steroid therapy. The TFTs and urinary iodine levels remained normal post steroid therapy. Conclusions: We suggest that in addition to the need for a thorough nutritional history, a trial of corticosteroids should be utilized in the management of IIT which can present with findings similar to AIT type 2 which is recalcitrant to thionamide therapy. If successful, corticosteroids may delay or prevent surgical management thus avoiding possible complications with the latter approach.

2021 ◽  
Vol 14 (1) ◽  
pp. e238145
Author(s):  
Darryl Portelli ◽  
Simon Mifsud ◽  
Alexia Abela ◽  
Stephen Fava

The authors present a case of a 55-year-old gentleman with a medical history of atrial fibrillation on amiodarone who presented with weight loss, palpitations and exertional dyspnoea. Thyroid function tests revealed thyrotoxicosis with a free thyroxine (T4) of 117 pmol/L and a thyroid-stimulating hormone (TSH) of <0.008 mIU/L. Interleukin-6 level was low. The negative TSH-receptor antibody status, the presence of a small thyroid gland with heterogeneous echotexture and decreased internal vascularity on ultrasound together with the relatively quick drop in free T4 and free tri-iodothyronine (T3) levels once prednisolone therapy was added to carbimazole suggested that this was typical of amiodarone-induced thyrotoxicosis (AIT) type 2. Subsequently, carbimazole was discontinued and treatment with prednisolone was continued. This case highlights that AIT management may be challenging and it is of paramount importance to establish the type of AIT present as this will guide management and is key to improving prognosis.


2020 ◽  
Vol 14 (1) ◽  
Author(s):  
Ahmad Al-Mousa ◽  
Mohammad Nour Shashaa ◽  
Mohamad Shadi Alkarrash ◽  
Mohamad Alkhamis ◽  
Lina Ghabreau ◽  
...  

Abstract Background Seminoma is the most common subtype of testicular cancer and occurs most commonly in patients aged 30–49 years, but decreases to a very low level in men in their 60s or older. Case presentation A 90-year-old Syrian man with a 6-year history of an increase in size of his right scrotum, presented to the urological clinic and, on clinical examination, the findings suggested testicular tumor. After orchiectomy and histology results based on microscopic and immunohistochemical examinations, a pure seminoma was diagnosed, so we describe in this case report the second-oldest patient with classical seminoma in the medical literature. Conclusion This case report has been written to focus on the probability of any type of testicular tumor occurring at any age or decade; urologists should consider seminoma as a differential diagnosis with any testicular swelling even in elderly patients.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A171-A172
Author(s):  
Abdul Mannan Khan ◽  
James Lightell ◽  
Corey Majors

Abstract Background: A Case of Hypocalcemia Secondary to Infection with SARS-CoV-2 Virus. Clinical Case: A 40 year-old obese male presented to the emergency department with a five day history of nausea, vomiting, shortness of breath, and nonproductive cough. Symptoms progressed culminating in a single episode of pre-syncope leading to his seeking medical care. Positive testing for the presence of SARS-CoV-2 as well as findings from computed tomography of the patient’s chest led to a diagnosis of COVID-19 and the patient’s admission to a COVID-19 ward, where treatment with dexamethasone, doxycycline, and 2 L oxygen via nasal cannula began. Blood testing on admission revealed profound hypocalcemia (6.2 mg/dL total and 3.5 mg/dL ionized) as well as newly diagnosed diabetes mellitus type 2 (T2DM) (HbA1c 13.0% on admission). Further electrolyte disturbances noted were consistent with his history of vomiting and untreated T2DM. Thyroid stimulating hormone and thyroxine levels showed primary hypothyroidism, but the patient’s parathyroid hormone level (16.5 pg/mL) was inappropriately normal. No other causes for hypocalcemia were identified. The patient’s hypocalcemia was treated with intravenous calcium gluconate and rose consistently through day six of hospitalization. Calcium fell sharply between day six and seven (7.6 mg/dL to 7.3 mg/dL) coinciding with worsening respiratory symptoms and requiring a doubling of oxygen dose from 2 to 4 L with subsequent improvement in hypocalcemia once underlying pulmonary function improved. Discussion: SARS-CoV-2 infection presenting with hypocalcemia has been well documented without definitive explanation [1]. Further, while the precise mechanism of SARS-CoV-2 virion export is unclear, the patient’s worsening hypocalcemia, respiratory symptoms, and concurrent presumable increased viral load suggests this is caused by a calcium-dependent exocytotic process [2]. 1: Marazuela, M., Giustina, A. & Puig-Domingo, M. Endocrine and metabolic aspects of the COVID-19 pandemic. Rev Endocr Metab Disord 21, 495–507 (2020). https://link.springer.com/article/10.1007/s11154-020-09569-22: Fehr A.R., Perlman S. (2015) Coronaviruses: An Overview of Their Replication and Pathogenesis. In: Maier H., Bickerton E., Britton P. (eds) Coronaviruses. Methods in Molecular Biology, vol 1282. Humana Press, New York, NY. https://link.springer.com/protocol/10.1007%2F978-1-4939-2438-7_1.


2019 ◽  
Vol 12 (8) ◽  
pp. e228936
Author(s):  
Navneet Kaur ◽  
Ulrich Schubart ◽  
Adel Mandl

A 56-year-old woman with a history of hypothyroidism and chronic constipation presented with an acute abdomen due to colonic pseudo-obstruction. Thyroid function tests were consistent with central hypothyroidism prompting intravenous administration of stress-dose glucocorticoids and levothyroxine. The patient then underwent emergency exploratory laparotomy with sigmoid resection and end-colostomy. The postoperative endocrine evaluation revealed that the patient had panhypopituitarism due to Sheehan’s syndrome (SS). The diagnosis had been missed by physicians who had been treating her for several years for presumed primary hypothyroidism with a low dose of levothyroxine, aimed at normalising a minimally elevated thyroid-stimulating hormone (TSH) level. This is the second reported case of SS presenting with colonic pseudo-obstruction and it illustrates the potential danger of relying on measurement of TSH alone in the evaluation and treatment of thyroid dysfunction.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kevin Kohm ◽  
Shivani Vekaria ◽  
Jack Xu ◽  
Carol Nasr ◽  
Lauren Hogshire

Abstract Introduction Myxedema 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 Case A 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. Conclusion Severe 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.


2020 ◽  
Vol 4 (3) ◽  
pp. 461-463
Author(s):  
Megan Gillespie ◽  
Patrick Flannery ◽  
Jessica Schumann ◽  
Nathan Dincher ◽  
Rebecca Mills ◽  
...  

Introduction: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2.1 COVID-19 first occurred in Wuhan, China, in December 2019, and by March 2020 COVID-19 was declared a global pandemic.1 Case Presentation: We describe a case of a 52-year-old female with past medical history of asthma, type 2 diabetes, and previous tobacco use who presented to the emergency department with dyspnea and was found to be positive for COVID-19. We discuss the computed tomographic finding of “crazy-paving” pattern in the patient’s lungs and the significance of this finding in COVID-19 patients. Discussion: Emergency providers need to be aware of the different imaging characteristics of various stages of COVID-19 to appropriately treat, isolate, and determine disposition of COVID-19 infected patients. Ground-glass opacities are the earliest and most common imaging finding for COVID-19.2-4 Crazy-paving pattern is defined as thickened interlobular septa and intralobular lines superimposed on diffuse ground-glass opacities and should be recognized by emergency providers as a radiographic finding of progressive COVID-19.2-4


Author(s):  
Doris Taha ◽  
Amita Adhikari ◽  
Leigh Anne Flore

AbstractObjectivesActivating germline mutations of the thyroid-stimulating hormone receptor (TSHR) are responsible for a rare form of neonatal nonautoimmune hyperthyroidism (NAH). We report the first case of familial neonatal neonatal nonautoimmune associated with c.1856A>G (p.Asp619Gly) variant in the TSHR gene.Case presentationWe describe an eight-year-old African-American female presenting with neonatal NAH associated with an inherited heterozygous c.1856A>G (p.Asp619Gly) variant in the TSHR gene. This variant was previously described in one patient presenting with sporadic NAH in adolescence. Our patient was diagnosed with hyperthyroidism in the neonatal period. The mother had a history of hyperthyroidism and had thyroidectomy at the age of 4 years. The patient had goiter and elevated free thyroxine (FT4) and free triiodothyronine (FT3) levels that normalized with methimazole treatment; however, TSH level remained suppressed. Thyroid antibodies were negative. The patient also had bilateral exotropia, a trait shared by the mother and may represent a new association.ConclusionsFamilial neonatal NAH is associated with heterozygous c.1856A>G (p.Asp619Gly) variant of the TSHR gene.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Rediet Ambachew ◽  
Tizita Yosef ◽  
Aklilu M. Gebremariam ◽  
Lishan Demere ◽  
Theodros Aberra ◽  
...  

Abstract Background Pretibial myxedema also known as localized myxedema, thyroid dermopathy, or infiltrative dermopathy and rarely as localized mucinosis is an infrequent manifestation of Graves’ disease. It can appear before, during, or after the thyrotoxic state. Euthyroid pretibial myxedema is a rare presentation with few case reports in the literature. This case highlights the importance of considering pretibial myxedema when characteristic skin lesions are observed in a euthyroid patient. Case presentation A 72-year old male Ethiopian patient with a very rare presentation of biopsy-proven pretibial myxedema in a euthyroid state without history of thyroid disease and absence of thyroid autoimmune markers. Resolution of skin lesion was achieved after topical corticosteroid application. Conclusion Absence of history of thyroid disorder and normal thyroid function tests should not exclude the diagnosis of pretibial myxedema.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A939-A940
Author(s):  
Anjani Pandya ◽  
Jawairia Shakil

Abstract Lenvatinib is an antineoplastic oral agent that acts as a multi-kinase inhibitor against vascular endothelial growth factor (VEGF). This drug is commonly known for its use against radioiodine-refractory differentiated thyroid cancer, but it is also approved for unresectable hepatocellular carcinoma (HCC). Side effects such as fatigue, hypertension, palmar-plantar erythrodysesthesia, diarrhea, decreased appetite, and hypothyroidism are frequently reported adverse effects. However, the incidence of hyperthyroidism is a less known phenomenon. This case describes a patient with HCC on lenvatinib therapy who develops destructive thyroiditis. A 69-year-old man with hepatitis c cirrhosis complicated by progressive hepatocellular carcinoma (Child-Pugh class A6) presented with generalized weakness, unintentional weight loss, heat intolerance, palpitations, and tremors. He had been started on chemotherapy with lenvatinib 12 mg/day four weeks prior to presentation. Endocrinology was consulted due to abnormal thyroid function tests (TFTs). He had no previous history of thyroid function abnormalities or family history of thyroid disease. Laboratory tests revealed a hyperthyroid state [total thyroxine (T4), 14.3 µg/dL (normal range 4.5-11.7); free thyroxine (FT4), 1.9 ng/dL (normal range 0.9-1.7); thyroid-stimulating hormone (TSH), 0.07 µIU/mL (normal range 0.27-4.20), and negativity for antibodies [anti-thyroid peroxidase antibody (TPO Ab), 0.8 IU/mL (normal range 0.0-9.0); thyroglobulin antibody (Tg Ab), &lt; 0.9 IU/mL (normal range 0.0-4.0); thyroid stimulating immunoglobulin (TSI), 90% (normal range &lt; 122)]. Ultrasonography revealed a mildly prominent thyroid gland, a homogenous echo texture, and no suspicious thyroid nodules. In addition, a 99m-technetium (99mTc) scintigraphy demonstrated reduced radioactive uptake that was consistent with thyroiditis. Therefore, this patient was diagnosed with lenvatinib-induced destructive thyroiditis. Palpitations improved with a beta-blocker and the patient was resumed on a lower dose of lenvatinib, 8 mg/day, one week later. About six weeks after the initial dose of lenvatinib, his TFT results normalized. Lenvatinib disrupts cell proliferation which can affect many organs, including the thyroid gland. Although several theories have been proposed, the exact underlying mechanism by which this occurs remains unknown. It is important to note that in addition to hypothyroidism, lenvatinib may also cause hyperthyroidism in the form of a transient destructive thyroiditis. This emphasizes the need to routinely check TFTs prior to the initiation of lenvatinib and throughout the course of therapy.


2020 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Tasleem Arif

Introduction: Linear atrophoderma of Moulin (LAM) is a rare dermatologic disorder characterized by hyperpigmented atrophic plaques following the Blaschko lines (BL). The trunk and limbs are the usual sites affected. Isolated facial involvement is an exceedingly rare entity. Despite a comprehensive medical literature search, the author could find only two cases of LAM where the lesions are exclusively localized to the face. In this article, the author presents the third case of LAM localized to face only. Case Presentation: A 26-year-old male complained of multiple linear non-pruritic pigmented lesions over the left side of the nose and glabellar area of six months’ duration. There was no history of erythema, thickening/hardening of skin, or violaceous border surrounding the lesions. On clinical examination, there were multiple hyperpigmented brownish lesions, the majority of which were depressed, involving the left ala and bridge of nose laterally and glabellar area in a Blaschkoid pattern. Diagnosis of LAM was established based on suggestive history and clinical examination. Conclusions: LAM is a rare disorder, and the facial localization makes it exceedingly rare. It should be kept in the differential diagnosis when hyperpigmented depressed lesions are present in a Blaschkoid pattern on the face.


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