scholarly journals Weight Loss-Based Nutraceuticals

2021 ◽  
Vol 16 (2) ◽  
pp. 49-54
Author(s):  
Shirley Shuster ◽  
Caitlyn Vlasschaert ◽  
Sara Awad

Thyrotoxic periodic paralysis (TPP) is characterized by muscle weakness, areflexia, and hypokalemia in the setting of thyrotoxicosis. We present the case of a 32-year-old male with multiple presentations to the emergency department for lower limb weakness, tremors, diaphoresis, and tachycardia. His initial blood work revealed T3-toxicosis and hypokalemia, and he was treated for TPP with intravenous fluids and potassium supplementation. He had been ingesting weight loss supplements containing iodine, kelp, licorice, and likely undeclared thyroid hormones or mimics. Following discontinuation of supplements, all laboratory investigations normalized and thyrotoxicosis symptoms resolved. This case illustrates that ingestion of thyroid hormone-based nutraceuticals should be considered as a cause of thyrotoxicosis and TPP. RésuméLa paralysie périodique thyréotoxique (PPT) se caractérise par de la faiblesse musculaire, une aréflexie et une hypokaliémie dans le contexte de la thyréotoxicose. Nous exposons le cas d’un homme de 32 ans qui s’est présenté au service des urgences pour de multiples symptômes, soit une faiblesse des membres inférieurs, des tremblements, une diaphorèse et une tachycardie. Son bilan sanguin initial a révélé une toxicose-T3 et une hypokaliémie, et il a été traité contre la PPT par des solutés intraveineux et une recharge en potassium. Il ingérait des suppléments pour la perte de poids contenant de l’iode, de la laminaire, de la réglisse et probablement des hormones thyroïdiennes ou leurs analogues non déclarés. Après l’arrêt des suppléments, tous les examens de laboratoire sont revenus à la normale et les symptômes de thyréotoxicose ont disparu. Ce cas montre que l’ingestion de nutraceutiques à base d’hormones thyroïdiennes devrait être considérée comme une cause de la thyréotoxicose et de la PPT.

Author(s):  
Suresh Sinha ◽  
Nagarajan Raghupathy

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.


2019 ◽  
Vol 12 (10) ◽  
pp. e229244 ◽  
Author(s):  
Kosar Hussain ◽  
Anil Xavier

We describe the case of a 76-year-old man who presented with bilateral lower limb weakness associated with decreased urine output. His initial blood results showed acute kidney injury (AKI) stage 3 with substantially raised serum creatine kinase concentration of 37 950 IU/L (normal range <171 U/L). He had been on high-dose rosuvastatin for 4 years with a recent brand change occurring 1 week prior to onset of symptoms. There was no history of pre-existing neuromuscular disease. Statin-related rhabdomyolysis was suspected and rosuvastatin was withheld. His muscle strength gradually improved. He required haemodialysis for 10 weeks. He was discharged home after a complicated course of hospitalisation. His renal function improved and he became dialysis-independent; however, he was left with residual chronic kidney disease.


2016 ◽  
Vol 15 (4) ◽  
pp. 209-211
Author(s):  
Suzanne R Harrogate ◽  
◽  
Edouard Mills ◽  
Asjid Qureshi ◽  
Jacob F de Wolff ◽  
...  

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.


2004 ◽  
Vol 22 (7) ◽  
pp. 544-547 ◽  
Author(s):  
Kuo-Cheng Lu ◽  
Yu-Juei Hsu ◽  
Jainn-Shiun Chiu ◽  
Yaw-Don Hsu ◽  
Shih-Hua Lin

Author(s):  
Clare E Bonnar ◽  
John F Brazil ◽  
Julie O Okiro ◽  
Louise Giblin ◽  
Yvonne Smyth ◽  
...  

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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