Thyrotoxic Periodic Paralysis Research Articles

Thyrotoxic periodic paralysis: A retrospective, observational study from India.

Background & objectives:Thyrotoxic periodic paralysis (TPP) is an endocrine emergency presenting with acute-onset flaccid paralysis in a patient having thyrotoxicosis accompanied by hypokalaemia. This study was conducted to evaluate the clinical profile of patients with TPP presenting to three centres in India.Methods:This retrospective, observational study was conducted at three tertiary care Armed Forces medical centres, located at Lucknow, Kolkata and Delhi. The history, clinical features, treatment details and outcomes were evaluated.Results:Of the 244 patients with thyrotoxicosis, 15 were diagnosed with TPP and included in the study. These 15 patients (14 male and 1 female) had 32 episodes of TPP which were analyzed. The mean age was 30.2±6.2 yr (range: 21-39), and overt thyrotoxicosis was seen in all patients except one who had subclinical hyperthyroidism. Graves’ disease was the most common cause of thyrotoxicosis (13/15) and the remaining two patients had subacute thyroiditis and gestational thyrotoxicosis. Hypokalaemia (serum potassium <3.5 mmol/l) was seen in 12 patients, and the mean serum potassium was 3.2±0.9 mmol/l (range: 2.1-4.9). All patients had flaccid weakness, predominantly involving the lower limb with no bulbar, respiratory or cranial nerve involvement. The average duration of paralysis was 10.6±5.7 h (range: 3-28 h).Interpretation & conclusions:Our study demonstrated an early age of presentation and presence of clinical and biochemical thyrotoxicosis in majority of patients with TPP. Hypokalaemia may not always be evident in patients with TPP.

THYROTOXIC PERIODIC PARALYSIS: CASE REPORT

Thyrotoxic periodic paralysis (TPP) represents an acquired form of hypokalemic periodic paralysis (HPP) in which attacs of weakness occur, often precipitated by rest after strenuous exercise or a high-carbohydrate load. TPP is more prevalent in Asians than non-asians. Despite a higher incidence of hyperthyroidism in females, over 95 percent of TPP occur in males. Any cause of hyperthyroidism can be associated with TPP. Graves’ disease is the underlying disorder in most of cases with TPP as it is the cause in most of cases with hyperthyroidism. We report a 28-year-old male presenting TPP with very low potassium level.

A case report on thyrotoxic periodic paralysis from Dhaka, Bangladesh

Thyrotoxic periodic paralysis (TPP) is a disorder comprising acute hypokalaemia, intermittent muscle weakness and thyrotoxicosis. TPP is a rare manifestation of thyrotoxicosis predominantly seen in Asian people. We reported a patient who was brought to the emergency department with acute onset of weakness of her lower limbs. After a series of investigations, the patient was diagnosed as a case of thyrotoxicosis. The patient was placed on carbimazole, which prevented further attacks. The patient's improvement was satisfactory, and she is currently symptom free. Because of the presenting feature, its precipitating factor, the absence of a family history of periodic paralysis and the improvement of a clinical parameter after the starting of the antithyroid treatment, the condition was diagnosed as thyrotoxic periodic paralysis. The physician should concern about thyrotoxic periodic paralysis in people who present with weakness and features of thyrotoxicosis. A high prediction, early diagnosis and treatment of the condition can prevent severe complications, such as cardiac dysrhythmia.

An unusual cause of periodic weakness

Sir, Thyrotoxicosis is a rare cause of periodic paralysis. It is a rare endocrine disorder found mainly in men of Asian origin. We report the case of a 32-year-old male patient who came with repeated episodes of bilateral lower limb weakness for the last 2 months. The weakness episodes were mostly early morning lasting from few hours to occasionally a day. The patient had difficulty walking, climbing stairs, and getting up from the squatting position. Weakness used to improve with rest. There was no history of preceding high-carbohydrate diet or exertion. He also gave a history of heat intolerance, palpitations, and weight loss for the last 1 year. There was no significant past illness or family history. On physical examination, he had tachycardia with normal blood pressure. There was no exophthalmos or goiter. Neurological examination revealed hypotonia in bilateral lower limbs. He had a proximal weakness (Grade 3/5) in bilateral lower limbs while distal motor strength was normal. There was generalized hyporeflexia. Plantar responses were bilaterally flexor. The rest of the neurological examination was unremarkable. Laboratory studies revealed hypokalemia (serum potassium – 2.8 mmol/l), thyroid-stimulating hormone <0.001 mU/l, and free T4 56.8 pmol/l (normal range 9–21 pmol/l). Antithyroid peroxidase levels were high (1630 U/ml; normal range 0–50 U/ml). Electrocardiogram was normal. The patient was managed with oral potassium supplementation. He was started on carbimazole and propranolol therapy. The patient gradually improved and discharged. Thyrotoxic periodic paralysis (TPP) is a rare syndrome, predominantly found in young men of Asian origin. Various precipitating factors, including a high-carbohydrate meal, warm weather, and increased physical exertion, have been identified.[1] It mainly affects the proximal group of muscles without any cranial nerve or sensory involvement. Patients can rarely have respiratory failure or cardiac arrhythmias.[23] In TPP, the primary defect is an intracellular accumulation of potassium.[4] Thyroid hormones increase the activity of Na-K-ATP pump, which changes the permeability of the plasma membrane to potassium.[5] Other mechanisms have also been proposed which cause intracellular shift of potassium. Patients suspected of having TPP should be kept under cardiac monitoring to check for arrhythmias. Furthermore, arterial blood gas pressures and spirometric assessment required to monitor respiratory function.[1] Potassium levels should be monitored. Potassium correction is the cornerstone in the emergency management of TPP. Primary illness has to be treated with antithyroid drugs. Furthermore, beta-blockers should be added to manage the peripheral effects of thyrotoxicosis. In conclusion, young men presenting with periodic paralysis should be evaluated for thyrotoxicosis. Early diagnosis and prompt treatment can prevent fatal complications. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Thyrotoxic Periodic Paralysis

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.

A case series of hypokalemic thyrotoxic periodic paralysis presenting in the North Eastern region of India

Hypokalemic periodic paralysis (HPP) with thyrotoxicosis is a rare but treatable cause of sudden onset paralysis. Its occurrence is more common in males particularly of Asian descent. Presentation is like those seen in HPP with an additional feature of a hyperthyroid state, where the symptoms of hyperthyroidism may often be mild and thus may be missed. We are reporting a series of 4 cases of HPP in two males and two females from the North eastern region of India who presented with sudden onset weakness of limbs. Although hyperthyroidism is not common in this region of the country, all of them had elevated thyroid hormone levels on further evaluation. This case series is to highlight the significance of thyroid function test in cases presenting with a history of periodic paralysis.

The three cases of Thyrotoxic periodic paralysis

The three cases of Thyrotoxic periodic paralysis

Contribution of Asian Haplotype of KCNJ18 to Susceptibility to and Ethnic Differences in Thyrotoxic Periodic Paralysis.

Thyrotoxic periodic paralysis (TPP) is an acute complication of thyrotoxicosis that can be lethal. TPP is rare in Caucasians but often affects young men in East Asian populations. This study aimed to clarify the contribution of KCNJ18 to susceptibility to TPP in East Asian populations. The study comprised 635 participants including 13 Japanese patients with TPP, 208 Japanese patients with Graves disease without TPP, and 414 healthy control subjects from the Japanese (n = 208), Korean (n = 111), and Caucasian populations (n = 95). DNA samples from 29 participants (13 with TPP, 8 with Graves disease, and 8 controls) were sequenced for KCNJ18, and all participants (n = 635) were genotyped for six variants of KCNJ18 and a polymorphism of KCNJ2 (rs312691). Six single-nucleotide variants (SNVs) with amino acid substitutions were identified by direct sequencing of KCNJ18. Among these, four SNVs comprised three haplotypes under strong linkage disequilibrium. Haplotype 1 (AAAG) of KCNJ18 was significantly associated with susceptibility to TPP in the Japanese population (OR = 19.6; 95% CI, 1.5 to 256.9; P = 0.013). Haplotype frequencies in the general East Asian (Japanese and Korean) and Caucasian populations differed significantly (haplotype 1: 80.8% vs 48.4%, P = 1.1×10-27). A major haplotype of KCNJ18 in East Asian populations is significantly associated with susceptibility to TPP. The haplotype is much more common in East Asian than Caucasian populations, suggesting its contribution to the high prevalence of TPP in East Asian populations.

Thyrotoxic Periodic Paralysis with Sensory Deficits in Young African American Male: A Case Report and Literature Review.

Thyrotoxic periodic paralysis is a sporadic entity characterized by hypokalemia and paralysis in the setting of hyperthyroidism. TPP is most commonly described in young Asian males. Studies have shown an association with mutations affecting inward rectifying potassium channels. The pathophysiology involves Na+-K+- ATPase channel causing an increased intracellular shift of potassium ions in the hyperthyroid state and in the presence of another precipitating condition. Most cases of thyrotoxic periodic paralysis are defined in young Asian males of 20–40 years of age, here we present an interesting case of thyrotoxic periodic paralysis in 32-year-old African American male, who presented with sudden onset weakness in the bilateral lower extremity and left upper extremity. Interestingly, the patient also has sensory deficits, a feature not known to be associated with thyrotoxic periodic paralysis.

Thyrotoxic hypokalemic periodic paralysis as a rare manifestation of Graves disease

The objectve of the study is to present a rare observation of thyrotoxic hypokalemic periodic paralysis in a Caucasian male. The article presents a clinical observation of 44-year-old man suffering from diffuse toxic goiter. The course of the disease was complicated by the development of attacks of periodic hypokalemic paralysis. The patient was repeatedly hospitalized to the neurological departments of different city hospitals with diagnosis of cerebrovascular disorders. Thyrotoxicosis as the cause of periodic paralysis was diagnosed in five months after the disease onset. Due to the risk of progression of thyrotoxic complications and worsening of neurological pathology, the patient underwent thyroidectomy. There were no complications. Working capacity restored on the 12thday. Attacks of muscle weakness were not observed. Replacement therapy with 100 mg of levothyroxine per day was prescribed. Parameters of potassium, total calcium were normal.Conclusion. A rare observation of genetically determined manifestations of diffuse toxic goiter – a thyrotoxic hypokalemic periodic paralysis is presented. Surgical treatment allowed to radically cure thyrotoxicosis and to eliminate episodes of paralysis, to return the patient’s workability.

Assessment of Molecular Subtypes in Thyrotoxic Periodic Paralysis and Graves Disease Among Chinese Han Adults

Thyrotoxic periodic paralysis (TPP) is a potentially lethal complication of hyperthyroidism. However, only 1 specific susceptibility locus for TPP has been identified. Additional genetic determinants should be detected so that a prediction model can be constructed. To investigate the genetic architecture of TPP and distinguish TPP from Graves disease cohorts. This population-based case-control study used a 2-stage genome-wide association study to investigate the risk loci of TPP and weighted genetic risk score to construct a TPP prediction model with data from a Chinese Han population recruited in hospitals in China from March 2003 to December 2015. The analysis was conducted from November 2014 to August 2016. Loci specifically associated with TPP risk and those shared with Graves disease and prediction model of joint effects of TPP-specific loci. A total of 537 patients with TPP (mean [SD] age, 35 [11] years; 458 male) 1519 patients with Graves disease and no history of TPP (mean [SD] age, 38 [13] years; 366 male), and 3249 healthy participants (mean [SD] age, 46 [10] years; 1648 male) were recruited from the Han population by hospitals throughout China. Two new TPP-specific susceptibility loci were identified: DCHS2 on 4q31.3 (rs1352714: odds ratio [OR], 1.58; 95% CI, 1.35-1.85; P = 1.24 × 10-8) and C11orf67 on 11q14.1 (rs2186564: OR, 1.50; 95% CI, 1.29-1.74; P = 2.80 × 10-7). One previously reported specific locus was confirmed on 17q24.3 near KCNJ2 (rs312729: OR, 2.08; 95% CI, 1.83-2.38; P = 8.02 × 10-29). Meanwhile, 2 risk loci (MHC and Xq21.1) were shared by Graves disease and TPP. After 2 years of treatment, the ratio of persistent thyrotropin receptor antibody positivity was higher in patients with TPP than in patients with Graves disease and no history of TPP (OR, 3.82; 95% CI, 2.04-7.16; P = 7.05 × 10-6). The prediction model using a weighted genetic risk score and 11 candidate TPP-specific single-nucleotide polymorphisms had an area under the curve of 0.80. These findings provide evidence that TPP is a novel molecular subtype of Graves disease. The newly identified loci, along with other previously reported loci, demonstrate the growing complexity of the heritable contribution to TPP pathogenesis. A complete genetic architecture will be helpful to understand the pathophysiology of TPP, and a useful prediction model could prevent the onset of TPP.

SAT-602 Thyrotoxic Periodic Paralysis Precipitated by Glucocorticoid Injection

Background: Thyrotoxic periodic paralysis (TPP) is a rare manifestation of hypokalemia that is driven by thyrotoxicosis. TPP is associated with any etiology of thyrotoxicosis, though Graves’ disease is the most common. Some of the provoking factors for these episodes are a high carbohydrate meal, rest after heavy exercise, fasting, stress, alcohol intake, and pulse steroid therapy. Clinical Case: A 48-year-old man presented with acute-onset lower extremity paralysis. He had been in his usual state of health until two days prior to admission when he developed a streptococcal throat infection. He was given IM injections of 80mg methylprednisolone and 1g ceftriaxone in an urgent care clinic and discharged. Soon after discharge, he developed progressively worsening bilateral lower extremity soreness and weakness resulting in a fall. He was taken to the hospital by EMS, where he was found to have bilateral lower extremity paresis. He was anxious, mildly tachycardic, and had a non-tender, 25-gram diffuse goiter. No thyroid nodules were palpated nor did the patient exhibit cervical lymphadenopathy. Lid lag, a fine tremor, and onycholysis were also detected. Basic metabolic panel revealed a serum potassium of 2.3 mmol/L (ref: 3.5-5.1 mmol/L). An ECG was normal. He was given 60 mEq of oral potassium chloride and started on propranolol 10mg TID and reported symptomatic improvement within several hours. During hospitalization, the patient remained asymptomatic and his serum potassium remained normal. Thyroid function testing revealed an undetectable TSH, a Free T4 of 4.41 ng/dL (ref: 0.61-1.18 ng/dL), and a Free T3 of 10.29 pg/mL (ref: 2.5-3.9 pg/mL). Radionucleotide uptake scan of the thyroid showed diffusely increased uptake (81%) with no nodules, consistent with Graves’ disease. Thyrotropin receptor antibody and Thyroid stimulating immunoglobulin levels were elevated. He underwent successful radioactive iodine ablation. Serial laboratory testing was done and within six weeks the patient became hypothyroid. He is now treated with levothyroxine for post-ablative hypothyroidism. A literature search reveals case reports implicating steroids in the precipitation of TPP. Corticosteroids, along with thyroid hormone, increase the activity of sodium-potassium ATPase channels in skeletal muscle. Steroids also lead to hyperglycemia and subsequent increased insulin release that causes an intracellular shift of potassium. Conclusion: Though rare, TPP is important to recognize, as failure to treat underlying hyperthyroidism can lead to repeated episodes of hypokalemia and paralysis. This case highlights TPP precipitated by pulse glucocorticoid injection, described rarely in the literature. The potential of glucocorticoids to precipitate paralysis should be recognized when considering steroid treatment for other medical conditions in hyperthyroid patients.

SUN-LB098 Mimic Presentation of Neuromuscular Symptoms in Thyrotoxic Periodic Paralysis in Hispanic Male

Introduction: Thyrotoxic periodic paralysis (TPP) is a rare condition characterized by sudden paralysis with profound hypokalemia. Clinical Case: A 34 year-old obese Hispanic male presented to ED with sudden onset of generalized weakness and numbness of bilateral upper & lower extremities for one day. The patient was not able to get up when he woke up in the morning. He described having blurry vision, more severe on the right side, which was associated with right retroocular pain. He reported over twenty pounds of weight loss within past two months, accompanied with intermittent episodes of watery diarrhea, palpitations, restlessness, mild headache, and dizziness. He denied loss of consciousness, urinary or fecal incontinence, fever, cough or recent respiratory infection. Past medical history included gastritis. He reported no recent trauma, injury or hospitalization. No smoking, alcohol abuse or illicit drug use. On physical examination, the patient was having mild respiratory distress. Right eye exophthalmos and normal cardiopulmonary examination were noted. Neck examination showed no thyroid gland enlargement. Neurological findings revealed cranial nerve and sensory examination intact, but all four limbs were flaccid and motor strength of all extremities was 1/5. Deep tendon reflex was absent. Initial blood test on admission showed Potassium 1.9 mmol/l, Phosphorus 2 mg/dl, Magnesium 1.9 mg/dl, Lactic acid 4.6 mmol/l, TSH 0.005 mIU/l, Free T3: 8.80 pg/ml, Free T4: 2.3 ng/ml, and TBG 14.1 mcg/dl. Thyroid peroxidase was positive. EKG revealed sinus tachycardia. ABG indicated primary respiratory acidosis. Lumbar puncture was normal and ruled out Guillain-Barré syndrome and, viral or bacterial meningitis. Thyroid sonogram showed heterogeneous thyroid with no nodules. CT head without contrast showed no evidence of intracranial hemorrhage. MRI brain revealed no intracranial mass. MRI lumbar & thoracic spine showed a normal finding. After the aggressive replacement of potassium chloride, the muscle weakness improved significantly, and methimazole was initiated. The patient was admitted to ICU for close monitoring and electrolyte management. Conclusion: Thyrotoxicosis periodic paralysis (TPP) is a rare condition that manifests through acute paralysis, and hypokalemia in the presence of hyperthyroidism (1). It is usually found in relatively young Asian population, but also the occurrence has increased in the Hispanic population recently. Early recognition of TPP in a patient with unexplained hypokalemia and painless generalized weakness, is imperative to demand thyroid studies to rule out this condition. Close electrolyte management is important rebound hyperkalemia and life-threatening arrhythmias. Reference: (1) Meseeha M et al. Thyrotoxic periodic paralysis: a case study and review of the literature. J Community Hosp Intern Med Perspect. 2017;7(2):103-106. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. s presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

MON-428 More Danger Than We Knew: Hypokalemic Periodic Paralysis Triggered by Alcohol Consumption

Introduction: Alcohol use disorder affects close to 20 million people in the United States. Alcohol causes long term damage in various organs including the muscles resulting in alcoholic myopathy. However, other less common etiologies for acute muscle weakness should be considered in these patients. Case presentation: Our patient is a 25 year-old Hispanic male, who presented with 2 hours of acute lower extremity weakness. He had difficulty walking, clothing, grasping and reported myalgia. He admitted to partying and binge drinking while consuming pizza and burgers the night before. He denied similar episodes in the past or any family history of weakness. His physical exam was remarkable for 2/5 strength in the hip flexors bilaterally, hip and knee extension was 4/5 bilaterally, knee flexion was 4/5 bilaterally. He had hyporeflexia, normal muscle bulk and tone and normal sensation. Diagnostic work up revealed a potassium of 1.9 mmol/L, phosphorus 1.9 mmol/L and CK of 176 IU/L (22-269 IU/L). Due to concern for thyrotoxic periodic paralysis, TSH was checked which was normal at 0.47 MCIU/ml (0.550-4.780 MCIU/ml). He was given 40meq IV potassium by slow infusion, followed by 40meq PO. His potassium improved to 2.4mmol/L after supplementation and there was a rapid recovery in his muscle weakness. Potassium levels were monitored for 24 hours. He had persistently normal potassium levels during his stay. His lower motor strength remained to be a 5/5 throughout the hospitalization. He was discharged with counseling and emphasis on alcohol cessation. Discussion: Beer contains 13 grams of CHO in 1 can. It’s high carbohydrate content can result in an insulin surge producing a rapid intracellular shift of potassium through N-K ATPase channels. This produces hypokalemic periodic paralysis (HPP) in predisposed patients. HPP is an uncommon neuromuscular disorder with 1 in 100,000 cases. It results from mutations in sodium, calcium and potassium channels in the skeletal muscles. It is an autosomal dominant disease and found predominantly in young Asian males. These patients are at risk for fatal cardiac arrhythmias due to their significantly low potassium levels on presentation. They carry the same risk for arrhythmias in the treatment period due to increased risk of over-correction resulting in hyperkalemia. Long term recurrent HPP can result in progressive proximal myopathy and reduced functional mobility that may affect quality of life. These short and long term complications in HPP can only be prevented by avoidance of triggers, in our case avoidance of alcohol consumption. Rapid recognition for close electrolyte monitoring and effective counseling by physicians to establish a clear understanding in patients is imperative for their long term health. (1)Vilarinho S, Siegel M D. Paralysis caused by a large carbohydrate meal. J Postgrad Med 2012;58:60-1

A case of thyrotoxic periodic paralysis

A CASE OF THYROTOXIC PERIODIC PARALYSIS Ankit Sakhuja, Pinky Patel, Aaron Dall. Medical College of Wisconsin, Milwaukee, WI, USA Thyrotoxic periodic paralysis is an uncommon disease affecting mostly young Asian males. It is usually associated with hyperthyroidism, mostly Grave’s disease. We present a case of thyrotoxic periodic paralysis in a young African American male with no significant past medical history. A 19 year old African American male with no significant past medical history presented to the emergency room with a history of significant weakness. He went to bed the night prior without any problems after a family dinner. He was however unable to get out of bed next morning and had to crawl out of bed. He denied any fever, diarrhea, URI, sick contacts, recent travel and insect or tick bites. His physical examination was significant for proximal muscle weakness more in lower extremities. Labs were significant for potassium of 2.6. meq/L, TSH 0.011 μIU/mL and fT4 2.71 ng/dL. His EKG showed U waves. Patient was diagnosed with thyrotoxic periodic paralysis, given 20 meq of potassium chloride and monitored in the hospital. His strength and potassium levels normalized within 24 hours. He was also started on propranolol and a thyroid scan confirmed Grave’s disease. Thyrotoxic periodic paralysis is an uncommon condition associated with hyperthyroidism. It usually presents in early morning and patients have significant hypokalemia on presentation. However the condition is usually self limited and potassium supplementation can lead to dangerous hyperkalemia. Propranolol has been shown to help abort the attack.

Thyrotoxic Periodic Paralysis: An Unusual Presentation of Hyperthyroidism in a 20 year-old Male (P5.4-020)

Thyrotoxic Periodic Paralysis: An Unusual Presentation of Hyperthyroidism in a 20 year-old Male (P5.4-020)

Thyrotoxic periodic paralysis with ventricular tachycardia

A 47-year-old man presented to our emergency department (ED) with limbs weakness for 2 h. His heart rate was 127 beats per minute and blood pressure was 95/49 mm Hg. He found weakness of limbs after 4-h sleep. Physical examinations revealed that the muscle strength of upper limbs is 3/5, and lower limbs are 2/5.Electrocardiogram (ECG) revealed wide QRS complex, monomorphic ventricular tachycardia (VT) with ST-segment depression and long QT interval. Serum potassium level was extremely low as 1.0 mEq/L. This led to periodic hypokalemic paralysis. Due to severe hypokalemia with possible atrioventricular block, the patient was admitted to the intensive care unit. During hospitalization, his potassium level returned to 5.1 mEq/L on the first day. He had a low level of thyroid stimulating hormone (TSH) of <0.03 micro-IU/mL (normal range: 0.25–4.00) and a high free thyroxine (T4) level of 2.43 ng/dL (normal range: 0.89–1.79 ng/dL). Therefore, hyperthyroidism was diagnosed, and 5 mg of methimazole was administered twice a day. The patient was discharged on the seventh day after admission. The final diagnosis is thyrotoxic periodic paralysis (TPP), also as known as nocturnal paralysis or night palsy.

Abstract #642 Thyrotoxic Periodic Paralysis in a Hispanic Male Resulting in Acute Respiratory Failure

Abstract #642 Thyrotoxic Periodic Paralysis in a Hispanic Male Resulting in Acute Respiratory Failure

Clinical and Etiological Spectrum of Hypokalemic Periodic Paralysis in a Tertiary Care Hospital in Pakistan.

IntroductionHypokalemic periodic paralysis (HPP) is characterized by muscle weakness secondary to low serum potassium levels. It may be primary in origin or there may be secondary causes like thyrotoxic periodic paralysis, renal or suprarenal causes, or non-renal causes like gastroenteritis.AimTo study the etiology, clinical manifestations, and outcome after therapy of patients with hypokalemic paralysis.MethodologyThe study was conducted from January 2016 to December 2016. Patients fulfilling the diagnostic criteria for hypokalemic paralysis, i.e., flaccid muscle weakness involving two or more limb muscles due to serum potassium < 3.5 mmol/L and with no objective sensory signs were included in the study. Relevant investigations were done. Those with other causes of flaccid weakness or on diuretic therapy were excluded from the study. Data was analyzed using SPSS Version 20.0 (IBM Corp., Armonk, NY).ResultsIn our study, 14 patients out of a total of 18 (14/18, i.e., 77.78%) were male and 4/18 (22.22%) were female [Male: Female ratio: 3.5:1]. The mean age of onset of HPP in males (29.5±10.14 yrs.) was lesser than that of females (41±10.8 yrs.), but this difference was statistically not significant (p<0.066). In the entire sample there were 15/18 cases (83.33%) of primary and 3/18 (16.67%) cases of secondary HPP [2/3 had thyrotoxic periodic paralysis and 1/3 had gastroenteritis]. Furthermore, 12/18 patients (66.66%) had symmetrical weakness (five cases of paraparesis and all were male; seven cases of quadriparesis: six males and one female) and 6/18 (33.33%) had asymmetrical weakness (two paraparesis: one male, one female; four quadriparesis: two males, two females). Statistically, no significant difference (p<0.709) was seen in those with symmetrical versus those with asymmetrical weakness. In this study 7/18 (38.89%) cases had absent, 1/18 (5.55%) had diminished, and 10/18 (55.55%) cases had intact deep tendon reflexes. None of the cases had cranial, bulbar, or respiratory involvement. The mean serum potassium of sample was 3.18±0.5 standard deviation (SD). The reduction in serum potassium was moderate (2.5-3.5 mmol/L) in primary and severe (<2.5 mmol/L) in secondary HPP. Those with quadriparesis had severe hypokalemia with a mean serum potassium of 2.1 mmol/L. Only 3/18 patients had concomitant magnesium deficiency. Patients given intravenous potassium replacement (except one with moderate hypokalemia and given oral replacement) recovered dramatically. The mean recovery time was 38.6±20.3 hours. The recovery time in quadriparesis was about 24 hours and in paraparesis was 12 hours. Only one patient with thyrotoxic periodic paralysis (TPP) and with severe serum potassium deficiency (0.9 meq/L) died due to cardiac arrhythmia. No atypical presentation was seen.ConclusionHPP has male preponderance. The age of onset of HPP is earlier in males than in females. Moreover, males are more prone to have symmetrical weakness. Asymmetrical weakness has almost an equal gender distribution. Primary hypokalemic paralysis is more frequent than secondary. Thyrotoxic periodic paralysis is the commonest cause of secondary periodic paralysis. The recovery time in quadriparesis is almost double the recovery time in paraparesis. Respiratory involvement is rare. HPP is an important differential in the diagnosis of acute flaccid muscle weakness. It should be promptly addressed to prevent recurrence of paralysis.

Thyrotoxic Periodic Paralysis with Hypokalemia in an Adult Male from Nepal: A Case Report

Thyrotoxic periodic paralysis is rare complication of hyperthyroidism characterized by the sudden onset of hypokalemia and muscle paralysis. It is typically present in young Asian males. There are very few literatures regarding the occurrence of thyrotoxic hypokalemic periodic paralysis in Nepal. We reported a case of a 35-year-old male presented with the chief complaints of weakness of all four limbs of 1 day duration. He was diagnosed as a case of hyperthyroidism in the past, received treatment for 6 months and left medications on his own 6 months ago. Evaluation during admission revealed severe hypokalemia with serum potassium level 1.3mEq/l and high serum Triiodothyronine (>20.00µg/L) and low serum Thyroid Stimulating Hormone (<0.01µg/L). Potassium supplements resolved muscle weakness and the patient was restarted with anti-thyroid drugs. Hence, hypokalemic paralysis is a reversible cause of paralysis and high index of suspicion as well as timely interventions are required to prevent potential harm. Keywords: hyperthyroidism; hypokalemia; muscle paralysis; thyrotoxic periodic paralysis.