RESUMEN
Angioedema is a rare but potentially lethal side effect of angiotensin-converting enzyme inhibitors (ACEIs). Most ACEI-induced angioedema (ACEI-AE) cases have been reported in adults, with few reports of cases in children. Posterior reversible encephalopathy syndrome (PRES) is a neurological disorder that presents with acute onset of symptoms, including headache, vomiting, visual disturbances, and seizures. We report the case of a patient who developed ACEI-AE after developing PRES during the treatment of steroid-resistant nephrotic syndrome. ACEI-AE is very rare, especially in children, but can be life-threatening if swelling of the tongue or the throat blocks the airway. Whenever ACEIs are used, even in children, clinicians should be aware of the possibility of the occurrence of ACEI-AE, particularly when accompanied by dry cough. Moreover, bradykinin may be associated with PRES onset in patients with ACEI-AE and may be a risk factor for PRES.
RESUMEN
Background: Hypercalcemic crisis caused by primary hyperparathyroidism (PHPT) in pediatric patients is very rare, and appropriate treatment approach for this condition has not been well demonstrated. Here, we report a case of PHPT-induced hypercalcemic crisis in a boy. Case Description: An 11-year-old boy visited the clinic with abdominal pain and nausea that lasted for 3 months, but the cause of his symptoms could not be identified. As these symptoms worsened after 1 month, he was referred to a nearby hospital. The boy's albumin-corrected serum calcium level was very high (14.3 mg/dL). Treatment was immediately started with the administration of normal saline, furosemide, and calcitonin to lower his serum calcium levels. Based on elevated intact-parathyroid hormone (i-PTH) (405 pg/mL) level and enlargement of the right superior parathyroid on diagnostic imaging, he was diagnosed with hypercalcemic crisis due to PHPT. As his albumin-corrected serum calcium level increased to 16.5 mg/dL and he could not take almost any foods due to severe nausea, he was transferred to our hospital and treated with pamidronate. Although his albumin-corrected serum calcium level decreased to 14.0 mg/dL, his symptoms did not improve completely. Therefore, 2 days after transfer to our hospital, he underwent emergency surgery to resect the enlarged right superior parathyroid gland. Fifteen minutes after removal of the enlarged parathyroid gland, the serum intact-PTH level decreased to 41.7 pg/mL. The histopathological diagnosis of the enlarged parathyroid gland was adenoma. The boy became asymptomatic, and his albumin-corrected serum calcium level was maintained within the normal limits for 6 months post operatively. Genetic testing performed after the surgery did not detect any pathogenic mutations in the MEN1 and CDC73 genes, and no genetic predisposition has been identified to date. Conclusions: Emergency focused parathyroidectomy prior to genetic testing might be an appropriate strategy when the pediatric patient presents with a PHPT-induced hypercalcemic crisis.