Ramen noodle neuropathy: an atypical case of partial paralysis from malnutrition.

INTRODUCTION: Due to a COVID-related job loss resulting in financial and food insecurity, a 28-year-old woman initiated a diet consisting solely of one cup of ramen noodles daily for twenty-two months, leading to 27 kg of weight loss. Ramen noodles are low in calories and lack key nutrients, including potassium, chloride, and vitamin B12. CASE DESCRIPTION: The patient presented to the emergency department with acute, worsening weakness and paresthesias in her left wrist and hand. Exam revealed no other abnormalities aside from a cachectic appearance. Labs revealed marked hypokalemia, hypochloremia, lactic acidosis, a mixed metabolic alkalosis with respiratory acidosis, and low levels of zinc and copper. An EKG revealed a prolonged QT interval. After a neurology and psychiatry consult, the patient was admitted for failure to thrive with malnutrition, peripheral neuropathy, hypokalemia, and an acid-base disorder. An MRI of the brain was unremarkable. Studies of other nutritional deficiencies, autoimmune conditions, and sexually transmitted infections were unremarkable. The patient received food and vitamin supplementation, was monitored for re-feeding syndrome, and had a significant recovery. DISCUSSION: After stroke, spinal injury, multiple sclerosis, and the most common focal mononeuropathies were ruled out, the clinical focus turned to nutritional deficiencies, the most significant of which was hypokalemia. Prior research has shown that severe hypokalemia can lead to weakness. It has also shown that chronically insufficient dietary intake is a common cause of hypokalemia. This case, with its partial paralysis of a unilateral upper extremity, may add to the known clinical manifestations of hypokalemia. We review the role of hypokalemia and hypochloremia in acid-base dynamics. Etiologies and clinical manifestations of cobalamin, thiamine, pyridoxine, and copper deficiencies, along with lead toxicity, are also discussed. Diagnostic clarity of mononeuropathies in the context of malnutrition and hypokalemia can be aided by urine potassium levels prior to repletion, neuroimaging that includes the cervical spine, and follow-up electromyography.

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.

A case report of Gitelman syndrome in children.

RATIONALE: Giltelman syndrome (GS) is an autosomal recessive infectious disease, which is caused by the mutation of SLC12A3 gene encoding thiazide diuretic sensitive sodium chloride cotransporter located in the distal convoluted tubule of the kidney. PATIENT CONCERNS: A 7-year-old and 3-month-old male patient has poor appetite, slow growth in height and body weight since the age of 3, body weight: 16 kg (-3 standard deviation), height: 110 cm (-3 standard deviation), normal exercise ability and intelligence. One year ago, he was diagnosed with hypokalemia. After potassium supplement treatment, the blood potassium returned to normal. The patient developed abdominal pain, vomiting, limb weakness, and tetany 1 day before admission. DIAGNOSES: After admission examination, the patient was found to have hypokalemia (2.27-2.88 mmol/L), hypomagnesemia (0.47 mmol/L), hypophosphatemia (1.17 mmol/L), hypocalcemia (1.06 mmol/24 hours), and metabolic alkalosis (PH 7.60). The blood pressure is normal, and the concentration of aldosterone is 791.63 pg/mL. The adrenocorticotropic hormone and cortisol detected at 8 am are 4.95 pmol/L and 275.09 nmol/L, respectively. Twenty-four hours of urine potassium is 32.52 mmol. Gene sequencing results showed 2 pathogenic variants in the GS-related SLC12A3 gene, which are related to the phenotype of the subject. INTERVENTIONS: After admission, the patients were given potassium and magnesium supplements, as well as oral spironolactone. The symptoms of limb weakness and tetany were significantly relieved. After discharge, the patients continued to maintain treatment to keep the blood potassium at more than 3.0 mmol/L, and the blood magnesium at more than 0.6 mmol/L. OUTCOMES: Follow-up at 1 month after discharge, in the patient's self-description, he had no symptoms such as limb weakness and tetany, and his height was increased by 1 cm and the body weight increased by 1.5 kg. LESSONS: For patients with hypokalemia, hypomagnesemia, and metabolic alkalosis, the possibility of GS should be given priority. After the diagnosed by gene sequencing of SLC12A3 gene, potassium and magnesium supplementation could significantly improve symptoms.

Recurrent hypokalemic paralysis in hypothyroidism.

Hypothyroidism, a commonly encountered thyroid disorder, usually manifests with readily recognizable typical features. However, an unusual presentation of a classic thyroid disorder may hinder accurate diagnosis in certain instances. One such rare initial presentation of hypothyroidism is recurrent hypokalemic paralysis, and existing reports in the literature are sparse. It has been more commonly reported in thyrotoxicosis. We report the case details and clinical outcomes of two middle-aged individuals (a 34-year-old male and a 37-year-old female) with recurrent episodes of hypokalemic paralysis. Their clinical examination revealed pure motor hyporeflexia quadriparesis with hypotonia and diminished deep tendon reflexes without any autonomic dysfunction. They had no significant previous medical history. Biochemical findings revealed hypokalemia in both cases (1.4 and 1.9 mEq/L, respectively) with elevated levels of thyroid­stimulating hormone and thyroid­related antibodies in both individuals, thus, confirming the diagnosis of autoimmune hypothyroidism. Immediate treatment with intravenous and oral potassium correction helped in the recovery. Thyroxine supplementation was considered a follow-up treatment, and for a one-year follow-up period there were no complaints of limb weakness reported in both individual.

Hypokalaemia associated with hydrochlorothiazide used in the treatment of hypertension in NHANES 1999-2018.

Hydrochlorothiazide is the most common thiazide diuretic used for hypertension in the US. Yet, hypokalaemia is a well-recognised adverse effect. To evaluate the prevalence and factors associated with hypokalaemia (serum potassium < 3.5 mmol/L) among hydrochlorothiazide users, we included US adults aged ≥20 years in the 1999-2018 National Health and Nutrition Examination Survey. Participants were categorised according to the use of hydrochlorothiazide and other antihypertensive agents. Factors associated with hypokalaemia, including demographics and prescription patterns (monotherapy vs single-pill fixed-dose combination vs polytherapy) were studied using multivariable logistic regression. Hypokalaemia was present in 12.6% of the hydrochlorothiazide users, equivalent to ~2.0 million US adults. Women (adjusted OR, 2.22; 95% CI, 1.74-2.83), non-Hispanic blacks (adjusted OR, 1.65; 95% CI, 1.31-2.08), underweight (adjusted OR, 4.33; 95% CI, 1.34-13.95), and participants taking hydrochlorothiazide for five years or more (adjusted OR, 1.47; 95% CI, 1.06-2.04) had a higher risk of hypokalaemia. Compared to monotherapy, fixed-dose combination therapy (adjusted OR, 0.32; 95% CI, 0.21-0.48) was associated with the lowest risk. Among those taking potassium supplements, hypokalaemia was found in 27.2% of participants on monotherapy and 17.9% on polytherapy. The prevalence of hypokalaemia among hydrochlorothiazide users was considerable, even among participants who also took potassium supplements. Women, ethnic minorities, underweight, monotherapy, and participants with long-term therapy are more likely to have hypokalaemia. Regular monitoring of potassium and combination with potassium-sparing drugs are needed.

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.

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 Paralysis Due to Primary Sjögren's Syndrome: Case Series.

BACKGROUND: Sjögren's syndrome (SS) is autoimmune disorder charaterized by exocrine glandular involvement and extra-glandular manifestations. Associations between hypokalemic paralysis and SS have not been emphasized enough. Present study evaluates hypokalemic paralysis as presenting feature in PSS. METHODS: A retrospective cross-sectional study from 2015 to 2020 was conducted to evaluate the clinical phenotype of primary Sjögren's syndrome (PSS) who presented to us with hypokalemic paralysis. RESULTS: Data of 13 patients were evaluated. All were female patients and mean age was 38 years. 61.5% (n= 8) had more than one episode of hypokalemic paralysis; 61.5% (n= 8) patients had oral dryness and 69% (n= 9) had dryness of eyes. 23% (n= 3) patients had inflammatory arthritis and 1 patient had Raynaud's phenomenon, myopathy respectively. 1 patient had chronic constipation and hypothyroidism was present in 61.5% (n= 8) patients. Other co-morbidity included hypertension, renal calculi and situs inversus present in 15%, 15% and 7% respectively. The mean ESR at presentation was 64 mm/hr; average serum potassium level was 2.04meq/dl and distal renal tubular acidosis was present in all patients. Paralysis was completely recovered in all patients after supplementation with potassium. CONCLUSION: The renal involvement in PSS can uncommonly present as hypokalemic paralysis in the absence of significant sicca symptoms or may precede sicca symptoms. A high index of suspicion for PSS should be kept in all patients with hypokalemic paralysis. This phenotype may represent a distinct subset. Serum electrolytes should be regularly monitored in all patients with SS.

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.

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.

Caffeine-induced hypokalemia: a case report.

BACKGROUND: With an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia. CASE PRESENTATION: A 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6-2.9 mmol/L) and low urine osmolality (100-130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized. CONCLUSIONS: An increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

Diagnosis and outpatient management of Gitelman syndrome from the first trimester of pregnancy.

A 32-year-old woman presented with an incidental finding of hypokalaemia on routine bloods at 9 weeks of a second pregnancy, on a background of lifelong salt craving. Her previous pregnancy was uncomplicated. She had no previous significant medical or family history. Venous blood gases showed a hypokalaemic, normochloraemic metabolic alkalosis. Urinary potassium was elevated. Escalating doses of oral supplementation of potassium, magnesium, sodium and potassium-sparing diuretics were required through the course of pregnancy, in response to regular electrolyte monitoring. These were later weaned and completely stopped post partum. Delivery was uneventful with no maternal or neonatal complications. Genetic testing performed post partum showed heterogenous mutation of SCL12A3 gene.

Hypokalaemic paralysis and metabolic alkalosis in a patient with Sjögren syndrome: a case report and literature review.

BACKGROUND: Acquired Gitelman syndrome is a very rare disorder reported in association with autoimmune disorders, mostly Sjögren syndrome. It is characterized by the presence of hypokalaemic metabolic alkalosis, hypocalciuria, hypomagnesaemia and hyper-reninaemia, in the absence of typical genetic mutations associated with inherited Gitelman syndrome. CASE PRESENTATION: A 20 year old woman who was previously diagnosed with primary Sjögren syndrome and autoimmune thyroiditis presented with two week history of lower limb weakness and salt craving. Examination revealed upper limb and lower limb muscle weakness with muscle power of 3/5 on MRC scale and diminished deep tendon reflexes. On evaluation, she had hypokalaemia with high trans-tubular potassium gradient, metabolic alkalosis and hypocalciuria, features suggestive of Gitelman syndrome. New onset hypokalaemic alkalosis in a previously normokalaemic patient with Sjögren syndrome strongly favored a diagnosis of acquired Gitelman syndrome. Daily potassium supplementation and spironolactone resulted in complete clinical recovery. CONCLUSIONS: Acquired Gitelman syndrome associated with Sjögren syndrome is rare. It should be considered as a differential diagnosis during evaluation of acute paralysis and hypokalaemic metabolic alkalosis in patients with autoimmune disorders, especially Sjögren syndrome.

Acute Trimethyltin Poisoning Caused by Exposure to Polyvinyl Chloride Production: 8 Cases.

This manuscript aimed to describe and analyze acute trimethyltin poisoning caused by exposure to polyvinyl chloride production and review the literature. Combined with an analysis of occupational hygiene survey data, the clinical data of 8 cases of acute trimethyltin poisoning were analyzed retrospectively. The clinical manifestations of acute trimethyltin poisoning are mainly related to central nervous system damage, hypokalemia and metabolic acidosis in patients with severe poisoning. Early positive potassium supplementation and symptomatic treatment are beneficial to the improvement of the condition. The early recognition of central nervous system manifestations and hypokalemia is beneficial for early diagnosis and correct treatment.

Distal Renal Tubular Acidosis due to Primary Sjögren's Syndrome: Presents as Hypoakalemic Paralysis with Hypokalemia-Induced Nephrogenic Diabetes Insipidus.

Classic distal renal tubular acidosis (dRTA) is characterized by inability to acidify the urine maximally (to

Distal renal tubular acidosis and nephrocalcinosis as initial manifestation of primary sjögren's syndrome.

There is a well-established association between primary Sjögren's syndrome and distal renal tubular acidosis (dRTA). dRTA is a relatively infrequent manifestation of primary Sjögren's syndrome which can present with life-threatening electrolyte abnormalities while, in some patients, it could be the first manifestation of the syndrome. We report the case of a 35-year-old woman who presented with unexplained episodes of generalized weakness, severe hypokalemia, nephrocalcinosis, and normal anion gap metabolic acidosis. Subsequent evaluation revealed primary Sjögren's syndrome as her underlying condition. The patient responded well to potassium supplementation, sodium bicarbonate, and oral prednisolone. After four years of follow-up, there were no other extraglandular manifestations, the renal function remained stable and the acidosis was partially improved without the need for oral bicarbonate. This case demonstrates that dRTA could be the initial manifestation of primary Sjögren's syndrome and highlights the necessity for increased vigilance for patients presenting with persistent hypokalemia or nephrocalcinosis so that an early diagnosis can be made allowing for better control and prevention of disease progression.

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.

Geriatric Patients Are at a High Risk of Hypokalemia Associated with Yokukansan Preparation: A Retrospective Cohort Study.

Although hypokalemia is an adverse effect of Yokukansan preparation, especially in geriatric patients, its association with age is unclear. We investigated whether age is a risk factor for hypokalemia. This single-center retrospective cohort study, conducted at Tokyo Women's Medical University, Medical Center East between June 2015 and May 2019, included patients who received the Yokukansan preparation. The primary outcome was hypokalemia (serum potassium level: < 3.0 mEq/L). A multivariate Cox proportional hazard model was used to determine risk factors, hazard ratio (HR) and 95% confidence interval (95% CI). The cut-off age was also examined. Of 665 patients (median age: 78 years; interquartile range: 68-84 years), 55 (8.3%) developed hypokalemia associated with Yokukansan preparation. Risk factors for hypokalemia were age (HR: 1.013, 95% CI: 1.006-1.021, p < 0.001), dementia (HR: 0.500, 95% CI: 0.357-0.682, p < 0.001), serum albumin level (HR: 0.754, 95% CI: 0.669-0.850, p < 0.001), and daily Yokukansan preparation dose ≥ 7.5 g (HR: 1.446, 95% CI: 1.144-1.850, p = 0.002). The cut-off ages were >75 and >80 years but not 65 years and >70 years. Clinicians should assess risk factors and monitor serum potassium levels to avoid hypokalemia associated with the Yokukansan preparation.

Ectopic ACTH syndrome of different origin-Diagnostic approach and clinical outcome. Experience of one Clinical Centre.

PURPOSE: Ectopic Cushing Syndrome (EAS) is a rare condition responsible for about 5-20% of all Cushing syndrome cases. It increases the mortality of affected patients thus finding and removal of the ACTH-producing source allows for curing or reduction of symptoms and serum cortisol levels. The aim of this study is to present a 20-year experience in the diagnosis and clinical course of patients with EAS in a single Clinical Centre in Southern Poland as well as a comparison of clinical course and outcomes depending on the source of ectopic ACTH production-especially neuroendocrine tumors with other neoplasms. METHODS: Twenty-four patients were involved in the clinical study with EAS diagnosed at the Department of Endocrinology between years 2000 and 2018. The diagnosis of EAS was based on the clinical presentation, hypercortisolemia with high ACTH levels, high dose dexamethasone suppression test and/or corticotropin-releasing hormone tests. To find the source of ACTH various imaging studies were performed. RESULTS: Half of the patients were diagnosed with neuroendocrine tumors, whereby muscle weakness was the leading symptom. Typical cushingoid appearance was seen in merely a few patients, and weight loss was more common than weight gain. Patients with neuroendocrine tumors had significantly higher midnight cortisol levels than the rest of the group. Among patients with infections, we observed a significantly higher concentrations of cortisol 2400 levels in gastroenteropancreatic neuroendocrine tumors. Chromogranin A correlated significantly with potassium in patients with neuroendocrine tumors and there was a significant correlation between ACTH level and severity of hypokalemia. CONCLUSION: EAS is not common, but if it occurs it increases the mortality of patients; therefore, it should be taken into consideration in the case of coexistence of severe hypokalemia with hypertension and muscle weakness, especially when weight loss occurs. Because the diagnosis of gastroenteropancreatic neuroendocrine tumor worsens the prognosis-special attention should be paid to these patients.