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Year : 2015  |  Volume : 18  |  Issue : 2  |  Page : 121-123

A case of type I diabetes mellitus and autoimmune thyroiditis presents with hypokalemic paralysis

1 Department of Endocrinology, Lala Lajpat Rai Memorial Medical College, Meerut, Uttar Pradesh, India
2 Department of Radiodiagnosis, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication9-Jun-2015

Correspondence Address:
Dr. Manish Gutch
D-15, Lala Lajpat Rai Memorial Medical College, Meerut - 250 004, Uttar Pradesh
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DOI: 10.4103/1119-0388.158411

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Hypokalemic periodic paralysis (HPP) is one form of periodic paralysis, a rare group of disorders that can cause acute onset weakness. Thyrotoxicosis is a well-known cause of periodic paralysis and has to be ruled out when a patient presents with HPP. Here, the authors report a case of recurrent episodes of acute onset quadriparesis attributed to hypokalemia ensuing from autoimmune thyrotoxicosis and he has also been diagnosed with type 1 diabetes mellitus. Although rare, periodic paralysis is to be differentiated from other causes of weakness and paralysis so that the proper treatment can be initiated quickly.

Keywords: Hypokalemic periodic paralysis, thyrotoxicosis, type 1 diabetes mellitus

How to cite this article:
Gutch M, Kumar S, Razi SM, Gupta A, Gupta KK, Nath M. A case of type I diabetes mellitus and autoimmune thyroiditis presents with hypokalemic paralysis. Trop J Med Res 2015;18:121-3

How to cite this URL:
Gutch M, Kumar S, Razi SM, Gupta A, Gupta KK, Nath M. A case of type I diabetes mellitus and autoimmune thyroiditis presents with hypokalemic paralysis. Trop J Med Res [serial online] 2015 [cited 2019 Oct 13];18:121-3. Available from: http://www.tjmrjournal.org/text.asp?2015/18/2/121/158411

  Introduction Top

There are several types of periodic paralysis associated with metabolic and electrolyte abnormalities. Of these, hypokalemic periodic paralysis (HPP) is the most common, with a prevalence of one in 100,000. [1] The clinical features of the syndrome vary somewhat depending on the underlying etiology but the most striking feature is the sudden onset of weakness ranging in severity from mild, transient weakness to severe disability resulting in life-threatening respiratory failure. Attacks may be provoked by stress such as a viral illness or fatigue, or certain medications such as beta-agonists, insulin, or steroids. A perturbation of sodium and calcium ion channels results in low potassium levels and muscle dysfunction. [2] Although the serum potassium level is often alarmingly low, other electrolytes are usually normal. Indeed, total body potassium is actually normal with the change in the serum level reflecting a movement of potassium into cells. [3] When possible, the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.

  Case Report Top

A 28-year-old male with no history of similar episodes of muscle weakness in the past presented to the emergency room with acute onset paralysis. The patient had gone to bed at 11 PM with no weakness and awakened in the morning, unable to move his upper or lower extremities. The weakness was bilateral and involved both the proximal muscles of the shoulders and hips as well as the distal extremities. He had no respiratory or swallowing difficulty and was able to move his neck and facial muscles. He denied any pain or paresthesia. Prior to this episode, the patient had been healthy and denied any recent diarrhea, chest pain, shortness of breath, or weight change. He did not take any medications, and denied the use of alcohol or drugs, or any significant changes in diet or activity levels. His mother had been diagnosed with hypothyroidism but his parents and brother had no history of similar episodes and no other significant illnesses.

On physical examination, the heart rate was 100/min and blood pressure was 140/80 mmHg. His height was 163 cm, weight was 75 kg, and body mass index (BMI) was 28.23 kg/m 2 , with a waist circumference of 91 cm but otherwise normal in overall appearance. His skin was cool and dry, and the oral mucosa was moist. No jugular venous distension, goiter, or lymphadenopathies were noted, and Pemberton's sign was negative. Cardiac examination revealed tachycardia with a regular rhythm and no murmurs. Examination of the lungs and abdomen were unremarkable. There were no deformities or oedema of the extremities, and distal pulses were present and equal bilaterally. Neurologic examination revealed flaccid paralysis of all extremities, which involved the proximal and distal muscles and included the hips and shoulders. Sensation was intact but deep tendon reflexes were absent. Cranial nerve function was grossly intact.

Investigations revealed a hemoglobin concentration of 10.3 gm%, total leukocyte count of 6700 per mm 3 (polymorphs 80%, lymphocytes 18%), and erythrocyte sedimentation rate of 30 mm at the end of 1 h. Serum protein concentration was 6.9 gm/dl, with a serum albumin concentration of 4.2 gm/dl. The level of blood urea nitrogen was 28, of serum creatinine was 0.9, of random blood sugar was 314, of serum sodium was 138, and of serum potassium was 1.36 (3.5-5 mmol/l); hepatic transaminases, tests for hepatitis B surface antigen, antinuclear antibodies, and antibodies against double-stranded DNA were negative. An electrocardiogram (ECG) revealed a heart rate of 75/min, with prolongation of PR interval, ST segment depression, T-wave inversion, and prominent U wave, which is a typical feature of hypokalemia.

Five hours after the initiation of intravenous potassium replacement, the patient's neurologic symptoms (weakness and reflexes) started improving and had completely resolved after 24 h, and a repeat ECG revealed a normal sinus rhythm and rate. On further evaluation, TSH-0.014 (0.3-5.5 IU/ml), T3-4.07 (0.8-2.0ng/ml), and T4-21.16 (4.5-12.5μg/dl); anti-TPO antibody assay >600 IU/ml (normal <34); anti-TgAb assay 767.8 IU/ml (normal <115); and positive for anti-insulin antibody test. Urine sodium and potassium, serum aldosterone, and renin levels were measured to rule out adrenal involvement and were found to be normal. The patient was diagnosed with HPP associated with autoimmune hyperthyroidism (confirmed with a technetium scan) and type 1 diabetes mellitus and was started on carbimazole and insulin for control of his underlying hyperthyroidism and type 1 diabetes mellitus. He was discharged on the 7 th day, with regular follow-ups. When we did regular follow-up for1 year, his thyroid functions and glycemic status had reverted to normal; in a period of 1 year, he did not have any episode of paralysis.

  Discussion Top

HPP occurs in several settings and the diagnosis may require an extensive search for the underlying etiology, since the treatment varies according to the cause. HPP may occur sporadically in the form of familial hypokalemic paralysis (FHP), a poorly understood disorder that may occur spontaneously or as the result of autosomal dominant inheritance. [1] This form of periodic paralysis is felt to be the result of disordered cellular potassium regulation, perhaps due to sodium or calcium channel abnormalities. [2],[4] Thyrotoxic periodic paralysis (TPP) occurs in the setting of hyperthyroidism. It is the most common form of HPP and is seen primarily in Asian males, occurring in 1.9% of Japanese hyperthyroid patients overall and in up to 8% of hyperthyroid Japanese men. [5],[6] The clinical features are similar to those seen with other forms of HPP but also include the symptoms of thyrotoxicosis such as weight loss, tachycardia, and anxiety. In patients who develop HPP, however, the symptoms of hyperthyroidism are often quite mild and may be overlooked. [7],[8] In contrast, our patient did not have any clinical feature suggestive of thyrotoxicosis besides episodic weakness. Paralytic episodes often occur at night, as was the case with this patient. [8] Any cause of hyperthyroidism can be associated with TPP, but Graves' disease is the most common. The major feature distinguishing TPP from other types of periodic paralysis is the association of paralytic episodes with the hyperthyroid state. Paralytic episodes can be induced in these patients by administering insulin and glucose but only when they are hyperthyroid. [3] Euthyroid patients are typically free from spontaneous and induced attacks. The underlying mechanism is not known but is thought to be different from that of FHP, since in that disorder, thyroid hormone levels are normal and the administration of exogenous thyroid hormone does not result in paralytic episodes. [9] Furthermore, the genetic abnormalities felt to be responsible for FHP have not been identified in patients with TPP. [4] Although acute paralytic episodes are treated with potassium replacement, the administration of prophylactic potassium or acetazolamide is not felt to benefit these patients, since potassium levels are normal between episodes and may result in dangerous hyperkalemia. [10] Rarely, HPP can result from substantial gastrointestinal or renal potassium losses. In such cases, total body potassium is depleted and requires aggressive replacement. Endocrine abnormalities such as hyperinsulinemia and primary hyperaldosteronism have been associated with HPP. [11]

  Conclusion Top

Periodic paralysis is important to consider when seeing patients with sudden onset weakness or paralysis, especially those with no history or evidence of other diseases and no significant risk factors for stroke.

  Acknowledgments Top

We owe thanks to the patient and her relatives for having patience and for their contribution to this undertaking.

  References Top

Fontaine B, Vale-Santos J, Jurkat-Rott K, Reboul J, Plassart E, Rime CS, et al. Mapping of the hypokalaemic periodic paralysis (HypoPP) locus to chromosome 1q31-32 in three European families. Nat Genet 1994;6:267-72.  Back to cited text no. 1
Jurkat-Rott K, Lerche H, Lehmann-Horn F. Skeletal muscle channelopathies. J Neurol 2002;249:1493-502.  Back to cited text no. 2
Lin SH, Lin YF, Chen DT, Chu P, Hsu CW, Halperin ML. Laboratory tests to determine the cause of hypokalemia and paralysis. Arch Intern Med 2004;164:1561-6.  Back to cited text no. 3
Wang W, Jiang L, Ye L, Zhu N, Su T, Guan L, et al. Mutation screening in Chinese hypokalemic periodic paralysis patients. Mol Genet Metab 2006;87:359-63.  Back to cited text no. 4
Okinaka S, Shizume K, Iino S, Watanabe A, Irie M, Noguchi A, et al. The association of periodic paralysis and hyperthyroidism in Japan. J Clin Endocrinol Metab 1957;17:1454-9.  Back to cited text no. 5
Shizume K, Shishiba Y, Kuma K, Noguchi S, Tajiri J, Ito K, et al. Comparison of the incidence of association of periodic paralysis and hyperthyroidism in Japan in 1957 and 1991. Endocrinol Jpn 1992;39:315-8.  Back to cited text no. 6
Kelley DE, Gharib H, Kennedy FP, Duda RJ Jr, McManis PG. Thyrotoxic periodic paralysis. Report of 10 cases and review of electromyographic findings. Arch Intern Med 1989;149:2597-600.  Back to cited text no. 7
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.   Back to cited text no. 8
Kung AW. Clinical review: Thyrotoxic periodic paralysis: A diagnostic challenge. J Clin Endocrinol Metab 2006;91:2490-5.  Back to cited text no. 9
Ogawa T, Kamikubo K.Hypokalemic periodic paralysis associated with hypophosphatemia in a patient with hyperinsulinemia. Am J Med Sci 1999;318:69-72.  Back to cited text no. 10
Cannon SC. An expanding view for the molecular basis of familial periodic paralysis. Neuromuscul Disord 2002;12:533-43.  Back to cited text no. 11


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