Steroid-induced hypokalemic periodic paralysis: a case report and literature review.

BACKGROUND: Hypokalemic periodic paralysis (HPP) is a rare channelopathy characterized by episodic attacks of acute muscle weakness concomitant with hypokalemia. The etiology of hypokalemia is the shift of potassium into the cells, and the clinical symptoms resolve when potassium starts to leak back to the serum. Most of the time, the underlying ion channel defects are well compensated, and an additional trigger is often required to initiate an attack. Well-known trigger factors include carbohydrate-rich meals, exercise followed by rest, stress, cold weather, and alcohol consumption. CASE PRESENTATION: Here, we present the case of a 26-year-old Asian man who suffered from an acute onset of bilateral lower limb weakness with hypokalemia following dexamethasone injection. He was diagnosed with HPP. CONCLUSIONS: We would like to remind physicians to think of steroids as an unusual precipitating factor while managing patients with HPP, per results of this case study.

Glucocorticoid-Induced Hypokalemic Periodic Paralysis after Short-Term Use of Tenofovir with Hypophosphatemia: A Case Report.

Hypokalemic periodic paralysis (HPP) is a neuromuscular disorder associated with muscular dysfunction caused by hypokalemia. There are various causes of HPPs and rarely, HPP appears to be relevant to tenofovir or glucocorticoid treatment. There have been several case reports of tenofovir-related nephrotoxicity or tenofovir-induced HPP. However, a case report of glucocorticoid-induced HPP in a patient using tenofovir temporarily has not been reported. Herein, we report a case of glucocorticoid-induced HPP with short-term use of tenofovir. A 28-year-old man visited the emergency room with decreased muscle power in all extremities (2/5 grade). In their past medical history, the patient was treated with tenofovir for two months for a hepatitis B virus infection. At the time of the visit, the drug had been discontinued for four months. The day before visiting the emergency room, betamethasone was administered at a local clinic for herpes on the lips. Laboratory tests showed hypokalemia, hypophosphatemia, and mild metabolic acidosis. However, urinalysis revealed no abnormal findings. Consequently, it can be postulated that this patient developed HPP by glucocorticoids after taking tenofovir temporarily. This is the first case report of glucocorticoid-induced HPP in a patient using tenofovir. Clinicians who prescribe tenofovir should be aware of HPP occurring when glucocorticoids are used.

A rare case of cephalexin-induced acute interstitial nephritis with hypokalemic periodic paralysis.

Drug-induced acute interstitial nephritis (AIN) is often encountered in clinical practice. Cephalexin is a first-generation cephalosporin with antimicrobial sensitivity ranging from Gram-positive to Gram-negative organisms. Cephalexin-induced AIN presenting with hypokalemic periodic paralysis (HPP) has been rarely reported. A 34-year-old female with recent history of oral cephalexin intake presented with acute onset paraplegia with deranged renal parameters and hypokalemia. She was treated conservatively with mechanical ventilator support. HPP could be a rare clinical presentation for cephalexin-induced AIN.

Severe hypokalaemia as a cause of acute transient quadriparesis.

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.

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.

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 hypokalemic periodic paralysis possibly precipitated by albuterol.

PURPOSE: An episode of acute hypokalemic paralysis associated with the use of inhaled albuterol is described. SUMMARY: A 34-year-old woman admitted to the emergency department reported the development of pain and diffuse paralysis of the extremities and torso shortly after using an albuterol inhaler. At age 18, she had been diagnosed with hyokalemic periodic paralysis (HPP), a disorder of muscle membrane excitability caused by serum potassium depletion that can lead to life-threatening neuromuscular and cardiovascular complications. After a 15-year period of episodically recurring HPP symptoms despite long-term acetazolamide use, she was switched to spironolactone therapy and had experienced no HPP exacerbations for about 1 year. On her arrival in the emergency department, the patient's serum potassium concentration was 1.8 meq/L and she was mildly tachycardic (heart rate of 125 beats/min). After careful supplementation to gradually increase the serum potassium concentration to 5.4 meq/L, the patient slowly regained movement and strength in her extremities. Application of the adverse drug reaction probability scale of Naranjo et al. to this case yielded a score of 3, indicating that albuterol was possibly the cause of the patient's HPP exacerbation. Beta-2-adrenergic agonists and several other medications can affect serum potassium levels; although the potential risks posed by the use of such drugs in patients with a history of HPP are unclear, cautious use in the context of known HPP is advised. CONCLUSION: A patient previously diagnosed with HPP experienced an exacerbation of HPP possibly induced by inhaled albuterol treatment.

A calcium channel mutant mouse model of hypokalemic periodic paralysis.

Hypokalemic periodic paralysis (HypoPP) is a familial skeletal muscle disorder that presents with recurrent episodes of severe weakness lasting hours to days associated with reduced serum potassium (K+). HypoPP is genetically heterogeneous, with missense mutations of a calcium channel (Ca(V)1.1) or a sodium channel (Na(V)1.4) accounting for 60% and 20% of cases, respectively. The mechanistic link between Ca(V)1.1 mutations and the ictal loss of muscle excitability during an attack of weakness in HypoPP is unknown. To address this question, we developed a mouse model for HypoPP with a targeted Ca(V)1.1 R528H mutation. The Ca(V)1.1 R528H mice had a HypoPP phenotype for which low K+ challenge produced a paradoxical depolarization of the resting potential, loss of muscle excitability, and weakness. A vacuolar myopathy with dilated transverse tubules and disruption of the triad junctions impaired Ca2+ release and likely contributed to the mild permanent weakness. Fibers from the Ca(V)1.1 R528H mouse had a small anomalous inward current at the resting potential, similar to our observations in the Na(V)1.4 R669H HypoPP mouse model. This "gating pore current" may be a common mechanism for paradoxical depolarization and susceptibility to HypoPP arising from missense mutations in the S4 voltage sensor of either calcium or sodium channels.

Betamethasone-induced hypokalemic periodic paralysis in pregnancy.

BACKGROUND: Acute hypokalemic periodic paralysis may be induced by betamethasone injections during pregnancy. CASE: A healthy 23-year-old gravid woman at 32 weeks of gestation with preterm premature rupture of membranes received two doses of 12-mg intramuscular betamethasone 24 hours apart to accelerate fetal lung maturation. She developed significant proximal muscle weakness within 16 hours after the initial dose. Her serum potassium was 1.6 mEq/L. Oral and parenteral potassium replacement restored her neuromuscular function over several days. She delivered by repeat cesarean at 34 weeks of gestation without complications for her or the neonate. CONCLUSION: Hypokalemic periodic paralysis, a rare cause of weakness, may be induced by betamethasone injections during pregnancy and is reversible with low-risk interventions.

Thyrotoxic hypokalemic periodic paralysis due to dietary weight-loss supplement.

Herbal and dietary supplements for weight loss and in treatment of obesity are growing in popularity and acceptance in the United States. Most of these supplements can be obtained over the counter and can have serious adverse effects associated with their consumption. We describe 2 patients who developed thyrotoxic hypokalemic periodic paralysis 2-3 weeks after consuming thyroxine-containing weight-loss supplements. This is the first known case of thyrotoxic hypokalemic periodic paralysis secondary to dietary supplements. It is important that patients and physicians are aware of the severe adverse reactions associated with dietary supplements. Physicians should as a routine inquire about herbal and dietary supplement consumption during all patient encounters.

[Pseudo-Conn's syndrome with hypokalemic paralysis due to diuretics and licorice abuse]. / Pseudo-Conn-Syndrom mit hypokaliämischer Lähmung bei Lakritzabusus und Diuretikatherapie.

Dyskalemic paralyses are characterised by single or periodic episodes with muscle weakness that affect mostly the proximal skeletal muscles. Symptoms may last for a few hours or persist for several days, spontaneous recovery is common. Familial cases can be distinguished from secondary, non-familial forms which are based on other diseases, for example, of the thyroid gland, kidneys or gastrointestinal tract. Familial cases are mostly inherited in an autosomal-dominant pattern and belong to the channelopathies. Both groups are characterised by changed potassium levels in the blood during an episode. A detailed and accurate medical history (plus family history, use of medication and eating habits) often easily leads to the diagnosis. Provoking tests or instrumental and histological investigations can help to solve difficult cases. Treatment focuses on relieving acute symptoms and attacks can be managed by correcting the blood potassium to a normal level. Changing eating and/or exercise habits and also permanent medical treatment helps to prevent further attacks.

Hypokalemic paralysis following administration of intravenous methylprednisolone in a patient with Graves' thyrotoxicosis and ophthalmopathy.

Glucocorticoids are commonly used in the treatment of patients with thyroid disorders, in particular Graves' ophthalmopathy. Thyrotoxic hypokalemic periodic paralysis (TPP) is an infrequent but potentially serious condition characterised by recurrent episodes of weakness associated with hypokalemia. We describe the development of acute hypokalemic paralysis in a middle-aged Caucasian man with recently diagnosed thyrotoxicosis and severe, active Graves' opthalmopathy who developed progressive flaccid paralysis 12 hours following intravenous administration of methylprednisolone. Rechallenge with the same dose after the patient had been rendered euthyroid did not provoke TPP. Clinicians should exercise caution when administering high-dose glucocorticoids during thyrotoxicosis as there is a risk of provoking hypokalemic paralysis in susceptible patients.

Thyrotoxic periodic paralysis due to excessive L-thyroxine replacement in a Caucasian man.

Thyrotoxic periodic paralysis is a potentially fatal complication of hyperthyroidism, more common in Asian races, which is defined by a massive intracellular flux of potassium. This leads to profound hypokalaemia and muscle paralysis. Although the paralysis is temporary, it may be lethal if not diagnosed and treated rapidly, as profound hypokalaemia may induce respiratory muscle paralysis or cardiac arrest. The condition is often misdiagnosed in the west due to its comparative rarity in Caucasians; however it is now increasingly described in Caucasians and is also being seen with increasing frequency in western hospitals due to increasing immigration and population mobility. Here we describe the case of a patient with panhypopituitarism due to a craniopharyngioma, who developed thyrotoxic periodic paralysis due to excessive L-thyroxine replacement. This disorder has been described in Asian subjects but, to our knowledge, thyrotoxic periodic paralysis secondary to excessive L-thyroxine replacement has never been described in Caucasians.

Glucocorticoids may trigger attacks in several types of periodic paralysis.

Hypokalemic periodic paralysis is a rare disorder characterized by episodic attacks of muscle flaccidity associated with low serum potassium levels. We report twelve patients with normokalemic and hypokalemic periodic paralysis due to various mutations who developed hypokalemic paralytic episodes following a single dose or short-term administration of glucocorticoids. We hypothesize that glucocorticoids cause hypokalemia due to their stimulation of the Na(+)-K(+) ATPase mediated by insulin and amylin and due to their side effect of insulin resistance resulting in hyperglycemia. This report adds to the clinical description of glucocorticoids as a trigger of attacks of hypokalemic periodic paralysis indicating that glucocorticoids should be administered with caution in patients with periodic paralysis.

An unusual cause of thyrotoxic periodic paralysis: triiodothyronine-containing weight reducing agents.

Thyrotoxic periodic paralysis resulting from exogenous thyroid hormone administration (thyrotoxicosis factitia) has been rarely reported. We describe a 23-year-old man who presented with limbs paralysis upon awakening in the morning. Pertinent history revealed that he took drugs containing triiodothyronine (64 mug) and propranolol (40 mg) twice daily for weight reduction in the past month and discontinued these drugs 3 days before admission. Physical examination showed systolic hypertension (160/76 mm Hg), relative tachycardia (98 bpm), and symmetrical flaccid paralysis of all extremities. The most striking laboratory finding was severe hypokalemia (1.6 mmol/L) with low urinary potassium excretion and normal blood acid-base status, suggesting acute potassium shifting into cells. Approximately, 174 mmol of potassium chloride was administrated to restore his muscle strength within 12 hours, but rebound hyperkalemia (6.1 mmol/L) developed upon recovery. Despite normal serum free triiodothyronine and thyroxine levels, the suppressed concentration of thyroid stimulating hormone indicated hyperthyroidism. The low radioiodine uptake (4%) and serum thyroglobulin level (2 ng/mL) were consistent with thyrotoxicosis factitia. This is the first reported case of exogenous triiodothyronine-induced thyrotoxic periodic paralysis, which may have been precipitated by the withdrawal of propranolol.

Thyrotoxic periodic paralysis induced by pulse methylprednisolone.

We present a young Thai man who developed acute flaccid paralysis after receiving pulse methylprednisolone for chronic inflammatory demyelinating polyneuropathy. Hypokalemia from intracellular shift was confirmed by calculation of transtubular potassium gradient (TTKG). His muscle strength and serum potassium fully recovered with a small amount of potassium replacement. Graves' disease was subsequently diagnosed and treated with radioactive iodine. We suggest that acute paralysis after the use of steroids should raise a suspicion of thyrotoxic periodic paralysis (TPP). The potential mechanisms of steroid-induced TPP are discussed.

Thyrotoxic hypokalemic periodic paralysis triggered by high carbohydrate diet.

Thyrotoxic hypokalemic periodic paralysis is an uncommon disorder characterized by elevated thyroid hormone, muscle weakness or paralysis, and intracellular shifts of potassium leading to hypokalemia. This article presents a case of thyrotoxic hypokalemic periodic paralysis in a 22-year old Hispanic man with nonfamilial thyrotoxic hypokalemic periodic paralysis triggered by a high carbohydrate diet. Laboratory studies showed elevated thyroid hormone, decreased thyroid-stimulating hormone, and hypokalemia. Rapid reduction in thyroid hormone levels by giving antithyroid drugs such as propylthiouracil and prompt potassium therapy with frequent measurements of serum potassium levels during therapy to avoid catastrophic hyperkalemia when potassium starts to shift back from intracellular to extracellular compartments can lead to successful outcome.

[Hypokalemic thyrotoxic periodic paralysis following rice consumption]. / Hypokaliämische thyreotoxische periodische Parese nach Reismahlzeit.

HISTORY AND ADMISSION FINDINGS: A 38-year-old previously healthy Swiss presented with acute onset of progressive weakness in his legs in the morning hours after a carbohydrate-rich meal the preceding evening. Examination on admission revealed symmetrical paresis affecting the upper and lower limbs without involvement of the respiratory muscles. Hyperthyroidism was suspected. Similar symptoms three weeks before admission had earlier resolved spontaneously. INVESTIGATIONS: Laboratory tests revealed severe hypokalemia of 1.4 mmol/l. Hyperthyroidism, caused by Grave's disease, was confirmed and a diagnosis of hypokalemic thyrotoxic periodic paralysis (TPP) was made. TREATMENT AND FOLLOW-UP: After initiating potassium replacement paresis was observed to disappear within three hours. Symptomatic treatment with propranolol and thyrostatic treatment with carbimazole prevented further episodes of paresis. CONCLUSION: Hypokalemic thyrotoxic periodic paresis is a rare but increasingly common medical condition among people living in Western Europe. Diagnostically one's attention should turn to TPP at the presentation of acute paresis in combination with hypokalemia, especially in young men. Serious cardio-pulmonary complications can be avoided with early diagnosis and treatment.