Electrolyte Abnormalities Research Articles

8104 Rare Case Of Ectopic Cushing’s Syndrome Secondary To Metastatic Parotid Pleomorphic Adenocarcinoma

Abstract Disclosure: B.S. Neutel: None. P. Manroa: None. Background: Pleomorphic adenocarcinoma of the parotid gland is a rare malignancy and ectopic ACTH secretion from these tumors is very rarely described. We report a case of ectopic Cushing’s syndrome (CS) in such a patient and describe the clinical course. Clinical Case: A 69-year-old female with left parotid pleomorphic adenocarcinoma status post surgery and adjuvant radiotherapy presented to her local hospital approximately 7 months after initial treatment with proximal muscle weakness and near-syncope. Workup revealed profound hypokalemia at 1.6 mmol/L (n 3.5-5.3 mmol/L) along with new-onset hypertension (BP 175/110 mm Hg) and hyperglycemia with a HbA1c 6.5 % (n <5.7%), as well as metabolic alkalosis with a bicarbonate level of >40 mmol/L (n 22-32 mmol/L). A CT scan showed multiple liver metastases and a biopsy confirmed metastatic parotid pleomorphic adenocarcinoma. She was then transferred to our comprehensive cancer center for further management. She reported muscle weakness, easy bruising, and facial edema. She denied acne, hirsutism, or abdominal striae. Endocrine workup revealed a random cortisol of 56 mcg/dL (n 3-18 mcg/dL) and ACTH of 378 pg/mL (n 7.2-63.3 pg/mL). Her AM cortisol level remained unsuppressed at 79.2 and 59.4 mcg/dL (n< 1.8 mcg/dL) after 1 mg and 8 mg overnight dexamethasone suppression tests respectively. Late-night salivary cortisol was 7.9 mcg/dL (n <0.112 mcg/dL). An MRI of the sella was negative for any pituitary lesions. After stabilizing her clinical condition and correcting electrolyte abnormalities, she was started on chemotherapy with paclitaxel and carboplatin by the oncologist. Based on clinical suspicion of ectopic CS, ketoconazole was started and titrated upwards with rapid improvement of blood pressure, hypokalemia, and hyperglycemia. She was discharged home and antihypertensives were tapered off. ACTH staining on the liver biopsy was unable to be performed due to paucity of the specimen. A Ga-68-DOTATATE PET CT revealed increased radiotracer uptake in the liver lesion suggestive of SSTR 2 receptor positivity. Despite initial clinical improvement, her disease progressed with widespread liver, lymph node, and osseous metastases within 3 months necessitating escalating doses of ketoconazole, spironolactone, and potassium supplementation. The patient elected to pursue hospice care due to intolerance to chemotherapy and passed away shortly afterward. Conclusion: Although ectopic CS caused by parotid pleomorphic adenocarcinoma is rare, prompt recognition and treatment is necessary because ectopic ACTH production is associated with poor prognosis in these patients. Presentation: 6/3/2024

7203 A case of undifferentiated shock found to be due to voriconazole-related primary adrenal insufficiency

Abstract Disclosure: K.X. Zhang: None. C. Bergwitz: None. Primary adrenal insufficiency can be a rare effect observed with azole antifungal therapy, classically ketoconazole, via inhibition of cortisol and aldosterone synthesis. Whether primary AI can be observed with newer triazole drugs used for neutropenic prophylaxis and treating invasive fungal infections is far less understood. We describe a case of a 65-year-old man with medical history notable for COPD and gout, who was on voriconazole for Aspergillus pneumonia, and admitted to the medical ICU with confusion and undifferentiated shock. His potassium was 6.5 mmol/L, sodium 133 mmol/L, bicarbonate 18 mmol/L, and blood pressure 72/63 requiring pressor support. Voriconazole was withdrawn. He also had a fever to 101.7F that was attributed to a gout flare, and he received a course of high dose prednisone. His shock and electrolyte abnormalities quickly resolved, and he was discharged on isavuconazole. At the 1 week mark, he was found to have a morning cortisol 2.3 ug/dL, potassium 5.4 mmol/L, and sodium 134 mmol/L, along with fatigue, nausea, and hypotension, which prompted resumption of steroid and mineralocorticoid replacement. One month after completing his course of isavuconazole, morning cortisol normalized to 11.0 ug/dL and ACTH 22.3 pg/mL. We present a convincing clinical story supporting the etiology of this patient’s initial shock as primary adrenal insufficiency related to a voriconazole effect. This case illustrates how iatrogenic AI can be a missed diagnosis in the emergency room setting. Primary AI has classically been reported following ketoconazole therapy, but there are only 4 reports of primary AI involving the newer triazole posaconazole, and none for voriconazole or isavuconazole. Due to the rarity of this effect, AI due to voriconazole was not on the initial shock differential and timely endocrine labs to seal the diagnosis (morning cortisol, ACTH, and renin/aldosterone levels) were not obtained. If our patient had not received steroids serendipitously for gout, he may have been at risk for adrenal crisis. Whereas central AI is more common and induced by chronic use of systemic steroids, it is important to also think about AI caused by antifungal therapy with newer azoles. Presentation: 6/3/2024

8690 Severe Hypocalcemia Following Treatment with Venetoclax for AML

Abstract Disclosure: K. Ruddiman: None. C. Price: None. Background: Venetoclax is a chemotherapeutic agent which has known side effects of tumor lysis syndrome, but few reports of isolated hypocalcemia. Clinical case: A 73 year old male with medical history pertinent for myeloproliferative and myelodysplastic disease was admitted for evaluation of failure to thrive. Workup revealed progression to acute myeloid leukemia. Following treatment with decitabine 34mg/day for 5 doses and initiation of venetoclax 100mg daily, he developed progressive, severe, symptomatic hypocalcemia with positive Trousseau and Chvostek sign. The patient was normocalcemic prior to admission with serum calcium ranging between 8.6-9.7mg/dL. Corrected calcium at admission was 8.8mg/dL. Serum calcium decreased steadily following venetoclax, requiring repletion with 3 doses of calcium chloride and gluconate 1gm IV and initiation of oral calcium carbonate 1900mg TID. At its nadir, corrected calcium was 6.1mg/dL on day 19 of treatment with venetoclax despite oral and IV repletion. Further workup showed undetectable 25 hydroxy vitamin D, PTH 62pg/mL, normal range uric acid, low phosphorus (lowest 2.2mg/dL), mild hypokalemia (lowest 3.2mg/dL), and mild hypomagnesemia of 1.8mg/dL. GFR was >90mL/min. Hypocalcemia improved after 3 infusions of calcium gluconate 10gm IV in 1 L normal saline to 7.2mg/dL. Oral repletion with calcium carbonate was transitioned to calcium citrate due to concomitant PPI use. PO calcium citrate titrated to 2850 mg TID to target corrected calcium 7.5 - 8.5 and limit further need for diuresis following calcium gluconate infusions. Ergocalciferol 50,000 IU was given thrice weekly in addition to daily cholecalciferol 5,000 IU with improvement in 25 hydroxy vitamin D to 17ng/mL. This patient was suspected to have multifactorial etiology for hypocalcemia, secondary to undetectable 25 hydroxy vitamin D as well as diuresis with furosemide during the admission, but the most strongly attributed factor was initiation of venetoclax prior to development of progressive hypocalcemia. FDA prescribing information reports hypocalcemia as a side effect of venetoclax when used in treatment for CML, but in phase 2 and 3 studies of venetoclax used alone and in combination with low dose cytarabine to treat AML, no significant episodes of hypocalcemia were reported. Tumor lysis syndrome (TLS) is a known adverse effect of venetoclax in which hypocalcemia is an expected feature, however, this patient did not have laboratory to support this diagnosis. His other electrolyte deficiencies were mild and transient. Conclusion: While electrolyte abnormalities associated with TLS are an expected side effect of venetoclax, isolated severe hypocalcemia is a rarely reported side effect. Calcium should be closely monitored during treatment. Presentation: 6/1/2024

Adverse outcomes and mortality in individuals with eating disorder-related electrolyte abnormalities in Ontario, Canada: a population-based cohort study

Individuals with eating disorders are at a higher risk of electrolyte abnormalities than the general population. We conducted the first representative cohort study assessing whether electrolyte abnormalities in people with eating disorders were associated with mortality and physical health outcomes. This was a retrospective population-based cohort study in Ontario including people aged 13 years or older with an eating disorder and an outpatient electrolyte measure within 1 year (between Jan 1, 2008 and June 30, 2019). An electrolyte abnormality was any of hypokalaemia, hyperkalaemia, hyponatraemia, hypernatraemia, hypomagnesaemia, hypophosphataemia, metabolic acidosis, or metabolic alkalosis. The primary outcome was all-cause mortality. Secondary outcomes were hospitalisation, a cardiac event, infection, acute or chronic kidney disease, fracture, and bowel obstruction. In additional analyses, we examined a younger cohort (<25 years old) and individuals with no previously diagnosed secondary outcome. We involved people with related lived or family experience in the study. 6163 patients with an eating disorder and an electrolyte measure within 1 year since diagnosis (mean age 26·8 years [SD 17·5]; 5456 [88·5%] female, 707 [11·5%] male; median follow-up 6·4 years [IQR 4-9]) were included. Ethnicity data were not available. The most common electrolyte abnormalities were hypokalaemia (994/1987 [50·0%]), hyponatraemia (752/1987 [37·8%]), and hypernatraemia (420/1987 [21·1%]). Overall, mortality occurred in 311/1987 (15·7%) of those with an electrolyte abnormality versus 234/4176 (5·6%) in those without (absolute risk difference 10·1%; adjusted hazard ratio 1·23 [95% CI 1·03-1·48]). Hospitalisation (1202/1987 [60·5%] vs 1979/4176 [47·4%]; 1·35 [1·25-1·46]), acute kidney injury (206/1987 [10·4%] vs 124/4176 [3%]; 1·91 [1·50-2·43]), chronic kidney disease (245/1987 [12·3%] vs 181/4176 [4·3%]; 1·44 [1·17-1·77]), bone fracture (140/1987 [7·0%] vs 167/4176 [4·0%]; 1·40 [1·10-1·78]), and bowel obstruction (72/1987 [3·6%] vs 57/4176 [1·4%]; 1·62 [1·12-2·35]) were associated with an electrolyte abnormality, but not infection or a cardiovascular event. Findings were consistent in young individuals (<25 years old) and those without secondary outcomes at baseline, by eating disorder type, and by sex. Electrolyte abnormalities are associated with death and poor physical health outcomes, supporting the importance of monitoring and possible interventions to prevent adverse outcomes. Findings also call for a refinement of the definition of severity of eating disorder and replication of these findings in other jurisdictions. None.

Metolazone Versus Chlorothiazide in Acute Heart Failure Patients With Diuretic Resistance and Renal Dysfunction: A Retrospective Cohort Study.

Guidelines recommend intravenous loop diuretics as first-line therapy for patients hospitalized with acute heart failure (AHF) and volume overload. Additional agents can be used for augmentation, but there is limited guidance on agent selection. The study objective was to determine if chlorothiazide or metolazone is associated with differences in diuretic efficacy or safety in loop diuretic-resistant patients with AHF and renal dysfunction (eGFR <45 mL/min/1.73 m²). We conducted a multicenter, retrospective cohort study of patients hospitalized with AHF and renal dysfunction who received metolazone or chlorothiazide in addition to intravenous loop diuretics. The primary end point was a comparison of 24-hour urine output (UOP) between the 24 hours before and after thiazide administration. Secondary and safety end points included weight change, requirement for vasopressors or inotropes, electrolyte abnormalities, and changes in renal function. A total of 221 patients were included. The mean daily diuretic doses were chlorothiazide 632 mg and metolazone 7 mg. The mean 24-hour UOP increased more among chlorothiazide-treated (from 1668 mL to 3826 mL) versus metolazone-treated patients (from 1672 mL to 2834 mL) ( P < 0.001) after the addition of the second diuretic. Statistically significant reductions in serum creatinine were observed in the chlorothiazide group following 72 hours of treatment ( P = 0.016). More hypomagnesemia was observed in the chlorothiazide group; no differences in other electrolytes or changes in weight were observed. Overall, chlorothiazide was associated with a greater increase in 24-hour UOP than metolazone without an excess of potassium or serum creatinine derangements. However, weight changes did not differ significantly between groups. Future prospective studies are needed to confirm potential differences in diuretic response and safety.

Development of deep learning algorithm for detecting dyskalemia based on electrocardiogram

Dyskalemia is a common electrolyte abnormality. Since dyskalemia can cause fatal arrhythmias and cardiac arrest in severe cases, it is crucial to monitor serum potassium (K+) levels on time. We developed deep learning models to detect hyperkalemia (K+ ≥ 5.5 mEq/L) and hypokalemia (K+ < 3.5 mEq/L) from electrocardiograms (ECGs), which are noninvasive and can be quickly measured. The retrospective cohort study was conducted at two hospitals from 2006 to 2020. The training set, validation set, internal testing cohort, and external validation cohort comprised 310,449, 15,828, 23,849, and 130,415 ECG-K+ samples, respectively. Deep learning models demonstrated high diagnostic performance in detecting hyperkalemia (AUROC 0.929, 0.912, 0.887 with sensitivity 0.926, 0.924, 0.907 and specificity 0.706, 0.676, 0.635 for 12-lead, limb-lead, lead I ECGs) and hypokalemia (AUROC 0.925, 0.896, 0.885 with sensitivity 0.912, 0.896, 0.904 and specificity 0.790, 0.734, 0.694) in the internal testing cohort. The group predicted to be positive by the hyperkalemia model showed a lower 30-day survival rate compared to the negative group (p < 0.001), supporting the clinical efficacy of the model. We also compared the importance of ECG segments (P, QRS, and T) on dyskalemia prediction of the model for interpretability. By applying these models in clinical practice, it will be possible to diagnose dyskalemia simply and quickly, thereby contributing to the improvement of patient outcomes.

STUDY OF SERUM SODIUM LEVELS AND ITS CLINICAL SIGNIFICANCE IN DECOMPENSATED CHRONIC LIVER DISEASE PATIENTS ADMITTED IN A TERTIARY CARE CENTRE OF NORTH EASTERN STATE, TRIPURA

Introduction: Chronic Liver Disease is a major source of death and morbidity globally. Hyponatremia is one of the most common electrolyte abnormalities in chronic liver disease patients. Various studies have established a correlation between serum sodium levels and survival in these patients. Hyponatremia is a marker of severity in CLD patients and studies have shown its relationship with MELD score and Child Pugh score. The complications of DCLD and mortality also increases with hyponatremia. The aim of this study was to study the serum sodium levels in patients with DCLD and to establish its significance. Materials And Methods: Data was collected from 100 patients admitted in medical wards. Patients were divided into 3 groups based on serum sodium levels and the relevant parameters analyzed among the groups. OBSERVATIONS: Among 100 patients, 45 had serum sodium levels ≥136 mEq/L, while 32 had serum sodium levels between 131 and 135 mEq/L and 23 patients had serum sodium level ≤130. No patients had serum sodium levels greater than 145. Serum sodium levels were associated strongly with the severity of liver disease as assessed by Child Pugh and MELD scores. Serum sodium ≤130 indicated the existence of Hepatic Encephalopathy, Hepatorenal Syndrome and Spontaneous Bacterial Peritonitis. Patients with serum sodium less than 130 mEq/L had increased frequency of complications than those with ≥136 mEq/L. Patient with serum sodium levels ≤130 had increased mortality. Conclusion: Hyponatremia is more common in DCLD and low serum sodium levels are associated with increased frequency of complications such as hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis and GI bleeding. Lower serum sodium levels were associated with increased MELD and Child Pugh score and mortality indicating the inverse relationship between serum sodium levels and severity of the disease.

Prevalence and Patterns of Electrolyte Imbalance in Children Diagnosed with Acute Severe Malnutrition at a Nutritional Stabilization Center

Malnutrition accounts for around 35% of all fatalities in Pakistan among children under five, making it the primary cause of childhood mortality in that country. The most severe type of malnutrition, known as severe acute malnutrition (SAM), was frequently linked to electrolyte abnormalities. The purpose of this study was to ascertain how frequently electrolyte imbalance occurred in children with SAM who were admitted to a tertiary care facility. Objective: To Determine the Prevalence and Patterns of Electrolyte Imbalance in Children Diagnosed with Acute Severe Malnutrition at a Nutritional Stabilization Center”. Methods: A cross-sectional study was carried out in Nawabshah at the Department of Pediatrics, Peoples University of Medical and Health Sciences, from May 16 to August 15, 2024. This study comprised 92 patients with severe acute malnutrition, ranging in age from 2 to 60 months. Non purposive sampling technique was used for data collection. Children with secondary causes of wasting were excluded, including those with congenital heart disease, chronic renal or liver illness, TB, cancer, and hemolytic anaemia. Weight-for-height was calculated using measurements of weight, length, and height. When the weight-for-height ratio fell below the -3 standard deviation (SD), children were diagnosed with SAM. The lab received blood samples that were taken for serum electrolytes. The chi-square test was used for stratification, and descriptive statistics were computed. Results: Participants' average ages ranged from 23.63± 12.71 months. A total of 85 (93.4%) of the 92 SAM patients had an electrolyte imbalance. The prevalence of hypokalemia (70.08%), hypocalcemia (56.52%), hyponatremia (32.60%), and hypomagnesemia (28.26%), respectively. Conclusions: Children with SAM experience dyselectrolytemia both with and without problems. In all cases of SAM, serum electrolyte levels may need to be assessed in order to identify hyponatremia and hypokalemia in the absence of symptoms. This will facilitate the inpatient treatment triage process for patients with asymptomatic hyponatremia and hypokalemia.

Exploring Acute Diarrhea in Infants: A Comprehensive Review of Infectious Agents and Laboratory Diagnostic Techniques

Introduction: acute diarrhea is one of the main causes of mortality in children under 5 years of age around the world. They disproportionately affect underdeveloped countries, where access to health services, drinking water and sanitation is limited. Objective: this review identifies the most relevant and recent studies associated with the topic, recognizes the most common infectious agents and determines the laboratory techniques used for their diagnosis. Methods: the literature was reviewed from sources such as Elsevier, PubMed, Scopus, SciELO and Google Scholar during the period March-May 2024, published in the last 5 years and several studies prior to 2019 that contributed relevant information to the topic. Results: previous studies reveal that acute childhood diarrhea is mainly characterized by its fecal-oral transmission, caused by Rotavirus and Adenovirus, and sometimes by Escherichia coli, Salmonella spp., Giardia lamblia and Entamoeba histolytica, among others. Acute diarrhea is characterized by the presence of three or more soft or liquid stools per day, and is classified according to its duration. Fecal increase, dehydration and electrolyte abnormalities are associated complications and constitute clinically useful elements for its diagnosis. For viruses, rapid tests and PCR are used, for bacteria, cultures and antibiograms, and for parasites, coproparasites, ELISA and PCR. Conclusion: These disorders represent a significant health challenge, with a considerable impact on morbidity and mortality, originating from viruses, bacteria and parasites. The diagnosis is made through physical, coprological examinations, immunochromatographic and molecular tests

Deciphering Familiar Conundrum of Cerebral Salt Wasting Syndrome vs Syndrome of Inappropriate Secretion of Antidiuretic Hormone and Establishing Role of Hyponatremia in Patients of Tuberculous Meningitis as a Predictor of Outcome.

Introduction: Hyponatremia is one of the most common electrolyte abnormalities [35-71%] associated with tuberculous meningitis [TBM]. It is an independent predictor of patient outcome. Cerebral salt wasting syndrome [CSWS] and syndrome of inappropriate secretion of antidiuretic hormones [SIADH] are two common causes of hyponatremia in patients with TBM. This study targets patients with tuberculous meningitis to provide a detailed analysis of hyponatremia in TBM patients and it’s predictive value in terms of outcome and also describes the distinguishing features of CSWS and SIADH. Materials and methods: This was a clinical, prospective study of 31 patients with TBM in which various parameters were analysed . Serial sodium levels were recorded on the day of admission, day 2, 7 and 28. Patients with hyponatremia were divided into CSWS and SIADH. Results: In this study, 24[77.42%] patients had hyponatremia. In 14 [58%], hyponatremia was due to CSWS and in 10[42%] of the patients with hyponatremia it was SIADH. Hyponatremia was related to disease severity, GCS score, hospital stay, ventilator stay and patient outcome. CSWS was more strongly associated with disease severity than SIADH. Conclusion: Hyponatremia is a common electrolyte imbalance in patients with TBM and a direct and valid predictor of disease outcome. CSWS should be differentiated from SIADH due to the different treatment strategies.

Exacerbation of Hepatic Damage in Endothelial Aquaporin 1 Transgenic Mice after Experimental Heatstroke.

Heatstroke induces fluid loss and electrolyte abnormalities owing to high ambient temperature (AT) and relative humidity (RH). Aquaporin 1 (AQP1) is a key protein for water homeostasis; however, its role in heatstroke remains unclear. This study examines endothelial AQP1 in Tie2-Cre/LNL-AQP1 double transgenic (dTG) mice with upregulated Aqp1 in endothelial cells. For experimental heatstroke, mice were exposed to 41 °C AT and >99% RH. Blood, brain, kidney, and liver samples were collected 24 h later. Blood was analyzed for electrolytes and tissue damage markers, and organs were examined using morphological and immunohistological staining for 3-nitrotyrosine (3-NT), AQP1, and Iba-1. No difference in Aqp1 expression was observed in the whole brain; however, it was detected in dTG mice after capillary deprivation. AQP1 immunostaining revealed immunoreaction in blood vessels. After heat exposure, wild-type and dTG mice showed electrolyte abnormalities compared with non-heatstroke wild-type mice. Hepatic damage markers were significantly higher in dTG mice than in wild-type mice. Hematoxylin-eosin staining and 3-NT immunoreactivity in the liver indicated hepatic damage. The number of Iba-1-positive cells adherent to hepatic vasculature was significantly higher in dTG mice than in wild-type mice. This study is the first to suggest that endothelial AQP1 contributes to hepatic damage after heatstroke.

Blood pressure alteration associated with abnormal body electrolyte and water balance in colitis mice.

Previous studies reported that there is an association between abnormal body fluid balance and prognosis in colitis patients. However, it remains to be clarified the effects of colitis on characteristics of body electrolytes or water content, including alternation in blood pressure. In this study, we examined the effects of colon injury on body water balance and blood pressure in the dextran sodium sulfate (DSS)-induced colitis mouse model. We evaluated body electrolytes and water content, blood pressure, and urea-associated water conservation in DSS mice. By 5 days after the treatment, DSS mice exhibited diarrhea but relatively maintained body weight and total body sodium, potassium, and water content by increases in water intake and hepatic ureagenesis. On 7 days after DSS treatment, when colitis becomes severe, DSS mice significantly decreased food and water intake, and body weight but significantly increased relative total body sodium, potassium, and water content per dry mass. Notably, DSS induced more total body dry mass loss relative to water loss. These body electrolytes and water accumulation on day 7 were associated with a reduction in urinary osmole excretion and urine volume accompanied by renal urea accumulation. DSS mice significantly increased blood pressure by day 5 and then decreased on day 7. These findings suggest that body electrolyte and fluid imbalance and alternations in blood pressure in colitis vary with the stage and severity of the condition. Assessment and correction of electrolyte and water content at the tissue level would be important to improve the prognosis of colitis.

Clinical examination findings and electrolyte abnormalities of dogs with marijuana/tetrahydrocannabinol toxicity: 223 cases (January 2017-July 2021).

The goal of this study was to describe the historical, physical, neurologic, and clinicopathologic findings in dogs with a definitive diagnosis of marijuana/tetrahydrocannabinol toxicity. A total of 223 dogs with known ingestion of marijuana or a positive tetrahydrocannabinol result on human urine multidrug test. Retrospective study from January 2017 to July 2021. Median age was 1 year (1 month to 12 years). A common history was becoming acutely neurologic after going outside or to a public place (62/223 [27.8%]). Most owners denied possibility of exposure (152/223 [68%]). Median vitals were normal, but hyperthermia (38/212 [22.6%]), tachycardia (82/222 [37%]), and systemic hypertension (37/61 [60.7%]) were common abnormalities. The most common clinical signs included ataxia (197/223 [88.3%]), hyperesthesia (168/223 [75.3%]), urinary incontinence (102/223 [45.7%]), lethargy (140/223 [62.5%]), and vomiting (58/223 [26%]). The most common combinations of neurologic signs included ataxia and hyperesthesia (157/223 [70.4%]) and ataxia, hyperesthesia, and urinary incontinence (81/223 [36.3%]). Mild hyperkalemia (39/76 [51.3%]) and mild hypercalcemia (53/67 [79.1%]) were common. Twenty-two dogs were hospitalized. Survival was 100%. A common presentation for marijuana toxicosis included young dogs with acute ataxia and hyperesthesia, with and without urinary incontinence, after going outside or to a public place. Vitals were often normal, but hyperthermia, tachycardia, and hypertension were common. Bloodwork was mostly normal, but mild hyperkalemia and mild ionized hypercalcemia were common. Marijuana should be high on the differential list with these history, physical examination, neurologic, and electrolyte abnormalities, regardless of owner denial or negative human urine multidrug test.

Failure to Thrive, Metabolic Acidosis, and Diarrhea in a 7-Week-Old Infant.

A 7-week-old infant presented to the emergency department with fussiness, decreased oral intake, loose stool, and respiratory distress for 2 days. The patient was born full-term with an uncomplicated birth history but had a history of slow weight gain. He was alert, but toxic-appearing at presentation, hypothermic with signs of dehydration, and with respiratory failure. He was found to have severe anion gap metabolic acidosis, hypokalemia, elevated lactate, and hyperammonemia. He responded well to initial resuscitation and was admitted to the ICU for intravenous electrolyte replacement, bowel rest, and respiratory support. A workup was pursued for failure to thrive with severe malnutrition, hyperammonemia, hyperlactatemia, anemia, vitamin D deficiency, and electrolyte abnormalities. After stabilization, he was restarted on enteral feeds and had a recurrence of loose stool and severe electrolyte abnormalities, which were refractory to enteral supplementations and required readmission to the ICU. His hospital course extended several weeks, included several subspecialty consultations, and ended with a surprising diagnosis of exclusion based on his clinical response to therapy.

Retrospective Outcomes Comparison by Treatment Location for Pediatric Mild and Moderate Diabetic Ketoacidosis.

Pediatric diabetic ketoacidosis (DKA) is often treated in a PICU, but nonsevere DKA may not necessitate PICU admission. At our institution, nonsevere DKA was treated on the floor until policy change shifted care to the PICU. We describe outcomes in pediatric mild to moderate DKA by treatment location. Patients aged 2 to 21 with mild to moderate DKA (pH <7.3 but >7.1), treated on the floor from January 1, 2018 to July 31, 2020 and PICU from August 1, 2020 to October 1, 2022 were included. We performed a single-center, retrospective cohort study; primary outcome was DKA duration (from emergency department diagnosis to resolution), secondary outcomes included hospital length of stay, and complication rates, based on treatment location. Seventy nine floor and 65 PICU encounters for mild to moderate pediatric DKA were analyzed. There were no differences in demographics, initial pH, or bicarbonate; PICU patients had more acute kidney injury on admission. Floor patients had a shorter DKA duration (10 hours [interquartile range 7-13] vs 11 hours [9-15]; P = .04), and a shorter median length of stay (median 43.5 hours [interquartile range 31-62] vs 49 hours [32-100]; P < .01). No patients had clinical signs of cerebral edema; other complications occurred at similar rates. PICU patients received significantly more intravenous electrolyte boluses, but there were no differences in dysrhythmia or electrolyte abnormalities on final serum chemistry. Our study did not find a clear benefit to admitting patients with mild to moderate DKA to the PICU instead of the hospital floor. Our findings suggest that some children with nonsevere DKA may be treated safely in a non-PICU setting.

Genotype-phenotype correlations in children with Gitelman syndrome.

This study aimed to analyze genotype-phenotype correlations in children with Gitelman syndrome (GS). This multicenter retrospective study included 50 Korean children diagnosed with SLC12A3 variants in one or both alleles and the typical laboratory findings of GS. Genetic testing was performed using the Sanger sequencing except for one patient. The median age at the diagnosis was 10.5years (interquartile range, 6.8;14.1), and 41 patients were followed up for a median duration of 5.4years (interquartile range, 4.1;9.6). A total of 30 different SLC12A3 variants were identified. Of the patients, 34 (68%) had biallelic variants, and 16 (32%) had monoallelic variants on examination. Among the patients with biallelic variants, those (n=12) with the truncating variants in one or both alleles had lower serum chloride levels (92.2±3.2 vs. 96.5±3.8mMol/L, P=0.002) at onset, as well as lower serum potassium levels (3.0±0.4 vs. 3.4±0.3mMol/L, P=0.016), and lower serum chloride levels (96.1±1.9 vs. 98.3±3.0mMol/L, P=0.049) during follow-up than those without truncating variants (n=22). Patients with monoallelic variants on examination showed similar phenotypes and treatment responsiveness to those with biallelic variants. Patients with GS who had truncating variants in one or both alleles had more severe electrolyte abnormalities than those without truncating variants. Patients with GS who had monoallelic SLC12A3 variants on examination had almost the same phenotypes, response to treatment, and long-term prognosis as those with biallelic variants.

Cost analysis of patiromer vs sodium zirconium cyclosilicate for the treatment of hyperkalemia in Spain and the UK

Background Hyperkalemia is an electrolyte abnormality with potentially life-threatening consequences. Published data have shown that potassium-binding polymer patiromer (Veltassa) is associated with reduced rates of severe edema and hospitalization for heart failure compared with sodium zirconium cyclosilicate (SZC, Lokelma) when treating hyperkalemia. The aim of this study was to evaluate the possible costs associated with these interventions in the Spanish and UK settings. Methods A cost-analysis model was developed in Microsoft Excel to compare the costs associated with patiromer and SZC for the management of hyperkalemia. Clinical event rates were taken from a published real-world comparative study, with the base case capturing the statistically significant reduction in severe edema with patiromer vs SZC and a sensitivity analysis also including the non-statistically significant reduction in hospitalization for heart failure. Country-specific costs, expressed in 2022 Euros (EUR) and British pounds sterling (GBP), were evaluated from a healthcare payer perspective and included pharmacy costs and costs of clinical events. Results Patiromer may be associated with cost savings of EUR 107 and GBP 630 per patient-year of treatment vs SZC in Spain and the UK, respectively. The majority of cost savings were due to the possible lower daily cost of patiromer compared with SZC. Including the difference in heart failure hospitalization rates in a sensitivity analysis led to greater cost savings with patiromer over SZC, increasing to EUR 460 and GBP 902 in Spain and the UK, respectively. Extrapolation of patient-level economic outcomes to a population level found that patiromer was associated with annual cost savings of EUR 30.6 million in Spain, and GBP 801.7 million in the UK vs SZC. Conclusions Patiromer has the potential to be cost saving vs SZC for the treatment of hyperkalemia in Spain and the UK based on the results of a real-world evidence analysis.

A case of Fanconi syndrome that developed following a year of consumption of a red yeast rice supplement.

Although some dietary supplements have been reported to cause renal dysfunction, there have been few reports of supplement-induced Fanconi syndrome. We present the case of a 56-year-old woman with Fanconi syndrome that developed after she consumed a red yeast rice supplement. She was referred to our hospital because of renal dysfunction, and was found to have electrolyte abnormalities, including hypophosphatemia and hypouricemia, renal diabetes, and hyperchloremic metabolic acidosis, and was, therefore, diagnosed with Fanconi syndrome. Renal biopsy revealed proximal tubular injury characterized by severely degenerated tubular epithelial cells as well as mild hypocellular fibrosis. We speculated that the red yeast rice supplement, which the patient had been consuming for approximately 1year, might be a cause of her syndrome, because reports of renal dysfunction associated with the consumption of red yeast rice supplements have emerged in Japan since 2024. After the supplement was discontinued and oral prednisolone treatment was initiated, the patient's renal function improved and her electrolyte abnormalities were ameliorated. Furthermore, even after tapering off and discontinuing the prednisolone over approximately 12weeks, her renal function remained. Because Fanconi syndrome may be caused by various exogenous substances, the taking of a thorough medical history is crucial, including with respect to the use not only of prescription medications, but also other substances, including supplements.

Hepatic cholera: a case report with literature review

BackgroundVasoactive intestinal peptide-secreting tumors (VIPomas), also known as WDHA syndrome (or “pancreatic cholera”), are rare neuroendocrine tumors (NETs) with an incidence of 0.05 to 2%. It secretes excessive amounts of VIP, leading to watery diarrhea, hypokalemia, and hypochlorhydria. In adults, they occur most commonly between the ages of 30 and 50 years and are mostly intrapancreatic, occurring in the tail of the pancreas, and rarely located in other segments of the gastrointestinal tract, such as the adrenal glands (35%), paraspinal retroperitoneal ganglia (30–35%), posterior mediastinum (20%), head and neck (1–5%), pelvis (2–3%), and rarely (1%) thymus, lung, kidney, anterior mediastinum, and liver.Case presentationOur patient, a 22-year-old man, was admitted with recurrent episodes of large-volume chronic watery diarrhea, generalized muscle weakness, and significant weight loss. After a complete workup, a solitary primary hepatic VIPoma was diagnosed. The patient underwent surgical resection of the liver lesion. Following surgery, there was immediate regression of diarrhea and electrolyte abnormalities, with no recurrence at the 1-year follow-up.ConclusionNeuroendocrine tumors, particularly VIPomas, are rare and mostly intrapancreatic. Solitary primary hepatic VIPoma is extremely rare, and to the best of our knowledge, only four cases without any evidence of a pancreatic lesion have been reported. Diagnosis remains challenging, as it is often not detected on conventional imaging. The prognosis mostly depends on tumor grade, stage, and surgical resectability.

Elucidating hematological profile and electrolyte balance in oral cancer patients.

Oral cancer is a serious health issue in both the developing and developed worlds, and it is one of the most common forms of cancer of the head and neck. In accordance with the 2017 World Health Organization classification, oral cancer can affect any part of the mouth, including the buccal mucosa, the front two-thirds of the tongue, the lip, the palate, the vestibule, the alveolus, the floor of the mouth, and the gingivae. Hematology and electrolyte balance have been proposed as tumor indicators and paths into cancer's genesis. Examining the patient's blood count and electrolyte levels in order to better understand their oral cancer. Electrolyte abnormalities are common in cancer patients and may be caused by the disease itself or by treatment. Hyponatremia is the most frequent electrolyte problem in cancer patients, and it is typically caused by the syndrome of improper ADH secretion. Although electrolyte problems are associated with a worse prognosis for cancer patients, timely and effective therapy has the potential to enhance both short- and long-term results and quality of life. Hematological tests on patients with oral cancer, including differential cell count, white blood cell count, and hemoglobin level. Compared to healthy controls, oral cancer patients show statistically significant differences in a number of biochemical parameters, including electrolytes (sodium, P<0.05; potassium, P=0.89; chloride, P<0.05); differential count (neutrophils, P<0.05; basophils, P<0.05). A significant risk factor for cancer patients is an electrolyte imbalance, which has been linked to inappropriate anti-diabetic hormone release. Clinicians will find these shifts in electrolytic level helpful in diagnosing and tracking oral cancer. Potentially malignant oral disorders and Oral squamous cell carcinoma may be better predicted using a combination of TLC, neutrophil, and lymphocyte counts, as shown in this study.