High Procalcitonin Levels in a Newborn with Erythroderma.

Abstract

To the Editor: Procalcitonin (PCT) is considered an excellent sepsis marker in the late neonatal period,1 but PCT can be increased in noninfectious conditions.2 We present a newborn with IgE-mediated cow’s milk protein allergy with a significant increase in serum PCT without associated infectious disease. A 17-day-old newborn, without infection risk factors in the peripartum period, presented to our emergency department with generalized erythroderma, which had begun 1 hour before, without urticarial, vesicular or petechial lesions. Vital signs were normal, and he had a good general condition. He had been exclusively breastfed until 2 days before the onset, when he started bottle feeding (2 bottles, the last one 10 minutes before the onset). The full blood count showed 5260 leukocytes/µL with a relevant left shift (20% bands, immature/total ratio: 0.31) and normal red blood cell and platelet counts. The biochemical tests were normal except for hyperglycemia (231 mg/dL) and elevated PCT (20.2 ng/mL), with C-reactive protein in the normal range (9.7 mg/L). Urinalysis, analysis of cerebrospinal fluid and blood, urine and cerebrospinal fluid cultures were normal. Based on the presumptive diagnosis of late-onset neonatal sepsis, the patient was treated with amikacin and vancomycin. Cow’s milk proteins were removed from the diet just in case. During the following days, the markers of inflammation became normal and the newborn became asymptomatic. On the seventh day of admittance, and without known cow milk exposure, he had a new episode of erythroderma. He started with vomiting without fever. Vital signs remained stable. Leukocytosis (30.080/µL) with left shift again and eosinophilia (eosinophils, 30%) with a slight rise in C-reactive protein (13.1 mg/L) and PCT (2.5 ng/mL) were noticed. Cultures were collected again, and the treatment was changed to ampicillin, gentamicin and clindamycin. In addition, the mother was advised to follow a strict cow’s milk protein-free diet and an elemental formula was prescribed, in case breast milk was not available. The erythroderma disappeared after 24 hours, and antibiotic therapy was stopped after negative results of the cultures were known. Immuno-CAP (ImmunoCap Phadia Sweden, Uppsala, Sweden) specific IgE test confirmed cow’s milk allergy: alpha-lactalbumin 3.56 KU/L (class 3), beta-lactoglobulin 11.6 KU/L (class 3) and cow’s milk 10.0 KU/L (class 3). There are few reports that correlate highly elevated serum levels of PCT with allergic, hypersensitivity or anaphylactic processes; although to our knowledge, none reported in the neonatal period.3–5 The pathophysiology of the marked increase in PCT levels in our patient remains to be defined. It is possible that the allergic IgE-mediated reaction produced a massive release of mediators that would stimulate a cellular response accountable for increasing proinflammatory cytokines, which induce the synthesis of PCT. However, this hypothesis has not been demonstrated in other allergic or anaphylactic pictures. It is interesting to point out that, although PCT is commonly used as a diagnostic and prognostic biomarker of bacterial infections in the neonatal period, IgE-mediated allergic reactions should be considered as a potential differential diagnosis in the absence of clinical or microbiologic data of severe bacterial infection. Beatriz Arizcun Aguilera, MD Sara Ruiz González, MD Department of Pediatrics Hospital Universitario Puerta de Hierro-Majadahonda Madrid, Spain Roberto Ortiz Movilla, MD Ana María Malalana Martínez, MD María del Carmen Muñoz Labián, MD Division of Neonatology Department of Pediatrics Hospital Universitario Puerta de Hierro-Majadahonda Madrid, Spain María Luz Cilleruelo Pascual, PhD Division of Pediatric Gastroenterology Department of Pediatrics Hospital Universitario Puerta de Hierro-Majadahonda Madrid, Spain