Oral Potassium Chloride Research Articles

Schizophrenia-like psychosis and gitelman syndrome: a case report and literature review.

IntroductionGitelman syndrome(GS) is a rare inherited tubular disorder which is characterized by hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. Here, we report a case of schizophrenia-like psychosis concomitant with GS and related literatures are reviewed.Case descriptionAn 18-year-old male patient with 1-week history of auditory hallucinations, sense of insecurity, delusions of reference and feelings of being followed and controlled by others unknown, insomnia was admitted to Psychiatry department in December, 2013. Hypokalemia and hypomagnesemia were noted. He was diagnosed as schizophrenia-like psychosis. Treatment with paliperidone at the dose of 6 mg/day and magnesium and potassium supplementations was commenced. However, electrolyte disturbances failed to improve following psychosis remission. Therefore, other underlying diseases resulting in electrolyte disturbances were suspected. Along with hypokalemia and hypomagnesemia, additional investigation showing metabolic alkalosis, hypocalciuria, renal loss of potassium, were consistent with GS. Gene analysis revealed this patient carried out c. 2687 G > A homozygous mutation of exon 23 in the SLC12A3 gene which led to p.Arg896Gln. Eventually, GS was identified. Thus, additional spironolactone (40 mg/day) combined with increased doses of oral potassium chloride sustained-release tablets (3.0 g/day) and potassium magnesium aspartate (0.3 g/day) were administered. During next half a year, fatigue resolved, paliperidone gradually tapered and eventually discontinued while psychosis maintained complete remission. His serum potassium was near normal (3.2–3.5 mmol/L), hypomagnesemia significantly improved (0.57–0.67 mmol/L).Discussion and evaluationElectrolyte abnormalities secondary to GS might cause or contribute to development of neuropsychiatric symptoms. In turn, hypokalemia was common among acute psychiatric inpatients. As a consequence, when concomitant with psychosis, GS was readily concealed.Conclusion Electrolyte disturbances are common in acute psychiatric patients. However, when electrolyte disturbances are not improved following psychosis remission, other underlying diseases such as GS should be considered.

Analysis of mutations of two Gitelman syndrome family SLC12A3 genes and proposed treatments using Chinese medicine.

To determine the gene location of two Gitelman syndrome (GS) family SLC12A3 genes and explore treatments using Chinese medicine (CM) prescriptions. In order to locate the two GS mutations, samples were collected from 11 people from two different pedigrees for direct genetic sequencing and comparison of the 26 exons of SLC12A3. Furthermore, the change of serum potassium was monitored throughout the therapy and those two probands undertook a sequential superposition of Western medicine (including potassium, Panangin and potassium-sparing diuretics) with CM prescription based on Buyang Huanwu Decoction () and Sijunzi Decoction (). The treatment included three stages, oral potassium chloride for the first 2 weeks (stage 1), potassium-sparing diuretic and Panangin with potassium chloride for the next 2 weeks (stage 2), CM along with the medicine in stage 2 for the final 2 weeks (stage 3). The three mutations occurring in proband 1 from pedigree I were Thr60Met, 965-1_976del13ins12 (small indels mutation) and Ala122Ala (homozygous silent mutation). Likewise, three mutations, Asn359Lys, Thr382Met and Arg913Gln, appeared in the proband 2 from pedigree II. The serum potassium levels increasing from baseline to sequential stages were 1.63 mmol/L (baseline), 2.5 mmol/L (stage 1), 3.1 mmol/L (stage 2) and 3.9 mmol/L (stage 3) in the proband 1, and 2.8 mmol/L (baseline), 3.1 mmol/L (stage 1), 3.5 mmol/L (stage 2) and 4.3 mmol/L (stage 3) in the proband 2, respectively. The symptoms (numbness of limbs, weakness, palpitations, etc.) of both probands were all alleviated. The mutations of both GS pedigrees can be defined as compound heterozygous mutations, most of which are known as missense mutations. Applying CM could be an appropriate choice for future intervention of GS.

Plasma exchange successfully treats central pontine myelinolysis after acute hypernatremia from intravenous sodium bicarbonate therapy

BackgroundOsmotic demyelination syndrome (ODS) primarily occurs after rapid correction of severe hyponatremia. There are no proven effective therapies for ODS, but we describe the first case showing the successful treatment of central pontine myelinolysis (CPM) by plasma exchange, which occurred after rapid development of hypernatremia from intravenous sodium bicarbonate therapy.Case presentationA 40-year-old woman presented with general weakness, hypokalemia, and metabolic acidosis. The patient was treated with oral and intravenous potassium chloride, along with intravenous sodium bicarbonate. Although her bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed hypernatremia with serum sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing hypernatremia, she exhibited tetraparesis, drooling, difficulty swallowing, and dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of hypernatremia after intravenous sodium bicarbonate therapy and treated her with plasma exchange. After two consecutive plasma exchange sessions, her neurologic symptoms were markedly improved except for mild diplopia. After the plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap metabolic acidosis, low blood bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a sodium bicarbonate loading test and diagnosed distal renal tubular acidosis (RTA). We also found that she had Sjögren’s syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer’s test and a lower lip biopsy. She was discharged and treated as an outpatient with oral sodium bicarbonate and potassium chloride.ConclusionThis case indicates that serum sodium concentrations should be carefully monitored in patients with distal RTA receiving intravenous sodium bicarbonate therapy. We should keep in mind that acute hypernatremia and CPM can be associated with intravenous sodium bicarbonate therapy, and that CPM due to acute hypernatremia may be effectively treated with plasma exchange.

Clinical Profile in Hypokalemic Periodic Paralysis Cases

The present article was aimed to study demographic and clinical pattern, periodicity and precipitating events for hypokalemic paralysis and to assess the response to treatment both during acute attacks and as prophylaxis in comparison with available literature. Forty patients with hypokalemic paralysis were admitted in Narayana Medical College and Hospital during the last two years, in all the medical units and neurology wards. Patients were assessed clinically, with symptomatology and precipitating factors were evaluated. There were total 40 patients in the present study. Younger more including male gender. Mean age was 30.95 years. Common precipitating factor were diarrhea, fever, strenuous activity, following dextrose administration, in patients with diabetic ketoacidosis, however in majority of the cases we could not identify the precipitating factors. Most common electrocardiographic change on ECG was U' wave (36 cases) followed by flat 'T' wave (14 patients) and ECG was normal in 4 patients. Hypokalemic paralysis was predominantly seen in younger males. Vomiting, diarrhea were important precipitating factors. The response to oral potassium chloride supplementation was good as only few patients requiring intravenous potassium chloride. The approach to hypokalemic paralysis patient includes a vigorous search for the underlying etiology and potassium replacement therapy.

Efficacy of oral potassium chloride administration in treating lactating dairy cows with experimentally induced hypokalemia, hypochloremia, and alkalemia

Hypokalemia occurs commonly in lactating dairy cows. The objectives of this study were to determine (1) whether a 24-h oral KCl dose of 0.4g/kg of body weight (BW) was effective and safe in hypokalemic cattle; (2) whether potassium was best administered as 2 large doses or multiple smaller doses over a 24-h period; and (3) the effect of oral KCl administration on plasma Mg concentration and urine Mg excretion in fasted lactating dairy cattle. Plasma K and Cl concentrations were decreased, and blood pH increased, in 15 lactating Holstein-Friesian cows by administering 2 intramuscular (i.m.) 10-mg injections of isoflupredone acetate 24h apart followed by 2 i.m. injections of furosemide (1mg/kg of BW) 8h apart and by decreasing feed intake. Cows were randomly assigned to 1 of 3 treatment groups with 5 cows/group: untreated control (group C); oral administration of KCl at 0.05g/kg of BW 8 times at 3-h intervals (group K3); and oral administration of KCl at 0.2g/kg of BW twice at 12-h intervals (group K12). A 24-h KCl dose rate of 0.4g/kg of BW increased plasma and milk K concentration and plasma Cl concentration, and corrected the metabolic alkalosis and alkalemia, with no clinically significant difference between 2 large doses (group K12) or multiple small doses (group K3) of KCl over 24 h. Oral KCl administration decreased peripheral fat mobilization in cattle with experimentally induced hypokalemia, as measured by changes in plasma nonesterified fatty acid concentration, and slightly augmented the fasting-induced decrease in plasma Mg concentration. Our findings support recommendations for a 24-h oral KCl dose of 0.4g/kg of BW for treating moderately hypokalemic cattle. Additional Mg may need to be administered to inappetant lactating dairy cattle being treated with oral KCl to minimize K-induced decreases in magnesium absorption.

Central pontine and extrapontine myelinolysis secondary to fast correction of severe hyponatremia and hypokalemia in an alcoholic patient

A 59-year-old white alcoholic female was transferred to ER by ambulance at 04:52 a.m. for lethargy, disorientation, weakness, falls, and headache for few days. She was only drinking alcohol for few days but not eating. She had history of hypertension, and she was taking Lorazepam 2 mg thrice daily, Ramipril 2.5 mg once daily and Hydrochlorothiazide 12.5 mg once daily. Her initial vital signs by paramedics revealed BP of 124/56 mmHg, pulse of 75 bpm, and temperature of 36.7 C. Her weight was 60 kg, and her height was 161 cm. Her Glasgow Coma Scale was 13/15. On examination, the patient was confused, only oriented to place and had slurred speech and multiple bruises of different ages. Her pupils were 5 mm, equal and reactive to light. No other significant findings were found. Initial laboratory results are shown in Table 1. Intravenous fluids were started as first line of 1 L of Normal Saline with 40 mEq of KCl at 100 mL/h and second line of 250 mL of Normal Saline with 40 mEq of KCl at 50 mL/h. Head CT scan was negative for acute hemorrhage, infarct, or edema. Thiamine 100 mg IVP was given, and third IV line was then initiated with 1 L of Saline with 40 mEq of KCl at 100 mL/h. Her blood pressure suddenly dropped to 82/44 mmHg, so a bolus of Normal Saline 500 mL was given, and her blood pressure improved to 152/87 mmHg within 15 min. She was transferred to ICU where she additionally received IV magnesium sulfate, oral potassium chloride, and oral sodium phosphate replacements. Serial blood chemistry tests were done, and IV fluid types and rates were adjusted accordingly. During the first day, she excreted a large amount of diluted urine which could be secondary to a quick decrease in serum vasopressin level when her A. G. Tarakji Aleppo University, Aleppo, Syria

Evaluation of Bedoradrine Sulfate (MN-221), a Novel, Highly Selective Beta2-Adrenergic Receptor Agonist for the Treatment of Asthma via Intravenous Infusion

Background. The number of hospitalizations or deaths due to asthma, most of which result from acute exacerbations of asthma, has remained the same for the past 20 years. MN-221 (bedoradrine sulfate) is a novel, highly selective beta2- (β2-) adrenergic agonist administered via intravenous (IV) infusion in development for the treatment for acute exacerbation of asthma. Objectives. Trial MN-221-CL-004 assessed the safety profile and preliminary efficacy of MN-221 in escalating doses in patients with stable mild-to-moderate asthma. Study MN-221-CL-005 assessed the safety profile and preliminary efficacy of MN-221 in patients with stable moderate-to-severe asthma when given as a fixed dose over 1- or 2- hr infusion. Methods. Two randomized, placebo-controlled clinical trials (n = 40) were performed to evaluate the pharmacokinetic (PK) and clinical effects of a novel, highly selective β2-agonist, MN-221, via IV infusion. Safety evaluations included vital signs, adverse events (AEs), clinical laboratory parameters, and electrocardiogram results. Efficacy evaluation included measurement of forced expiratory volume in 1 second (FEV1) and PK parameters were additionally monitored. The study was reviewed and approved by the Institutional Review Board at each site. Results. Adverse effects were mild or moderate and there were no serious AEs or deaths during the studies. The most frequently reported AEs were tremor, hypokalemia, and headache. There were no consistent dose-dependent effects of MN-221 on any safety parameters, with the exception of heart rate, which was not considered to be clinically significant and did not require any treatment. Moderate hypokalemia occurred once in one subject in the MN-221-CL-004 study and twice in one subject in the MN-221-CL-005 study and were transient and returned to normal range following single oral potassium chloride treatments. PK assessments indicated a linear response in MN-221 plasma concentrations for the doses evaluated. Dose escalation results showed that mean changes in FEV1 from pre-infusion were significantly greater than placebo and an overall dose response was statistically significant (p < .0001). Post-infusion FEV1 improvements appeared to plateau at the 30 μg/min dose level despite a higher peak plasma concentration at 60 μg/min. Dose-rate escalation results demonstrated greater mean increases in change in FEV1 compared to the placebo group with the largest increase associated with the higher MN-221 dose rate and peak plasma concentration. Conclusions. The safety profile of MN-221 and evidence of dose- and plasma-concentration-related bronchodilation supports further clinical development and suggests the potential for clinical benefit without increased clinical risk, particularly for patients where inhaled or nebulized therapy is not adequate or possible. Trial registry name and registration number:Name: MN-221-CL-005Number: NCT00679263

Idiopathic thrombocytopenic purpura and hypokalaemic dRTA with compensated haemolysis and striking acanthocytosis in a band 3 (SLC4A1/AE1) A858D homozygote

Dear Editor, The pleiotropic effects of mutations of the band 3 (SCL41/ AE1) gene which result in familial distal renal tubular acidosis (dRTA) and red cell abnormalities are now wellestablished [1]. The occurrence of dRTA and haemolytic anaemia in A858D homozygotes was first reported recently in children from India [2] and Oman [3]. This letter describes certain unusual features in an Omani adolescent A858D homozygote. A 17-year-old Omani Arab youth, son of a consanguineous marriage presented with complaints of bleeding gums and easy bruising for a few weeks. Also, he reported experiencing progressively severe muscle weakness which, after several weeks, culminated in his inability to rise out of bed. He was of normal stature and weight with mild scleral icterus, generalised skin purpura, buccal mucosal petechiae and mild splenomegaly; hypotonia, hyporeflexia and quadriparesis were additional findings. Investigations showed a normal haemoglobin (Hb— 131 g/L), haematocrit (0.39) and white blood cell count, but an increased reticulocyte count (373.5×10/L) and a very low platelet count (6.0×10/L). Freshly drawn blood films revealed polychromasia, a striking predominance of acanthocytes (70–85 %), a moderate number of ovalocytes and a few other poikilocytes (Fig. 1). Ahaptoglobinaemia, unconjugated hyperbilirubinaemia, normal serum immunoglobulins and a negative antiglobulin test provided supportive evidence for a non-immune-compensated haemolysis. The bleeding problem was diagnosed as autoimmune idiopathic thrombocytopenic purpura (ITP) despite negative results of platelet and other relevant autoantibody tests [4]. Associated autoimmune diseases such as SLE and Sjogren's syndrome [5] were ruled out. Quadriparesis was due to hypokalaemia (serum K, 2.5 mmol/L) secondary to complete dRTA characterised essentially by hyperchloraemic acidosis (Cl, 117 mmol/ L), reduced serum HCO3 − (18 mmol/L) concentration and normal values of serum anion gap, blood urea, serum creatinine, arterial blood pH and blood gases, coupled with a positive urine anion gap and a persistent urine pH >6.0; the patient refused a urine acidification test. DNA analysis revealed a homozygous A858D (alanine → aspartic acid) mutation of the SLC41/AE1 gene. Following a 3-week course of oral prednisolone, bleeding symptoms ceased, platelet count was normalised (317×10/ L) and muscle weakness improved considerably on oral potassium chloride, sodium bicarbonate and spironolactone. During the ensuing years, because of poor drug compliance, he was hospitalised several times with hypokalaemic limb pareses (serum K levels varying between 2.0 and 3.1 mmol/L), but his blood counts have remained normal throughout. Ultrasonography later revealed bilateral J. U. Rehman : S. Al Zadjali :N. A. Fawaz : S. Al Kindi Department of Haematology, College of Medicine & Health Sciences, Sultan Qaboos University, PO Box 35, Muscat 123, Sultanate of Oman

Comparison of two ways of oral therapy for hypokalemia

Objective To compare the effect of two ways of oral therapy for mild hypokalemia.Methods We retrospectively analyzed the clinical data of 116 cases treated by oral therapeutics for mild hypokalemia between March 2010 and March 2011.58 cases were treated by potassium chloride sustained-release tablets,the other 58 cases by oral potassium chloride solution.We retested the serum potassium level two days after treatment.Results After treatment,serum potassium level elevated in all the 116 cases compared with baseline.The serum potassium level elevation magnitude in patients who took potassium chloride solution were larger than in patients who took potassium chloride sustained-release tablets,and there was statistically significant difference between the two methods [ (0.492 ± 0.242 ) mmol/L vs (0.219 ± 0.131) mmol/L; t =2.543,P ＜0.05 ].Conclusions For mild hypokalemic patients,oral potassium chloride solution treatment is safe and more effective compared with oral potassium chloride sustained-release tablets. Key words: Nursing; Hypokalemia; Potassium chloride; Oral

Renal tubular dysfunction and lactic acidosis: Questions

A 10-year-old girl presented with a 3-week history of lethargy and weight loss with associated polyuria and polydypsia. There was no significant past medical or family history. On examination she was appropriately grown for age, with no organomegaly or lymphadenopathy, but was noted to be peripherally mottled. Serum electrolyte and venous blood gas levels indicated marked metabolic acidosis (pH 7.29, bicarbonate 12 mmol/L) and hypokalaemia (potassium 1.8 mmol/L). Lactic acid was also elevated (6.4 mmol/L; normal <2 mmol/L). Urinary potassium was 9.9 mmol/L and urinary pH was 6.0 on admission. Calcium, magnesium and phosphate levels were within normal limits, and the results of a full blood examination were normal. She was admitted to the ward and her hypokalaemia corrected using oral supplementation with a mixture of oral potassium chloride and potassium citrate. The serum phosphate decreased to 0.73 mmol/L, requiring supplementation. Glycosuria was noted on dipstick, and there was associated aminoaciduria. The spot calcium:creatinine ratio was elevated at 1.30 mmol/mmol (<0.7 mmol/L). Ultrasound examination identified a right kidney measuring 12.1 cm and a left kidney measuring 13.2 cm, both greater than the 97th centile for age, with preserved corticomedullary differentiation; Doppler waveforms were normal. There was no nephrocalcinosis. Despite appropriate bicarbonate supplementation, the patient remained severely acidotic with bicarbonate levels of between 7 and 13 mmol/L and there was a persistent elevation of lactate of between 5 and 10 mmol/L. The initial diagnosis was considered to be secondary to a combination of proximal renal tubular acidosis with features of distal tubular dysfunction. An underlying mitochondrial disorder was proposed due to the persistently elevated lactic acidosis. Other causes suggested as differential diagnoses of the tubular acidosis, including heavy metal poisoning, were considered but did not explain the persistent lactic acidosis. Initial haematological findings were normal with no associated organomegaly and a malignant cause was thought to be unlikely. Our patient underwent skin, liver and muscle biopsies for the suspected mitochondrial disorder. One month post-initial presentation, our patient progressively developed anaemia with a decrease in haemoglobin from 116 to 75 g/L. The total white cell count was slightly depressed at 3.9×10/L, but the neutrophil and lymphocyte counts were normal at 1.5×10/L and 2.6×10/L, respectively. The platelet count was also within normal range. Bone marrow examination revealed that blasts accounted for 38 % of all nucleated cells and that these had the morphology of The answers to these questions can be found at doi:10.1007/s00467012-2180-2.

Persistent acidosis at presentation in a patient with type 1 diabetes: Concomitant diagnosis of type 1 distal renal tubular acidosis

We present a rare case of a 7-year-old boy who was diagnosed with type 1 diabetes mellitus and type 1 distal renal tubular acidosis concomitantly. The proband presented with history of polyuria, polydipsia and lethargy. He was found to be severely dehydrated. Initial pH value was 7.025 with bicarbonate level of 5.3 mmol/L, and serum glucose of 23 mmol/L. Despite adequate rehydration and insulin therapy (0.1 U/kg/hr), he continued to have persistent metabolic acidosis with normal bicarbonate. Other causes for acidosis were thought off, and with further inquiry, the parents revealed that the father and two other siblings are treated for renal tubular acidosis. Our patient had urine pH of 8, serum potassium 2.9 - 3.7 (3.5 - 5.4 mmol/L), chloride 110 - 116 (98 - 110 mmol/L). The diagnosis of type 1 renal tubular acidosis was made, and the acidosis was corrected with oral sodium bicarbonate and potassium chloride. The patient was discharged on subcutaneous multiple daily insulin injections.

Eplerenone Improved Hypokalemia in a Patient with Gitelman's Syndrome

A 47-year-old woman presented with hypokalemia (2.4 mmol/L). She also had hypomagnesemia, hypocalciuria, and hyperreninemic hyperaldosteronism. Sequence analysis revealed a compound heterozygous mutation, R655C and R955Q, in the SLC12A3 gene. These findings were compatible with Gitelman's syndrome (GS). Eplerenone, a selective aldosterone blocker, in combination with oral potassium chloride improved serum potassium level (3.6 mmol/L) with no apparent adverse effect. Although eplerenone has an advantage over spironolactone for its selective affinity for the aldosterone receptor, the efficacy and safety of eplerenone for GS is little understood. Our observation suggests that eplerenone is a useful treatment option for GS.

Aldosterone Blockade in Diabetic Nephropathy

In the 1950s, electrocortin, as aldosterone was then known,1 was a relatively novel hormone, the importance of which in human pathophysiology was established by reports of cases of aldosterone excess by Conn in 1955.2 Despite more than 50 yr of study, the breadth of many actions of aldosterone continues to unfold in basic, translational, and clinical milieus. From a basic aspect, aldosterone has typical genomic effects. After receptor binding, aldosterone exposure initiates transcriptional processes, which increase protein synthesis in pathways that enhance sodium retrieval from tubular lumens, salivary and sweat glands, and colon. Nongenomic aspects have been reported in which aldosterone infusion reduces the caliber of isolated afferent and efferent arterioles3 through the activation of systems that inhibit endothelial nitric oxide action.4 From a translational aspect, the synthetic pathways detailing aldosterone production offer the opportunity for studying genes such as CYP11B2 , which regulates production of 11β-hydroxylase, a key enzyme in corticosteroid production.5 Population studies of polymorphisms in the CYP11B2 gene suggest that compensation for reduced activity of CYP11B2 , through modest increases in the release of ACTH, results in upregulation of other …

Bartter's Syndrome with Type 2 Diabetes Mellitus

We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patients condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin), oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions.

Syndrome de Gitelman et grossesse: à propos d'un cas et revue de la littérature

Gitelman syndrome (GS) is a tubulopathy characterized by hypokaliemia, hypomagnesiemia, metabolic alkalosis and hypocalciuria. We report a case of a 33-year-old pregnant woman with Gitelman Syndrome. Oral potassium chloride and magnesium citrate were prescribed and the course of the pregnancy was uneventful with vaginal delivery at term. The impact of GS on the physiologic adaptations to pregnancy is not well-known, with few reports to date. Monitoring of serum potassium and magnesium levels with supplementation, amniotic fluid and fetal growth is required to prevent obstetrical and fetal complications in a patient with GS.

Oral Solid Potassium Chloride and Anticholinergic Medications: A New Drug Interaction for an Old Drug?

Oral Solid Potassium Chloride and Anticholinergic Medications: A New Drug Interaction for an Old Drug?

Causes of Hypocitraturia in Recurrent Calcium Stone Formers: Focusing on Urinary Potassium Excretion

Multiple factors associated with hypocitraturia have been identified. However, limited studies addressing the causal relationship to hypocitraturia are available. We therefore conducted this study to determine factors associated with hypocitraturia and show their causal relationship in recurrent calcium stone formers. Dietary review and 24-hour urine samples were obtained from all recurrent calcium stone formers referred for metabolic workup in the stone clinic. One month of oral potassium chloride supplementation was prescribed to stone formers to determine the causal relationship between urinary potassium and citrate levels. Eighty-three subjects, 44 men and 39 women, were recruited to participate in this study. Hypocitraturia (citrate < 300 mg/d [<1.43 mmol/d]) was found in 50.6% of subjects. Four independent urinary variables associated with hypocitraturia were identified, including potassium level, net gastrointestinal alkaline absorption, calcium level, and titratable acid. Urinary potassium level was the strongest predictor of urinary citrate level. Hypocitraturic subjects also had lower fruit intake compared with subjects with high urinary citrate levels. Potassium chloride supplementation to a subgroup of this population (n = 58) resulted in a significant increase in urinary citrate excretion (350.73 +/- 27.25 versus 304.15 +/- 30.00 mg/d [1.67 +/- 0.13 versus 1.45 +/- 0.14 mmol/d]; P < 0.02), but no alteration in fractional excretion of citrate (19.7% +/- 2.7% versus 23.1% +/- 2.4%; P > 0.05). Hypocitraturia was found to be a common risk factor associated with recurrent calcium stone formation and low urinary potassium level, low alkaline absorption, low urinary calcium level, and high titratable acid excretion. Hypocitraturia is predominantly of dietary origin. Estimation of fruit intake should be included in the metabolic evaluation for recurrent calcium stone formation.

Pseudomembranous colitis due to Salmonella enterica serotype infantis

A 75-year-old woman with severe mixed connective tissue disorder and hypertension presented with worsening diarrhea, nausea and vomiting. On admission she complained of 10 - 12 episodes of watery diarrhea which also occurred at night. The patient had suffered from diarrhea for 2 months, and during these last 2 months she had received antibiotic therapy twice, first to treat a pneumonia and then to treat a urinary tract infection. When she first developed diarrhea it was assumed that it was antibiotic-associated and she was given empiric therapy for Clostridium difficile infection. Her diarrhea had improved slightly, but the stool had remained soft until a week prior to the present admission, when worsening watery diarrhea had begun again. The bowel movements were associated with tenesmus but without passage of blood or mucus. The patient was taking the following medications: oral corticosteroids, CellCept, amlodipine, metoprolol, torasemid, and potassium chloride. She was admitted with clinical and laboratory evidence of dehydration. Physical examination was notable for a low-grade fever (37.9 °C). The abdomen was tympanitic, with normal bowel sounds, tenderness to palpation in both lower quadrants, but no rebound pain. Digital rectal examination revealed liquid yellow, guaiac-positive stool. Laboratory values (normal values in parentheses) on admission were notable for white blood cell count of 12 800/ml (4.300 - 10.000/ml), hemoglobin 6.5 g/dl (12.0 - 16.0), albumin 2.3 g/dl (3.5 - 5.5), creatinine 208 µmol/ml (< 120), and C-reactive protein of 230.2 (< 5). Stool studies for ova and parasites, culture and sensitivity, fecal leukocytes, and C. difficile toxin were obtained. Stool tests for C. difficile toxin were negative on three occasions. Colonoscopy revealed multiple pseudomembranes (Figure [1]). These were most prominent in the rectum and sigmoid but extended to the right colon. Histological findings were consistent with pseudomembranous colitis. There were no histologic findings suggestive of inflammatory bowel disease, ischemic colitis or viral infection [1]. Imunohistological stains were negative for cytomegalovirus (CMV). Based on the endoscopic findings, treatment with oral metronidazole was initiated. Immunosuppressive therapy was temporarily discontinued. Despite therapy with metronidazole, the patient had persistent diarrhea. Final stool culture results disclosed Salmonella enterica serotype infantis colitis. Antibiotic therapy was changed to ceftriaxone, after which she showed gradual improvement. Colonoscopy performed 4 weeks later was entirely normal. At follow-up, 4 months later, she did not have any diarrhea. Our case has potential important clinical implications because it demonstrates that pseudomembranous colitis may occur secondary to other micro-organisms besides C. difficile. A C. difficile cytotoxin assay that has 94 % to 100 % sensitivity was negative on these occasions. A review of the literature revealed that there can be other etiologies for pseudomembranous colitis, such as CMV, Shigella, and Plesiomonas shigelloides, as well as ischemia, and medicines such as gold and diclofenac [2] [3] [4] [5]. In a recent endoscopic study, Yuani et al. suggested that pseudomembranes can also be part of the spectrum of collagenous colitis itself [6]. Our case, like others, emphasizes that pseudomembranes may not be pathognomonic for C. difficile colitis. We believe that Salmonella colitis should be added to the list of potential etiologies of pseudomembranous colitis [2] [3] [4] [5]. In summary, in the presence of pseudomembranous colitis and negative C. difficile assays, further investigations should be performed to try to establish an alternative etiology and institute appropriate therapy.

Recurrent paralysis in a young man

A 22-year-old man presented in July, 1997, with 1 day history of weakness of both legs that progressed to involve his arms over a few hours. He was breathless, with no sensory abnormalities or sphincter involvement. He had had more than 200 similar episodes of weakness over the past 9 years, requiring multiple admissions. He had hypokalaemia during at least five admissions. He was diagnosed with hypokalaemic periodic paralysis (HOPP). Every time he became weak he would treat himself with potassium chloride, and the weakness would respond. He denied any precipitating factors. Previously he had been given acetazolamide, but he stopped taking this drug because it increased episodes of weakness. On examination he was drowsy, irritable, cyanosed, with grade 2 motor quadriparesis. Respiratory rate was 56/min with chest expansion of 0·5 cm. There were no signs of meningeal irritation or cranial nerve, sensory, cortical, or sphincter involvement. Full blood count was normal. The serum sodium was 136 mmol/L, potassium 1·8 mmol/L, chloride 112 mmol/L, and bicarbonate 9·2 mmol/L. Arterial blood gas analysis showed pH 7·26, a PaO2 of 23·3 mm Hg with an O2 saturation of 76·9%. Urine pH was 7·0, dipstick was negative for protein and glucose and microscopy was normal. The serum concentrations of urea, creatinine, glucose, uric acid, calcium, phosphate, liver function tests, creatinine kinase, and lactose dehydrogenase were normal. The patient was ventilated and potassium chloride and sodium bicarbonate were given. He had a rapid recovery over the next 24 hours. Urine pH remained alkaline. 24-hour excretion of phosphate, uric acid, and calcium was normal. There was no aminoaciduria or glycosuria. Urinary sodium was 43·2 mmol/L, potassium 32·6 mmol/L, chloride 69 mmol/L. Fractional excretion of bicarbonate at induced serum bicarbonate of 21·2 mmol/L (after a bicarbonate infusion) was 3·2% and U-B pCO2 11·2 mm Hg. Serum and urinary osmolality were normal. Radiographs of the chest, and bones showed osteopenia. Electrocardiogram showed U waves initially which became normal after correction of serum potassium. Radiological examination of the kidneys were normal. Viral serology was negative. Thyroid function was normal. Nerve conduction studies were normal. Electromyography showed a diminution of interference pattern. The patient was discharged on oral sodium bicarbonate and potassium chloride, when his pH was 7·34 with bicarbonate of 19·2 mmol/L. Over the next 2 years, he had only two episodes of weakness, each brought about by discontinuation of the therapy, and both responded to reinstitution of potassium chloride and bicarbonate. A screen of the family members was negative for any acidification defect.

Hypergastrinemia, Dysuria-Hematuria and Metabolic Alkalosis: Complications Associated with Gastrocystoplasty

Purpose To help determine the etiology and most appropriate treatment regimen for hypergastrinemia, dysuria-hematuria and metabolic alkalosis following augmentation gastrocystoplasty. Materials and Methods Two patients who presented with refractory metabolic alkalosis (1 with dysuria-hematuria) underwent extensive laboratory evaluation, complete upper gastrointestinal evaluation and intravesical pH probe placement. Results Both patients eventually required high dose oral potassium chloride supplementation. Bladder mucosal pH was not reflected by buffered urinary pH. Both patients demonstrated significant gastroesophageal reflux and diminished overall gastric acid output. Conclusions Outpatient maintenance on potassium chloride supplementation may be warranted in select patients and appears to be preferable to histamine blockade or omeprazole. Postoperative screening esophagogastroscopy and an additional surgical maneuver might be indicated to prevent possible adverse sequelae of reflux esophagitis. Gastrocystoplasty may be an inappropriate operation in children with renal insufficiency who have not had metabolic acidosis.