Case Of Hypokalemic Periodic Paralysis Research Articles

Sjogren’s syndrome presenting as hypokalemic periodic paralysis, a rare manifestation: A case series

Sjogren’s syndrome is a chronic and slowly progressing autoimmune disease characterized by lyphocytic infiltration of exocrine glands resulting in Sicca syndrome (xerostomia and keratocunjuntivitis sicca). The disease can present alone or along with other autoimmune diseases leading to significant organ specific and systemic disease. Middle aged women (Female: Male: 9:1) are primarily affected. Extraglandular (systemic) manifestations are seen in one third of patients with Sjogren’s syndrome. Among the extraglandular manifestations, renal involvement is commonly seen. Renal involvement in the form of tubulointerstitial nephritis (TIN) is more common compared to glomerular involvement. Distal renal tubular acidosis (RTA) is more common manifestation of TIN presenting as mild hypokalemia, metabolic acidosis, and rarely with hypokalemic periodic paralysis. We report three cases of hypokalemic periodic paralysis with metabolic acidosis, two in respiratory paralysis, diagnosed as distal RTA. On further evaluation of distal RTA, the patient diagnosed to have Sjogren’s syndrome and managed accordingly. Our report shows that Sjogren’s syndrome is a rare but important cause of hypokaemic periodic paralysis due to RTA.

A Case of Hypokalemic Periodic Paralysis Requiring Intravenous Injection of Large Doses of Potassium due to Repeated Ventricular Fibrillation

A Case of Hypokalemic Periodic Paralysis Requiring Intravenous Injection of Large Doses of Potassium due to Repeated Ventricular Fibrillation

SUN-518 Graves’ Disease Newly Diagnosed in the Setting of Hypokalemic Periodic Paralysis in an HIV+ Patient

Relevance: A rare yet distinct cause of sudden onset paralysis is severe hypokalemia associated with thyrotoxicosis. This is thought to be associated with mutations in genes encoding cellular potassium channels. We report a case of acute onset paralysis with profound hypokalemia and a new diagnosis of Graves’ thyrotoxicosis in a previously asymptomatic African American, HIV+ man on highly active antiretroviral therapy (HAART) for over 8 years. Clinical case: A 49-year-old man with hypertension and HIV presented with acute paralysis of his bilateral upper and lower extremities. His initial potassium was 1.8 mEq/L (3.5-5.0). Prior to sudden onset loss of motor strength, he denied any preceding palpitations, tremor, anxiety, diaphoresis, hyper-defecation, weight loss, heat or cold intolerance, neck pain, increase in neck girth or difficulty swallowing, proptosis or other ocular symptoms. He has no family history of thyroid disease. He had an enlarged palpable thyroid without nodules and no audible bruit. There was no periorbital edema or proptosis, and no signs of dermopathy. A thyroid ultrasound showed a hyperemic and diffusely enlarged thyroid gland without nodules. Labs included a TSH of 0.007 mCU/mL (0.43-3.8), Free T4 2.1 ng/dL (0.71-1.85), Total T3 229.6 ng/dL (58-194), and thyrotropin receptor antibody 2.6 IU/L (0-1.75). The CD4+ count was 146 in 2010 with a slow gradual rise to 673 in 2019, and HIV viral load was undetectable. There were no offending medications or supplements identified. With aggressive potassium repletion, the serum potassium improved to 4.6 mEq/L and he regained normal strength within several hours. He was started on Methimazole 10mg daily and propranolol 10mg TID. At one month, the thyroid function tests normalized. Methimazole 10mg daily was continued and propranolol was tapered off. He remains euthyroid. Genetic testing is pending. Conclusions: Graves’ disease is the most common thyroid disease triggered by immune reconstitution in HIV + individuals on HAART. The incidence of thyroid disease in HIV patients on HAART is higher in women and Africans with a 1.5-2 fold increase compared with the general population [Muller et. al, Eur Thyroid J 2019;8:173-185]. Despite a higher incidence of hyperthyroidism in women, over 95% of cases of hypokalemic periodic paralysis have been reported in men, with a 10-fold higher incidence among Asians compared to Westerners. There has been one prior case report of Thyrotoxic Periodic Paralysis in an HIV + patient and this was in a Polynesian male (Brown JD et al. Hawaii Med J 2007). To our knowledge, this is the first case report of an African American HIV+ patient with this disorder. An association with mutations in the Kir2.6 gene (encodes a potassium channel, is expressed in skeletal muscle, and is transcriptionally regulated by thyroid hormone) has been proposed [Ryan et. al, Cell 2010 January 8; 140(1):88-98].

SUN-507 Fueling the Fire: A Case of Hypokalemic Periodic Paralysis Associated with Type I Renal Tubular Acidosis and Thyrotoxicosis in Pregnancy

Background: Hypokalemic periodic paralysis (HPP) related to thyrotoxicosis, though rare, is more often seen in Asian males. Type 1 renal tubular acidosis (T1 RTA), which can also cause HPP, is typically managed with alkali therapy and potassium supplementation, though there are no well-established guidelines for management in pregnancy.Clinical Case: A 27-year-old Puerto Rican woman, at 32 weeks gestation, presented to the hospital with sudden onset muscle weakness, and was found to have 1/5 muscle strength in her lower extremities. She had no personal or family history of similar illness. Laboratory analysis revealed hypokalemia (potassium 2.0 mmol/L, range: 3.5 – 5); non-gap metabolic acidosis (sodium 137mmol/L, range 136 – 145; chloride 113 mmol/L, range 98- 107; and bicarbonate 8 mmol/L, range 22 – 29); and an arterial pH of 7.09. Urine studies demonstrated a urine pH of 6.5 and a urine sodium of 32 mmol/L which was diagnostic of T1 RTA in the context of her metabolic derangements. She was treated emergently with potassium and bicarbonate infusions, with improvement in her symptoms. Subsequent thyroid function testing revealed: a low TSH of 0.01 uIU/ml, normal free T4 of 1.66 (range: 0.9 - 1.7) ng/dl, normal free of T3 3.7 (range: 2.0 -4.4) pg/ml and elevated total T4 of 16.5 (range: 4.5 - 11.7) ug/dl. Renal ultrasound demonstrated medullary nephrocalcinosis. She was discharged on potassium and sodium citrate tablets. At 37 weeks, the patient was readmitted for induction of labor due to pre-eclampsia, and delivered a healthy male baby. Several months later, she presented to the Endocrinology clinic with symptoms of increased frequency bowel movements, palpitations and heat intolerance, which had been ongoing since pregnancy. On review, a metabolic panel prior to pregnancy had demonstrated non-gap acidosis and mild hypokalemia. Further testing demonstrated the following: TSH < 0.01 uIU/ml, Free T4 1.71 ng/dl, Free T3 4.8 pg/ml, TSI 280%, and a thyroid uptake scan with homogenous radiotracer uptake, with a 24-hour uptake of 40%. She was started on methimazole therapy, and continued on potassium and sodium citrate tablets with clinical and biochemical improvement.Conclusion: Thyrotoxicosis can augment hypokalemia in T1 RTA, and can increase the risk of HPP. Our patient had biochemical evidence of RTA prior to pregnancy, though without episodes of HPP, and we believe that her hyperthyroidism, triggered by pregnancy, may have been the additional insult that precipitated her paralysis. This is the first reported case of HPP related to co-existing thyrotoxicosis and T1 RTA in a pregnant individual.Reference:1. Tu ML, Fang YW, Leu JG, Tsai MH. An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report. BMC Nephrol. 2018;19(1):160. Published 2018 Jul 4. doi:10.1186/s12882-018-0971-9

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.

Abstract #545 A Case of Hypokalemic Periodic Paralysis on a Hispanic Male Presenting with Lower Extremities Paralysis and Subtle Signs & Symptoms of Thyrotoxicosis

Abstract #545 A Case of Hypokalemic Periodic Paralysis on a Hispanic Male Presenting with Lower Extremities Paralysis and Subtle Signs & Symptoms of Thyrotoxicosis

Atypical Presentation of Periodic Paralysis: A Case Report

Hypokalemic periodic paralysis (HPP) is a kind of periodic paralysis, which is a heterogeneous group of muscle diseases. It is characterized by episodes of flaccid and sudden muscle weakness.Here, we present a case of HPP. The patient was referred to our department because of severe dizziness and fall. After a comprehensive evaluation, a markedly low potassium was detected. The patient’s symptoms resolved after replacement of potassium and he was discharged without deficits. Even though the literature reports an association with exercise, carbohydrate load, and stress, further workup in our patient revealed no association with these precipitants. A proper differential diagnosis should rule out other causes of weakness and paralysis, thus allowing a timely treatment.

Hypokalemic Periodic Paralysis: Reports of Two Cases and Brief Review

Hypokalemic periodic paralysis (HPP) is a rare autosomal dominant channelopathy characterized by skeletal muscle weakness or paralysis when there is a fall in potassium levels in blood. Weakness may be mild and limited to certain muscle groups or more severe causing generalized paralysis. During an attack, reflexes may be diminished or absent. Attacks may last for a few hours or persist for several days, ultimately resulting in complete recovery. Some patients may develop chronic muscle weakness later in life. Recurrent muscle weakness accompanied by hypokalemia and exclusion of other causes help establish the diagnosis. Potassium supplementation is the mainstay of treatment of acute illness. Lifestyle modification with or without pharmacotherapy in the form of carbonic anhydrase inhibitors and/ or spironolactone can prevent future attacks. Here, we present two cases of HPP, the first one had no positive family history and responded to oral potassium and spironolactone, while the second case had family history suggestive of HPP and was managed with potassium and eplerenone.&#x0D; Birdem Med J 2019; 9(1): 74-79

Abstract #1061 Gravely Paralyzed: A Case of Hypokalemic Periodic Paralysis in a Patient with Graves’ Disease

Abstract #1061 Gravely Paralyzed: A Case of Hypokalemic Periodic Paralysis in a Patient with Graves’ Disease

A possible association of hypokalaemic periodic paralysis, autoimmune thyroiditis and neuromyotonia

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.

Hypokalemic Periodic Paralysis Accompanied with Myasthenia Gravis: A Case Report

Myasthenia gravis and hypokalemic periodic paralysis are commonly related with hyperthyroidism but rarely occur together. Here, in this article a case of hypokalemic periodic paralysis in a north Indian male accompanied with myasthenia gravis has been reported. He had motor weakness despite a normal level of serum potassium. Edrophonium test was positive. He dramatically improved after pyridostigmine treatment. Autoantibodies to nicotinic AchR-Ab and dihydropyridine receptor or L-type voltage gated calcium channel were postulated to explain these associated diseases.

그레이브씨 병에 동반된 저칼륨 혈증성 주기성 마비 1예

그레이브씨 병에 동반된 저칼륨 혈증성 주기성 마비 1예

Thyrotoxic periodic paralysis in Caucasian patients: A diagnostic challenge

Secondary hypokalemic periodic paralysis is rare. However, when it occurs, it is usually associated with Graves' disease and it is mostly diagnosed in Asiatic male patients. In this report, we analyze the diagnostic procedure in three cases of hypokalemic periodic paralysis associated with Graves' disease, diagnosed in three different emergency care units over the last 3 years. Three Caucasian men (26, 30, and 39 years of age) came to the emergency care unit for acute tetraparesia. One of them had suffered 15 stereotypical episodes of tetraparesia during the last 2 years. Goiter was present in each case. Kalemia was 1.8, 2.1, and 3 mmol/l, respectively. Triggering events such as considerable sugar intake and physical exercise were present in two cases. In all cases, low TSH levels, high FT4 levels, and anti-TSH receptor antibodies led to the diagnosis of Graves' disease. All patients were treated with potassium supplementation and neomercazole. Outcome was good with a follow-up of 6, 9, and 24 months, respectively. Emergency care practitioners should be aware of this diagnosis, which may affect Caucasian patients presenting with transient tetraparesia in a primary care unit.