Making weight: acute muscle weakness and hypokalaemia exacerbated by thyrotoxicosis factitia in a bodybuilder

Summary A 32-year-old Caucasian male presented to the emergency department with a one-day history of acute severe bilateral lower limb weakness, three days after competing in a bodybuilding competition. He consumed large quantities of carbohydrate-rich foods following the competition. His past medical history was significant for anxiety, and family history was non-contributory. Examination was normal except for reduced power and hyporeflexia in both legs, despite his muscular physique. He was noted to have severe hypokalaemia (K+= 1.9 mmol/L). His thyroid function tests were consistent with thyrotoxicosis. He reported taking thyroxine and several other agents to facilitate muscle mass generation before the bodybuilding competition. His presentation was reminiscent of thyrotoxic periodic paralysis, albeit uncommon with Caucasian ethnicity. He also had transient hyperglycaemia at presentation with concomitant hyperinsulinaemia, which could be attributed to the carbohydrate load and may have exacerbated his hypokalaemia through a transcellular shift. Urine toxicology screen subsequently ruled out the use of diuretics but confirmed the presence of a long-acting beta agonist (clenbuterol) which, along with other substances, may have aggravated the hypokalaemia further. After 12 h of i.v. replacement, the potassium level normalised and leg weakness resolved. The patient agreed to stop taking thyroxine and beta agonists and was well during the clinic visit at one month follow-up. This case highlights the potential for thyrotoxicosis factitia to exacerbate hypokalaemia and muscle weakness from other causes in bodybuilders presenting with acute severe weakness, irrespective of ethnicity. Learning points In patients presenting with muscle weakness and hypokalaemia, early consideration of thyrotoxicosis is essential, even in the absence of a past history of thyroid disease or specific symptoms of thyrotoxicosis, in order to allow prompt initiation of appropriate treatment and to prevent recurrence. Bodybuilders may constitute a uniquely ‘at-risk’ group for thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia, especially where there is concomitant use of beta-adrenergic agonists, even in the absence of diuretic use. Although rare and usually described in patients of Asian or Polynesian ethnicity, this case highlights that thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia can also occur in patients with Caucasian ethnicity. We speculate that consuming large quantities of carbohydrates may induce hyperinsulinaemia, which could theoretically contribute to worse hypokalaemia, though mechanistic studies would be needed to explore this further.

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Thyrotoxic Periodic Paralysis in Young Caucasian Male

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.1974 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A966-A966

Author(s):

Sujata Panthi ◽

Rajib Kumar Bhattacharya

Keyword(s):

Muscle Weakness ◽

Past History ◽

Lower Extremities ◽

Asian Population ◽

Periodic Paralysis ◽

Medical Emergency ◽

Graves Disease ◽

Free T4 ◽

Thyrotoxic Periodic Paralysis ◽

Caucasian Male

Abstract Background: Thyrotoxic periodic paralysis (TPP) can be a medical emergency as delay in diagnosis can lead to life-threatening arrhythmia. Periodic paralysis is more prevalent in the Asian population. We report a case of thyrotoxic periodic paralysis in a young Caucasian male. Case: A 24-year-old male with a past history of Graves’ disease, hypertension, and asthma was brought to the hospital due to leg weakness and fall. He was initially diagnosed with Graves’ disease 2 years ago. The patient could not take methimazole or metoprolol due to the affordability issue for the last 18 months. On presentation, he fell on the floor while attempting to stand up from the couch. He could not stand up or pick his cell phone. He remained on the floor for 2-3 hrs. A review of the system was positive for palpitation and fatigue and negative for diarrhea, weight loss, anxiety, sleep problem, and dry eyes. On arrival, he had a pulse of 100/min, BP of 157/85 mmHg with rest of vitals signs normal. Motor strength on bilateral lower extremities were 2/5. Upper extremity strength was normal. No thyromegaly or thyroid bruit was noted in the exam. The rest of the physical exam was normal. Labs showed Potassium 1.9 with a normal reference range (RR) of 3.5 - 5.1 mmol/l. His TSH was < 0.01 (RR 0.35 - 5.00 MCU/ML), Free T4 was 5.0 (RR 0.6- 1.6 NG/DL), Total T3 was 425 (RR 87 - 180 NG/DL) and CK was 70 (RR 35- 232 U/L). EKG showed sinus rhythm at 90 bpm with no PR, T/ST, or QT abnormalities. He was given IV potassium and was also started on methimazole 10mg TID and metoprolol. His weakness and tachycardia were improved the next day. We discussed with him the options of medical management vs. surgery. He underwent a total thyroidectomy. Biopsy showed nodular hyperplasia consistent with graves’ disease. Discussion: Thyrotoxic periodic paralysis (TPP) is characterized by hypokalemia and episode of acute muscle weakness in lower extremities in the setting of hyperthyroidism. The pathophysiology of TPP remains uncertain. Hyperthyroidism is a hyperadrenergic state in which beta-2-adrenergic stimulation in muscle cells directly induces cellular K+ uptake by increasing cAMP, leading to activation of Na/K ATPase. The increase in the influx of intracellular K+ leads to hypokalemia and skeletal muscle weakness. Some studies show pathophysiology can be different in Caucasians compared to the Asian population that there could be abnormalities in Na and K channels other than Na/K ATPase. Potassium replacement should be done with caution as hypokalemia is due to intracellular shift and rebound hyperkalemia is common during the management. Beta-blocker may reverse adrenergic overstimulation of Na/K ATPase. It can help rapidly improve paralytic symptoms.

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Thyrotoxic Periodic Paralysis

JOURNAL FOR CLINICAL AND DIAGNOSTIC RESEARCH ◽

10.7860/jcdr/2020/44218.13836 ◽

2020 ◽

Author(s):

Suresh Sinha ◽

Nagarajan Raghupathy

Keyword(s):

Sudden Onset ◽

Periodic Paralysis ◽

Lower Limbs ◽

Limb Weakness ◽

Thyrotoxic Periodic Paralysis ◽

Asian Origin ◽

Sodium Potassium ◽

Lower Limb Weakness ◽

History Of ◽

Hormone Sensitive

Thyrotoxic periodic paralysis is not uncommon in people of Asian origin. It presents as sudden onset paralysis resulting from hypokalemia due to intracellular shift of potassium because of thyroid hormone sensitive Sodium-Potassium ATPase. A 34-year-old male with history of weight loss, palpitation and increased sweating for three months presented with sudden onset weakness of both lower limbs, two hours post-dinner. On investigation, he was found to be having hypokalemia as well as thyrotoxicosis. His potassium was corrected and was put on non-selective beta blocker and carbimazole. The patient improved within 24 hours and was discharged with advice to continue with Inderal and Carbimazole and report after one month. Hyperthyroidism should be included in differential diagnosis of sudden onset lower limb weakness.

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Thyrotoxic Periodic Paralysis Causing Back Pain and Leg Weakness: An Unusual Presentation of Hyperthyroidism

Case Reports in Endocrinology ◽

10.1155/2021/6622658 ◽

2021 ◽

Vol 2021 ◽

pp. 1-4

Author(s):

Henrik Elenius ◽

Marie Cesa ◽

Corina C. Nava Suarez ◽

Abhishek Nimkar ◽

Prasanta Basak ◽

...

Keyword(s):

Muscle Weakness ◽

Periodic Paralysis ◽

Close Monitoring ◽

Respiratory Compromise ◽

Thyrotoxic Periodic Paralysis ◽

Asian Populations ◽

Life Threatening ◽

Common Etiology ◽

Leg Weakness ◽

Hispanic Male

Thyrotoxic periodic paralysis (TPP) is a rare muscular disorder, characterized by muscle weakness and hypokalemia triggered by thyrotoxicosis. In Asian populations, 2% of patients with thyrotoxicosis are affected, compared to only 0.1–0.2% of non-Asians. The vast majority of patients are male. Muscle weakness ranges in severity from very mild to life-threatening, due to respiratory compromise. We present a case of a previously healthy 39-year-old Hispanic male who presented with sudden quadriparesis and quickly recovered after being treated for hypokalemia and thyrotoxicosis. TPP, although unusual, is important to recognize as it is a potentially fatal condition that requires close monitoring and is readily reversible with appropriate therapy. Any cause of thyroid hormone excess can cause TPP, with Graves’ disease being the most common etiology. Acute treatment includes potassium repletion, while long-term management focuses on determining and treating the cause of thyrotoxicosis, since maintaining a euthyroid state will prevent further episodes of TPP.

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Rhabdomyolysis Induced by Nonstrenuous Exercise in a Patient with Graves’ Disease

Case Reports in Endocrinology ◽

10.1155/2014/286450 ◽

2014 ◽

Vol 2014 ◽

pp. 1-3 ◽

Cited By ~ 1

Author(s):

Sarawut Summachiwakij ◽

Issac Sachmechi

Keyword(s):

Differential Diagnosis ◽

Periodic Paralysis ◽

Graves Disease ◽

Past Medical History ◽

Thyrotoxic Periodic Paralysis ◽

Radioiodine Uptake ◽

Thyroid Stimulating Immunoglobulins ◽

History Of ◽

Brown Urine ◽

Thyroid Ophthalmopathy

Hyperthyroidism can result in several musculoskeletal conditions such as thyrotoxic periodic paralysis, thyrotoxic myopathy, and thyroid ophthalmopathy. Rhabdomyolysis has been rarely reported to be associated with hyperthyroidism. We describe a 33-year-old man who presented with bilateral thigh pain and dark brown urine after regular squatting. He had a past medical history of hyperthyroidism but stopped taking it 2 months prior to admission. He was found to have rhabdomyolysis, myoglobinuria, and thyrotoxicosis. Presence of thyroid-stimulating immunoglobulins (TSI) and high radioiodine uptake confirmed a diagnosis of Graves' disease. He received aggressive fluid resuscitation and sodium bicarbonate intravenously along with monitoring fluid and electrolyte. Methimazole was also resumed. The patient responded to treatment and rhabdomyolysis gradually resolved. Therefore, nonstrenuous exercise can potentially induce rhabdomyolysis in patients with hyperthyroidism. Although hyperthyroidism is not widely recognized as a cause of rhabdomyolysis, it should be considered in the differential diagnosis of rhabdomyolysis.

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Thyrotoxic periodic paralysis in new-onset hyperthyroidism – a case report and review of the literature

Revista de Ciências Médicas e Biológicas ◽

10.9771/cmbio.v12i4.9207 ◽

2014 ◽

Vol 12 (4) ◽

pp. 531

Author(s):

Joaquim Custódio da Silva Junior ◽

Helton Estrela Ramos

Keyword(s):

Case Report ◽

Previous History ◽

Rare Condition ◽

Periodic Paralysis ◽

Emergency Physicians ◽

Review Of The Literature ◽

Font Size ◽

Thyrotoxic Periodic Paralysis ◽

History Of ◽

New Onset

Thyrotoxic periodic paralysis (TPP) is a rare condition related to hyperthyroidism, with specific clinical and physiopathological features. In this article, we discuss a case report of a patient that develops TPP with no previous history of thyroid illness, highlighting semiological characteristics that can help Emergency physicians to suspect of this condition. Subsequently, we review the recent articles about TPP, with focus in the molecular basis of ion channelopathies and predisposing factors, and discuss the therapeutic approach at acute phase of TPP and prevention of crisis recurrence.

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A Case of Nonfatal Ventricular Arrhythmia Due to Thyrotoxic Periodic Paralysis in a Saudi Patient as an Initial Presentation of Graves’ Disease

Clinical Medicine Insights Case Reports ◽

10.4137/ccrep.s34560 ◽

2016 ◽

Vol 9 ◽

pp. CCRep.S34560 ◽

Cited By ~ 1

Author(s):

Osamah Hakami ◽

Maswood M. Ahmad ◽

Naji Al Johani

Keyword(s):

Muscle Weakness ◽

Early Recognition ◽

Periodic Paralysis ◽

Graves Disease ◽

Thyrotoxic Periodic Paralysis ◽

Asian Populations ◽

Definitive Therapy ◽

Life Threatening ◽

Acute Paraparesis ◽

Saudi Male

Thyrotoxic periodic paralysis (TPP) is a potentially lethal complication of hyperthyroidism characterized by recurrent muscle weakness and hypokalemia. It has been commonly reported in non-Asian populations. Four cases were reported in Saudis so far, and one had a life-threatening arrhythmia. We describe an additional case of a 28-year-old apparently healthy Saudi male patient, who presented with acute paraparesis associated with hypokalemia (K: 2.0 mmol/L), complicated by ventricular tachycardia and cardiac arrest. He was successfully resuscitated and his hypokalemia was corrected. A diagnosis of Graves’ disease associated with TPP was made. He was initially treated with carbimazole and β-blockers and then given a definitive therapy with radioactive iodine, which showed a good response. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness. A brief review of TPP and associated arrhythmia is included.

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An Unusual Case of Acute Muscle Weakness

Acute Medicine Journal ◽

10.52964/amja.0638 ◽

2016 ◽

Vol 15 (4) ◽

pp. 209-211

Author(s):

Suzanne R Harrogate ◽

◽

Edouard Mills ◽

Asjid Qureshi ◽

Jacob F de Wolff ◽

...

Keyword(s):

Muscle Weakness ◽

Unusual Case ◽

Beta Blockers ◽

Periodic Paralysis ◽

Beta Blockade ◽

Proximal Muscle ◽

Thyrotoxic Periodic Paralysis ◽

Potassium Supplementation ◽

Leg Weakness ◽

Hypokalaemic Periodic Paralysis

A previously healthy 35-year old man presented to hospital with acute leg weakness following an alcohol binge. On assessment, tachycardia, urinary retention and bilateral upper and lower limb proximal weakness with preserved peripheral power were noted. Biochemistry revealed marked hypokalaemia, which responded to intravenous replacement, and biochemical thyrotoxicosis, leading to the diagnosis of Thyrotoxic Periodic Paralysis (TPP). Anti-thyroid therapy and beta-blockers were commenced and his neurological symptomatology resolved as he became progressively euthyroid. TPP is a rare acquired subtype of hypokalaemic periodic paralysis, typically causing proximal muscle weakness associated with thyrotoxicosis. It is most common in young Asian males. Acute treatment requires cautious oral potassium supplementation, beta-blockade, and anti-thyroid therapy. TPP is prevented by maintaining euthyroidism; otherwise recurrence is likely.

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When Your Thyroid Causes Muscle Paralysis

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.1987 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A972-A973

Author(s):

Anand Gandhi ◽

Ahmad Al-Maradni ◽

Karyne Lima Vinales ◽

Ricardo Rafael Correa

Keyword(s):

Muscle Weakness ◽

Young Male ◽

Sudden Onset ◽

Periodic Paralysis ◽

Adrenergic Stimulation ◽

Free T4 ◽

Thyrotoxic Periodic Paralysis ◽

Beta Adrenergic ◽

Thyroid State ◽

Altered Thyroid

Abstract Background: Periodic paralysis represents a spectrum of disorders characterized by ion channel dysfunction, mainly Na-K-ATPase channels. Thyrotoxic periodic paralysis (TTP) is defined by the presence of hypokalemia and diffuse muscular paralysis in a pre-existing hyperthyroid state. Diagnosis can be challenging, especially in cases of undiagnosed hyperthyroidism due to the non-specific presentation of this illness. We present a case of a young male who presented with recurrent, spontaneous paralysis found to have Graves’ disease. Clinical Case: A 38-year-old Asian male presented with sudden onset diffuse weakness, numbness, and tingling. The weakness was so severe that he could barely walk more than a few steps. However, his symptoms resolved in less than 24 hours without any intervention. Five months later, the patient experienced a recurrent episode of this similar constellation of diffuse muscle weakness and paresthesia. The patient was taken to a nearby hospital, where he was provided with intravenous fluid resuscitation. Initial laboratory workup was notable for hypokalemia to 1.4 mmol/L (n: 3.6 - 5.3 mmol/L), hypophosphatemia to 0.6 mmol/L (n: 2.4 – 4.8 mmol/L), and elevated creatinine kinase to 807 U/L (n: 22 – 198 U/L). Additionally, TSH was <0.001 mU/L (n: 0.45 – 4.5 mU/L) along with free T4 3.4 ng/dL (n: 0.80 – 1.70 ng/dL. The patient denied any other symptoms or a family history of similar symptoms. Lumbar puncture and brain/spine MRIs were unremarkable. Symptoms gradually improved throughout hospitalization with fluid and electrolyte repletion. Hyperthyroidism was treated with methimazole 5mg twice daily, later changed to PTU 50mg every eight hours due to recurrent headaches. Thyroid uptake scan showed diffuse bilateral uptake to 39.11% at 4 hours and 61.8% at 24 hours. Follow up labs revealed: TSH 0.3 mU/L, free T4 1.44 ng/dL, free T3 3.5 pg/mL (n: 2.3 – 4.1 pg/mL). Patient denied recurrent episodes of weakness or paresthesia. Definitive hyperthyroidism treatment with RAI was planned. Conclusions: The prevalence of TPP is higher in Asian males compared to other ethnic groups. TPP manifests as a sporadic onset of muscle weakness ranging from mild weakness to flaccid paralysis. It has been described that thyroid hormone itself augments the activity of the Na-K-ATPase channel and increases its responsiveness to beta-adrenergic stimulation. In addition, hyperthyroidism is associated with insulin resistance leading to hyperinsulinemia. Both beta-agonism and insulin promote potassium to be driven into cells resulting in hypokalemia. As such, activities which increase beta adrenergic stimulation, like stress and exercise, and promote the secretion of insulin, such as heavy carbohydrate intake, are well described triggers of TPP. Treatment revolves around acutely treating hypokalemia followed by preventing subsequent attacks via regulation of the altered thyroid state.

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SUN-514 Thyrotoxic Periodic Paralysis in Adolescence Patient a Case Report and Literature Review

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.652 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Luke He ◽

Veronica Lawrence ◽

Wayne V Moore ◽

Yun Yan

Keyword(s):

Emergency Department ◽

Muscle Weakness ◽

Periodic Paralysis ◽

Adolescent Male ◽

Conduction Delay ◽

Graves Disease ◽

Adult Males ◽

Thyrotoxic Periodic Paralysis ◽

Intraventricular Conduction ◽

Potassium Replacement

Abstract BACKGROUND: Thyrotoxic periodic paralysis (TPP) is an uncommon disorder characterized by acute flaccid paralysis due to hypokalemia. It is diagnosed primarily in Asian adult males and is rare in children and adolescents. Here we report an adolescent male patient of Vietnamese descent who presented to the emergency department with an episode of syncope, muscle weakness, and shortness of breath one day after the initiation of methimazole treatment for Graves’ disease. The laboratory revealed significant hypokalemia. In this report we also included and summarized the reported cases of TPP in adolescent patients since 1997. Clinical Case: A 17-year-old Vietnamese American male who was recently diagnosed with Graves’ disease presented to the emergency department after an episode of syncope, muscle weakness, and difficulty breathing. Two months previously, he began having episodes of tachycardia. He was diagnosed with hyperthyroidism with a TSH of 0.007 mIU/mL and free T 4 > 7 ng/dL (0.8-1.9). He was subsequently evaluated by Cardiology and started on atenolol. He was then seen by Endocrinology 5 days after and started on methimazole 15 mg twice daily. On the next morning after starting methimazole, he reported feeling weak and passed out. His father had found him on the floor, weak and unable to move, approximately 30 minutes after his father “heard a thud upstairs”. The patient recalled that his legs gave out and he “hitting his face on a table”. In the emergency department, he was tachycardic at 116 bpm, widened pulse blood pressure of 131/50 mmHg with normal respiratory rate 24 BR/min. He had diffused and significant muscle weakness on his all extremities including grip strength. His potassium was 1.6 mmol/L (3.5 - 5.2) and magnesium 1.6 mmol/L (1.6-2.3). The rest of his chemistry panel was unremarkable. He had EKG changes consistent with hypokalemia with U waves, also revealing atrial rhythm with first degree AV block, intraventricular conduction delay, and QTc prolongation at 588 (<450). His chest x-ray was normal. Normal saline was administered, and potassium replacement was given with 40 mEq of KCl followed by D5 NS with 40 meq/L KCl at maintenance. He continued taking atenolol and methimazole. He was also given an IV dose of magnesium. His muscle strength returned completely and potassium level returned to normal range at 4.6 mmol/L after 24 hours of treatment. Conclusion: TPP is a rare cause of acute paralysis and can lead to cardiac arrhythmia and death without accurate diagnosis and prompt treatment. Our case should raise awareness of this disorder among pediatricians, emergency department physicians and endocrinologists. Acute paralysis with hypokalemia should also prompt the physician to consider evaluating thyroid function as a differential diagnosis in young Asian men.

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Management Thyroid Disease in Pregnancy: Preconception, and the postpartum complications

Endocrinology and Disorders ◽

10.31579/2640-1045/012 ◽

2017 ◽

Vol 1 (3) ◽

pp. 01-04

Author(s):

R F Gross man

Keyword(s):

Thyroid Function ◽

Thyroid Disease ◽

Postpartum Period ◽

Past History ◽

First Trimester ◽

Thyroid Function Tests ◽

Specialist Referral ◽

Thyrotropin Receptor Antibodies ◽

History Of ◽

In Pregnancy

Pregnancy has a profound impact on the thyroid gland and thyroid function since the thyroid may encounter changes to hormones and size during pregnancy. The diagnosis and treatment of thyroid disease during pregnancy and the postpartum is complex but knowledge regarding the interaction between the thyroids and pregnancy/the postpartum period is advancing at a rapid pace. For women known to have hypothyroidism, an increase in thyroxine dose by 20–40% when pregnancy is confirmed usually ensures they remain euthyroid. Treatment of subclinical hypothyroidism is recommended if the woman has antithyroid antibodies. Treatment of hyperthyroidism, unless it is related to human chorionic gonadotrophin, involves propylthiouracil in the first trimester. Carbimazole may be used in the second trimester. Thyroid function tests are checked every month and every two weeks following a change in dose. Women with a current or a past history of Graves’ disease who have thyrotropin receptor antibodies require early specialist referral as there is a 1–5% risk of fetal hyperthyroidism. Women with thyroid disorders in pregnancy should be followed up by their GP in the postpartum period. Postpartum thyroiditis may present months after delivery.

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