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An epileptic seizure is a common neurological presentation in the Emergency Department (ED). Electrolyte disturbances are an important cause of neurological symptoms like seizures and hypomagnesemia is one of them. PPI's can cause hypomagnesemia and are readily prescribed. Therefore patients taking PPI's are at risk of developing neurological symptoms due to hypomagnesemia.A 82-year old woman was seen in ED with a history of nausea, vomiting and vertigo. A vertical nystagmus was observed with attacks of mydriasis followed by a phase of encephalopathy and restlessness. These were recognized as epilepsy. Hypokaliemia, hypocalcemia and a deep hypomagnesemia were present. The PPI accounted for hypomagnesemia. After 2 days of intravenous magnesium suppletion all symptoms disappeared.PPI's can cause hypomagnesemia and magnesium levels should be obtained in patients presenting with encephalopathy or atypical neurological symptoms.

Liquorice consumption can cause pseudohyperaldosteronism and potentially lead to life-threatening complications. Besides correcting hypokalemia and hypertension, finding the triggering factor for pseudohyperaldosteronism is essential to prevent recurrence.A 68-year-old Syrian man presented in the Emergency Department with complaints of fatigue, weakness and exercise-related shortness of breath. Blood tests revealed severe hypokalemia for which suppletion and cardiac rhythm surveillance was necessary. Talking to the patient's son, it occurred that our patient drank copious amounts of Erk Sous, a thirst-quenching drink made from liquorice. The diagnosis pseudohyperaldosteronismwas confirmed by a high level of glycyrrhetinic acid in the patient's urine. After correction of the hypokalemia, our patient recovered successfully.Erk Sous is a thirst-quenching drink that can cause pseudohyperaldosteronism. The drink is popular in the Middle East during summer and Ramadan. If a patient from the Middle East presents with hypokalemia and/or hypertension, ask for consumption of Erk Sous.

Primary aldosteronism (PA) is characterized by autonomic aldosterone production, usually leading to severe hypertension and hypokalaemia. PA is a heterogeneous condition caused by sporadic adrenal adenoma, bilateral adrenal hyperplasia or rare familial forms. Familial aldosteronism type 1 is caused by a hybrid gene that codes for an ACTH-sensitive form of aldosterone synthase. Familial aldosteronism type 3 was recently recognized as a new form of PA caused by mutation in KCNJ5. The clinical manifestations vary from life-threatening PA and pronounced adrenal hyperplasia to milder forms. In addition to germline mutations in KCNJ5, somatic KCNJ5 mutations are present in about 40% of aldosterone-producing adrenal adenomas. Mutations in three other genes are also regularly observed. All these mutations cause increased aldosterone synthase activity, eventually leading to PA. In patients under 20 with PA, familial forms must be excluded before proceeding to adrenalectomy.

Hypokalaemic periodic paralysis is an autosomal, dominantly inherited disorder, characterised by attacks of partial or total muscle weakness and serum hypokalaemia. The mutations responsible are located in the CACNA1S gene (type 1) and in the SCN4A gene (type 2), and are all missense mutations where arginine is mostly replaced by histidine or sometimes glycine. The mutation has been localised in the voltage sensor of the transmembrane segment of calcium channel (type 1) and sodium channel (type 2) respectively. How muscle weakness develops is not known. Oral or intravenous administration of potassium is helpful in treating partial or complete attacks. Acetazolamide can reduce the frequency of attacks in type-1 hypokalaemic periodic paralysis.

Apparent mineralocorticoid excess (AME) is an autosomal recessive disease caused by deficiency of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). 11beta-HSD2 converts cortisol into inactive cortisone and prevents the stimulation of the mineralocorticoid receptor by cortisol. In patients with AME, an enhanced stimulation of mineralocorticoid receptors by cortisol in the distal nephron causes an elevated sodium reabsorption and increased potassium excretion. Sodium retention leads to severe low renin hypertension. The diagnosis of AME is based on the detection of an increased concentration of cortisol metabolites and a low or undetectable concentration of cortisone metabolites in urine. Molecular analysis of the HSD11B2 gene confirms the diagnosis. AME is successfully treated by potassium-sparing diuretics, sometimes in combination with loop diuretics (furosemide). Mild forms of AME might occur more frequently than is currently known and should be suspected in patients with hypertension, hypokalemia and decreased plasma renin concentration. Since liquorice can induce the clinical symptoms of AME due to reversible inhibition of the 11beta-HSD2 enzyme by glycyrrhetinic acid, the active ingredient of liquorice, patients suspected of having AME should not consume liquorice.

Hypokalaemic periodic paralysis is an autosomal, dominantly inherited disorder, characterised by attacks of partial or total muscle weakness and serum hypokalaemia. The mutations responsible are located in the CACNA1S gene (type 1) and in the SCN4A gene (type 2), and are all missense mutations where arginine is mostly replaced by histidine or sometimes glycine. The mutation has been localised in the voltage sensor of the transmembrane segment of calcium channel (type 1) and sodium channel (type 2) respectively. How muscle weakness develops is not known. Oral or intravenous administration of potassium is helpful in treating partial or complete attacks. Acetazolamide can reduce the frequency of attacks in type-1 hypokalaemic periodic paralysis.

Two alcoholic patients, a woman aged 64 and a man aged 69 years, were admitted with tetany. Both had severe electrolyte disorders, with low plasma levels of calcium, magnesium and potassium. Following mineral supplementation both patients recovered. Hypomagnesaemia plays a central role in the pathophysiology of this syndrome. Chronic alcohol abuse results in hypomagnesaemia in 30% of patients by decreasing renal tubular reabsorption. Hypomagnesaemia leads to suppression of parathyroid-hormone secretion, parathyroid-hormone resistance and vitamin-D suppression, resulting in hypocalcaemia. Hypomagnesaemia also causes kaliuresis leading to hypokalaemia. Supplementation with magnesium is crucial in the treatment of this combined electrolyte disorder.

A 39-year-old woman had been investigated elsewhere due to symptomatic hypokalaemia, renal potassium wasting and metabolic alkalosis. Vomiting was considered to be the underlying cause but the patient repeatedly denied this behaviour. After extensive investigations, Bartter's syndrome was finally diagnosed. Eighteen months later the patient was readmitted due to progressive renal insufficiency. On the basis of a very low urinary chloride excretion and the aforementioned laboratory results, it was concluded that the metabolic disturbances were due to vomiting and the diagnosis of Bartter's syndrome was rejected. Upon being confronted with these findings, the patient finally admitted to vomiting, but stated that this happened involuntarily after meals. She had a stenotic ulcer in the pylorus and a gastric biopsy demonstrated the presence of Helicobacter pylori associated gastritis. Eradication therapy was given and the symptoms disappeared. The renal insufficiency was partly accounted for by hypovolaemia and partly by tubulointerstitial nephropathy (demonstrated by kidney biopsy) which was probably due to the chronic hypokalaemia. This case illustrates the difficulty of establishing the differential diagnosis of hypokalaemia, especially in the case of denied vomiting. However, it also shows that in such cases the correct diagnosis can be made if objective parameters are used.

A 41-year-old woman, who presented with (apparent) essential hypertension, was treated with atenolol and candesartan. This treatment, however, was unsuccessful. After the addition of hydrochlorothiazide (HCT) to the combination, she developed hypokalaemia with muscle cramps and weakness. This hypokalaemia persisted for more than 4 weeks after discontinuation of HCT and starting potassium suppletion. As a result of polyuria (4000 ml/day) found in a 24-hour urine collection, it was discovered that the patient drank at least 3 litres of liquorice tea a day. She had denied eating liquorice sweets, a well-known cause of hypertension in the Netherlands, but no one had thought of asking her if she drank liquorice tea. Blood pressure and serum potassium normalized about 2 months after she stopped drinking liquorice tea, and medication was withdrawn. In a patient presenting with hypertension and hypokalaemia, who denies eating liquorice sweets, one should consider the consumption of other products containing liquorice such as liquorice tea. In the Netherlands liquorice tea is increasingly popular and has recently become available on a large scale. Therefore more cases such as the one described may be expected in coming years.

Patients with anorexia nervosa or bulimia nervosa may try to compensate weight gain due to binge eating by purging: vomiting or use of diuretics, laxatives or diet pills. Purging may reduce the body weight through volume depletion, but has hardly any effect on the food uptake. Frequent vomiting is revealed by enlargement of the submandibular and parotid glands and rise of the serum amylase. Use of laxatives leads to electrolyte imbalances, lesions of intestinal mucosa and chronic obstipation. Physical effects of diuretics are dehydration and electrolyte imbalance; oedema may be a sign of their discontinuation. Frequent or major effects of purging are: disorders of cardiac conduction (caused by hypokalaemia), insults and cerebral dysfunction (both due to hyponatraemia). A normal serum potassium concentration does not exclude intracellular hypokalaemia; accordingly, electrocardiography is indicated.

A 2-year-old female Burmese cat was referred to the University Hospital of Companion Animals of Utrecht University because of periodic muscle weakness and cervical ventroflexion. Laboratory examinations revealed hypokalemia. The combination of breed, clinical signs and hypokalemia warranted the diagnosis of 'periodic hypokalemic myopathy', a homozygote recessive hereditary disease in Burmese cats. Potassium supplementation resulted in complete disappearance of the signs. Possible causes of hypokalemia in the cat are discussed.

Gitelman's syndrome was diagnosed in five siblings. The parents were relatives in the third remove. Gitelman's syndrome is a rare autosomal recessive hereditary magnesium reabsorption defect in the distal tubule. It is characterized by episodes of muscle weakness, usually accompanied by abdominal pain and vomiting. Tetany may occur during a febrile illness. Patients are of normal height and weight and have normal blood pressures. Sometimes eczematous skin lesions are found. Biochemically there is hypokalaemia, hypomagnesaemia and alkalosis. Urinary excretion rates of potassium and magnesium are elevated, the excretion of calcium is diminished. Treatment consists of oral suppletion of magnesium, sometimes also with oral potassium. A potassium-sparing diuretic may be used. The prognosis appears to be good.

In a 38-year-old woman who was hospitalized because of hypertension and hypokalaemic alkalosis, the intake of liquorice (200 g per day) was proven to be the cause. A liquorice provocation test produced all the expected clinical and biochemical abnormalities. Some kinds of liquorice contain glycyrrhetic acid which inhibits the enzyme 11-beta-hydroxysteroid dehydrogenase (e.g. in the kidney) leading to decreased transformation of cortisol into cortisone. The mineralocorticoid action of cortisol causes a drop in serum potassium and an increase in serum sodium concentration, together with a metabolic alkalosis, which in the patient described led to retention of water resulting in weight increase and hypertension.

Hypopotassaemic periodic paralysis as the sole manifestation of hyperthyroidism. Hypopotassaemic periodic paralysis is a rare disorder that is found in certain families, sporadically or in association with certain diseases. The association with hyperthyroidism is almost wholly restricted to south-east Asian males. It is characterized by attacks of subacute paralysis, starting most often early in the morning and lasting some hours to a few days. We present a 42-year-old patient of Indonesian origin, who experienced four attacks of paralysis before underlying hyperthyroidism was diagnosed. The mechanism is based on potassium shift into the muscle cell due to higher activity of the Na-K-ATP-ase pump, under the influence of beta-adrenergic stimulation and thyroid hormone. Treatment with antithyroidal medication and beta-blockers led to the complete abolition of attacks.

Small-cell lung cancer may be accompanied by hypercortisolism due to secretion of adrenal stimulating peptides. This occurs almost exclusively in case of extensive disease. The neuroendocrine cell, from which these tumours may originate, plays an important part in the production of these peptides. Four patients are described with small-cell lung cancer and clinical presentation of hypercortisolism, particularly manifesting itself with hypokalaemia.

A female patient aged 45 years is described with a rare form of chondrocalcinosis caused by hypomagnesaemia due to excessive renal loss of magnesium. The patient also had impaired renal conservation of potassium leading to a hypokalemia. She most probably had an idiopathic renal tubular dysfunction. Magnesium supplementation prevented further symptoms. Therefore in young patients with chondrocalcinosis it can be of therapeutic importance to search for an underlying treatable metabolic disorder.

Rhabdomyolysis, secondary to chronic small bowel obstruction. The authors report the case of a 48-year old man, who developed rhabdomyolysis based only upon hypokalemia secondary to a chronic gastro-intestinal disorder (chronic obstruction of the small bowel). They would like to point out that despite the rare occurrence of rhabdomyolysis associated with hypokalemia, this pathological condition cannot be underestimated. Complaints of acute myalgia and general muscle weakness are characteristic. Early recognition of this syndrome is mandatory because myoglobinuria could provoke acute renal failure with eventual fatal outcome.

A girl with periodic weakness since the age of two, is presented. Not until four years after the first symptoms appeared hypokalaemic periodic paralysis was diagnosed. Some aspects of this disease are discussed.