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Purpose: Thyrotoxic periodic paralysis (TPP) is characterized by muscle paralysis and significant intracellular potassium movement resulting in hypokalemia. Since TPP is a rare condition, only a few studies have explicated the clinical characteristics of patients with this disease. This study aimed to elucidate the clinical characteristics of patients with TPP by comparing them with those with thyrotoxicosis without paralysis (non-TPP) and sporadic periodic paralysis (SPP)., Methods: This was a single-center retrospective cohort study. Clinical data of patients with hyperthyroidism (n = 62) or periodic paralysis (n = 92) who were emergently admitted to our hospital was extracted from the electronic medical records and analyzed., Results: All patients in the TPP group (15 males and 2 females) had Graves' disease, with 14 being newly diagnosed. The average serum potassium level on admission was 2.3±0.75 mEq/L. No significant correlation was observed among serum potassium level, amount of potassium required for normalization, and thyroid hormone levels. The TPP group showed significantly younger age, higher male ratio and body mass index (BMI), and lower serum potassium and phosphorus levels than the non-TPP group, which comprised 36 patients with Graves' disease. No significant differences were observed between the TPP and SPP (n = 11) groups in terms of age, sex, BMI, serum electrolyte levels, potassium requirement for normalization, and recovery time., Main Conclusions: Considering that most patients with TPP have undiagnosed Graves' disease, distinguishing TPP from SPP based on clinical information and course alone is difficult in emergency settings. Therefore, for early detection and launch of specific treatment of Graves' disease, screening for thyroid hormone and anti-thyroid stimulating hormone receptor antibody levels is necessary when treating patients with periodic paralysis., Competing Interests: The authors declare that this study was conducted in the absence of any commercial or financial relationships that could be construed as potential conflicts of interest., (Copyright: © 2024 Yamada et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

A 21-year-old man presented with hyperthyroidism and hypokalemia and was treated for thyrotoxic hypokalemic periodic paralysis caused by Graves' disease. Thyroid function soon normalized but hypokalemia persisted. Laboratory data revealed hyperreninemic hyperaldosteronism and metabolic alkalosis consistent with Gitelman Syndrome. The patient was found to have a previously unreported compound heterozygous mutation of T180K and L858H in the SLC12A3 gene, and Gitelman Syndrome was diagnosed. He was started on eplerenone to control serum potassium level. Alternative diagnoses should be considered when electrolyte imbalances persist after disease resolution.

Bilateral symmetrical weakness of acute onset is not very uncommon and the differential varies widely from life-threatening neurological illnesses to metabolic and electrolyte derangements. We report the case of a young female with severe muscle weakness, respiratory distress and hypokalemia who required immediate intubation on arrival to emergency department. During hospital course, even after normalisation of serum potassium and some improvement in limb weakness, patient failed multiple attempts of extubation because of type II respiratory failure. Subsequently, acetyl cholinesterase antibodies were checked which came out positive, and diagnosis of myasthenia gravis and hypokalemic periodic paralysis was made. She was successfully extubated after intravenous pulse steroids, pyridostigmine and plasmapheresis. Patient was finally discharged home on oral steroids, pyridostigmine and azathioprine. In a patient presenting with hypokalemic weakness, the suspicion of a second disorder should be very high if weakness fails to resolve following correction of hypokalemia., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Hypokalemic periodic paralysis (HypoKPP) is characterized by transient episodes of flaccid muscle weakness. We describe the case of a teenaged boy with HypoKPP and hyperthyroidism due to Hashimoto's thyroiditis with initial manifestation of renal tubular acidosis. This combination is rare and little described previously in men. Case presentation : A 17-year-old boy was admitted after three days of muscular weakness and paresthesia in the lower limbs with an ascending evolution, leading to prostration. Decreased strength was found in the lower limbs without a defined sensory level, reduced patellar and ankle reflexes. Positive antithyroid antibodies were found. He received hydration treatment, IV potassium and levothyroxine, with which there was a clinical improvement. Other examinations led to the diagnosis of type 1 renal tubular acidosis. Conclusion : HypoKPP is a rare disorder characterized by acute episodes of muscle weakness. Type 1 renal tubular acidosis can occur as a consequence of thyroiditis, which is explained by the loss of potassium. This combination is unusually rare, and has not been described before in men. The etiopathogenesis of the disease as well as a dynamic explanation of what happened with the patient are discussed in this report., Competing Interests: No competing interests were disclosed.

Hypokalaemic periodic paralysis is a rare skeletal muscle channelopathy causing flaccid paralysis, which predominantly presents in adolescents and young adults. I report a case of a 33-year-old Caucasian man who presented with sudden onset paralysis, following previous similar presentations without investigation. Blood tests revealed undetectable serum potassium levels in the context of paralysis. Other causes of hypokalaemia were excluded, and the patient was treated with planned lifelong prophylactic potassium replacement for a diagnosis of primary hypokalaemic periodic paralysis. This case demonstrates that, although rare, hypokalaemic periodic paralysis should be considered as a differential diagnosis in young patients who present with sudden flaccid paralysis and can easily be excluded by checking serum potassium levels at presentation.

We report a case of a 9-year-old boy who developed hypokalaemic periodic paralysis (HypoPP) following a prodrome of persistent fatigue and muscle aches associated with mildly elevated creatine kinase (CK) levels.HypoPP is usually associated with a sudden onset of weakness and hypokalaemia at presentation. A review of published cases failed to identify any other reports of individuals with a similar onset of symptoms and elevated CK levels prior to the development of frank HypoPP.In the case described above, the association of these symptoms with elevated levels of CK may have been related to the underlying mutation in the skeletal muscle calcium channels that was subsequently identified.In cases of persisting fatigue and myalgia associated with elevated CK levels it may be helpful to consider HypoPP in the differential diagnosis., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Hypokalaemic paralysis covers a heterogeneous group of disorders caused either by an enhanced shift of potassium into the cells or following a significant renal or gastrointestinal loss of potassium. We present the case of a 48-year-old Caucasian man with paralysis of both upper and lower extremities. ECG showed sinus rhythm and characteristic changes of hypokalaemia with depression of the ST segment, prolonged QTc interval of 581ms and U waves seen as a small positive deflection at the T wave in the middle precordial leads. We suspected the cause of hypokalaemia leading to paralysis to be due to administration of high doses of furosemide without oral potassium supplementation coupled with regular use of insulin. Initial therapy included both oral and intravenous potassium replacement and close monitoring of cardiac rhythm and serum potassium levels. Twenty-four hours after admission, the potassium level had normalised and the patient slowly recovered and gained strength. The patient was discharged after 1 week of careful follow-up and did not experience any serious degree of rebound hyperkalaemia. At the time of discharge, all laboratory tests were normal and ECG revealed a normal sinus rhythm and normal QTc intervals., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objective: To study the clinical profile of hypokalemic flaccid paralysis (HKFP) and to evaluate its causes., Methods: Fifty cases of hypokalemic flaccid paralysis (HKFP) admitted between November 2012 to October 2014 were taken up in the study. Serum potassium level < 3.5 mmol/ltr has been taken as hypokalemia. All cases were studied for spot and/or 24 hour urinary sodium / potassium, serum potassium / calcium / magnesium. Hypokalemic periodic paralysis (HPP) were diagnosed if there was spot/24 hour urine potassium excretion < 20mmol/ltr in presence of hypokalemia and flaccid weakness without other causes. EMG and nerve conduction study were done to exclude polyneuropathy and myopathic cases., Results: Out of 50 cases of HKFP, male gender predominated (88%). Maximum number of cases (70%) occurred in 21 to 40 years of age. It occurred in all seasons but more in summer (58%). The precipitating factors were present in 76% of cases out of which high carbohydrate meal (28%), vomiting (16%), excessive sweating (8%), diarrhea (8%) and increased urination (12%) were present. Twenty percent of cases had recurrence (2 to 3 episodes most often) and 6% of cases had family history. Quadriparesis was seen in (54%), paraparesis (36%), hemiparesis (10%) and neck muscle weakness (32%). No case was present with respiratory paralysis or cranial nerve palsy. Twenty-one cases (42%) have very low potassium < 2.5 mmol/ltr, 11 cases (22%) with potassium level between 2.5 to 2.9 mmol/ltr and 18 cases (36%) with 3 to 3.5 mmol/ltr. There was no correlation between severity weakness and potassium level. Eleven cases (22%) had thyrotoxicosis and 3 cases (6%) were hypothyroid. Thirteen cases (26%) have excess urinary loss of potassium (≥20 mmol/ltr) of which 5 cases (10%) were distal renal tubular acidosis (dRTA), four cases (8%) were Gitelman's syndrome (GS) and in 4 cases exact cause could not be diagnosed. Non-renal / prior renal loss of potassium like diarrhea and excessive sweating was responsible in 8% cases each and vomiting in 10% of cases. One unique case of hypernatraemic hypokalemic paralysis (HHP) was found. Only 9 (18%) cases are hypokalemic periodic paralysis (HPP)., Conclusions: HKFP is a hetergenous group of disease of which a significant number of patients had thyroid disorders mostly in the form of thyrotoxicosis followed by renal tubular dysfunctions like dRTA and GS; non-renal and prior renal loss of potassium like diarrhea, excessive sweating and vomiting respectively. Early recognition and prompt management of these conditions will give gratifying result and prevent further attacks in some cases.

Periodic thyrotoxic paralysis is a genetic condition, rare in the West and in Caucasians. Thyrotoxicosis, especially in western hospitals, is an easily overlooked cause of sudden-onset paralysis. We present a case of a 40-year-old man who awoke one morning unable to stand. He had bilateral lower limb flaccid weakness of 0/5 with reduced reflexes and equivocal plantars; upper limbs were 3/5 with reduced tone and reflexes. ECG sinus rhythm was at a rate of 88/min. PR interval was decreased and QT interval increased. Bloods showed potassium of 1.8 mEq/L (normal range 3.5-5), free T4 of 29.2 pmol/L (normal range 6.5-17) and thyroid-stimulating hormone (TSH) of <0.01 mIU/L (normal range 0.35-4.94). Random urinary potassium was 8.8 mEq/L (normal range 12.5-62.5). The patient was admitted initially to intensive therapy unit and given intravenous potassium. His symptoms resolved within 24 h. He was diagnosed with thyrotoxic periodic paralysis. He was discharged on carbimazole and propanolol, and follow-up was arranged in the endocrinology clinic., (2015 BMJ Publishing Group Ltd.)

A 26-year-old Hispanic man with no significant medical history presented to our emergency room with gradual onset weakness of his lower extremities. He was haemodynamically stable and examination revealed loss of motor function in his lower limbs up to the level of hips. Laboratory data revealed hypokalaemia. The patient was started on potassium supplementation and he recovered his muscle strength. Differential diagnosis included familial hypokalaemic periodic paralysis and thyrotoxic periodic paralysis (TPP). Further investigations revealed a low thyroid-stimulating hormone and high free thyroxine levels. Radio iodine 123 scan revealed an enhanced homogeneous uptake in the thyroid suggesting Graves' disease. Thyroid stimulating antibodies were also found to be elevated. The patient was started on methimazole and propranolol and he never had another attack of TPP even at 1 year follow-up.

Hypokalaemic periodic paralysis (HPP) is a life-threatening condition. Our aim was to study the clinical profile and laboratory parameters of HPP patients and to develop an algorithm to determine the causes of HPP. 84 patients presented with HPP over a 3 year period. 58 (69.0%) were found to have renal tubular acidosis (RTA). The other causes were idiopathic HPP (8 (9.5%)), acute gastroenteritis (4 (4.8%)), suspected primary hyperaldosteronism and familial HPP (2 each (2.4%)) and suspected Gitelman/Bartter Syndrome and thyrotoxic periodic paralysis (1 each (1.2%)). The number of cases peaks in the hot season. Over a third of the patients (35.7%) had recurrent episodes. 80% had secondary HPP and therefore a biochemical evaluation is mandatory. A simple algorithm was developed. Both health professionals and patients need further education regarding this problem in order to improve diagnosis and treatment and to improve compliance.

Thyrotoxic periodic paralysis is a reversible metabolic disorder that is characterized by acute muscle weakness and hypokalemia. It predominantly affects males of Asian descent. We describe the youngest such patient yet reported, a 13-year-old Asian male with a history of transient attacks of weakness who presented to our emergency department with weakness in his extremities and mild tachycardia. Laboratory test results initially revealed marked hypokalemia and later confirmed associated hyperthyroidism. Correction of the hypokalemia reversed the patient's weakness in the emergency department.

Acute hypokalemic periodic paralysis (HPP), a clinical syndrome characterised by acute systemic weakness and low serum potassium (K+), is a rare but treatable cause of acute limb weakness. Hypokalemia can be caused by K+ loss via the kidneys or extra renal routes mainly the gut, or due to transcellular potassium shifts where extracellular K+ will move into the cell. In the latter situation, although there is hypokalaemia, there is no deficit of K+ in the body. The main causes for intracellular shift of K+ are familial hypokalemic periodic paralysis, thyrotoxic periodic paralysis, barium poisoning, insulin excess and alkalosis. Although the association between thyrotoxicosis and HPP is known, HPP with hypothyroidism is extremely rare. We report a case of hypokalemic periodic paralysis associated with hypothyroidism and neuromyotonia.

We report an unusual case of 5-yrs-old girl presenting with recurrent episodic weakness with documented hypokalemia, polyuria and failure to thrive. The child was finally diagnosed as having distal renal tubular acidosis. Imaging studies revealed associated hypoechoic spaces in renal medulla. Long term treatment with alkali and maintenance of normokalemia lead to regression of these morphological changes.

Background: A recent genome-wide association study of Thai patients with thyrotoxic periodic paralysis (TPP) identified a novel genetic variant rs623011 located in chromosome 17q24.3, which may potentially reduce the transcription of Kir2.1 and total Kir current., Purpose: The aim of this study was to evaluate whether this genetic variant was present in Chinese patients with TPP and sporadic periodic paralysis (SPP), the second leading cause of non-familial hypokalemic periodic paralysis (hypoKPP) in Asia., Methods: Ninety patients with TPP, 61 SPP, and 100 age and sex-matched healthy subjects were performed. Genomic DNA was isolated from blood leukocytes and analysis of rs623011 was performed by polymerase chain reaction and direct sequencing., Results: Compared with normal control, the frequency of the risk allele A of rs623011 was significantly higher in both TPP and SPP patients (73.9% versus 53.5%, p=0.001; 82.0% versus 53.5%, p<0.001, respectively) with the Odds ratios (95% confidence interval) 2.426 (1.348-4.369) and 4.488 (2.265-8.891), respectively. The frequency of the A allele of rs623011 was similar between TPP and SPP., Conclusions: TPP and SPP have the same susceptible gene variant rs623011 and may share the pathogenic mechanism of reduced Kir current in skeletal muscle independent of thyroid hormone., (Copyright © 2012 Elsevier B.V. All rights reserved.)

We report a case of a 39 year-old Asian man in whom profound lower limb paralysis, along with severe hypokalemia and electrocardiographic changes, were the presenting features of Graves' disease (GD)-related thyrotoxicosis. Rapid recognition and management of the disorder were the key factors to avoid fatal hypokalemia-induced cardiac arrhythmias and promptly restore patient's capacity to ambulate.

Thyrotoxic Periodic Paralysis (TPP) is a rare complication of thyrotoxicosis and is up to 20 times more common in males. Cases usually present with painless muscle weakness precipitated by heavy exercise, fasting, an alcohol binge or large carbohydrate meal. Serum potassium is low in the majority, but normokalaemic (or even hyperkalaemic) TPP is recognised. Acute treatment of any electrolyte disorder, administration of a beta-blocker and treatment of the thyrotoxicosis leads to complete resolution. This rare diagnosis should be considered by the Acute Physician when confronted with any case of muscle weakness.

Background: Acute flaccid paralysis is a common neurological emergency with diverse causes and variable outcome. There is a paucity of reports documenting the spectrum of hypokalaemic paralysis in neurological practice., Objective: To report the clinical features, aetiology, and outcome of patients with hypokalaemic paralysis in a tertiary care teaching hospital in India., Methods: Consecutive patients with acute flaccid paralysis with hypokalaemia from 2008 to 2010 were included in the study. Patients with Guillain-Barré syndrome, porphyria, polio and non-polio enterovirus infection and myositis were excluded. Detailed clinical examination, urinalysis, renal function tests, arterial blood gas analysis, thyroid hormones, and electrocardiogram were carried out. Patients received intravenous or oral potassium supplementation and their underlying causes were treated., Results: Thirty patients aged 17-52 years, including three females, were included. Secondary causes of hypokalaemic paralysis were present in 13 patients and included thyrotoxic paralysis in five and renal tubular acidosis (RTA) and Gitelman syndrome in four each. All the patients had quadriparesis and 10 had severe weakness (MRC grade <2). Tendon reflexes were reduced in eight and brisk in four patients. Respiratory paralysis was present in six patients and one needed artificial ventilation. Fifteen patients had severe hypokalaemia (<2 mmol/l), four had acidosis, and six had alkalosis. The secondary group had more severe hypokalaemia and needed longer time to recover., Conclusion: 43.3% of patients with hypokalaemic paralysis had a secondary cause for their condition. Patients with severe hypokalaemia with acidosis or alkalosis should be investigated for secondary causes as their management differ.

Thyrotoxic periodic paralysis is a rare complication associated with hyperthyroidism. It is most common in the Asian population. We describe a case of a 28-year-old Sudanese man who presented with ascending lower extremity paralysis after treatment of hyperthyroidism with prednisone and methimazole. This case report reviews the literature looking at pathophysiology, causes, and treatment recommendations for this rare complication of hyperthyroidism.

Objectives: To analyze the independent factors for the severity of paralysis in the patients with hypokalemic periodic paralysis (HOPP)., Methods: Eighty patients admitted with HOPP were reviewed. Using univariate analysis and multivariate analysis, the independent factors for the severity of paralysis were revealed., Results: A total of 76 cases were male and 4 female with a mean age of (26.3 +/- 4.5) years. Univariate analysis showed that patients with low serum magnesium level, low serum potassium level, high serum creatine kinase level, changes of electrocardiogram, chest distress and palpitation, nausea and vomiting as well as muscular soreness had more severe paralysis, while multivariate analysis revealed that serum magnesium < 0.8 mmol/L (OR 8.3, 95%CI 1.0 - 68.4, P < 0.05), serum potassium 1.5 - 1.8 mmol/L (OR 1.3, 95% CI 1.1 - 16.0, P < 0.01) and serum creatine kinase > 200 U/L (OR 1.1, 95%CI 1.0 - 1.1, P < 0.01) were the independent factors for the severity of paralysis., Conclusion: Low serum magnesium level, low serum potassium level and high serum creatine kinase level are the independent risk factors for more severe paralysis in patients with HOPP.

Thyrotoxic Periodic Paralysis (TPP) is a rare manifestation of hyperthyroidism characterized by muscle weakness and hypokalemia. Thyroid-Stimulating Hormone (TSH)-secreting pituitary adenoma is a rare cause of hyperthyroidism. Even more rare is the occurrence of TPP as the first manifestation of a TSH-secreting pituitary adenoma. We report a 31-year-old Asian male patient suffering from TPP caused by a TSH-secreting adenoma, who was evaluated for persistent episodes of muscle paralysis. Laboratory investigation revealed hypokalemia as well as elevated levels of both thyroid hormones and TSH. The Magnetic Resonance Imaging (MRI) of the pituitary gland revealed a microadenoma, thus suggesting the presence of a TSH-secreting adenoma. The patient underwent transphenoidal resection and the pathological investigation confirmed the diagnosis of TSH-secreting pituitary adenoma. After the adenomectomy and the restoration of euthyroidism, the patient did not experience any episode of hypokalemic paralysis or weakness. Despite its rarity, TSH-secreting pituitary adenoma should be included in the differential diagnosis of TPP.

Objective: Thyrotoxic periodic paralysis (TPP) occurs predominantly in Asian males, but there are few reports about TPP in the mainland of the People's Republic of China. The purpose of this study was to report the clinical features of cases of TPP in mainland China., Methods: Forty-five cases of TPP, admitted to Zhongnan Hospital of Wuhan University during a 5-year period, were retrospectively reviewed., Results: Patients typically presented with acute paralysis of the limbs, almost half (48.6%) initiated with legs, while the rest (51.4%) with both arms and legs. Twenty of 45 patients (44.4%) who had been diagnosed with hyperthyroidism suffered sudden attacks, while the remaining 25 patients were newly diagnosed with TPP. 16 patients had low potassium serum concentrations (1.44-3.00 mmol/L). There was a correlation between the lowest muscle strengths of the proximal and distal legs and serum potassium concentrations (Spearman correlation, r=0.556, P=0.049)., Conclusions: TPP is not an uncommon disease in mainland China. Thyrotoxic patients need to improve medication compliance and follow-up. At the time of the TPP attack, a detailed interview and inquiry with a thorough physical examination usually provide clues to the diagnosis. Leg muscle strength evaluation may be useful to assess the severity of hypokalemia.

Objectives: In this study we describe the clinical presentation and electrolyte disturbances of thyrotoxic periodic paralysis (TPP) in patients admitted to the Department of Medicine at Hamad General Hospital., Methods: Retrospective descriptive study involving patients admitted to the medical department of Hamad General Hospital with paralysis and hyperthyroidism., Results: Eighteen patients with TPP were identified over a three-year period (2004-2007). Their mean age was 32.4 +/- 8.52 years (range 21 to 48 years); all were males. Eleven patients were from the Philippines, five were from Nepal, one was Indian and one was from Sri Lanka. Fourteen patients (77.8%) had the attack in the summer while the remaining four in winter. Nine had a history of severe exertion, five had ingested a heavy carbohydrate meal, two had a sore throat, one had ingested alcoholic and one was without a precipitating cause. Fifteen patients had no previous history of hyperthyroidism. Later on, all patients proved to have hyperthyroidism. All patients were hypokalaemic, while seven patients had hypophosphataemia and three had hypomagnesaemia. Urinary potassium was <20 mmol/l in all patients. Fifteen patients had ECG changes. All patients had proximal myopathy. Twelve patients had signs of hyperthyroidism in the form of goitre, warm sweaty palms, tachycardia, and tremor. Nine patients had attacks of paralysis before diagnosis. After discharge, ten patients had recurrences within one to seven months., Conclusion: The causes of hypokalaemia and lower-extremity paralysis are numerous; TPP should be taken into consideration in the differential diagnosis of all acute episodes of motor paralysis, especially in young Asian male patients.

Thyrotoxic, hypokalaemic periodic paralysis is an uncommon, potentially life-threatening endocrine emergency. Because of the acute onset of neurological symptoms patients often initially present to hospital ED. To reduce patient morbidity and costs of unnecessary investigations, early recognition and appropriate treatment is required. The case of a young man of Singaporean origin is presented to highlight current treatment, management and pathophysiology of this condition.

Background: Periodic paralysis is classified into hypokalemic (hypoPP) and hyperkalemic (hyperPP) periodic paralysis according to variations of blood potassium levels during attacks., Objective: To describe new mutations in the muscle sodium channel gene SCN4A that cause periodic paralysis., Methods: A thorough clinical, electrophysiologic, and molecular study was performed of four unrelated families who presented with periodic paralysis., Results: The nine affected members had episodes of muscle weakness reminiscent of both hyperPP and hypoPP. A provocative test with potassium chloride was positive in two patients. However, repeated and carefully performed tests of blood potassium levels during attacks resulted in normal potassium levels. Remarkably, two patients experienced hypokalemic episodes of paralysis related to peculiar provocative factors (corticosteroids and thyrotoxicosis). Similarly to hyperPP, electromyography in nine patients revealed increased compound muscle action potentials after short exercise and a delayed decline during rest after long exercise as well as myotonic discharges in one patient. With use of molecular genetic analysis of the gene SCN4A, three new mutations were found affecting codon 675. They resulted in an amino acid substitution of a highly conserved arginine (R) to either a glycine (G), a glutamine (Q), or a tryptophan (W). Interestingly, hypoPP is caused by both mutations affecting nearby codons as well as the change of an arginine into another amino acid., Conclusion: A potassium-sensitive and normokalemic type of periodic paralysis caused by new SCN4A mutations at codon 675 is reported.

Introduction: Profound hypokalemic conditions resulting from cisplatin therapy have been known to produce hypokalemic paralysis in rare cases. We describe such a case of cisplatin-induced hypokalemic paralysis., Case Summary: A 15-year-old Persian girl with ovarian dysgerminoma presented with severe generalized weakness and paraplegia 1 week after the fourth course of cisplatin-based chemotherapy. On physical examination, there was symmetric flaccid paralysis and areflexia in all of the extremities and particularly in the lower limbs. Her serum potassium concentration was 1.7 mmol/L. Metastatic disease was excluded by a comprehensive systemic evaluation. Complete clinical and paraclinical recovery was achieved after short-term administration of potassium supplement., Discussion: Adverse drug reactions are common with cisplatin, but the drug is only rarely associated with hypokalemic paralysis. Based on the Naranjo causality algorithm, an objective assessment revealed cisplatin to be a probable cause of hypokalemic paralysis in this case. This adverse drug event--whether isolated or secondary to hypomagnesemia--may be deceptive, leading to a fatal mistake in the oncology setting, and should therefore be precisely differentiated from cancer-related complications., Conclusions: This case suggests that cisplatin should be added to the list of agents causing hypokalemic paralysis. Regular serum electrolyte measurement, the early detection of cation deficiency, and appropriate replacement of cations are all recommended.

Hypokalaemic periodic paralysis is an autosomal, dominantly inherited disorder, characterised by attacks of partial or total muscle weakness and serum hypokalaemia. the mutations responsible are located in the CACNA1S gene (type 1) and in the SCN4A gene (type 2), and are all missense mutations where arginine is mostly replaced by histidine or sometimes glycine. The mutation has been localised in the voltage sensor of the transmembrane segment of calcium channel (type 1) and sodium channel (type 2) respectively. How muscle weakness develops is not known. Oral or intravenous administration of potassium is helpful in treating partial or complete attacks. Acetazolamide can reduce the frequency of attacks in type-1 hypokalaemic periodic paralysis.

Acute hypercapnic respiratory failure is a potentially life-threatening complication of profound hypokalemia usually seen in patients with large total-body potassium (K+) deficits. It has rarely been reported in thyrotoxic periodic paralysis (TPP), which is due to intra-cellular shifts of K+. The authors report on a 29-year-old man who presented with sudden onset of muscle paralysis in all extremities and acute progressive respiratory insufficiency requiring artificial respiratory support. He was treated with intravenous KCl. After six hours, muscular strength had returned to normal, with plasma K+ concentration of 3.0 mmol/L. At the eighth hour, rebound hyperkalemia (6.6 mmol/L) developed with high-tented T waves, even after the KCl was discontinued. Ventilatory support was uneventfully weaned at 14 hours. Elevated free thyroxine and undetectable thyroid-stimulating hormone confirmed the diagnosis of TPP. TPP should be kept in mind as a cause of acute respiratory failure in association with acute muscle weakness to avoid delayed diagnosis and improper management.

The aetiology of schizophrenia and the other psychoses is not yet established. The Knight model, based on genetic and other evidence, proposes that schizophrenia is an autoimmune disease, caused by the development of forbidden clones of B lymphocytes that secrete autoantibodies that accidentally stimulate cell surface receptors on certain neurons, affecting the limbic system of the brain. An unusual defect in a Maori man with Graves' disease rendered him unresponsive to the usually effective antithyroid drugs, prompting his being treated with prednisone, a non-specific immunosuppressant agent. This was highly successful, reducing the blood level of the causative thyroid-stimulating autoantibodies with reduction of thyroid hormone levels and thyroid gland size. Unfortunately, high dosage prednisone can be used for only a month, because of steroid toxicity. A research pathway to effective therapy of receptor-mediated autoimmune diseases, which probably include the psychoses, is now apparent. It involves finding the autoantibodies, then cloning of their antigenic targets, as has been done for Graves' disease. This will provide knowledge of the peptide sequences necessary for constructing therapeutic agents for selectively destroying the pathogenic forbidden clones. Meanwhile, usage of short-term therapy with prednisone could be helpful in the management of schizophrenia and should be explored.

Hypokalemia with paralysis (HP) is a potentially reversible medical emergency. It is primarily the result of either hypokalemic periodic paralysis (HPP) caused by an enhanced shift of potassium (K(+)) into cells or non-HPP resulting from excessive K(+) loss. Failure to make a distinction between HPP and non-HPP could lead to improper management. The use of spot urine for K(+) excretion rate and evaluation of blood acid-base status could be clinically beneficial in the diagnosis and management. A very low rate of K(+) excretion coupled with the absence of a metabolic acid-base disorder suggests HPP, whereas a high rate of K(+) excretion accompanied by either metabolic alkalosis or metabolic acidosis favors non-HPP. The therapy of HPP requires only small doses of potassium chloride (KCl) to avoid rebound hyperkalemia. In contrast, higher doses of KCl should be administered to replete the large K(+) deficiency in non-HPP.

Thyrotoxic periodic paralysis (TPP) and sporadic periodic paralysis (SPP) are the most common causes of hypokalemic periodic paralysis (HPP) in EDs in Asia. Their neuromuscular presentations are almost indistinguishable. We conducted this study to identify clinical clues that can help EPs distinguish between TPP and SPP. Thirty-four patients presenting to the ED with HPP were enrolled during a 3-year period. They did not have known hyperthyroidism before the attack and no family history of paralysis. They all had low K(+) excretion rates. Vital signs and blood biochemistry, including acid-base and electrolytes, were measured. TPP was subsequently established by thyroid function tests. Twenty patients had TPP and 14 patients had SPP. There was no significant difference in age and sex distribution between them. Systolic (SBP) but not diastolic blood pressure (SBP 145 +/- 4 vs 128 +/- 4 mm Hg, P < 0.001) and heart rate (106 +/- 3 vs 73 +/- 3 beats/min, P < 0.001) were significantly higher in those experiencing TPP than SPP. Among the biochemical factors, only plasma phosphate concentration (2.2 +/- 0.2 vs 3.2 +/- 0.2 mg/dL, P < 0.001) was significantly lower in those experiencing TPP than SPP. Systolic hypertension, tachycardia, and hypophosphatemia are clinical clues favoring the diagnosis of TPP.

Objective: To investigate whether patients with thyrotoxic hypokalaemic periodic paralysis (THPP) have the same molecular defect in the calcium channel gene described in familial hypokalaemic periodic paralysis (FHPP), as the symptoms of both diseases are comparable, we analysed, in patients with THPP, the presence of mutations R528H, R1239H and R1239G on the S4 voltage-sensing transmembrane segment of the alpha1 subunit of the calcium channel gene (Cav1.1)., Design and Patients: Genomic DNA was extracted from peripheral blood from 14 patients with THPP, 13 sporadic cases and one with a family history. An FHPP family was selected as a positive control. The exons bearing the described mutations were amplified by PCR, screened by single-strand conformation polymorphism (SSCP), and further sequenced., Measurements: THPP was diagnosed both clinically and through laboratory tests, all patients having elevated levels of thyroid hormones (T4, T3 or free T4), suppressed TSH and plasma potassium below 3 small middle dot5 mmol/l., Results: No evidence of the described mutations was found in patients with THPP. Furthermore, we did not detect any mutations in any of the four full S4 voltage-sensing transmembrane segments of Cav1 small middle dot1 (DIS4, DIIS4, DIIIS4 and DIVS4) by direct sequencing. However, close to the R528H mutation, we identified two single nucleotide polymorphisms at nucleotides 1551 and 1564 in both familial and sporadic cases with THPP. In addition, we were able to detect the R528H mutation in the DIIS4 transmembrane segment in all members of the FHPP family., Conclusion: Mutations linked to familial hypokalaemic periodic paralysis in the calcium channel alpha1 subunit gene (Cav1.1) are not associated with thyrotoxic hypokalaemic periodic paralysis. However, polymorphisms in nucleotides 1551 and 1564 in the exon 11 were found in patients with familial hypokalaemic periodic paralysis and thyrotoxic hypokalaemic periodic paralysis in higher frequency than in controls. The polymorphisms identified within the Cav1.1 gene are associated with thyrotoxic hypokalaemic periodic paralysis and represent a novel finding.

Objective: To investigate the relationships between the changes of plasma angiotensin I (AT I). Angiotensin II (AT II). serum aldosterone (Ald) levels and hypokalemic periodic paralysis (THPP) complicating hyperthyroid Graves' disease., Methods: The levels of serum potassium, TT3, TT4, FT3, FT4, Ald and the plasma AT I, AT II and 24 hours urine potassium output were determined in 73 cases of hyperthroid Graves' disease, of which 43 were complicated by THPP and the other 30 were grouped as NTHPP cases., Results: The mean level of serum potassium in THPP group was significantly lower than that in NTHPP group (P = 0.000), and the mean level of 24 hours urine potassium output in THPP group was significantly higher than that in NTHPP group(P = 0.000); The mean levels of plasma AT II and serum Ald in THPP group in upright position were significantly higher than those in NTHPP group (P = 0.008 and 0.013, respectively). The mean levels of 24 hours urine potassium output, plasma AT II and serum Ald in upright position were negatively correlated to serum potassium in both groups. The level of serum Ald in upright position was positively correlated to the level of 24 hours urine potassium out-put. The mean levels of plasma AT I and AT II in supine position were positively correlated to serum T3, and the level of plasma AT II in upright position was positively correlated to serum FT3., Conclusion: The level of 24 hours urine potassium output rises in THPP patients; the high levels of AT and Ald may contribute to the pathogenesis of the disease.

Hypokalemia and hypophosphatemia are commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. Potassium and phosphate supplements have been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective beta-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium and phosphate. We describe two patients who had an acute attack of TPP with characteristic hypokalemia and hypophosphatemia associated with low urinary potassium and phosphate excretion. After oral propranolol, 3 mg/kg, serum potassium and phosphate concentrations increased promptly in 2 hours in both patients, and there was complete amelioration of paralysis. No rebound hyperkalemia or hyperphosphatemia was detected. Given their efficacy in this pilot study, they should be considered as a first-line therapy for TPP.