Bartter syndrome-like phenotype in a patient with type 2 diabetes mellitus.

Bartter syndrome (BS) is a rare genetic tubulopathy affecting the loop of Henle leading to salt wasting. It is commonly seen in utero or in the early neonatal period. Rare cases of acquired BS are reported in association with infections like tuberculosis, granulomatous conditions like sarcoidosis, autoimmune diseases and drugs. The mainstay of management includes potassium, calcium and magnesium supplementation. We report the case of a woman in her 50s with a history of type 2 diabetes mellitus for the last 10 years, who presented with diabetic foot ulcers and generalised weakness with ECG changes suggestive of hypokalaemia. She had severe hypokalaemia with high urine potassium excretion and hypochloraemic metabolic alkalosis. She poorly responded to intravenously administered potassium supplements and had persistent hypokalaemia. On further evaluation of the persistent hypokalaemia, a diagnosis of idiopathic Bartter-like phenotype was made. She responded well to tablet indomethacin and is presently asymptomatic and is being maintained on tablet indomethacin after 6 months of follow-up.

Interpreting epigenetic causes of recurrent hypokalemia and seizures: Gitelman syndrome co-exist with pseudohypoparathyroidism type 1B.

We describe a unique case of 27-year-old male with Gitelman syndrome (GS) co-exist with pseudohypoparathyroidism type 1B (PHP1B). The patient presented with a 5-year history of seizures, tetany, and numbness of the extremities. Further examinations showed recurrent hypokalemia, inappropriate kaliuresis, hypocalcemia, hyperphosphatemia, and elevated PTH levels. A novel variant of autosomal recessive GS (p.Val287Met SLC12A3) and a novel 492.3Kb deletion containing the whole of STX16, were discovered by a whole-exome sequencing. Following the diagnosis, calcitriol, calcium, and potassium supplements were started. Hematuria calcium and phosphorus levels, as well as blood potassium levels, have recovered and remained within normal ranges after 3 years of follow-up. Our findings have important consequences for supporting the idea that heterozygosity for variants have effects on the patients' clinical performance with autosomal recessive inheritance disorders. Further study is need for the putative effects of the variant. Likewise, further investigation with regards to the gene-gene interaction relations between GS and other electrolyte imbalance disorders is warranted.

Concomitant hypokalemia and hypocalcemia: a very rare but life-threating combination of reversible causes of cardiac arrest - an unusual first manifestation of coeliac disease.

The causes of cardiac arrest are extremely heterogeneous. Among these, both hypokalemia and hypocalcemia are known reversible factors that can lead to cardiac arrest. In this report, we present a unique case report of a patient with previously undiagnosed coeliac disease who experienced cardiac arrest due a combination of hypokalemia and hypocalcemia resulting from malabsorption. A 66-year-old male presented to the emergency department with symptoms of malaise, weakness, weight loss, and persistent diarrhea. The patient exhibited characteristic signs of hypokalemia and hypocalcemia, including fasciculations, weakness, and swelling. An electrocardiogram showed a normal rhythm, and blood tests confirmed the electrolyte imbalances. Despite initial treatment, the patient experienced sudden cardiac arrest. Prompt resuscitation efforts were successful in restoring spontaneous circulation. However, recurrent episodes of ventricular arrhythmias and cardiac arrest occurred. Large doses of intravenous potassium chloride, in conjunction with magnesium, were needed prior to restore electrolyte balance. The concomitant severe hypocalcemia required caution calcium supplementation, to avoid further decreases in serum potassium levels. Appropriate ion replacements ultimately led to successful resuscitation with good functional recovery. During the hospital stay, the patient was diagnosed with coeliac disease. This case is noteworthy for its uniqueness, as there are no documented instances in the scientific literature linking cardiac arrest directly to coeliac disease. It is important to emphasize the need for investigating potential reversible causes of cardiac arrest, such as hypokalemia and hypocalcemia, and implementing appropriate interventions to address these factors.

The Impact of Obesity on the Resolution of Hypertension Following Adrenalectomy for Primary Hyperaldosteronism.

BACKGROUND: This study aims to determine the impact of patient obesity on the resolution of hypertension and pill burden post-adrenalectomy for PA. Primary hyperaldosteronism (PA) is the most common cause of secondary hypertension that may be remedied with surgery (unilateral adrenalectomy). Obesity may independently cause hypertension through several mechanisms including activation of the renin-angiotensin-aldosterone pathway. The influence of obesity on the efficacy of adrenalectomy in PA has not been established. METHODS: This is a retrospective analysis of prospectively collected data on patients undergoing adrenalectomy for PA at a single, tertiary-care surgical centre from January 2015 to December 2020. Electronic health records of patients were screened to collect relevant data. The primary outcomes of the study include post-operative blood pressure, the reduction in the number of anti-hypertensive medications and potassium supplementation burden post-adrenalectomy. RESULTS: Fifty-three patients were included in the final analysis. There was a significant reduction in the blood pressure and the number of anti-hypertensive medications in all patients after adrenalectomy (p < 0.001). Of the 34 patients (64.2%) with pre-operative hypokalaemia, all became normokalaemic and were able to stop supplementation. However obese patients required more anti-hypertensive medications to achieve an acceptable blood pressure than overweight or normal BMI patients (p < 0.01). Multivariate logistic regression analysis showed that male gender and BMI were independent predictors of resolution of hypertension (p <0.01). CONCLUSION: Unilateral adrenalectomy improves the management of hypertension and hypokalaemia when present in patients with PA. However, obesity has an independent deleterious impact on improvement in blood pressure post-adrenalectomy for PA.

Case report: Gitelman syndrome with diabetes: Confirmed by both hydrochlorothiazide test and genetic testing.

RATIONALE: Gitelman syndrome (GS) is an autosomal recessive tubulopathy caused by mutations of the SLC12A3 gene. It is characterized by hypokalemic metabolic alkalosis, hypomagnesemia and hypocalciuria. Hypokalemia, hypomagnesemia, and increased renin-angiotensin-aldosterone system (RAAS) activity can cause glucose metabolism dysfunction. The diagnosis of GS includes clinical diagnosis, genetic diagnosis and functional diagnosis. The gene diagnosis is the golden criterion while as functional diagnosis is of great value in differential diagnosis. The hydrochlorothiazide (HCT) test is helpful to distinguish GS from batter syndrome, but few cases have been reported to have HCT testing. PATIENT CONCERNS: A 51-year-old Chinese woman presented to emergency department because of intermittent fatigue for more than 10 years. DIAGNOSES: Laboratory test results showed hypokalemia, hypomagnesemia, hypocalciuria and metabolic alkalosis. The HCT test showed no response. Using next-generation and Sanger sequencing, we identified 2 heterozygous missense variants (c.533C > T:p.S178L and c.2582G > A:p.R861H) in the SLC12A3 gene. In addition, the patient was diagnosed with type 2 diabetes mellitus 7 years ago. Based on these findings, the patient was diagnosed with GS with type 2 diabetic mellitus (T2DM). INTERVENTIONS: She was given potassium and magnesium supplements, and dapagliflozin was used to control her blood glucose. OUTCOMES: After treatments, her fatigue symptoms were reduced, blood potassium and magnesium levels were increased, and blood glucose levels were well controlled. LESSONS: When GS is considered in patients with unexplained hypokalemia, the HCT test can be used for differential diagnosis, and genetic testing can be continued to confirm the diagnosis when conditions are available. GS patients often have abnormal glucose metabolism, which is mainly caused by hypokalemia, hypomagnesemia, and secondary activation of RAAS. When a patient is diagnosed with GS and type 2 diabetes, sodium-glucose cotransporter 2 inhibitors (SGLT2i) can be used to control the blood glucose level and assist in raising blood magnesium.

Thyrotoxic periodic paralysis associated with lactic metabolic acidosis: Case report of an African man and review of literature.

BACKGROUND: Thyrotoxic periodic paralysis (TPP) is a rare and most often acquired subtype of hypokalemic periodic paralysis. The association of varying degrees of muscle weakness, hyperthyroidism and hypokalemia characterizes it. The treatment requires potassium supplementation, control of hyperthyroidism and prevention measures. It is a frequent disease in Asian men, but much rare in Caucasian or African populations. This is the first report of TPP associated with lactic metabolic acidosis in an African man. CASE PRESENTATION: A 23 year-old African man, native from Morocco, with recurrent episodes of tetraparesis for eleven months, and abdominal pain, was referred for evaluation. Biochemical investigations showed severe hypokalemia associated with hyperthyroidism and lactic metabolic acidosis. His EKG showed signs of hypokalemia such as sinus tachycardia and U waves. After potassium supplementation, neurological recuperation was quick and complete. Thyroid ultrasound identified a hypoechogenic and hypervascularized goiter, associated with high levels of thyroid antibodies, in favor of Grave's disease. With antithyroid drugs and life-style changes, the patient did not have any other attack. REVIEW OF LITERATURE: In addition to the case report, this article presents an extended review of literature, from the first large study reporting the diagnosis and incidence of TPP in 1957 to nowadays. Are reported here the latest information concerning epidemiology, clinical manifestations, complementary examinations, management and genetic finding. The lactic acidosis observed initially is exceptional, never described in TPP. TPP is a diagnostic and therapeutic emergency, requiring careful potassium supplementation, in order to avoid the risk of the onset of rebound hyperkalemia, to be maintained until the etiological treatment is effective. Paraclinical assessment with emergency EKG and electromyogram are essential to assess the impact. DISCUSSION: It is essential in the face of any hypokalaemic periodic paralysis, including in non-Asian subjects, to search hyperthyroidism. CONCLUSIONS: This report demonstrates the importance of thyroid testing in case of acute muscle weakness, even in non-Asian patients in order to diagnose TPP. This is a rare but possible etiology, to be distinguished from the familial form of hypokalemic periodic paralysis. It also questions on the impact of TPP on energetic metabolism, in particular on lactic metabolism.

[Intraoperative management of potentially fatal arrhythmias after anesthesia induced by severe hypokalemia: A case report].

Severe hypokalemia is defined as the concentration of serum potassium lower than 2.5 mmol/L, which may lead to serious arrhythmias and cause mortality. We report an unusual case of potentially fatal ventricular arrhythmias induced by severe hypokalemia in a patient undergoing laparoscopic partial nephrectomy in Peking University Third Hospital due to irregular use of indapamide before operation. Indapamide is a sulfonamide diuretic with vasodilative and calcium antagonistic effects, which enhances sodium delivery to the renal distal tubules resulting in a dose-related increase in urinary potassium excretion and decreases serum potassium concentrations. The electrolyte disorder caused by the diuretic is more likely to occur in the elderly patients, especially those with malnutrition or long-term fasting. Hence, the serum potassium concentration of the patients under indapamide therapy, especially elderly patients, should be monitored carefully. Meanwhile, the potassium concentration measured by arterial blood gas analysis is different from that measured by venous blood or laboratory test. According to the previous research, the concentration of potassium in venous blood was slightly higher than that in arterial blood, and the difference value was 0.1-0.5 mmol/L. This error should be taken into account when rapid intravenous potassium supplementation or reduction of blood potassium level was carried out clinically. In the correction of severe hypokalemia, the standard approach often did not work well for treating severe hypokalemia. The tailored rapid potassium supplementation strategy shortened the time of hypokalemia and was a safe and better treatment option to remedy life-threatening arrhythmias caused by severe hypokalemia with a high success rate. Through the anesthesia management of this case, we conclude that for the elderly patients who take indapamide or other potassium excretion diuretics, the electrolyte concentration and the general volume state of the patients should be comprehensively measured and fully evaluated before operation. It may be necessary for us to reexamine the serum electrolyte concentration before anesthesia induction on the morning of surgery in patients with the history of hypokalemia. For severe hypokalemia detected after anesthesia, central venous cannulation access for individualized rapid potassium supplementation is an effective approach to reverse the life-threatening arrhythmias caused by severe hypokalemia and ensure the safety of the patients.

Acquired autoimmune Bartter syndrome in a patient with primary hypothyroidism.

We describe an unusual clinical presentation of autoimmune Bartter syndrome in a patient with primary hypothyroidism. A 65-year-old female patient was admitted with neuromuscular weakness associated with hypokalemia and metabolic alkalosis. She had a suboptimal response to potassium supplementation and potassium-sparing diuretic resulting in re-hospitalization with the same symptoms. A detailed serum and urinary biochemistry analysis in the absence of other causes of potassium wasting helped diagnose Bartter syndrome, a rare entity in adults. An autoimmune profile showed anti-Scl-70 antibody to be positive, although she did not develop other systemic features of the disease. Our patient responded to a steroid-based regimen potassium supplement, Indomethacin, and aldosterone antagonist with remarkable resolution of symptoms and correction of electrolyte derangement. We reviewed the literature to search for similar cases and included twenty-seven full-length publications on acquired and autoimmune causes of Bartter syndrome. Our case highlights the fact that hypokalemia with metabolic alkalosis in an adult patient should prompt clinicians to evaluate for common and uncommon conditions. While assessing for abnormal conditions, acquired Bartter syndrome should be considered if a patient has an underlying autoimmune, endocrine, or connective tissue disease.

Hypokalaemia - an active contributor to hepatic encephalopathy?

Patients with cirrhosis are prone to electrolyte disorders, including hypokalaemia. The available evidence suggests that hypokalaemia facilitates hyperammonaemia and thus increases the risk for hepatic encephalopathy (HE). In case studies, plasma potassium decrements were followed by plasma ammonia increments and HE progression, which was reversed by potassium supplementation. The explanation to the hyperammonaemia may be that hypokalaemia both stimulates renal ammonia production and reduces hepatic ammonia elimination by urea synthesis. Further, hypokalaemia eases the entrance of the increased ammonia into the central nervous system because the lower potassium ion concentration favours the competition of NH4+ ions for potassium transporters across the blood brain barrier, and because hypokalaemia-induced metabolic alkalosis increases the amount of gaseous ammonia, which freely passes the barrier. Potassium depletion thus seems to be a mechanistic contributor to HE, supporting the clinical notion of routinely correcting low potassium in patients with cirrhosis.

Intraoperative management of potentially fatal arrhythmias after anesthesia induced by severe hypokalemia: A case report / 北京大学学报(医学版)

Severe hypokalemia is defined as the concentration of serum potassium lower than 2.5 mmol/L, which may lead to serious arrhythmias and cause mortality. We report an unusual case of potentially fatal ventricular arrhythmias induced by severe hypokalemia in a patient undergoing laparoscopic partial nephrectomy in Peking University Third Hospital due to irregular use of indapamide before operation. Indapamide is a sulfonamide diuretic with vasodilative and calcium antagonistic effects, which enhances sodium delivery to the renal distal tubules resulting in a dose-related increase in urinary potassium excretion and decreases serum potassium concentrations. The electrolyte disorder caused by the diuretic is more likely to occur in the elderly patients, especially those with malnutrition or long-term fasting. Hence, the serum potassium concentration of the patients under indapamide therapy, especially elderly patients, should be monitored carefully. Meanwhile, the potassium concentration measured by arterial blood gas analysis is different from that measured by venous blood or laboratory test. According to the previous research, the concentration of potassium in venous blood was slightly higher than that in arterial blood, and the difference value was 0.1-0.5 mmol/L. This error should be taken into account when rapid intravenous potassium supplementation or reduction of blood potassium level was carried out clinically. In the correction of severe hypokalemia, the standard approach often did not work well for treating severe hypokalemia. The tailored rapid potassium supplementation strategy shortened the time of hypokalemia and was a safe and better treatment option to remedy life-threatening arrhythmias caused by severe hypokalemia with a high success rate. Through the anesthesia management of this case, we conclude that for the elderly patients who take indapamide or other potassium excretion diuretics, the electrolyte concentration and the general volume state of the patients should be comprehensively measured and fully evaluated before operation. It may be necessary for us to reexamine the serum electrolyte concentration before anesthesia induction on the morning of surgery in patients with the history of hypokalemia. For severe hypokalemia detected after anesthesia, central venous cannulation access for individualized rapid potassium supplementation is an effective approach to reverse the life-threatening arrhythmias caused by severe hypokalemia and ensure the safety of the patients.

Hypokalemia Related to Distal Renal Tubular Acidosis as an Initial Presentation of Primary Sjogren's Syndrome.

Hypokalemia due to loss of potassium through the kidneys can be caused by distal Renal Tubular Acidosis (dRTA). The etiology of dRTA can be primary due to genetic defects or secondary to autoimmune diseases, especially Sjogren's syndrome (SS). The occurrence of dRTA in SS patients is low, at only 5% of cases. This case was interesting because dRTA was the initial clinical manifestation that led to the diagnosis of SS in the patient. A 48-year-old woman came with complaints of recurrent weakness. The patient was routinely hospitalized with severe hypokalemia and received potassium supplementation. The diagnosis of dRTA was based on repeated weakness, normal blood pressure, severe and recurrent hypokalemia, high urinary potassium, alkaline urine, low plasma bicarbonate, and standard anion gap metabolic acidosis. The diagnosis of SS in this patient was confirmed based on dry eyes, dry mouth, positive Schirmer's test, and positive autoantibodies to SS-A and Ro-52. There was a delay in the diagnosis of SS for two years in this patient because the complaints were initially subtle and non-specific. The hypokalemia in this patient was secondary to dRTA associated with primary SS. The possibility of an underlying autoimmune disorder should be considered in a patient presenting with recurrent severe hypokalemia. dRTA, as the etiology of hypokalemia, can be a gateway to the diagnosis of SS. In this patient, complaints related to dRTA appeared before the onset of sicca symptoms, and the diagnosis of SS was established.

Distal renal tubular acidosis presenting with an acute hypokalemic paralysis in an older child with severe vesicoureteral reflux and syringomyelia: a case report.

BACKGROUND: Distal renal tubular acidosis (dRTA) is the most common type of renal tubular acidosis (RTA) in children. Pediatric dRTA is usually genetic and rarely occurs due to acquired issues such as obstructive uropathies, recurrent urinary tract infections (UTIs), and chronic kidney disease (CKD). Although persistent hypokalemia frequently occurs with dRTA, acute hypokalemic paralysis is not frequently reported, especially in older children. CASE PRESENTATION: An eight-year-old girl presented with an acute first episode of paralysis. A physical examination revealed normal vital signs, short stature consistent with her genetic potential, and decreased muscle strength of her upper and lower extremities. Preexisting conditions included stage 4 CKD due to recurrent UTIs, severe vesicoureteral reflux and bilateral hydronephrosis, neurogenic bladder, and multisegment thoracic syringomyelia. Her laboratory work-up revealed hypokalemic, hyperchloremic metabolic acidosis with a normal anion gap. She also had a urine osmolal gap of 1.9 mOsmol/kg with a high urine pH. Intravenous potassium replacement resulted in a complete resolution of her paralysis. She was diagnosed with dRTA and discharged with oral bicarbonate and slow-release potassium supplementation. CONCLUSIONS: This case report highlights the importance of considering dRTA in the differential diagnosis of hypokalemic acute paralysis in children. Additionally, in children with neurogenic lower urinary tract dysfunction and recurrent UTIs, early diagnosis of spinal cord etiology is crucial to treat promptly, slow the progression of CKD, and prevent long-term complications such as RTA.

Hypokalemic Paresis in a 26-Year-Old Man After Recreational Cannabis Use.

BACKGROUND Hypokalemia (serum potassium level below 3.5 mmol/L) is present in approximately 11% of patients admitted to emergency departments. Hypokalemia can be a manifestation of many underlying causes and if untreated can be fatal. A careful approach to work-up and management is required in hypokalemic patients. CASE REPORT Here we report a 26-year-old previously healthy male patient who was admitted to the Emergency Department with rapidly progressing paresis of the lower and upper extremities. Initial laboratory results revealed severe hypokalemia of 2.1 mmol/l, which aggravated to 1.6 mmol/l before receiving treatment with intravenous potassium chloride supplementation. In addition, the patient developed rhabdomyolysis secondary to prolonged paralysis and immobilization induced by hypokalemia. Following this treatment, the patient's symptoms eased rapidly, and his potassium concentration was normalized. The patient admitted to smoking cannabis the day before admission. In this case report, we systematically elaborate and exclude the causes of hypokalemia in this otherwise healthy young adult, including medication, gastrointestinal symptoms, licorice consumption, and genetical testing. Cannabis has been associated with hypokalemia, proposedly through activation of the cannabinoid receptor 1 (CB1)-mediated activation of G protein-coupled inwardly rectifying potassium (GIRK) channels. CONCLUSIONS This case report emphasizes that hypokalemia can cause paralysis and cannabis should be included in the diagnostic mindset.

Childbirth with epidural analgesia in a pregnant woman with hypokalemic periodic paralysis.

Familial hypokalaemic periodic paralysis (FHPP) is an uncommon genetic disease characterized by muscle weakness associated with hypokalaemia. Episodes are precipitated by drugs, stress, metabolic diseases, hypothermia or infection. We report the case of a 38-year-old pregnant women with FHPP who underwent epidural analgesia for labour. Pregnant women with FHPP require multidisciplinary management involving an anaesthesiologist, a gynaecologist and a paediatrician. It is important to maintain normothermia, prevent hyperventilation, monitor electrolytes, avoid glucose infusions and medications that cause hypokalaemia, and administer potassium supplements when required. Locoregional techniques should be preferred over general anaesthesia. Early epidural analgesia reduces the risk of pain that could trigger an episode of FHPP. In the case of general anaesthesia, drugs that can cause malignant hyperthermia should be avoided, and short-acting non-depolarizing neuromuscular blockers with blockade-depth monitoring should be used.

Hypokalemia-induced rhabdomyolysis as the first symptom of primary aldosteronism: a case report and literature review.

Primary aldosteronism (PA) is a well-documented cause of secondary hypertension, often accompanied by hypokalemia. However, PA with normal blood pressure and hypokalemic rhabdomyolysis (RM) is rare. We report a case of hypokalemia-induced RM as the first symptom of PA. A 65-year-old woman was admitted due to intermittent limb weakness and myalgia. She denied a history of hypertension. Laboratory findings showed profound hypokalemia (1.8 mmol/L) and extreme elevation of creatinine kinase (CK) levels (18,370 U/L), suggestive of hypokalemia-induced RM. She was administered intravenous fluids as well as active oral and intravenous potassium supplements. CK and myoglobin levels gradually decreased, but the serum potassium recovery was poor. Further evaluations strongly suggested PA by an aldosterone-producing adenoma, which was surgically removed. After surgery, the patient recovered well. The systolic blood pressure decreased by approximately 10-20 mmHg and the diastolic blood pressure decreased by approximately 5-10 mmHg. After discontinuation of spironolactone and oral potassium supplementation, the patient had normal serum potassium levels. This case indicates that PA is a cause of hypokalemic RM, even in patients with normal blood pressure. In addition, attention should be paid to changes in serum aminotransferase levels associated with RM. If the patient had no liver disease, it might be a marker for skeletal muscle injury instead of hepatocyte damage.

Diuretic-induced hypokalaemia: an updated review.

Diuretic-induced hypokalaemia is a common and potentially life-threatening adverse drug reaction in clinical practice. Previous studies revealed a prevalence of 7%-56% of hypokalaemia in patients taking thiazide diuretics. The clinical manifestations of hypokalaemia due to diuretics are non-specific, varying from asymptomatic to fatal arrhythmia. Diagnosis of hypokalaemia is based on the level of serum potassium. ECG is useful in identifying the more severe consequences. A high dosage of diuretics and concomitant use of other drugs that increase the risk of potassium depletion or cardiac arrhythmias can increase the risk of cardiovascular events and mortality. Thiazide-induced potassium depletion may cause dysglycaemia. The risk of thiazide-induced hypokalaemia is higher in women and in black people. Reducing diuretic dose and potassium supplementation are the most direct and effective therapies for hypokalaemia. Combining with a potassium-sparing diuretic or blocker of the renin-angiotensin system also reduces the risk of hypokalaemia. Lowering salt intake and increasing intake of vegetables and fruits help to reduce blood pressure as well as prevent hypokalaemia.

Thyrotoxic periodic paralysis in two sexagenarian men: A case report.

RATIONALE: Thyrotoxic periodic paralysis (TPP) characterized by the triad of muscle paralysis, acute hypokalemia, and the presence of hyperthyroidism is often reported in young adults but rarely reported in age >60 year-old. PATIENT CONCERNS: Two sexagenarian males (age 61 and 62) presenting to the emergency department with progressive muscle paralysis for hours. There was symmetrical flaccid paralysis with areflexia of lower extremities. Both of them did not have the obvious precipitating factors and take any drugs. DIAGNOSIS: Their Wayne scores, as an objective index of symptoms and signs associated with thyrotoxicosis, were <19 (7 and 14, respectively). Their blood pressure stood 162/78 and 170/82 mm Hg, respectively. Their thyroid glands were slightly enlarged. Both of them had severe hypokalemia (1.8 and 2.0 mmol/L). Their presumptive diagnosis of mineralocorticoid excess disorders with severe potassium (K+) deficit were made. However, low urine K+ excretion and relatively normal blood acid-base status were suggestive of an intracellular shift of K+ rather than K+ deficit. Hormone studies confirmed hyperthyroidism due to Graves disease. INTERVENTIONS: A smaller dose of K+ supplementation (only a total of 50 and 70 mmol K+, respectively) were prescribed for the patient. OUTCOMES: After treatment, their serum K+ levels became normal with a full recovery of muscle strength. LESSONS: Our 2 cases highlight the fact that thyrotoxic periodic paralysis must be still kept in mind as the underlying cause of hypokalemia with paralysis and hypertension in elderly patients to avoid missing curable disorders.

Association between potassium supplementation and the occurrence of acute kidney injury in patients with hypokalemia administered liposomal amphotericin B: a nationwide observational study.

BACKGROUND: Hypokalemia and acute kidney injury (AKI) occur in patients administered liposomal amphotericin B (L-AMB), a wide-spectrum anti-fungicidal drug. However, the association between potassium supplementation and the occurrence of AKI in patients with hypokalemia who were administered L-AMB is not well understood. METHODS: Using nationwide claims data and laboratory data, the occurrence of AKI during L-AMB treatment was retrospectively compared between patients with hypokalemia who were or were not supplemented with potassium and between those adequately or inadequately supplemented with potassium (serum potassium levels corrected to ≥3.5 mEq/L or remained < 3.5 mEq/L, respectively) before or after L-AMB treatment initiation. RESULTS: We identified 118 patients who developed hypokalemia before L-AMB treatment initiation (43 received potassium supplementation [25 adequate and 18 inadequate supplementation] and 75 did not receive potassium supplementation), and 117 patients who developed hypokalemia after L-AMB initiation (79 received potassium supplementation [including 23 adequate and 15 inadequate supplementation] and 38 did not receive potassium supplementation). The occurrence of any stage of AKI was similar between patients with hypokalemia, regardless of potassium supplementation (i.e., before L-AMB treatment initiation [supplementation, 51%; non-supplementation, 45%; P = 0.570] or after L-AMB initiation [supplementation, 28%; non-supplementation, 32%; P = 0.671]). After adjusting for confounding factors, we found that the occurrence of any stage of AKI was not associated with potassium supplementation before L-AMB initiation (odds ratio [OR]: 1.291, 95% confidence interval [CI]: 0.584-2.852, P = 0.528) or after L-AMB initiation (OR: 0.954, 95% CI: 0.400-2.275, P = 0.915). The occurrence of any stage of AKI tended to decline in patients with hypokalemia who were adequately supplemented with potassium (44%) before, but not after, L-AMB initiation relative to that in patients inadequately supplemented with potassium (61%), however this result was not significant (P = 0.358). CONCLUSION: Potassium supplementation was not associated with any stage of AKI in patients with hypokalemia who were administered L-AMB.

A rare case of ectopic ACTH syndrome with rhabdomyolysis.

BACKGROUND: Manifestations of hypokalaemia in ectopic adrenocorticotropic hormonesyndrome(EAS) vary from mild muscle weakness to life-threatening arrhythmia. Herein, we present a rare case of EAS with concomitant rhabdomyolysis(RM) as a result of intractable hypokalaemia. CASE PRESENTATION: A 64-year-old man was admitted for limb weakness and facial hyperpigmentation for 2 weeks. Lab tests revealed intractable hypokalaemia (lowest at 1.8 mmol/L) and metabolic alkalosis. The diagnosis of RM was based on a creatine kinase(CK)level of 5 times the upper limit. The elevated CK and myohemoglobin (Mb) levels returned to within the normal range after the alleviation of hypokalaemia. The patient was diagnosed with ACTH-dependent Cushing's syndrome (CS) based on unsuppressed serum cortisol after a low-dose dexamethasone suppression test(LDDST) and remarkably elevated ACTH levels. The diagnosis of EAS was made based on the results of a high-dose dexamethasone suppression test(HDDST) and bilateral inferior petrosal sinus sampling(BIPSS). Multiple lymph nodes in the left supraclavicular fossa, right root of neck, mediastinum and bilateral hili of the lung were found with abnormal uptake of 68Ga-DOTA-NOC. Mediastinoscopic lymph node biopsy was performed. The pathological diagnosis was small-cell and large-cell neuroendocrine carcinoma with positive ACTH staining. The patient was prescribed mifepristone and received one cycle of chemotherapy. The patient could not tolerate subsequent chemotherapy and died of dyscrasia. CONCLUSIONS: RM is a rare complication of EAS with insidious onset and atypical clinical manifestations. Serum potassium levels should be vigilantly monitored to avoid RM in EAS.

Low-dose oral propranolol for treatment of thyrotoxic periodic paralysis with hypokalaemia in the emergency department: A case report.

WHAT IS KNOWN AND OBJECTIVE: Thyrotoxic periodic paralysis (TPP) with hypokalaemia is a rare acute phenomenon. Reports of the use of high-dose non-selective ß-blockers describe symptom resolution, but often administration does not occur promptly enough in the treatment course and patients may experience overcorrection and hyperkalaemia. CASE DESCRIPTION: A 37-year-old Hispanic male developed TPP. Patient was successfully treated with low-dose oral propranolol and potassium supplementation with no overcorrection. WHAT IS NEW AND CONCLUSION: Delay in the administration of non-selective ß-blockers may lead to overcorrection of potassium with exogenous supplementation. Low-dose propranolol administered in the Emergency Department was successful in preventing overcorrection of potassium.