Unusual causes of hypokalaemia and paralysis

Alazami, M.; Lin, Shih‐Hua; Cheng, Chih-Jen; Davids, Mogamat Razeen; Halperin, Mitchell L.

doi:10.1093/qjmed/hcl011

Cited by 20 publications

(29 citation statements)

References 27 publications

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“…Drugs prescribed to some of our prematurely born Gitelman-patients, including β-lactams, aminoglycosides and especially caffeine, may sometimes cause hypokalemia [13,14]. The persistence of hypokalemia after the withdrawal of these drugs and the clear-cut results of genotype analysis indicate that the prescribed drugs played a relatively minor role in our patients as the cause of hypokalemia during early infancy.…”

Section: Discussionmentioning

confidence: 80%

Early appearance of hypokalemia in Gitelman syndrome

Tammaro¹,

Bettinelli²,

Cattarelli³

et al. 2010

Pediatr Nephrol

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Inactivating mutations in the SLC12A3 gene that encodes the thiazide-sensitive co-transporter causes Gitelman syndrome. The main features of this syndrome include normal or low blood pressure, hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, and hyperreninemia. These patients are at low risk for preterm birth and do not present with symptoms before school age. As a consequence, the condition is usually diagnosed in late childhood or in adult life. We report on four patients, two pairs of prematurely born twins, in whom hypokalemia was demonstrated early in life. In these children, a tendency towards hypokalemia was first noted during the third week of life. Overt hypokalemia subsequently appeared associated with normal blood pressure, hypochloremia, hyperreninemia, and an inappropriately high fractional excretion of potassium and chloride. Molecular biology studies failed to detect mutations in the SLC12A1, KCNJ1, and CLCNKB genes responsible for the Bartter syndromes type I, II and III, respectively. Compound heterozygous mutations in the SLC12A3 gene were detected in both pairs of twins: a frameshift mutation in exon 10 (c.1196_1202dup7bp), leading to the truncated protein p.Ser402X, and a missense mutation in exon 11, p.Ser475Cys (c.1424C>G) in the first pair; two missense mutations, p.Thr392Ile (c.1175C>T) in exon 9 and p.Ser615Leu in exon 15 (c.1844C>T), in the second pair. In conclusion, the diagnosis of Gitelman syndrome deserves consideration in infants with unexplained hypokalemia.

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Section: Discussionmentioning

confidence: 80%

Early appearance of hypokalemia in Gitelman syndrome

Tammaro¹,

Bettinelli²,

Cattarelli³

et al. 2010

Pediatr Nephrol

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“…Usually, the affinity of the drug for the enzyme is high, but its maximum velocity is not that large and the effect can be prolonged. 7 For these reasons, we suggest that patients who present with hypokalemia due to large and prolonged caffeine oral intake should be monitored for at least 18 hours after normalization of potassium serum levels and after all symptoms have disappeared because of the delayed recurrence of hypokalemia. Particular attention should also be paid to athletes, as they are potentially greater users of different energy drinks that, even if permitted, could contain large amounts of caffeine.…”

Section: Case Reportmentioning

confidence: 99%

“…6 The positive effect on prolonged exercise performance should be related to the adenosine antagonist action of caffeine, which leads to a release of Ca++ from skeletal muscle sarcoplasmic reticulum. 7 Other effects are determined by the increase of lipolysis, by a modest raise of muscle glycogen, 8 and by the indirect increase in catecholamine release. 1 …”

Section: Introductionmentioning

confidence: 99%

Severe Hypokalemia in 2 Young Bicycle Riders Due to Massive Caffeine Intake

Rigato¹,

Blarasin²,

Kette³

2010

Clinical Journal of Sport Medicine

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“…An increased shift of K + into cells can occur in a number of conditions that are associated with increased catecholamines and in states with hyperinsulinemia or rapid anabolism (e.g., recovery from DKA) [47,48]. High adrenergic states include asthma or drugs used to suppress appetite or bronchoconstriction or the intake of a large quantity of caffeine, exacerbation of chronic obstructive pulmonary disease, acute myocardial infraction, head injury, and delirium tremens among others [49][50][51]. In contrast, barium intoxication and chloroquine overdose may cause hypokalemia via closure of cellular membrane K + channels [52,53].…”

Section: Urine Flow Ratementioning

confidence: 99%

Hypokalemia: A Practical Approach to Diagnosis and its Genetic Basis

Lin¹,

Halperin²

2007

CMC

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Hypokalemia is a common and important finding in hospitalized patients because it may provoke cardiac arrhythmias and/or respiratory arrest. Our aim is to suggest better diagnostic tools and therapeutic principles, and summarize new molecular advances that are linked to hypokalemia. Measurements in freshly-voided urine to evaluate potassium (K+) excretion and an assessment of the acid-base status in blood can help differentiate between the various causes of hypokalemia. In patients with a low rate of K+ excretion, hypokalemia can be explained by an acute shift of K+ into cells, intestinal K+ loss, or prior renal K+ excretion. Patients with a high rate of K+ excretion usually have metabolic acid-base disorders. In patients with hyperchloremic metabolic acidosis, an assessment of the rate of excretion of ammonium (NH4+) in the urine separates those with renal tubular acidosis (RTA) (low NH4+ excretion) from those with causes other than RTA. In patients with metabolic alkalosis, a high blood pressure helps to distinguish between a state with high mineralocorticoid activity from others with extracellular fluid (ECF) volume contraction. Measurement of renin activity, aldosterone, and cortisol levels in plasma help to differentiate between the causes with mineralocorticoid excess whereas the urine chloride (Cl-) concentration may reveal the basis for renal Na+ wasting and distinguish it from non-renal Na+ loss. The treatment of hypokalemia is guided by the risk imposed by hypokalemia, magnitude of the K+ deficit, route of the K+ administration, available K+ preparations, adjuncts to therapy, and special associated conditions. Recent molecular advances in inherited hypokalemic disorders affecting transcellular K+ shift, gastrointestinal and renal K+ excretion are also discussed.

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Unusual causes of hypokalaemia and paralysis

Cited by 20 publications

References 27 publications

Early appearance of hypokalemia in Gitelman syndrome

Early appearance of hypokalemia in Gitelman syndrome

Severe Hypokalemia in 2 Young Bicycle Riders Due to Massive Caffeine Intake

Hypokalemia: A Practical Approach to Diagnosis and its Genetic Basis

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