Proton pump inhibitors (PPIs) are frequently used medications to treat a wide variety of gastrointestinal conditions. By irreversibly inhibiting the hydrogen-potassium ATPase pump, they remarkably reduce gastric acid secretion. However, chronic PPI intake can result in serious complications, including severe hypomagnesemia. The following case report presents a severe case of refractory PPI-induced hypomagnesemia (PPIH), resistant to continuous oral and intravenous magnesium replacement, in a 70-year-old male patient, with a long history of PPI use due to persistent epigastric pain. Upon each of the 10 admissions to the hospital, he presented with severe signs and symptoms of hypomagnesemia, such as nausea, muscle fasciculation, diffuse cramps, weakness, neuromuscular irritability, and ECG disturbances, including non-specific T-wave abnormalities. In fact, PPIH has been reported for the first time in 2006. It is believed that the excessive, chronic intake of PPIs can disturb the normal functioning of the transient receptor potential melastatin 6/7 (TRPM 6/7), which is the main pathway of active intestinal magnesium absorption, leading to hypomagnesemia. PPIH is typically characterized by stubborn resistance to oral and intravenous magnesium replenishment but usually resolves after PPI withdrawal. Hence, despite being among the safest and most commonly prescribed drugs, PPI intake should be closely monitored when prolonged usage is planned. Additionally, continuous follow-up and regular assessment of serum magnesium levels are crucial to avoid the occurrence of PPIH and to prevent its potentially deleterious complications, including life-threatening arrhythmias.

We present the case of a woman of 50 years of age who experienced widespread bone pain along with digestive symptoms, including nausea and vomiting. She had been prescribed tenofovir disoproxil fumarate (TDF) tablets for the treatment of hepatitis B. Laboratory testing revealed low circulating phosphorus and potassium concentrations and acidosis. A whole-body bone scan revealed abnormal bone metabolism. Rheumatologic and urologic conditions were ruled out, and therefore TDF-induced Fanconi syndrome (FS) and related bone pain was diagnosed. After the TDF was discontinued, the patient\'s symptoms and laboratory indices significantly improved. In this manuscript, we highlight the clinical manifestations of and laboratory test results associated with FS and summarize the cases of TDF-induced FS reported on PubMed between 2013 and 2022 to improve understanding of FS.

Abiraterone, an androgen biosynthesis inhibitor drug approved by the Food and Drug Administration (FDA) in 2011 for the treatment of metastatic prostate cancer, has seen an increase in prescriptions over the years, owing largely to the aging population and the association of prostate cancer with increasing age. As the rate of abiraterone prescription increases, it is important for physicians to be aware of its adverse effects profile to improve patient outcomes. This case report explains the mechanism, clinical presentation, and management of abiraterone-induced hypokalemia in a 67-year-old male with prostate cancer and highlights the importance of close monitoring and management of electrolyte levels for patients on abiraterone.

Children with sellar and/or suprasellar lesions may develop central diabetes insipidus with subsequent inappropriate antidiuretic hormone secretion. An increased incidence of polyuria, natriuresis, and hyponatremia has been reported in some cases, which make up the diagnostic triad of cerebral salt wasting syndrome. Here we report the clinical course of 7 patients with a history of acute central nervous system injury and central diabetes insipidus followed by cerebral salt wasting syndrome. Treatment included the sequential use of parenteral saline solution, oral sodium chloride, desmopressin, mineralocorticoids, and even thiazides. Due to persistent polyuria and hyponatremia, ibuprofen was added. As a result of this sequential therapeutic regimen, daily urine output reduced significantly from 10 mL/kg/h to 2 mL/kg/h over an average period of 5 days, together with a normalization of natremia (from 161 mEq/L to 143 mEq/L) over an average period of 9 days. No treatment-related adverse effects were observed in any case.
Los niños con lesiones selares y/o supraselares pueden presentar diabetes insípida central con posterior secreción inadecuada de hormona antidiurética. Nosotros observamos, en algunos casos, aumento de la incidencia de poliuria, natriuresis e hiponatremia, tríada diagnóstica del síndrome cerebral perdedor de sal. Aquí comunicamos la evolución de 7 pacientes con antecedentes de daño agudo del sistema nervioso central y diabetes insípida central seguida por síndrome cerebral perdedor de sal. Como tratamiento aportamos secuencialmente fluidos salinos parenterales, cloruro de sodio oral, desmopresina, mineralocorticoides e incluso tiazidas. Ante la persistencia de poliuria con hiponatremia, agregamos ibuprofeno. Como resultado de este esquema terapéutico secuencial, este grupo redujo significativamente los valores de diuresis diaria de 10 ml/kg/h a 2 ml/kg/h en un tiempo promedio de 5 días, normalizando también las natremias (de 161 mEq/L a 143 mEq/L) en un tiempo promedio de 9 días. En ningún caso observamos efectos adversos asociados al tratamiento.

Long QT syndrome is a type of disease caused by ion channels in the heart not working properly. It is a rare condition that can affect up to one in 2000 people. Many people with this condition do not develop any symptoms; however, this can lead to heart rhythm abnormality, known as torsades de pointes, and can sometimes be fatal. The cause of this condition is often inherited; however, it can also be triggered by certain medications. But the latter tends to affect those who already tend to develop this condition. The medications causing this condition include antiarrhythmics, antibiotics, antihistamines, antiemetics, antidepressants, antipsychotics, and many more. In this case report, we will be discussing a 63-year-old female who developed long QT syndrome as a result of the multiple drug therapy which is associated with long QT syndrome. Our patient was admitted to the hospital with dyspnoea, fatigue, and weight loss and was diagnosed with acute myeloid leukaemia. The patient was commenced on several medications leading to a prolonged QTc interval which resolved after stopping the culprit medications.

An adenoma is the most typical large bowel tumor found in 30% of all screening colonoscopies. However, it is often asymptomatic but sometimes might lead to abdominal pain or bleeding of the rectum. Critical electrolyte disbalance and acute kidney injury caused by secretory diarrhea is an untypical clinical manifestation of adenoma. It has rarely been reported in the literature and is defined as McKittrick-Wheelock syndrome. A 61-year-old patient was hospitalized for heavy dyselectrolytemia, diarrhea, acute kidney injury, sepsis, and fever. After the renal function was corrected and electrolyte imbalance persisted, visual instrumental diagnostics tests revealed a large tumor in the sigmoid colon. Subsequently, the patient underwent surgical resection, which exhibited evidence of tubulovillous adenoma on pathology. The atypical signs of McKittrick-Wheelock syndrome and comorbidities can make the diagnostics challenging. When severe hyponatremia and hypokalemia are followed by persistent mucous diarrhea, the clinicians should suspect MWS as a possible reason for it.

Porphyria is a challenging metabolic disease due to its heterogeneous presentation symptoms and its difficult diagnosis. Many affected individuals can complain of recurrent neuro-visceral attacks per year, some of which may be persistent and life-threatening, which is confusing if there is no established diagnosis. Although the motor manifestations, autonomic changes and seizure are highly suggestive, the diagnosis is often overlooked and needs confirmatory genetic testing. To the best of our knowledge, the acute intermittent porphyria (AIP) reported in this case, involving severe electrolyte disturbances and rapid severe weakness is a challenging neuro-metabolic case and is extremely rare worldwide. Here, we reported a case of AIP in a young girl who presented to the emergency department of Al-Araby international Hospital, Monufia, Egypt with severe abdominal pain, constipation, and headache which had started 10 days ago. It seems that the diagnosis of porphyria should be considered particularly in those patients with abdominal complaints associated with electrolyte disturbances, seizures, and severe progressive neuropathy.

BACKGROUND: Epidermolysis bullosa is a rare inherited connective tissue disorder compromising cellular junctions. Blister formation is the first manifestation of epidermolysis bullosa. As cellular adhesion is affected, it can affect many organs. Due to compromised skin integrity, water loss and electrolyte imbalances are prevalent in these patients. However, hypernatremia is the usual observed sodium imbalance rather than hyponatremia.
METHODS: The patient was a 48-day-old Iranian male infant born near term. He was diagnosed with epidermolysis bullosa at 1 month of age. The patient was brought to the pediatrics center with apnea and respiratory distress, and was intubated and admitted to the pediatric intensive care unit. His symptoms started 4 days before the admission with vomiting and poor feeding, and the patient later developed loss of consciousness. Vital signs revealed a pulse rate of 154 beats per minute, respiratory rate of 70 per minute, a temporal temperature of 36.5 °C, nondetectable blood pressure, and oxygen saturation of 96%. The patient was anuric at presentation and was rehydrated. Physical examination showed bolus eruptions all over the body but not in mucosal membranes. Important laboratory findings were white blood cell count of 41,000/mm3 with 68% neutrophils, hemoglobin of 10.8 g/dL, platelet count of 856,000/mm2, negative C-reactive protein (CRP), blood sugar of 514 mg/dL, urea of 129 mg/dL, sodium of 98 mg/dL, corrected sodium of 105 mg/dL, potassium of 5.5 mg/dL, serum creatinine of 1.7 mg/dL, and serum procalcitonin of more than 75 ng/mL. Urine analysis revealed many red blood cells. Brain computed tomography demonstrated loss of differentiation between gray and white matter and effacement of cortical sulci suggesting severe cytotoxic edema. We administered 3% hypertonic saline and corrected the plasma sodium levels, and provided the patient with multiple doses of mannitol as well as antibiotics due to the leukocytosis. Subsequently, after 3 days in pediatric intensive care unit, the symptoms of brain edema resolved, and after 4 days, he was weaned from the ventilator and extubated. Later he was discharged from the pediatric intensive care unit.
CONCLUSIONS: This study illustrates the possibility of severe hyponatremia in patients with epidermolysis bullosa to clinicians. Although uncommon, knowledge on such possibilities is vital due to the possible detrimental outcomes for patients.

BACKGROUND: Classic electrocardiographic manifestations of hyperkalemia starting with peaked symmetrical T-waves are widely recognized in daily clinical practice but little evidence is documented how quickly it can evolve in real-time.
METHODS: An elderly diabetic and hypertensive male presented with acute renal failure and rhabdomyolysis. He experienced cardiac arrest with moderate hyperkalemia despite medical treatment and hemodialysis. Telemetry changes were retrospectively studied and found to have significant rhythm changes that occurred just less than 10 minutes prior to the cardiac arrest.
CONCLUSIONS: In hyperkalemia, telemetry rhythm can change instantaneously in a significant way. Rapidly rising potassium could be life threatening and may require more than medical treatment.

Refeeding syndrome can occur in malnourished patients with acute pancreatitis who have electrolyte imbalances. Refeeding syndrome is characterized by severe electrolyte imbalances (mainly hypophosphatemia, hypomagnesemia, and hypokalemia), vitamin deficiency (mainly thiamine deficiency), fluid overload, and salt retention resulting in organ dysfunction and cardiac arrhythmias. We herein report a case involving a patient with severe pancreatitis and gallbladder stones who developed refeeding syndrome with shock and loss of consciousness. The patient was treated by opportune vitamin and electrolyte supplementation therapy and showed substantial improvement after 2 weeks of hospitalization, gaining the ability to eat small bites of solid food orally. Early diagnosis and treatment of refeeding syndrome may reduce morbidity and mortality in patients with acute pancreatitis. Patients should be fasted only if alimentation is contraindicated, and electrolyte values must be closely monitored.