Thyrotoxic periodic paralysis presenting with quadriparesis and hyperreflexia.

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that manifests as painless flaccid paralysis. An East Asian man in his late 20s presented to the emergency department with an acute onset of quadriparesis associated with hypertonia and hyperreflexia. His initial symptoms and signs suggested involvement of the brain and spinal cord; however, MRI of the neuroaxis was normal. His serum potassium concentration was low, and thyroid test results were consistent with hyperthyroidism. The patient was diagnosed with TPP associated with Graves' disease and was treated with potassium supplementation, propranolol and methimazole. Motor strength improved to his baseline level of power; bulk was normal, and tone was increased. Although flaccid paralysis is a typical presentation of TPP, brisk reflexes and muscle spasticity cannot rule out this condition. This case highlights the importance of considering TPP as a possible diagnosis in patients presenting with acute quadriparesis.

Thyrotoxic periodic paralysis associated with lactic metabolic acidosis: Case report of an African man and review of literature.

BACKGROUND: Thyrotoxic periodic paralysis (TPP) is a rare and most often acquired subtype of hypokalemic periodic paralysis. The association of varying degrees of muscle weakness, hyperthyroidism and hypokalemia characterizes it. The treatment requires potassium supplementation, control of hyperthyroidism and prevention measures. It is a frequent disease in Asian men, but much rare in Caucasian or African populations. This is the first report of TPP associated with lactic metabolic acidosis in an African man. CASE PRESENTATION: A 23 year-old African man, native from Morocco, with recurrent episodes of tetraparesis for eleven months, and abdominal pain, was referred for evaluation. Biochemical investigations showed severe hypokalemia associated with hyperthyroidism and lactic metabolic acidosis. His EKG showed signs of hypokalemia such as sinus tachycardia and U waves. After potassium supplementation, neurological recuperation was quick and complete. Thyroid ultrasound identified a hypoechogenic and hypervascularized goiter, associated with high levels of thyroid antibodies, in favor of Grave's disease. With antithyroid drugs and life-style changes, the patient did not have any other attack. REVIEW OF LITERATURE: In addition to the case report, this article presents an extended review of literature, from the first large study reporting the diagnosis and incidence of TPP in 1957 to nowadays. Are reported here the latest information concerning epidemiology, clinical manifestations, complementary examinations, management and genetic finding. The lactic acidosis observed initially is exceptional, never described in TPP. TPP is a diagnostic and therapeutic emergency, requiring careful potassium supplementation, in order to avoid the risk of the onset of rebound hyperkalemia, to be maintained until the etiological treatment is effective. Paraclinical assessment with emergency EKG and electromyogram are essential to assess the impact. DISCUSSION: It is essential in the face of any hypokalaemic periodic paralysis, including in non-Asian subjects, to search hyperthyroidism. CONCLUSIONS: This report demonstrates the importance of thyroid testing in case of acute muscle weakness, even in non-Asian patients in order to diagnose TPP. This is a rare but possible etiology, to be distinguished from the familial form of hypokalemic periodic paralysis. It also questions on the impact of TPP on energetic metabolism, in particular on lactic metabolism.

Recurrent hypokalemic paralysis in hypothyroidism.

Hypothyroidism, a commonly encountered thyroid disorder, usually manifests with readily recognizable typical features. However, an unusual presentation of a classic thyroid disorder may hinder accurate diagnosis in certain instances. One such rare initial presentation of hypothyroidism is recurrent hypokalemic paralysis, and existing reports in the literature are sparse. It has been more commonly reported in thyrotoxicosis. We report the case details and clinical outcomes of two middle-aged individuals (a 34-year-old male and a 37-year-old female) with recurrent episodes of hypokalemic paralysis. Their clinical examination revealed pure motor hyporeflexia quadriparesis with hypotonia and diminished deep tendon reflexes without any autonomic dysfunction. They had no significant previous medical history. Biochemical findings revealed hypokalemia in both cases (1.4 and 1.9 mEq/L, respectively) with elevated levels of thyroid­stimulating hormone and thyroid­related antibodies in both individuals, thus, confirming the diagnosis of autoimmune hypothyroidism. Immediate treatment with intravenous and oral potassium correction helped in the recovery. Thyroxine supplementation was considered a follow-up treatment, and for a one-year follow-up period there were no complaints of limb weakness reported in both individual.

Vitamin D inhibits bone loss in mice with thyrotoxicosis by activating the OPG/RANKL and Wnt/ß-catenin signaling pathways.

Objective: Vitamin D and thyroid hormones have crucial roles in bone metabolism. This study aims to explore the effects of vitamin D on bone metabolism in mice with thyrotoxicosis and its mechanisms. Methods: 12-week-old mice were randomly divided into 6 groups (6 mice/group), the control (CON) group, vitamin D (VD) group, low-dose LT4 (Low LT4) group, low-dose LT4+VD (Low LT4+VD) group, high-dose LT4 (High LT4) group, high-dose LT4+VD (High LT4+VD) group, LT4 was provided every day and vitamin D3 every other day for 12 weeks. Thyroid function, 25-hydroxy vitamin D, type I collagen carboxy-terminal peptide (CTX), and type I procollagen amino-terminal peptide were determined. In addition, microcomputed tomography, bone histology and histomorphometry, a three-point bending test, and the mRNA expression of osteoprotegerin (OPG), receptor activator of nuclear factor-κB ligand (RANKL) and ß-catenin in bone were conducted. Results: The BMD of lumbar vertebrae and femur decreased and the bone microstructure was destroyed significantly in thyrotoxicosis mice. Addition of vitamin D improved the BMD and bone microstructure only in the low LT4+VD group. Mice with thyrotoxicosis had a significantly higher level of CTX (P<0.05), which was decreased by treatment with vitamin D (P<0.05). The eroded surface per bone surface (Er. S/BS) of the cancellous bone and elongated surface/endocortical perimeter (Er. S/E Pm) of the cortical bone significantly increased in the Low LT4 and High LT4 groups (P<0.05). Treatment with vitamin D significantly decreased the Er. S/BS and Er. S/E Pm. But, treatment with vitamin D did not significantly improve the toughness and rigidity of bones. The ratio of OPG to RANKL and mRNA expression of ß-catenin in the Low LT4+VD group were higher than that in the Low LT4 group (P<0.05). Conclusion: In mice with thyrotoxicosis, treatment with vitamin D can inhibit bone resorption and improve the BMD and trabecular bone architecture by increasing the ratio of OPG to RANKL and upregulating the expression of Wnt/ß-catenin.

[Multimodal anesthesia in a patient with Graves' disease and thyrotoxicosis: A case report]. / Anestesia multimodal en paciente con enfermedad de Graves y tirotoxicosis: reporte de caso.

Background: Hyperthyroidism is the increase in the synthesis and secretion of thyroid hormones. It is rare but serious in children and constitutes approximately 5% of all cases; 15% manifests before 10 years of age. The peak of presentation and the majority of cases (80%) are diagnosed around 10-15 years of age. Adolescence is usually the stage with the highest incidence and it is more frequent in women (5:1). Acute thyrotoxic crisis or thyroid storm is rare and only occurs in a poorly controlled hyperthyroid patient or in a hyperthyroid patient undergoing emergency surgery. It is manifested by fever, extreme tachycardia, tachyarrhythmia with atrial fibrillation, vomiting, diarrhea, agitation and mental confusion. Clinical case: 17-year-old adolescent with Graves' disease with uncontrolled clinical manifestations that did not respond to medical treatment and was scheduled for radical thyroidectomy. 35 points were obtained on the Burch and Wartofsky Scale. It was managed with general anesthesia, reducing stimuli for airway and regional control to reduce surgical stimuli. Adjuvant medications such as magnesium sulfate for intraoperative stability were used. Conclusion: Multimodal anesthesia managed to avoid thyroid storm, postoperative pain, as well as other complications.

Introducción: el hipertiroidismo es el incremento en la síntesis y secreción de hormonas tiroideas. Es raro pero grave en la edad pediátrica y constituye aproximadamente el 5% de todos los casos; el 15% se presenta antes de los 10 años. El pico de presentación y la mayoría de los casos (80%) se diagnostican hacia los 10-15 años. La adolescencia es la etapa de mayor incidencia y más frecuente en mujeres (5:1). La crisis tirotóxica aguda o tormenta tiroidea es rara y solo se presenta en un hipertiroideo mal controlado o en un paciente hipertiroideo intervenido de urgencia. Se manifiesta con fiebre, taquicardia extrema, taquiarritmia con fibrilación auricular, vómito, diarrea, agitación y confusión mental. Caso clínico: adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria. Conclusión: la anestesia multimodal logró evitar la tormenta tiroidea, el dolor postoperatorio, así como otras complicaciones.

Thyrotoxic periodic paralysis in two sexagenarian men: A case report.

RATIONALE: Thyrotoxic periodic paralysis (TPP) characterized by the triad of muscle paralysis, acute hypokalemia, and the presence of hyperthyroidism is often reported in young adults but rarely reported in age >60 year-old. PATIENT CONCERNS: Two sexagenarian males (age 61 and 62) presenting to the emergency department with progressive muscle paralysis for hours. There was symmetrical flaccid paralysis with areflexia of lower extremities. Both of them did not have the obvious precipitating factors and take any drugs. DIAGNOSIS: Their Wayne scores, as an objective index of symptoms and signs associated with thyrotoxicosis, were <19 (7 and 14, respectively). Their blood pressure stood 162/78 and 170/82 mm Hg, respectively. Their thyroid glands were slightly enlarged. Both of them had severe hypokalemia (1.8 and 2.0 mmol/L). Their presumptive diagnosis of mineralocorticoid excess disorders with severe potassium (K+) deficit were made. However, low urine K+ excretion and relatively normal blood acid-base status were suggestive of an intracellular shift of K+ rather than K+ deficit. Hormone studies confirmed hyperthyroidism due to Graves disease. INTERVENTIONS: A smaller dose of K+ supplementation (only a total of 50 and 70 mmol K+, respectively) were prescribed for the patient. OUTCOMES: After treatment, their serum K+ levels became normal with a full recovery of muscle strength. LESSONS: Our 2 cases highlight the fact that thyrotoxic periodic paralysis must be still kept in mind as the underlying cause of hypokalemia with paralysis and hypertension in elderly patients to avoid missing curable disorders.

Thyrotoxic Channelopathies.

Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. Early recognition of TPP is vital to initiating appropriate treatment and to avoiding the risk of rebound hyperkalemia that may occur if high-dose potassium replacement is given. Here we present a case of 31 year old male with thyrotoxic periodic paralysis with diagnostic and therapeutic approach.

A hypothesis on the mechanism of action of high-dose thyroid in refractory mood disorders.

Multiple lines of evidence suggest the hypothesis that high dose thyroid therapy corrects for cellular hypothyroidism found in bipolar disorders. Evidence indicates that bipolar disorders are associated with mitochondrial dysfunction which results in low cellular adenosine 5'-triphosphate (ATP) levels. Transport of thyroid hormones into cells is energy intensive and dependent on ATP except in the pituitary gland. Inadequate ATP levels makes it difficult to get thyroid hormone into cells leading to cellular hypothyroidism. This creates a condition where the blood and pituitary levels of thyroid hormone are normal but low in other tissues. High dose thyroid therapy produces a gradient that is sufficient for thyroid hormone to diffuse into cells correcting cellular hypothyroidism. If this hypothesis is correct there are number of implications. The two most important are: On average patients suffering from a bipolar disorder die 10-20years earlier than the general population. The medical sequelae associated with bipolar disorders cause far more deaths than suicide. If high dose thyroid corrects for cellular hypothyroidism it could well decrease the medical morbidity and mortality associated with bipolar disorders that are the result of cellular hypothyroidism. Thus high dose thyroid would be a first treatment that decreases the considerable medical morbidity and mortality associated with the bipolar disorders. This would stand in stark contrast to most psychiatric medications that can that increase morbidity and mortality. It would also reinforce the safety of HDT. The second implication is thyroid hormone blood levels in patients suffering from a bipolar disorder do not accurately reflect the true thyroid status.

The confounding effect of the development of idiopathic orthostatic edema and thyrotoxcosis on weight fluctuation related to effects on free water clearance in a woman with long-standing surgically induced panhypopituitarism and diabetes insipidus.

PURPOSE: To evaluate the effect of idiopathic orthostatic edema and the effect of thyrotoxicosis on weight fluctuation and fluid retention in the presence of surgically induced panhypopituitarism and diabetes insipidus controlled with hormone replacement. MATERIALS AND METHODS: Dextroamphetamine sulfate was used for weight gain when no other etiologic factor was found. Methimazole was used when weight loss occurred when serum T4 and free T4 indicated thyrotoxicosis. RESULTS: Sympathomimetic amine therapy very effectively controlled the weight gain and methimazole controlled the weight loss. CONCLUSIONS: Hypopituitarism and diabetes insipidus controlled with hormone replacement do not protect against fluid retention from idiopathic edema.

The multiple effects of thyroid disorders on bone and mineral metabolism.

Differently from most hormones, which commonly are specialized molecules able to influence other cells, tissues and systems, thyroid hormones (TH) are pleiotropic peptides, whose primordial function is difficult to identify. The complex action of TH on human economy can be easily witnessed by examining the diverse consequences of TH excess and deficiency during development and after maturity. In particular, different manifestations in bone modeling and remodeling reflect the circumstantial consequences of thyroid disturbances, which are age dependent. While hyperthyroidism during childhood enhances bone mineralization and accelerates epiphyseal maturation, in adults it induces bone loss by predominant activation of osteoclast activity. Furthermore, the syndrome of TH resistance is a multifaceted condition in which different sites exhibit signs of hormone excess or deficiency depending on the configuration of the TH receptor isoform. The investigation of the impact of TH resistance on the skeleton still remains to be elucidated. We present here a thorough review of the action of TH on bone and of the impact of thyroid disorders, including hyper- and hypothyroidism and the syndrome of TH resistance, on the skeleton.

The multiple effects of thyroid disorders on bone and mineral metabolism / Os múltiplos efeitos das disfunções tireoidianas sobre o metabolismo osteomineral

Differently from most hormones, which commonly are specialized molecules able to influence other cells, tissues and systems, thyroid hormones (TH) are pleiotropic peptides, whose primordial function is difficult to identify. The complex action of TH on human economy can be easily witnessed by examining the diverse consequences of TH excess and deficiency during development and after maturity. In particular, different manifestations in bone modeling and remodeling reflect the circumstantial consequences of thyroid disturbances, which are age dependent. While hyperthyroidism during childhood enhances bone mineralization and accelerates epiphyseal maturation, in adults it induces bone loss by predominant activation of osteoclast activity. Furthermore, the syndrome of TH resistance is a multifaceted condition in which different sites exhibit signs of hormone excess or deficiency depending on the configuration of the TH receptor isoform. The investigation of the impact of TH resistance on the skeleton still remains to be elucidated. We present here a thorough review of the action of TH on bone and of the impact of thyroid disorders, including hyper- and hypothyroidism and the syndrome of TH resistance, on the skeleton.

Diferentemente da maioria dos hormônios, que usualmente são moléculas especializadas capazes de influenciar outras células, tecidos e sistemas, os hormônios da tireoide (HT) são peptídeos pleiotrópicos, cuja função primordial é difícil de identificar. A ação complexa dos HT na fisiologia humana pode ser facilmente reconhecida ao observar as diversas consequências do excesso e da deficiência de HT durante e após o pleno desenvolvimento. Em particular as diferentes manifestações na modelação e remodelação óssea refletem que as consequências esqueléticas das disfunções tireoidianas dependem das circunstâncias e variam com a idade. Enquanto o hipertireoidismo durante a infância aumenta a mineralização óssea e acelera a maturação epifisária, em adultos induz a perda óssea pela ativação predominante da ação osteoclástica. Além disso, a síndrome de resistência ao HT é uma condição multifacetada na qual diferentes tecidos apresentam sinais de excesso ou deficiência hormonal, dependendo da predominância da expressão das diversas isoformas do receptor de HT. O impacto da resistência ao HT sobre o esqueleto ainda é motivo de investigação. Apresentamos aqui uma revisão abrangente sobre as ações ósseas dos HT e o impacto no esqueleto dos distúrbios da tireoide, incluindo hipo e hipertireoidismo e síndrome de resistência ao HT.

Thyrotoxic periodic paralysis: an endocrine cause of paraparesis.

Periodic paralysis is a muscle disorder that belongs to the family of diseases called channelopathies, manifested by episodes of painless muscle weakness. Periodic paralysis is classified as hypokalemic when episodes occur in association with low potassium levels. Most cases are hereditary. Acquired cases have been described in association with hyperthyroidism. Diagnosis is made on clinical and biochemical grounds. Patients may be markedly hypokalemic during the episode and respond well to potassium supplementation. Episodes can be prevented by achieving a euthyroid state. This report describes a young gentleman presenting with thyrotoxic hypokalemic paraparesis. The condition needs to be considered in the differential diagnosis of neuromuscular weakness in the context of hypokalemia by the treating physicians.

Thyrotoxic periodic paralysis triggered by ß2-adrenergic bronchodilators.

Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by ß2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled ß2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110 mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that ß2-adrenergic bronchodilators should be considered a potential precipitant of TPP.

Thyrotoxic hypokalaemic periodic paralysis: a rare presentation of Graves' disease in a Hispanic patient.

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.

Parálisis periódica hipopotasémica tirotóxica: a propósito de un caso / Thyrotoxic hypokalemic periodic paralysis. A case report

La parálisis periódica hipopotasémica tirotóxica (PPT) es una rara complicación de la tirotoxicosis caracterizada por la aparición de episodios de debilidad muscular asociados a hipopotasemia en pacientes con hipertiroidismo, más frecuentemente con enfermedad de Graves-Basedow. El tratamiento con antitiroideos y suplementos de potasio revierte la sintomatología de debilidad muscular y evita la reaparición de estos síntomas (AU)

Thyrotoxic hypokalemic periodic paralysis is an uncommon complication of thyrotoxicosis, characterized by attacks of generalized muscular weakness associated with hypokalemia in patients with hyperthyroidism, most frequently with Graves-Basedow disease. Treatment with antithyroid drugs and potassium supplements reversed the symptoms and the episodes of acute muscular weakness did not reappear (AU)

[Thyrotoxic periodic paralysis: a case series of four patients and literature review]. / Paralysie périodique thyréotoxique hypokaliémique : quatre observations et revue de la littérature.

PURPOSE: Periodic thyrotoxic hypokalemic paralysis (TPP) is a neuromuscular complication of hyperthyroidism. It is more common in young Asian males than in Caucasian and African patients. We report four new cases and review the literature. CASE REPORTS: Four consecutive patients were diagnosed with TPP. They were all men with a median age of 34.5 years at presentation. Two patients originated from the Philippines, one was African and one was Caucasian ethnic background. They all presented with a paresis or flaccid paralysis, without respiratory failure. Previous similar episodes in their past medical history, the presence of profound hypokalemia (mean serum potassium level of 2 mmol/L) and the presence of clinical and biological signs of hyperthyroidism led to the diagnosis of TPP. All four patients were diagnosed with Graves' disease. Outcome was favourable in all four patients with the symptomatic treatment of TPP and treatment of Graves' disease. CONCLUSION: TPP is a severe condition, due to a dysfunction of the Na(+)-K(+) ATPase pump. Initial management relies on ß-blocker treatment and careful potassium supplementation. Then, medical or surgical etiological treatment of the thyrotoxicosis is essential to prevent a recurrence. The disease is probably underdiagnosed: it must be suspected when a profound hypokaliema resolves very quickly (<12hours); hyperthyroidism should always be included in the differential diagnosis of a paresis associated with hypokalemia.

Thyrotoxic periodic paralysis: clinical and molecular aspects.

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that most often affects young East Asian males but increasingly also in other ethnic groups. The typical presentation is acute attacks varying from mild weakness to total paralysis starting at night or in the early morning a few hours after a heavy meal, alcohol abuse or strenuous exercise with complete recovery within 72 h. Signs and symptoms of hyperthyroidism may not be obvious. The hallmark is hypokalemia from increased cellular sodium/potassium-ATPase pump activity with transport of potassium from the extracellular to the intracellular space in combination with reduced potassium output. Recently, KCNJ18 gene mutations which alter the function of an inwardly rectifying potassium channel named Kir2.6 have been detected in 0-33 % of cases. Hence, the pathophysiology in TPP includes a genetic predisposition, thyrotoxicosis and environmental influences and the relative impact from each of these factors may vary. The initial treatment, which is potassium supplementation, should be given with caution due to a high risk of hyperkalemia. Propranolol is an alternative first-line therapeutic option based on the assumption that hyperadrenergic activity is involved in the pathogenesis. If thyroid function tests are unobtainable in the acute situation the diagnosis is supported by the findings of hypokalemia, low spot urine potassium excretion, hypophosphatemia with hypophosphaturia, high spot urine calcium/phosphate ratio, and electrocardiographic abnormalities as tachycardia, atrial fibrillation, high QRS voltage, and atrioventricular block. Definitive treatment is cure of the hyperthyroidism. The underlying mechanisms of TPP remain, however, incompletely understood awaiting further studies.

Spectrum of hypokalaemic periodic paralysis in a tertiary care centre in India.

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.

Hypokalemic periodic paralysis: a case series, review of the literature and update of management.

The objective of this study was to present a case series of patients with hypokalemic periodic paralysis. We described all patients with diagnosis of hypokalemic periodic paralysis admitted to the Al Ain Hospital (UAE) during the year 2006. Seventeen patients, all males and mostly Asians, were presented to the Al Ain Hospital over a 12-month period. The majority were admitted during the summer months. Four were thyrotoxic. All of the 17 patients received oral potassium supplements and recovered well without any major complications. In conclusion, clinicians should have a high index of suspicion, especially among Asians presenting with flaccid paralysis and hypokalemia. The main steps in the management include exclusion of other causes of hypokalemia, potassium replacement, hydration and close monitoring of the cardiac rhythm and serum potassium levels. When possible, the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.

[Hypokalaemia and paralysis: think about the thyroid]. / Hypokaliémie et paralysie: penser à la thyroïde.

Periodic hypokalemic paralysis can be of genetic origin or secondary to other causes of hypokalaemia. The thyreotoxic hypokalemic periodic paralysis (THPP) usually occurs among asian subjects. It is a diagnostic and therapeutic emergency which may lead to life-threatening complications due to hypokalaemia and muscle weakness. The potassium supplementation is followed by a complete recovery after a few hours. We underlined the interest of thyroid assays in patients having an acute muscular paralysis associated with hypokalaemia.