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Unusual presentation of thyrotoxicosis with paraparesis in a young male: a rare case report.

INTRODUCTION:

Even though it is commonly seen in Graves' disease, TPP is not related to the etiology, severity, and duration of thyrotoxicosis. (1)

The pathogenesis of hypokalaemic periodic paralysis in certain populations with thyrotoxicosis is unclear. Transcellular distribution of potassium is maintained by the Na+/K+--ATPase activity in the cell membrane, and it is mainly influenced by the action of insulin and beta-adrenergic catecholamines. (2) Hypokalemia in TPP results from an intracellular shift of potassium and not total body depletion. It has been shown that the Na+/K+- ATPase activity in platelets and muscles is significantly higher in patients with TPP. (3) Hyperthyroidism may result in a hyperadrenergic state, which may lead to the activation of the Na+/K+- ATPase pump and result in cellular uptake of potassium. (2, 4, 5) Thyroid hormones may also directly stimulate Na+/K+- ATPase activity and increase the number and sensitivity of beta receptors. (2, 6) Patients with TPP have been found to have hyperinsulinemia during episodes of paralysis. This may explain the attacks after high-carbohydrate meals. (7)

CASE REPORT:

A 19 year old male patient presented to our emergency room with sudden onset weakness of lower limbs. He was not able to stand or walk. Power of 0/5 in both lower limbs and 3/5 in upper limbs was noticed on examination. Routine investigations revealed to have severe hypokalemia with a serum potassium of 1.6 meq/l (normal range 3.5-5.0 meq/l), a serum phosphorus level of 3.4 mg/dl (normal range 3-4.5 mg/dl) and mild hypomagnesemia with serum magnesium level of 1.5mg/dl (normal range 1.8-3.0 mg/dl). ECG showed hypokalemic changes with prolonged PR interval, increased P-wave amplitude and widened QRS complexes. He was managed on intravenous as well oral potassium and history revealed weight loss, increased appetite and tremors from past 4 months. He had a multinodular goiter and radioactive iodine uptake scan (Iodine 131) showed a toxic nodule (Toxic nodule shows increased iodine uptake while the rest of the gland is suppressed) with no exophthalmos, sensory or cranial nerve deficits. Thyroid function tests revealed thyrotoxicosis with free T4 of 4.3ng/dl (normal range 0.8-1.8ng/dl), T3 of 279 ng/dl (normal range = 60--181 ng/dl) and a TSH level of <0.15milliunits/L (normal range = 0.3--4 milliunits/L). He was managed on intravenous potassium & propanolol. The patient showed dramatic improvement of his symptoms. The patient was discharged home on carbamazole with the diagnosis of TPP secondary to toxic nodular goiter.

In this case there was a significant family history as one of his elder brother had a sudden death (cause not known) and his mother was primary hypothyroid on levothyroxin replacement therapy.

DISCUSSION:

TPP is seen most commonly in Asian populations, with an incidence of approximately 2% in patients with thyrotoxicosis of any cause. (1,8,9,10) The attacks of paralysis have a well-marked seasonal incidence, usually occurring during the warmer months.1 Pathogenesis of hypokalaemia has been explained by some authors to be due to an intracellular shift of body potassium, which is catecholamine mediated. (11,12) Shizume and his group studied total exchangeable potassium which revealed that patients with thyrotoxic periodic paralysis were not significantly different from controls when the value was related to lean body mass. (11) The paralytic symptoms and signs improve as the potassium returns from the intracellular space back into the extracellular space. (13) The diurnal variation in potassium movement where there is nocturnal potassium influx into skeletal muscle would explain the tendency for thyrotoxic periodic paralysis to occur at night. (14) Hypophosphataemia and hypomagnesaemia are also known to occur in association with thyrotoxic periodic paralysis. (14,15,16,17,18) The correction of hypophosphataemia without phosphate administration supports the possibility of intracellular shift of phosphate. (16) Electrocardiographic findings supportive of a diagnosis of TPP rather than sporadic or familial periodic paralysis are sinus tachycardia, elevated QRS voltage and first-degree AV block (sensitivity 97%, specificity 65%). (20) In addition to ST-segment depression, T-wave flattening or inversion and the presence of U waves are typical of hypokalaemia.

The management is to deal with the acute attack as well as treatment of the underlying condition to prevent future attacks. Rapid administration of oral or intravenous potassium chloride can abort an attack and prevent cardiovascular and respiratory complications.4 A small dose of potassium is the treatment of choice for facilitating recovery and reducing rebound hyperkalaemia due to release of potassium and phosphate from the cells on recovery. (1,2,3) Rebound hyperkalaemia occurred in approximately 40% of patients with TPP, especially if they received >90 mmol of potassium chloride within the first 24 hours. (4) Another mode of treatment is to give propranolol, a nonselective b-blocker, which prevents the intracellular shift of potassium and phosphate by blunting the hyperadrenergic stimulation of Na+/K+--ATPase. (20) Hence, initial therapy for stable TPP should include propranolol. (21,22,23) The definitive therapy for TPP includes treatment of hyperthyroidism with antithyroid medications, surgical thyroidectomy, or radioiodine therapy.

REFERENCES

(1.) McFadzean AJ, Yeung R. Periodic paralysis complicating thyrotoxicosis in Chinese. BMJ. 1967; 1 (538):451^55.

(2.) Gennari FJ. Hypokalemia. N Engl J Med. 1998; 339 (7):451--458.

(3.) Chan A, Shinde R, Chow CC, Cockram CS, Swaminathan R. In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis. BMJ. 1991; 303 (6810):1096--1099.

(4.) Lin SH. Thyrotoxic periodic paralysis. Mayo Clin Proc. 2005; 80 (1):99-105.

(5.) Levey GS, Klein I. Catecholamine-thyroid hormone interactions and the cardiovascular manifestations of hyperthyroidism. Am J Med. 1990; 88 (6):642--646.

(6.) Ginsberg AM, Clutter WE, Shah SD, Cryer PE. Triiodothyronine-induced thyrotoxicosis increases mononuclear leukocyte beta-adrenergic receptor density in man. J Clin Invest. 1981; 67 (6):1785--1791.

(7.) Lee KO, Taylor EA, Oh VM, Cheah JS, Aw SE. Hyperinsulinemia in thyrotoxic hypokalemic periodic paralysis. Lancet. 1991; 337 (8749): 1063-1064.

(8.) Stedwell RE, Allen KM, Binder LS. Hypokalemic paralysis: a review of the etiologies, pathophysiology, presentation, and therapy. Am J Emerg Med. 1992; 10:143-8.

(9.) Magsino CH Jr, Ryan AJ Jr. Thyrotoxic periodic paralysis. South Med J. 2000; 93: 996-1003.

(10.) Mellgren G, Bleskestad HI, Aanderud S, Bindoff L. Thyrotoxicosis and paraparesis in a young woman: case report and review of the literature. Thyroid. 2002; 12:77-80.

(11.) Shizume K, Shishiba Y, Sakuma M, et al. Studies on electrolyte metabolism in idiopathic and thyrotoxic periodic paralysis. II. Total exchangeable sodium and potassium .Metabolism. 1966; 15: 145-52.

(12.) Shizume K, Shishiba Y, Sakuma M, et al. Studies of electrolyte metabolism in idiopathic and thyrotoxic periodic paralysis. I. Arteriovenous differences of electrolytes during induced paralysis. Metabolism. 1966; 15: 138-44.

(13.) Ober KP. Thyrotoxic periodic paralysis in the United States: report of 7 cases and review of the literature. Medicine. 1992; 71: 109-20.

(14.) Manoukian MA, Foote JA, Crapo LM. Clinical and 1. metabolic features of thyrotoxic periodic paralysis in 24 episodes. Arch Intern Med. 1999; 159:601-6.

(15.) Tinker TD, Vannatta JB. Thyrotoxic hypokalemic periodic paralysis: report of four cases and review of the literature. J Okla State Med Assoc. 1987; 80:76-83.

(16.) Norris KC, Levine B, Ganesan K. Thyrotoxic periodic paralysis associated with hypokalemia and hypophosphatemia. Am J Kidney Dis. 1996; 28:270-3.

(17.) Nora NA, Berns AS. Hypokalemic, hypophosphatemic thyrotoxic periodic paralysis. Am J Kidney Dis. 1989; 13:247-9.

(18.) Guthrie GP Jr, Curtis JJ, Beilman KM. Hypophosphatemia in thyrotoxic periodic paralysis. Arch Intern Med. 1978; 138:1284-5.

(19.) Hsu Y, Lin Y, Chau T, Liou JT, Kuo SW, Lin SH. Electrocardiographic manifestations in patients with thyrotoxic periodic paralysis. Am J Med Sci. 2003; 326:128-32.

(20.) Yeung RT, Tse TF. Thyrotoxic periodic paralysis: effect of propranolol. Am J Med. 1974; 57:584-90.

(21.) Tassone H, Moulin A, Henderson SO. The pitfalls of potassium replacement in thyrotoxic periodic paralysis: a case report and review of the literature. J Emerg Med. 2004; 26:157-61.

(22.) Shayne P, Hart A. Thyrotoxic periodic paralysis terminated with intravenous propranolol. Ann Emerg Med. 1994; 24:736-40.

(23.) Huang TY, Lin SH. Thyrotoxic hypokalemic periodic paralysis reversed by propranolol without rebound hyperkalemia. Ann Emerg Med. 2001; 37:415-6.

(24.) Charness ME, Johns RJ. Hypokalemic periodic paralysis. Johns Hopkins Med J. 1978; 143:48-53

Competing Interests None Declared

Author Details

HAKIM IRFAN SHOWKAT, Postgraduate scholar, Dept of Internal medicine, SKIMS, India. ARIF HUSSAIN SARMAST, Postgraduate scholar, Dept of Surgery, SKIMS, India. RUBINA LONE, Assistant Professor, Dept of microbiology, SKIMS Medical College, India. MEHMOOD IQBAL QADRI, Senior resident, Dept of Internal medicine, SKIMS Medical college, India. MANZOOR AHMED WANI, Senior resident, Dept of Internal medicine, SKIMS Medical college, India.

CORRESSPONDENCE: HAKIM IRFAN SHOWKAT, Postgraduate scholar, Dept of Internal medicine, SKIMS, India. Email: docirfanshahi512@gmail.com
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Article Details
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Author:Showkat, Hakim Irfan; Sarmast, Arif Hussain; Lone, Rubina; Qadri, Mehmood Iqbal; Wani, Manzoor Ahmed
Publication:British Journal of Medical Practitioners
Article Type:Case study
Geographic Code:9INDI
Date:Mar 1, 2012
Words:1456
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