Thyrotoxic Periodic Paralysis Research Articles

Hypokalaemic Periodic Paralysis in a Patient with Subclinical Hyperthyroidism: A Rare Case

Thyrotoxic Periodic Paralysis (TPP) is an uncommon disorder. Though many cases of hypokalaemic periodic paralysis are reported in overt hyperthyroidism, hypokalaemic paralysis in subclinical hyperthyroidism is very rare. Subclinical hyperthyroidism is characterised by circulating TSH levels below reference range and normal thyroid hormone levels. We describe a case of 32-year-old Asian male who presented to the emergency department with acute onset weakness and hypokalaemia with no previous history of thyroid disorder or any signs and symptoms suggestive of hyperthyroidism. He was subsequently diagnosed with Graves' disease with subclinical hyperthyroidism.

THYROTOXIC HYPOKALEMIC PERIODIC PARALYSIS – A CASE REPORT

Thyrotoxic hypokalemic periodic paralysis is a medical emergency which presents with muscular weakness, hypokalemia and features of thyrotoxicosis. Urgent treatment is very important; since, very low potassium levels can lead to cardiaccomplications. Here, we present a case where features of hyperthyroidism were missed on initial assessment and were picked up subsequently in the second presentation of paralysis. This emphasizes the importance in recognizing the subtle features of hyperthyroidism from both history and clinical examination. Acute management consisted of administering intravenous potassium chloride and then treatment of thyrotoxicosis.

Size of quadriceps femoris may contribute to thyrotoxic periodic paralysis

Thyrotoxic periodic paralysis (TPP) frequently occurs on male individuals at their third and forth decades. The major site of involvement is the proximal muscles of lower limbs. Increasing evidence has shown that the occurrence of TPP is determined by multiple factors. We hypothesized that apart from hormonal fluctuations, skeletal muscle itself may explain for the age and sex variance as well. Our study was established to explore whether the size of lower limb skeletal muscles were related to TPP. We conducted a clinical experiment including 43 patients diagnosed with TPP (Group 1) and 39 pure hyperthyroidism individuals (Group 2). Current age, body mass index (BMI), thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), average girth of bilateral upper arm and thigh, physical activity level (PAL) were measured. We also adopted B mode ultrasound to quantify the muscle thickness (MT) of the major muscle involved in the disease, the quadriceps femoris (QF, including rectus femoris, RF; vastus intermedius, VI; vastus medialis, VM and vastus lateralis, VL). Patients were matched in TSH, FT4 and FT3. PAL was also statistically identical between groups. Age, BMI, thigh girth, the average of bilateral MT of QF were statistically different. After adjusting for age, BMI and girth, Group 1 still presented with larger MT of QF than Group 2, regardless of their current thyroid hormone level. There indeed exists an independent relationship between muscle thickness and TPP.

Graves' Disease and Periodic Paralysis

Thyrotoxic periodic paralysis represents a rare neurological emergency of an endocrine disorder. It poses a diagnostic challenge to the clinicians, as it is an uncommon disorder and its clinical presentation is similar to the more common hypokalemic paralysis. Adding to the diagnostic dilemma is that most patients do not have prior history of thyroid disorder and only have subtle features of hyperthyroidism. Hence, the diagnosis can be easily missed without a high clinical index of suspicion. These patients usually present to the emergency department with acute flaccid paralysis and all physicians should be aware of this clinical entity. The disease can be life-threatening if early diagnosis and prompt therapy is not initiated. We report three interesting cases in which periodic paralysis was the initial manifestation of underlying Graves’ disease in two and occurred in the third case who was previously diagnosed with thyrotoxicosis due to non-adherence to drug therapy.

Single Nucleotide Polymorphisms associated with Angleûs Class I and III Occlusal Relationship in Thais with Thyrotoxic Hypokalemic Periodic Paralysis

Single Nucleotide Polymorphisms associated with Angleûs Class I and III Occlusal Relationship in Thais with Thyrotoxic Hypokalemic Periodic Paralysis

Mutation analysis of CACNA1S and SCN4A in patients with hypokalemic periodic paralysis.

Mutations in CACNA1S (calcium channel, voltage‑dependent, L type, alpha 1S subunit) and SCN4A (sodium channel, voltage‑gated, type IV, alpha subunit) are associated with hypokalemic periodic paralysis (HPP). The aim of the current study was to investigate CACNA1S and SCN4A mutations in patients with HPP. Mutations in CACNA1S and SCN4A were detected in three familial hypokalemic periodic paralysis (FHPP) pedigrees and in two thyrotoxic hypokalemic periodic paralysis (THPP) pedigrees using polymerase chain reaction, DNA sequencing and sequence alignment with GenBank data. A single base mutation from cytosine to guanine at site 1582 was identified in exon 11 of CACNA1S in one FHPP pedigree, resulting in an arginine to glycine (R528G) substitution. A single base mutation from thymine to cytosine at site 2012 was identified in exon 12 of SCN4A in one THPP pedigree, resulting in a phenylalanine to serine (F671S) substitution. No mutations in CACNA1S or SCN4A were identified in the remaining three pedigrees. The present study indicated that CACNA1S and SCN4A mutations are relatively rare in patients with HPP, and further studies are required to determine whether these mutation‑associated substitutions are representative of patients with HPP.

Abstract #1072: Clinical and Biochemical Characteristics of Patients with Thyrotoxic Periodic Paralysis in a National Hospital of Lima-Peru from 2011 to 2014

Abstract #1072: Clinical and Biochemical Characteristics of Patients with Thyrotoxic Periodic Paralysis in a National Hospital of Lima-Peru from 2011 to 2014

Rare KCNJ18 variants do not explain hypokalaemic periodic paralysis in 263 unrelated patients

ObjectiveTo examine rare KCNJ18 variations recently reported to cause sporadic and thyrotoxic hypokalaemic periodic paralysis (TPP).MethodsWe sequenced KCNJ18 in 474 controls (400 Caucasians, 74 male Asians) and 263 unrelated patients...

The clinical and genetic features in a cohort of mainland Chinese patients with thyrotoxic periodic paralysis.

BackgroundThyrotoxic periodic paralysis (TPP) is a life-threatening channelopathy manifesting as recurrent episodes of hypokalemia and muscle weakness in the presence of hyperthyroidism. Recent findings indicate defects of inward rectifying K+ (Kir) channels are associated with some TPP patients. The associations are not only found in Caucasian population (mainly Brazilian), but also in Singaporean population. However, potential genetic risk factors for mainland Chinese patients, the largest group of TPP cases in the world, have been largely unexplored.MethodsSamples of DNA from 127 individuals with TPP and 102 hyperthyroidism male controls self-reported as mainland Chinese were collected from 5 clinical centers from Jan 2011 to Jan 2014. The KCNJ2 gene, KCNJ18 gene, as well as loci polymorphisms (rs623011and rs312691) at 17q24.3 were directly sequenced in TPP patients and controls. Clinical data were summarized from TPP participants for genotype/phenotype correlations.Results3.1% of TPP cases harbored KCNJ18 gene mutations in mainland Chinese patients. Patients with KCNJ18 mutation had shorter attack duration, higher prevalence of muscle soreness and weakness recurrence than patients without KCNJ18 mutation. The alleles at 17q24.3 (rs623011and rs312691) were more common in patients with TPP than in controls, and therefore were significant risk factors for TPP (odds ratio, 11.94 and 10.57; 95% CI, 5.93-24.05 and 5.48-20.40; P = 1.81 × 10−14 and 1.07 × 10−14 respectively).ConclusionsThis study demonstrates that the KCNJ18 variants are only responsible for a small proportion of TPP patients in mainland China. There are significant clinical differences between patients with KCNJ18 mutations and patients without KCNJ18 mutations. In addition, the rs623011and rs312691 loci are significantly associated with TPP patients in mainland China, and highlight the Kir2.1 channel as a causative target in TPP.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-015-0290-8) contains supplementary material, which is available to authorized users.

THANKSGIVING MEAL PARALYSIS? A RARE CASE OF THYROTOXIC PERIODIC PARALYSIS WITH CARDIAC ARREST

Thyrotoxic periodic paralysis(TPP) is an endocrinopathy related to increased Na+/K+ ATPase activity, triggered by hyperadrenergic, hyperthyroid, or hyperinsulinemic states. It is characterized by transient, recurrent episodes of flaccid muscle paralysis affecting proximal more severely than distal

Thyrotoxic Periodic Paralysis: A Review of Cases in the Last Decade

ABSTRACT Objective: Thyrotoxic periodic paralysis (TPP) is a rare condition characterized by severe muscle weakness and life-threatening hypokalemia in uncontrolled hyperthyroidism. Given the life-threatening potential of this condition, it is important to better characterize its presentation, management, and likelihood for complications to aid in quicker diagnosis and optimize medical management. Methods: We retrospectively reviewed cases of TPP that occurred at 3 hospitals from 2004 to 2014. Patients included were those presenting with weakness and hypokalemia who were found to have thyrotoxicosis. Results: Nine cases of TPP were identified including 7 Hispanic males and 1 African American male. Six patients developed complications of therapy with rebound hyperkalemia. TPP was the first presentation of thyrotoxicosis for 5 patients. The remaining 4 patients with known hyperthyroidism admitted to several weeks of medication nonadherence prior to their episode of TPP. Conclusion: Our study suggests that TPP may be more common in other ethnicities than previously described, with the majority of our cases occurring in Hispanic males. Physicians should be wary of rebound hyperkalemia as it is a common complication of therapy. Because hypokalemia is related to a transcellular shift and not total body depletion of potassium, supplementation with potassium should be done slowly. Early concurrent treatment with nonselective beta-blockers should be employed, and standardized hospital potassium replacement protocols should be avoided. TPP may be the first sign of thyrotoxicosis. All patients with weakness and hypokalemia should undergo thyroid function testing. Abbreviations: ICD International Classification of Disease ICU intensive care unit TPP thyrotoxic periodic paralysis

A Case Report of Thyrotoxic Periodic Paralysis; Serial Nerve Conduction Studies before and after Recovery

A Case Report of Thyrotoxic Periodic Paralysis; Serial Nerve Conduction Studies before and after Recovery

I Lost Weight, but I Became Weak and Cannot Walk—A Case of Nutraceutical (T3)-Induced Thyrotoxic Periodic Paralysis

Thyrotoxic periodic paralysis (TPP) is a rare reversible cause of paralysis and cramping. TPP is usually precipitated by common causes of thyrotoxicosis such as Grave disease or multinodular goiter. TPP precipitated by exogenous triiodothyronine (T3) intake is an extremely rare occurrence with only 3 cases reported to date. We now report a 24-year-old healthy manual laborer who developed quadriparesis during a period of rest after heavy exertion and carbohydrate intake. He had severe hypokalemia (potassium level 1.9 mmole/L). Correction of his hypokalemia reversed the paralysis without rebound hyperkalemia. After a detailed history review, he reported that he had been consuming nutraceuticals containing T3 for 1 month to lose weight, and laboratory studies confirmed factitious T3 toxicosis. There was no evidence of renal or gastrointestinal potassium wasting. This episode of TPP was the first manifestation of thyrotoxicosis in this patient, and avoidance of T3 intake prevented more episodes.

Acute Paralysis Recovered Within 24 Hours in a Young African American Man: A Case of Thyrotoxic Hypokalemic Periodic Paralysis

Acute Paralysis Recovered Within 24 Hours in a Young African American Man: A Case of Thyrotoxic Hypokalemic Periodic Paralysis

The insulin-sensitivity sulphonylurea receptor variant is associated with thyrotoxic paralysis.

Thyrotoxicosis is the most common cause of the acquired flaccid muscle paralysis in adults called thyrotoxic periodic paralysis (TPP) and is characterised by transient hypokalaemia and hypophosphataemia under high thyroid hormone levels that is frequently precipitated by carbohydrate load. The sulphonylurea receptor 1 (SUR1 (ABCC8)) is an essential regulatory subunit of the β-cell ATP-sensitive K(+) channel that controls insulin secretion after feeding. Additionally, the SUR1 Ala1369Ser variant appears to be associated with insulin sensitivity. We examined the ABCC8 gene at the single nucleotide level using PCR-restriction fragment length polymorphism (RFLP) analysis to determine its allelic variant frequency and calculated the frequency of the Ala1369Ser C-allele variant in a cohort of 36 Brazilian TPP patients in comparison with 32 controls presenting with thyrotoxicosis without paralysis (TWP). We verified that the frequency of the alanine 1369 C-allele was significantly higher in TPP patients than in TWP patients (61.1 vs 34.4%, odds ratio (OR)=3.42, P=0.039) and was significantly more common than the minor allele frequency observed in the general population from the 1000 Genomes database (61.1 vs 29.0%, OR=4.87, P<0.005). Additionally, the C-allele frequency was similar between TWP patients and the general population (34.4 vs 29%, OR=1.42, P=0.325). We have demonstrated that SUR1 alanine 1369 variant is associated with allelic susceptibility to TPP. We suggest that the hyperinsulinaemia that is observed in TPP may be linked to the ATP-sensitive K(+)/SUR1 alanine variant and, therefore, contribute to the major feedforward precipitating factors in the pathophysiology of TPP.

Periodic Paraplegia as the First Time Presentation of Thyrotoxicosis

Hyperthyroidism presents with a myriad of symptoms and signs, periodic paralysis is rare among them. Thyrotoxic periodic paralysis is a condition in which there are acute episodes of muscle weakness in patients with high levels of thyroid hormones. Hypokalemia is the commonest cause of muscle weakness in this disorder, but potassium (K+) levels may be normal in between the attacks. Normal K+ levels can also be seen in thyrotoxic normokalemic periodic paralysis where K+ levels are normal even during the paralysis. A patient presenting with paralysis as the first presentation in thyrotoxicosis is extremely rare. Here we present a case of twenty one year old male patient presenting with thyrotoxic normokalemic periodic paraplegia as the first presentation.

Molecular cloning of ion channels in Felis catus that are related to periodic paralyses in man: a contribution to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis.

ABSTRACTNeck ventroflexion in cats has different causes; however, the most common is the hypokalemia associated with flaccid paralysis secondary to chronic renal failure. In humans, the most common causes of acute flaccid paralysis are hypokalemia precipitated by thyrotoxicosis and familial forms linked to mutations in sodium, potassium, and calcium channel genes. Here, we describe the sequencing and analysis of skeletal muscle ion channels in Felis catus that could be related to periodic paralyses in humans, contributing to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis. We studied genomic DNA from eleven cats, including five animals that were hyperthyroid with hypokalemia, although only one presented with muscle weakness, and six healthy control domestic cats. We identified the ion channel ortholog genes KCNJ2, KCNJ12, KCNJ14, CACNA1S and SCN4A in the Felis catus genome, together with several polymorphic variants. Upon comparative alignment with other genomes, we found that Felis catus provides evidence for a high genomic conservation of ion channel sequences. Although we hypothesized that neck ventroflexion in cats could be associated with a thyrotoxic or familial periodic paralysis channel mutation, we did not identify any previously detected human channel mutation in the hyperthyroid cat presenting hypokalemia. However, based on the small number of affected cats in this study, we cannot yet rule out this molecular mechanism. Notwithstanding, hyperthyroidism should still be considered as a differential diagnosis in hypokalemic feline paralysis.

Thyrotoxic periodic paralysis triggered by β2- adrenergic bronchodilators

ABSTRACT 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 β2-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 β2-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 110mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP.

Thyrotoxic periodic paralysis as the first manifestation of hyperthyroidism

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Thyrotoxic periodic paralysis in new-onset hyperthyroidism – a case report and review of the literature

&lt;p class="MsoNormal" style="margin-bottom: 0.0001pt; text-align: justify;"&gt;&lt;em&gt;&lt;span style="font-size: 10.0pt; font-family: ";Times New Roman";,";serif";; mso-ansi-language: EN-US;" lang="EN-US"&gt;Thyrotoxic periodic paralysis (TPP) is a rare condition related to hyperthyroidism, with specific clinical and physiopathological features. In this article, we discuss a case report of a patient that develops TPP with no previous history of thyroid illness, highlighting semiological characteristics that can help Emergency physicians to suspect of this condition. Subsequently, we review the recent articles about TPP, with focus in the molecular basis of ion channelopathies and predisposing factors, and discuss the therapeutic approach at acute phase of TPP and prevention of crisis recurrence.&lt;/span&gt;&lt;/em&gt;&lt;/p&gt;