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Journal of Medical Case Reports Feb 2024Hydroxychloroquine and azathioprine have been routinely used to control and treat primary and secondary Sjögren's syndrome, which potentially triggered some overdoses...
INTRODUCTION
Hydroxychloroquine and azathioprine have been routinely used to control and treat primary and secondary Sjögren's syndrome, which potentially triggered some overdoses by these drugs. Toxicity from hydroxychloroquine and azathioprine manifests in the form of cardiac conduction abnormalities, nausea, vomiting, and muscle weakness. Recognizing these unique drug overdoses and management of these toxicities is important. This case report aims to expand our current understanding of these drug overdoses and their management and also underscores the importance of anticipating and identifying fewer common complications, such as hypocalcemia.
CASE REPORT
A 34-year-old Persian woman with a history of Sjögren's syndrome presented to the emergency department 3.5-4 hours after an intentional overdose of hydroxychloroquine and azathioprine and severe hypotension and loss of consciousness. Although the patient was regularly taking other medications, such as fluoxetine, naproxen, and prednisolone, she explicitly clarified that these were not the substances involved in her overdose. Early investigations showed hypokalemia (2.4 mEq/L), hypocalcemia (7.5 mg/dL), and hypoglycemia (65 mg/dL). She was also diagnosed with metabolic acidosis and respiratory alkalosis. The electrocardiogram showed changes in favor of hypokalemia; other lab tests were run on the patient. Supportive treatments were applied, including rapid intravenous fluid dextrose 5%, normal saline, potassium chloride 30 mEq, and calcium gluconate 100 mg. The patient was managed and monitored overnight in the emergency room and recovered without residual side effects.
CONCLUSION
Hydroxychloroquine and azathioprine toxicity are considered rare, but it is likely to increase in frequency given the prevalence and increase in autoimmune diseases and the increasing usage of these drugs in treating such diseases. We found hypocalcemia as the presentation to this patient, which needs further investigation into the probable mechanism. Clinicians need to consider the unique effects of hydroxychloroquine and azathioprine poisoning and initiate appropriate emergency interventions to improve the outcomes in similar patients.
Topics: Female; Humans; Adult; Hydroxychloroquine; Azathioprine; Hypocalcemia; Sjogren's Syndrome; Hypokalemia; Drug Overdose; Drug-Related Side Effects and Adverse Reactions
PubMed: 38409169
DOI: 10.1186/s13256-024-04390-w -
Case Reports in Endocrinology 2024The triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with ingesting high doses of calcium and absorbable bases characterizes the...
INTRODUCTION
The triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with ingesting high doses of calcium and absorbable bases characterizes the calcium-alkali syndrome. . We report the case of a patient with postthyroidectomy hypoparathyroidism 15 years ago due to differentiated thyroid cancer who presented with severe hypercalcemia. He had adequate control of calcemia for many years on treatment with calcitriol and calcium carbonate and hypertension treated with amlodipine, losartan, and hydrochlorothiazide. After a period of loss to follow-up, he suddenly presents with severe hypercalcemia, metabolic alkalosis, and loss of renal function. Upon hydration and withdrawal of calcitriol and calcium replacements, hypercalcemia resolved. The etiological investigation identified no granulomatous or neoplastic diseases, but an aldosterone-producing adrenal incidentaloma was found. The cause of hypercalcemia in this patient was calcium-alkali syndrome due to calcium carbonate replacement potentiated by hydrochlorothiazide and primary aldosteronism. Six months after the hospitalization and suspension of calcium and vitamin D, the patient returned to hypocalcemia, reinforcing the diagnosis.
CONCLUSION
Although seldom described, the calcium-alkali syndrome is an expected complication for individuals with postoperative hypoparathyroidism, as they require lifelong calcium and vitamin D supplementation. This case also shows the importance of hydrochlorothiazide use and primary aldosteronism as possible triggers of life-threatening hypercalcemia.
PubMed: 38404648
DOI: 10.1155/2024/3067354 -
Gastric outlet obstruction due to an intragastric balloon in a patient returning from the Caribbean.Clinical Case Reports Feb 2024Gastric outlet obstruction can be a dangerous complication of intragastric balloons, as it can result in severe metabolic alkalosis. As weight loss procedures and...
KEY CLINICAL MESSAGE
Gastric outlet obstruction can be a dangerous complication of intragastric balloons, as it can result in severe metabolic alkalosis. As weight loss procedures and medical tourism become more popular, physicians should have a high index of suspicion for complications of invasive procedures, particularly in returning travelers.
ABSTRACT
Intragastric balloons for weight loss have decreased in frequency in the United States. However, they are still frequent in low- and middle-income countries. Severe complications occur in less than 3% of patients who undergo this procedure. Herein, we present a case of gastric outlet obstruction, severe metabolic alkalosis, and refeeding syndrome in a patient returning from the Dominican Republic. She presented with 2 weeks of emesis and obstipation, followed by a pre-syncope and altered mental status. An intragastric mass was observed on computerized tomography, which was characterized as an intragastric balloon and retrieved endoscopically. All metabolic derangements were corrected, and the patient improved without sequelae. As weight loss procedures and medical tourism become more popular, physicians should have a high index of suspicion for complications of invasive procedures, particularly in returning travelers.
PubMed: 38333653
DOI: 10.1002/ccr3.8509 -
Radiology Case Reports Apr 2024Typhoid fever, caused by Salmonella Typhi, is a severe bacterial infection prevalent in developing countries, and can result in life-threatening complications if...
Typhoid fever, caused by Salmonella Typhi, is a severe bacterial infection prevalent in developing countries, and can result in life-threatening complications if untreated. Nutcracker Syndrome is a rare vascular disorder involving compression of the left renal vein between the aorta and the superior mesenteric artery. It can lead to various symptoms and poses diagnostic and management challenges. We present a case study of a patient diagnosed with typhoid fever in a Unit of Critical Emergency Care. Coincidentally, the evaluation through CT-scan revealed the presence of Nutcracker Syndrome. This report underscores the incidental discovery of Nutcracker Syndrome during the assessment of a patient with typhoid fever in a critical emergency care setting.
PubMed: 38327558
DOI: 10.1016/j.radcr.2024.01.034 -
Cureus Jan 2024Abiraterone acetate causes an adrenocorticotropic hormone (ACTH)-mediated mineralocorticoid excess. We present a 77-year-old man with prostate adenocarcinoma who...
Abiraterone acetate causes an adrenocorticotropic hormone (ACTH)-mediated mineralocorticoid excess. We present a 77-year-old man with prostate adenocarcinoma who developed signs and symptoms of mineralocorticoid excess while on abiraterone and discuss its pathophysiology and treatment options. The patient developed hypokalemia, metabolic alkalosis, and hypertension, indicative of increased mineralocorticoid activity, confirmed by elevated ACTH, corticosterone, and deoxycorticosterone levels. Abiraterone inhibits cytochrome P450c17 (CYP17A1), thus inhibiting testosterone and cortisol synthesis. Diminished cortisol synthesis, in turn, leads to excessive mineralocorticoid precursor production mediated by ACTH, leading to enhanced sodium absorption and potassium excretion. Abiraterone is often prescribed with low-dose prednisone to suppress ACTH; however, this strategy may not provide physiological glucocorticoid levels, resulting in ACTH-mediated mineralocorticoid excess in some patients. High-dose steroids or mineralocorticoid antagonists may activate mutant androgen receptors in prostate cancer tissue; therefore, amiloride is suggested for managing residual mineralocorticoid activity. This case highlights the importance of being vigilant for the signs and symptoms of mineralocorticoid excess in patients on abiraterone.
PubMed: 38318572
DOI: 10.7759/cureus.51757 -
CEN Case Reports Feb 2024Gitelman syndrome is a rare, autosomal recessively inherited tubulopathy manifesting with hypokalemia, hypomagnesemia, hypocalciuria, and metabolic alkalosis. Common...
Gitelman syndrome is a rare, autosomal recessively inherited tubulopathy manifesting with hypokalemia, hypomagnesemia, hypocalciuria, and metabolic alkalosis. Common symptoms include fatigue, myalgia, reduced performance capacity, tetany, paresthesia, and delayed growth. However, as reported in the literature, diagnosis in some patients is prompted by an incidental finding of hypokalemia. GS develops due to mutations in the SLC12A3 gene, which encodes the thiazide-sensitive Na-Cl cotransporter. Many variants in the SLC12A3 gene causing GS have been reported in literature. A new pathogenic homozygous mutation (c.2612G > T), absence of hypomagnesemia, and accompanying autoimmune thyroiditis are remarkable in our patient. There are a few Gitelman syndrome cases that are complicated with autoimmune thyroiditis in the literature. In this study, we present a case of Gitelman syndrome with a novel homozygous mutation and accompanying autoimmune thyroiditis and review of the literature.
PubMed: 38308744
DOI: 10.1007/s13730-023-00845-z -
CEN Case Reports Feb 2024Pseudo-Bartter/Gitelman syndrome (PBS/PGS) is a disorder that presents with hypokalemia and metabolic alkalosis resembling Gitelman syndrome (GS) due to secondary...
Pseudo-Bartter/Gitelman syndrome (PBS/PGS) is a disorder that presents with hypokalemia and metabolic alkalosis resembling Gitelman syndrome (GS) due to secondary factors, such as lifestyle and /or medicines. Notably, PBS/PGS is more likely to cause renal dysfunction than GS. We report the first case of PBS/PGS due to long-term laxative abuse leading to end-stage kidney disease (ESKD). The patient was a 49-year-old woman with a history of constipation since school, who had used excessive doses of laxatives on her own judgment for nine years at least from 22 years of age. Two years later, blood tests revealed hypokalemia (serum K 3.1 mEq/L), and nine years later, the patient's renal function began to deteriorate (Cr-eGFR 48.7 mL/min/1.73 m). Since abuse of laxatives was suspected as the cause, it was changed to the proper dosage of laxatives. At 33 years, the patient developed acute kidney injury (AKI), due to a urinary tract infection, and required intensive treatment, including hemodialysis. Although the patient was eventually weaned off dialysis, the renal function did not recover to pre-AKI levels. In suspected GS, comprehensive genetic testing for renal disease-related genes was performed; however, no obvious pathogenic variants were identified. Thereafter, despite decreasing the laxative doses and potassium supplementation, her renal function continued to decline. At 49 years, the patient developed ESKD and was started on maintenance hemodialysis. PBS/PGS is a disease that can lead to ESKD. An early diagnosis of PBS/PGS is crucial to prevent renal function deterioration, and the underlying causes should be removed immediately.
PubMed: 38306007
DOI: 10.1007/s13730-024-00851-9 -
AJP Reports Jan 2024We describe a pregnant patient with severe compulsive water ingestion and vomiting that lead to metabolic alkalosis and preterm delivery. A 21-year-old patient was...
We describe a pregnant patient with severe compulsive water ingestion and vomiting that lead to metabolic alkalosis and preterm delivery. A 21-year-old patient was hospitalized multiple times throughout pregnancy for symptoms initially thought to be related to hyperemesis gravidarum. Overtime, it became apparent that the patient induced vomiting by rapidly drinking large volumes of water. At 32 weeks' gestation, rapid ingestion of water caused 3 days of vomiting with findings of hyponatremia, hypokalemia, hypochloremia, metabolic alkalosis, and compensatory respiratory acidosis. Fetal monitoring showed minimal variability and recurrent decelerations; subsequent biophysical profile score of 2/10 prompted urgent cesarean section. A male newborn was delivered and cord blood gases reflected neonatal metabolic alkalosis and electrolyte imbalances identical to those of the mother. Compensatory hypoventilation in both mother and fetus were treated with assisted ventilation. With saline administration and repletion of electrolytes, metabolic alkalosis resolved for both patients within days. Metabolic alkalosis was transplacentally acquired by the fetus. This case demonstrates the development of metabolic alkalosis in a pregnant woman caused by vomiting severe enough to prompt preterm delivery for nonreassuring fetal status. It also demonstrates fetal dependence on both placenta and mother to maintain physiologic acid-base and electrolyte balance.
PubMed: 38269119
DOI: 10.1055/s-0043-1778113