Recurrent Hypokalemia leading to Flaccid Quadriparesis: A Renal or Connective Tissue Disorder.

Hypokalemic periodic paralysis (hypoKPP) is a clinical entity characterized by recurrent skeletal muscle paralysis due to a decrease in serum potassium levels; hypoKPP can have either a primary (familial) or a secondary cause. One of the secondary causes of hypoKPP is distal renal tubular acidosis (dRTA). Distal renal tubular acidosis (dRTA) is diagnosed when the urinary pH is greater than 5.3 and in the presence of hyperchloremic metabolic acidosis and hypokalemia, with one of the causes being primary Sjögren's syndrome (pSS). PSS can have both glandular and extra glandular manifestations, with dryness of the eyes and mouth being the most common presenting symptoms. DRTA arising from pSS is very unusual, occurring in fewer than 2% of the cases of Sjogren's syndrome (SS). Here, we report on a case of recurrent flaccid quadriparesis that appears to have been caused by distal RTA, resulting in hypokalemia; upon further investigation and clinical evaluation, the patient was diagnosed with pSS.

Role of diuretics and lipid formulations in the prevention of amphotericin B-induced nephrotoxicity.

PURPOSE: To collect available clinical data to define the role of diuretics and lipid formulations in the prevention of amphotericin B (AmB)-induced nephrotoxicity (AIN) in human populations. METHOD: A literature search was performed in the following databases: Scopus, Medline, Embase, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systematic Reviews. RESULTS AND CONCLUSION: Co-administration of mannitol failed to show any clinically significant benefit in preventing AIN. Potassium-sparing diuretics, such as amiloride and spironolactone, have been shown to have beneficial effects as an alternative or adjunct to oral/parenteral potassium supplements in preventing hypokalemia due to AmB. Lipid-based formulations of AmB are clinically effective and safe in preventing AIN. However, due to their high cost and limited accessibility, these formulations are generally used as second-line antifungal therapy in cases of conventional AmB refractoriness and/or intolerance or pre-existing renal dysfunction. The potential effects of other nephroprotective agents, such as N-acetylcysteine, AIN merit further considerations and investigations.

Severe Hypokalemia Complicated by Acute Myopathy: Initial Manifestation of Primary Sjögren's Syndrome-Associated Renal Tubular Acidosis.

BACKGROUND Severe hypokalemia, which often causes life-threatening malignant arrhythmias, is usually first diagnosed in the Emergency Department (ED). It is important to note that hypokalemia is often closely and complexly related to renal tubular acidosis (RTA) associated with autoimmune diseases such as Sjögren's syndrome (SS), especially in females with acute myopathy or acute liver injury (ALI). Severe hypokalemia can directly cause muscle injury, which can lead to hyper-creatine kinaseemia (HCK) and ALI, while SS can also directly cause hypokalemia, HCK, and even ALI and renal tubular/interstitial injury. Therefore, by reporting a rare case of SS-associated RTA (SS-RTA), we systematically reviewed the relationship between SS-RTA and severe hypokalemia, which may be beneficial to increase attention on this topic. CASE REPORT A 35-year-old female patient who presented to the ED primarily for limb weakness symptoms was initially diagnosed with severe hypokalemia, acute myopathy, and ALI. She was eventually diagnosed with primary SS (pSS) and SS-RTA, although she did not present with the typical dry mouth, dry eyes, and other clinical manifestations of SS. CONCLUSIONS Severe hypokalemia is a serious life-threatening emergency, and although the differential diagnosis is very broad, we should be aware of RTA associated with autoimmune diseases such as SS in female patients, especially when combined with clinical manifestations such as acute myopathy and ALI that cannot be explained by other causes. Simultaneously, we hope to be able to guide emergency physicians encountering similar patients to complete the diagnostic and therapeutic process.

Hypokalemic Paralysis Revealing Primary Sjogren's Syndrome: A Case Report.

Sjogren's syndrome is a rare chronic autoimmune disease characterised by dry eyes and dry mouth due to autoimmune destruction of the lacrimal and salivary glands, which can occur concurrently with other autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, or thyroiditis. It can lead to renal complications such as interstitial nephritis and glomerulonephritis, with distal/ type 1 renal tubular acidosis which may result in life-threatening electrolyte imbalance. We present a case of a 35-year-old female who presented with complaints of multiple episodes of muscle weakness. Type 1 renal tubular acidosis was discovered to be the cause of her symptoms which lead to the subsequent diagnosis of Sjogren's syndrome. This is rare presentation of Sjogren's syndrome, and it poses a challenge to diagnosis. Early detection and diagnosis of Sjogren's syndrome might be difficult due to existing diagnostic criteria, which contributes to a higher likelihood of missed diagnosis. Keywords: case reports; hypokalemia; renal tubular acidosis; Sjogren's syndrome.

[Mediastinitis in a patient with eating disorder]. / Syömishäiriöpotilaan mediastiniitti.

Mediastinitis is a rare but life-threatening disorder. This infection, spreading from outside of the chest to the mediastinum, is most commonly derived from the pharynx or the teeth. In our patient, mediastinitis resulted from an eating disorder. She attempted to control her body weight by vomiting and damaged her pharynx by provoking vomiting. Eating disorder is exceptional as a cause of mediastinitis. This condition should be kept in mind in some common somatic symptoms and findings. An example of these is vomiting induced hypokalemia.

A Case of Kidney Involvement in Primary Sjögren's Syndrome.

BACKGROUND Sjögren's syndrome is an autoimmune disorder caused by the infiltration of monocytes in epithelial glandular and extra-glandular tissues. Hallmark presentations include mouth and eye dryness. Although renal involvement is uncommon in primary Sjögren's syndrome (pSS), patients may experience renal tubular acidosis type I (RTA I), tubulointerstitial nephritis, diabetes insipidus (DI), nephrolithiasis, and Fanconi syndrome. However, it is atypical to see more than 1 of these manifestations in a single patient. CASE REPORT We present the case of a 24-year-old woman with polyuria and polydipsia, who was initially diagnosed with nephrogenic diabetes insipidus. She also had chronic hypokalemia and nephrolithiasis. Based on clinical presentation and work up, she was diagnosed with pSS and treated accordingly. CONCLUSIONS This was a pSS patient with tubulointerstitial nephritis, diabetes insipidus, renal tubular acidosis, hypokalemia, and nephrolithiasis, who was receiving symptomatic treatment for diabetes insipidus. Diagnosis and treatment of pSS led to significant improvement in systemic and renal presentations of the patient. pSS should be considered as one of the differential diagnoses in patients with diabetes insipidus and renal tubular acidosis.

Hypokalaemia in Sjögren's syndrome: the missing piece.

A 58-year-old Chinese woman with well controlled type 1 diabetes mellitus presented with acute and progressive bilateral lower limb weakness. Investigations revealed severe hypokalaemia (1.3 mmol/L) and hypophosphataemia (<0.32 mmol/L) with rhabdomyolysis and electrocardiogram changes, without other concurrent biochemical abnormalities. Immediate intravenous and oral potassium and phosphate replacement was initiated with objective improvement in weakness with replenished electrolyte levels. Urine studies confirmed renal potassium wasting. Further history revealed frequent dental caries, xerostomia and recent weight loss. A computerised tomography scan showed atrophy of her salivary glands and a skin lesion biopsied by her GP in the past had been histologically characterised as anetoderma. The constellation of these findings and subsequent positive anti-SSA/SSB levels confirmed her diagnosis of primary Sjögren's syndrome (PSS). PSS has a wide spectrum of renal involvement and should be a differential diagnosis when investigating interstitial nephritis and electrolyte abnormalities, particularly in patients with coexisting autoimmune conditions.

Diagnosing bulimia nervosa with parotid gland swelling.

BACKGROUND: The authors describe bulimia nervosa, or BN, and its effect on the parotid gland. The associated asymptomatic bilaterally enlarged parotid glands often present a diagnostic dilemma. CASE DESCRIPTION: The authors present a case of a 22-year-old woman with BN who had bilateral parotid gland swelling, serum electrolyte alteration and no dental stigmata. Her principal concern was the associated cosmetic deformity. CLINICAL IMPLICATIONS: Because patients with BN who have parotid gland swelling usually are secretive about their purging, the diagnosis may be confirmed by conducting a clinical examination and a serum electrolyte study. Prompt diagnosis can avoid serious medical complications.

[Rhabdomyolysis and arterial hypertension caused by apparent excess of mineralocorticoids: a case report]. / Rabdomiolisi e ipertensione arteriosa da apparente eccesso di mineralcorticoidi: descrizione di un caso clinico.

We report the case of a 61-year-old man who was referred to our Institution because of severe hypokalemia, rhabdomyolysis and high blood pressure. Severe hypokalemia may lead to rhabdomyolysis. The plasma aldosterone concentrations were low and the plasma renin activity was suppressed. A diagnosis of apparent mineralocorticoid excess, attributable to licorice and grapefruit juice ingestion, was made. Glycyrrhizic acid and glycyrrhetinic acid, its hydrolytic product, in licorice extracts, and polyphenols, in grapefruit juice, can inhibit 11 beta-hydroxysteroid dehydrogenase type 2, the enzyme that converts cortisol to cortisone. Moreover, having suspended licorice and grapefruit juice ingestion, the plasma K+ levels and blood pressure values progressively and simultaneously returned to normal. We would like to stress the diagnostic weight of a careful history taking.

[Bulimia during adolescence]. / Les crises de boulimie à l'adolescence.

Binge eating, bulimia nervosa, binge eating disorder, anorexia-bulimia are terms often used without really knowing what precisely one is referring to. Otherwise, there are many articles concerning anorexia nervosa in medical literature, a disease, which can be seen and fascinates. These eating disorders are frequent in today's society; medical, psychological and social consequences are important.

[Somatic and biochemical complications in bulimia]. / Somatiske og biokjemiske komplikasjoner ved bulimi.

Bulimia is an eating disorder characterized by binge eating followed by purging, i.e. self-induced vomiting, abuse of cathartic or diuretic drugs, increased activity or periods of restrictive dieting. Studies show that persons with bulimia are prone to a number of medical complications as a result of binge-eating, vomiting and drug abuse. Vomiting is the most harmful in terms of medical risk, and also the most common source of complications. Both vomiting and purging lead to loss of body fluids and electrolytes, often resulting in hypokalemia. Vomiting also leads to sore throats and dental problems such as destruction of enamel. Gastric dilatation is the only complication directly associated with binge-eating. Harmless symptoms, such as abdominal pain, diarrhoea, constipation and neuromuscular symptoms are common. This article discusses the pathophysiology behind the complications and their treatment.

Medical consequences of eating disorders.

While much has appeared in the recent literature about various psychotherapeutic techniques used to treat eating disorders, little attention has been paid to the medical complications. Prominent among these are heart damage, failure of the endocrine system, infarction and perforation of the stomach after acute dilatation, multiple suicide attempts, aspiration, injury or rupture of the esophagus, severe bleeding per rectum causing anemia due to laxative abuse, hypokalemic nephropathy, depressive disorders due to starvation, and severe erosion of the enamel of the teeth resulting in extensive loss of teeth. I decry the sudden trend of nonmedically trained personnel rushing into the treatment of eating disorders, particularly anorexia nervosa and bulimia, because they know little about the possibly fatal consequences of their failure to attend to some of these medical phenomena. I also note with grave concern the identification of the medical profession with the "thin is better" mentality of our culture, which blinds them to the serious medical consequences of eating disorders.

Fecal and salivary electrolytes in the diagnosis of primary aldosteronism.

Fecal and salivary sodium and potassium concentrations were measured in 22 hypertensive patients with hypokalemia who were undergoing investigation for primary aldosteronism due to an adrenocortical adenoma (Conn's syndrome). Of eight patients with a high aldosterone secretion rate, five had clearly low fecal Na/K ratios, (including all four patients with Conn's syndrome), in three the ratios were equivocal. Of 14 patients with hypertension and a normal aldosterone secretion rate, none had a sufficiently low fecal Na/K ratio strongly to suggest hyperaldosteronism, although two were borderline. Salivary electrolyte concentrations were not as consistent an indicator of mineralocorticoid hormone excess. Estimation of fecal sodium and potassium concentrations may be useful in the diagnosis of mineralocorticoid hormone excess and in assessing the results of therapy.

[Acute monoblastic leukemia. Clinical and therapeutic aspects in 20 cases]. / Leucémie aiguë monoblastique. Aspects cliniques et thérapeutiques de 20 cas

Twenty cases of acute monoblastic leukemia are studied according to definite criterias: cytology, cytochemical staining, lysozyme production. The study points out the tumoral characters: hematodermy, gingivitis, central nervous system leukemia and the lack of important bone marrow incompetence. 47 per cent of complete remissions are obtained with daunorubicin, aracytin combination therapy. Other useful chemical agents, and prospects for maintenance therapy are discussed.

[Longterm potassium therapy in angina pectoris (author's transl)]. / Kaliumlangzeit- therapie bei Angina pectoris

The effect of a two month potassium therapy on maximum performance was systematically investigated in 12 patients with overt angina pectoris. The patients received 40 mEq potassium daily by mouth. The average maximum performance increased by 85% after 8 weeks' administration of potassium. The rise in the performance curve fell after 6 weeks to attain a steady state after 8 weeks. In particular it must be emphasized that the heart rate was reduced under maximum capacity in spite of considerable increase in performance. Furthermore, a comparison of heart rates after 8 weeks' potassium administration showed that in each case for the same level of performance the heart rate was 15% less than before potassium. The results of the investigation support longterm therapy with potassium in angina pectoris.