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Background Posterior reversible encephalopathy syndrome is characterized by a combination of clinical-radiological findings and pathophysiologically by localized brain vasogenic edema. Many clinical illnesses may trigger the onset of posterior reversible encephalopathy syndrome and hypertension is present in about 80% of patients. Methods We describe a child with high consumption of licorice toffees who developed systemic hypertension followed by posterior reversible encephalopathy syndrome. Results This boy was hospitalized following a cluster of generalized tonic-clonic seizures. Monitoring his clinical parameters, we detected constant high blood pressure and a brain magnetic resonance scan showed a localized vasogenic edema; these symptoms suggested posterior reversible encephalopathy syndrome. He had been eating licorice toffees for a period of 4 months, consuming an estimated 72 mg of glycyrrhizic acid per day; this led to our assumption of the reason for his hypertension. Conclusion There are several reported examples of posterior reversible encephalopathy syndrome–induced licorice hypertension in adults, but none related to children. Our report examines a possible link between licorice consumption and hypertension/posterior reversible encephalopathy syndrome in children.

Background: Menetrier's disease is a rare form of acquired gastropathy characterized by giant rugal folds in the stomach lining and protein-losing gastropathy; in children, it rarely needs aggressive treatment and resolves spontaneously within 2–10 weeks with support therapy. Many cases of pediatric Menetrier's disease associated with cytomegalovirus (CMV) infection have been reported. Clinical findings include nausea, vomiting, abdominal pain, peripheral edema, ascites, and pleural effusion. Gastroduodenal endoscopy is useful in confirming the diagnosis and excluding other similar conditions as lymphoma, eosinophilic gastropathy, gastric varices, Zollinger-Ellison syndrome and lymphangectasia. Specific aim: We describe a case of protein-losing gastropathy, associated with primary CMV infection. Case report: An 18-month-old male presented with periorbital swelling, vomiting and food refusal. Blood tests on admission showed hypoalbuminemia, IgG hypogammaglobulinemia, hypocalcemia and a high peripheral blood eosinophil count. Metabolic, allergologic and autoimmune diseases were ruled out. His immunological profile was normal. Tests for infectious diseases revealed a primary CMV infection. The Guthrie card test for CMV PCR was negative. Endoscopy revealed a normal macroscopic picture of the digestive sections examined and histological examination of multiple oesophageal, gastric and duodenal biopsies was normal. In contrast, the ultrastructural examination of the biopsies revealed signs of viral infection. Considering the diagnostic hypothesis of protein-losing gastropathy associated with CMV infection, a proton pump inhibitor with support therapy and a dose of IgG immunoglobulins to treat the IgG hypogammaglobulinemia were administered. The child was discharged in good clinical condition, with monthly outpatient follow-up for 6 consecutive months. Conclusions: Although CMV infection appears to be the major cause of Menetrier's disease in infants, in our case, the lack of endoscopic and histological features suggestive of Menetrier's disease led us to consider a form of protein-losing gastropathy associated with CMV infection. It is important for pediatric emergency departments to consider the often misdiagnosed Menetrier's disease, together with the other causes of protein-losing enteropathy, in the differential diagnosis for edema and low albumin levels.