A case of primary sjogren`s syndrome with distal renal tubular acidosis presenting as hypokalemic paralysis.

Renal tubular acidosis secondary to autoimmune interstitial nephritis is quite common in patients with Sjogren`s syndrome. Here we present a case of 24 year old female who presented with Acute Hypokalemic Quadriparesis and was later diagnosed with distal RTA. Patient did not have features of xerostomia or xerophthalmia but was diagnosed to have Primary Sjogren`s syndrome fromserological findings,in this case renal involvement preceded subjective Sicca syndrome.Patient recovered after giving i.v potassium. Patient was treated with corticosteroids and is asymptomatic during the one year follow up period.

Acute Onset Hypokalemic Quadriparesis with Dengue Fever: A Case Report.

Dengue fever is an acute viral disease caused by dengue virus (DENV1- 4) and is endemic to India. It commonly presents as fever along with headache, bodyache, rashes, polyserositis, bleeding manifestations and rarely as cardiovascular, gastrointestinal, renal or neurological manifestations. Here, we report a case of dengue fever with hypokalemic quadriparesis. A 38-year-old male admitted with history of fever of 3-day duration and weakness of all four limbs of 1-day duration. His investigations showed Hb - 16.20 g/dL, platelet - 37,000/mm3, serum Na+ - 150.00 mmol/L, serum K+ - 2.50 mmol/L and positive dengue serology. Hypokalemic quadriparesis secondary to dengue fever should be considered as a differential diagnosis in a case of acute febrile illness with muscle weakness in tropical countries.

Etiology of Hypokalemic Paralysis in Korea: Data from a Single Center

Recognizing the underlying causes of hypokalemic paralysis seems to be essential for the appropriate management of affected patients and their prevention of recurrent attacks. There is, however, a paucity of documented reports on the etiology of hypokalemic paralysis in Korea. We retrospectively analyzed 34 patients with acute flaccid weakness due to hypokalaemia who were admitted during the 5-year study period in order to determine the spectrum of hypokalemic paralysis in Korea and to identify the differences in clinical parameters all across the causes of hypokalemic paralysis. We divided those 34 patients into 3 groups; the 1st group, idiopathic hypokalemic periodic paralysis (HPP), the 2nd, thyrotoxic periodic paralysis (TPP), and the 3rd group, secondary hypokalemic paralysis (HP) without TPP. Seven of the patients (20.6%) were diagnosed as idiopathic HPP considered the sporadic form, and 27 patients (79.4%) as secondary HP. Among the patients diagnosed as secondary HP, 16 patients (47.1%) had TPP. Patients of secondary hypokalemic paralysis without TPP required a longer recovery time compared with those who had either idiopathic HPP or TPP. This is due to the fact that patients of secondary HP had a significantly negative total body potassium balance, whereas idiopathic HPP and TPP were only associated with intracellular shift of potassium. Most of the TPP patients included in our study had overt thyrotoxicosis while 3 patients had subclinical thyrotoxicosis. This study shows that TPP is the most common cause of hypokalemic paralysis in Korea. And we suggest that doctors should consider the presence of TPP in patients of hypokalemic paralysis even if they clinically appear to be euthyroid state.

A Case of Hypokalemic Paralysis Provoked after Trigger Point Injection with Dexamethasone and Lidocaine

Acute hypokalemic paralysis is characterized by acute systemic weakness and low serum potassium. Trigger point injection (TPI) is frequently performed for myofacial pain relief with rare complications. 34-year-old male was admitted with quadriparesis after TPI with dexamethasone and lidocaine before 24 hours. Hypokalemia was found with compatible findings on nerve conduction studies and electromyography. Hypokalemia and weakness were fully recovered after potassium replacement. Steroid and lidocaine can provoke iatrogenic hypokalemic paralysis, therefore, TPI with these medications should be cautiously performed.

Licorice-nduced Hypokalemia and Myopathy / 대한신장학회잡지

Chronic ingestion of licorice or licorice-like compounds induces a syndrome with typical findings of mineralocorticoid excess such as hypertension, hypokalemia, metabolic alkalosis, low plasma renin activity. The only unique feature is that plasma aldosterone concentration is decreased. We described a 79-year-old woman who, with a plasma K+ 1.75 mEq/L, showed a paralysis and severe rhabdomyolysis after the habitual comsumption of licorice in the form of a herbal medication. Following potassium replacement therapy and discontinuation of licorice ingestion, complete clinical recovery was observed within ten days. It is important for physicians to keep licorice consumption in mind as a cause for hypokalemic paralysis and rhabdomyolysis.

A Case of Licorice Induced Hypokalemic Paralysis with Rhabdomyolysis / 대한내분비학회지

Prolonged ingestion of licorice can cause hypermineralocorticoidism, with sodium retention, potassium loss and hypertension. Nevertheless, its initial presentation with a very severe degree of hypokalemic paralysis and rhabdomyolysis are exceedingly rare. We describe a patient who experienced hypokalemic paralysis and rhabdomyolysis after licorice ingestion. The patient's initial blood pressure was 160/80mmHg. The major biochemical abnormalities included; hypokalemia(K+ 1.3mEq/L), metabolic alkalosis, with a pH of 7.64, and urine myoglobin > 3000ng/mL. The plasma rennin activity and aldosterone level were suppressed. The 24 hour urine cortisol concentration was normal. The patients, over a 1 month period, had ingested 500g of licorice boiled in water. After quitting the licorice, the hypokalemia and muscle paralysis gradually improved and blood pressure returned to normal

A Case of Primary Sjorgen's Syndrome Presenting as Hypokalemic Periodic Paralysis / 대한류마티스학회지

We describe a 46-year-old woman with hypokalemic paralysis as the initial manifestation of Sjorgen's syndrome. Sjorgen's syndrome is an autoimmune exocrinopathy, characterized by keratoconjuntivitis sicca and xerostomia. Among the extraglandular manifestations of Sjorgen's syndrome, renal tubular involvement, especially renal tubular acidosis, is the most often latent or minimally symptomatic. Renal tubular acidosis is estimated to be present in 25~30 percent of the cases. Hypokalemic paralysis may serve as a clinical marker for more severe renal disease in patient who has primary Sjorgen's syndrome with renal tubular acidosis, even though it is a rare manifestation of Sjorgen's syndrome.

Systematic analysis of concomitant-infectious hypokalemic paralysis / 临床神经病学杂志

Objective To study the relationship between infection and hypokalemic paralysis and its clinical features.Methods A systemic analysis was made on the infection courses,clinical manifestations, serum levels of potassium and creatine phosphokinase,the results of electrophysiological and virological examinations in present 34 patients and 115 cases reported in literature with hypokalemic paralysis.Results There were differences in the clinical manifestations and denominations among the present and reported cases. No definite evidences for virus infections were found among patients who were characterized by acute flaccid paralysis accompanied with hypokalemia in the infection curses. The prognosis of the disorder was better after the patients were given potassium, and most of them didn't recur.Conclusion No enough evidences showed that this disorder was an independent disease.It should be named as "concomitant infectious hypokalemic paralysis" appropriately. It was probably a syndrome accompanied by infection on the base of hereditary susceptibility.

A Case of Primary Sjiigren's Syndrome with Hypokalemic Paralysis and Renal Tubular Acidosis / 대한류마티스학회지

A 36-year old woman with Sjogren's syndrome, distal renal tubular acidosis and hypokalemic muscle paralysis is described. The main manifestation was muscle paralysis due to hypokalemia secondary to renal tubular acidosis. Review of English literatures revealed 13 cases of hypokalemic paralysis due to Sjogren's syndrome. The data from those reports have indicated that hypokalemic paralysis was seen more often in patients with primary Sjogren's syndrome than secondary one and that it might precede the classic sicca comple. Hypokalemic paralysis may serve as a clinical marker for more severe renal disease in patients who have primary Sjogren's syndrome and renal tubular acidosis, even though it is a rare manifestation of Sjogren's syndrome.