scholarly journals Thyrotoxic Dysphagia in an 82-Year-Old Male

2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Konstantinos Parperis ◽  
Ramona Dadu ◽  
Sheikh Hoq ◽  
Vivian Argento

Dysphagia is a common problem in elderly patients and a rare manifestation of Graves' disease. We report a case of an 82-year-old male who presented with a 4-week history of dysphagia and weight loss. Workup for his dysphagia with upper endoscopy, MRI brain, electromyography, acetyl-cholinesterase receptor antibodies, and voltage-gated calcium channel antibodies were negative. Modified Barium swallow test showed oropharyngeal dysphagia. Thyroid function tests that revealed hyperthyroidism and antibodies to TSH-receptor were positive. Based on the above findings, we considered Graves' disease as the most likely diagnosis. Patient was treated with methimazole and beta-blockers and subsequently his dysphagia resolved. This paper highlights the importance to clinicians of considering thyrotoxicosis as possible diagnosis in an elderly patient presenting with unexplained dysphagia.

2021 ◽  
Vol 20 (1) ◽  
pp. 68-73
Author(s):  
Avinash Aujayeb ◽  
◽  
James Dundas ◽  

A 30-year-old female patient with a past medical history of pernicious anaemia presented with pleuritic chest pain, palpitations, fatigue, coryzal symptoms and a high temperature. She was hypoxic and tachycardic and was extensively investigated as well as aggressively treated. A type 1 ‘gut feeling’ assessment by the admitting medical registrar made the diagnosis possible as thyroid function tests were grossly deranged and pointed to Graves’ disease causing heart failure, complicated by pneumonia. The patient was discharged on carbimazole, antibiotics and beta blockers. Due to a resultant thrombocytopaenia, she has now been swapped onto propylthiouracil and is under active follow up.


2020 ◽  
Vol 13 (3) ◽  
pp. e231337
Author(s):  
Michael S Lundin ◽  
Ahmad Alratroot ◽  
Fawzi Abu Rous ◽  
Saleh Aldasouqi

A 69-year-old woman with a remote history of Graves’ disease treated with radioactive iodine ablation, who was maintained on a stable dose of levothyroxine for 15 years, presented with abnormal and fluctuating thyroid function tests which were confusing. After extensive evaluation, no diagnosis could be made, and it became difficult to optimise the levothyroxine dose, until we became aware of the recently recognised biotin-induced lab interference. It was then noticed that her medication list included biotin 10 mg two times per day. After holding the biotin and repeating the thyroid function tests, the labs made more sense, and the patient was easily made euthyroid with appropriate dose adjustment. We also investigated our own laboratory, and identified the thyroid labs that are performed with biotin-containing assays and developed strategies to increase the awareness about this lab artefact in our clinics.


2019 ◽  
Vol 65 (6) ◽  
pp. 830-833 ◽  
Author(s):  
Roberto Vita ◽  
Valeria Cernaro ◽  
Salvatore Benvenga

SUMMARY OBJECTIVE Even though stress has been long known as a provocative factor for Graves’ disease, its relationship with Hashimoto's thyroiditis is more controversial. Studies on this topic are scanty. This paper aims to report a case of stress-induced Hashitoxicosis. RESULTS Here we report a case of Hashitoxicosis induced by a psychological stressful event in a 28-year-old woman with Hashimoto's thyroiditis. She had remained stably euthyroid for 12 years. She was first observed in April 2016, while euthyroid. She came back after 11 months because of fatigue and palpitations, in the absence of neck pain. Thyroid function tests revealed moderate thyrotoxicosis (undetectable TSH; FT4 36.94 pmol/L, normal values 9.0-24.46; FT3 13.50 pmol/L, normal values 3.07-6.14) with negative TSH-receptor antibodies. In the previous three months, she had experienced a psychological stressful event. Inflammatory markers were negative, and the white cell count was normal. Thyroid ultrasound revealed a modest increase in vascularization. Transient subclinical hypothyroidism ensued after seven weeks and spontaneously recovered. On the last visit, the patient was still on euthyroidism. (TSH 1.01 mU/L; FT4 9.22 pmol/L; FT3 3.98 pmol/L). We also performed HLA serotyping and genotyping. CONCLUSION This case demonstrates that, similarly to Graves’ disease, Hashitoxicosis can also be triggered by stressful life events.


1993 ◽  
Vol 128 (2) ◽  
pp. 156-160 ◽  
Author(s):  
Brita Winsa ◽  
Agneta Mandahl ◽  
F Anders Karlsson

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.


2019 ◽  
Vol 5 (6) ◽  
pp. e369-e371 ◽  
Author(s):  
Nicolas Perini ◽  
Roberto Bernardo Santos ◽  
João Hamilton Romaldini ◽  
Danilo Villagelin

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.


2020 ◽  
Vol 13 (3) ◽  
pp. e230989
Author(s):  
Abubakar Sharif ◽  
Lucinda Carr ◽  
Efstratios Saliakellis ◽  
Himadri Chakraborty

We present a case of Sandifer syndrome in a 3-year-old girl who initially presented with a history of recurrent paroxysmal head drops associated with ataxia-like symptoms and recurrent falls sustaining a clavicular fracture on one occasion. She was referred to and seen by the paediatric neurologist. Physical examination, electroencephalogram, MRI brain, electromyograph single fibre study and blood tests were all normal. With the history of hiccups and choking-like episodes she was referred to the speech and language therapist (SALT). SALT assessment did not reveal indications of swallowing impairment or possible aspiration. A barium swallow later showed small amount of reflux into the distal oesophagus. This prompted a trial of lansoprazole and she was referral to the gastroenterologists. Endoscopy and oesophageal manometry were essentially normal. However, the pH impedance study revealed severe gastro-oesophageal reflux disease. She continued with lansoprazole and dairy-free diet and her symptoms resolved.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A908-A909
Author(s):  
Ally Wen Wang ◽  
Geeti Mahajan ◽  
Aaron Etra ◽  
Shira R Saul

Abstract Introduction: Graves’ disease has been associated with cytopenias, most commonly anemia. Pancytopenia is a rare complication and is not often encountered. Case Presentation: A 54-year-old woman with history of multiple sclerosis on alemtuzumab was referred for abnormal thyroid function tests. At the initial visit, the patient reported a 20-pound unintentional weight loss, tremors, sweating and heat intolerance. She was 3 years post-menopausal and had no history of recent viral illness, contrast exposure or family history of thyroid disease. Physical exam revealed an anxious appearing woman with fine tremors in both hands, hyperreflexia but no lid lag or exophthalmos. Labs included TSH &lt;0.005 uIU/mL (0.400-4.2), free T4 2.89 ng/dL (0.80-1.50), TSH receptor binding antibody 8.24 IU/L (&lt; 2.00), TSI 7.27 IU/L (&lt;0.56), WBC 2900/uL (4500-11000), ANC 1746/uL (1900 - 8000), hemoglobin 11.4 g/dL (11.7-15.0) and platelet 207,000/uL (150,000-450,000). Thyroid ultrasound noted sub-centimeter hypoechoic/cystic nodules and 24-hour thyroid uptake showed 56.4% symmetric uptake (upper limit of normal 30%). Due to leukopenia, the patient was started on propranolol and underwent radioiodine ablation with 14.8 mCI. Two weeks later, she reported easily bruising and gum bleeding and her blood work was significant for pancytopenia. The patient was referred to hematology and two bone marrow samples were obtained. Though MDS/MPN was initially suspected based on atypia in both specimens, there were no immunophenotypic, cytogenetic or molecular abnormalities suggesting a neoplastic process. Instead the patient was thought to have autoimmune pancytopenia secondary to Graves’ and the atypia was believed to be secondary to peripheral consumption. She was started on prednisone 1 mg/kg/day with resolution of her cytopenias. Discussion: Graves’ disease has been associated with hematological abnormalities including isolated anemia (the most common), thrombocytopenia or leukopenia. Pancytopenia is an uncommon complication and is rarely described in the literature. The exact mechanism remains unclear, but may be related to either reduced production of hematopoietic cells from the bone marrow or increased destruction of mature hematopoietic cells due to autoantibodies. Since thyroid hormones are known to increase erythropoietin, this leads to an exaggerated consumption of iron, folic acid and vitamin B12 and can cause various forms of anemias. Leukopenia may be secondary to immunologic destruction whereas thrombocytopenia may be due to antiplatelet antibodies or increased splenic sequestration. Pancytopenia is rare. Our patient was treated with high dose prednisone with resolution of her pancytopenia, which suggests an autoimmune process as the mechanism. Our case showcases a rare complication of Graves’ disease and highlights that high dose steroid therapy may improve cytopenias associated with this condition.


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 (Supplement_1) ◽  
Author(s):  
Isabelle Daneault Peloquin ◽  
Matthieu St-Jean

Abstract Clinical vignette ENDOCRINE SOCIETY 2020 Title: A case of T3 thyrotoxicosis induced by a dietary supplement. A 24 yo man consulted for a 2 weeks history of diaphoresis, fatigue, insomnia, palpitations and headache associated with a 20 pounds lost. The patient didn’t have a goiter or any signs of orbitopathy. The results revealed a free T3 level of 45.8 pmol/L upon arrival (normal (N) 3.4- 6.8 pmol/L), free T4 level of 6.4 pmol/L (N 11.0–22.0 pmol/L) and TSH level less than 0.005 mUI/L (N: 0.35 to 3.50 mUI/L). Facing those results, a complete review of the patient medication and natural product consumption was done. The patient revealed that he was using, since a month, a vegetable extracts nutritional supplement that didn’t included iodine. He was asked to stop the nutritional supplement and propranolol 10 mg twice daily was prescribed. Thyroid function tests were done 3 days after. The results demonstrate a fT3 level of 4.6 pmol/L, a fT4 level of 5.6 pmol/L and a TSH that still suppressed. A thyroid scintigraphy was performed 7 days later and showed a homogeneous uptake of 18.5% (N 7.0% – 35.0%). We saw the patient 2 weeks later and we ordered another thyroid function test with TSH receptor antibodies, TPO antibodies and thyroglobulin. The results were the following: fT3 of 5.1 pmol/L, fT4 of 12.1 pmol/L, TSH of 2.31 mUI/L, thyroglobulin of 19.8 ug/L (N: 1.4 – 78) and normal levels of antibodies against TPO and TSH receptors. To confirm the contamination of the nutritional supplement by fT3 we used a plasma pool of normal patients in which we measured thyroid function tests at baseline and after we have added the nutritional supplement powder to reflect the dose suggested by the manufacturer. The results showed that fT3 level increased by 36.5%, fT4 by 11.2% and TSH didn’t changed. The powder was then analyzed by an external laboratory that wasn’t able to demonstrate the presence of fT3 nor fT4. The two diagnostic possibility facing those results were that the powder induced an interference with immunoassay used to measure fT3 and fT4 but not TSH or thyrotoxicosis induced by the nutritional supplement with limitation in the technique that tried to identify fT3 in the powder. Given the presentation of the patient, we are convinced that this case represents a thyrotoxicosis induced by a nutritional supplement. In conclusion, Graves’ disease is responsible for 60–80% of the cases of hyperthyroidism. However, there are few cases reports of thyrotoxicosis induced by nutritional supplement1,2, but some studies demonstrate the presence of thyroid hormone in significant amounts in some commercially available health supplements3. This case highlights the importance of verifying exposition to medications and natural products when confronted to cases of thyrotoxicosis. 1.Regina A et al. MMWR Morb Mortal Wkly Rep. 2016 2. Panikkath R et al. Am J Ther. 2014 3. Kang GY et al. Thyroid. 2013


2020 ◽  
pp. 1-2
Author(s):  
Showkat Nazir Wani ◽  
Anish Garg Atul Kaushik ◽  
Atul Kaushik ◽  
Naveen Tariq

We report a case of dengue fever with features of encephalitis from Northern India. A 22 years female presented with history of high-grade fever with chills for 2 days followed by altered sensorium and MRI brain, revealed characteristic changes consistent with Encephalitis with hemorrhage mainly involving the bilateral thalami. The diagnosis of dengue was confirmed by the presence of dengue antigen in the serum and the presence of dengue antibodies in the serum as well as cerebrospinal fluid. Dengue is not primarily a neurotropic virus and encephalopathy is an uncommon finding in dengue. This case explains the importance of considering dengue encephalitis as the differential diagnosis of fever with altered sensorium, especially in countries like India where dengue is rampant.


Sign in / Sign up

Export Citation Format

Share Document