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PP-055 Congenital chagas disease. a case report
  1. C Marti-Gil1,
  2. I Martin-Niño1,
  3. L Recuero-Galve1,
  4. E Cueto-Calvo2,
  5. J Sanchez-Gundin1,
  6. D Barreda-Hernandez1
  1. 1Virgen de la Luz Hospital, Pharmacy, Cuenca, Spain
  2. 2Virgen de la Luz Hospital, Paediatrics, Cuenca, Spain

Abstract

Background Congenital infection with Trypanosoma cruzi occurs in an average of 5% of children born of mothers with chronic infection.

Purpose To describe a case report of a newborn with Chagas disease (CD) acquired by vertical transmission in a non=endemic zone.

Material and methods Medical history review and literature research.

Results The case was a 10-day-old girl, born after spontaneous gestation of normal evolution and eutocic birth (Apgar test 8/10, 3100 g, 49 cm), whose mother (40-year-old South-American) had negative serologies and SBAgalactiae test, immune rubella and toxoplasma, but had IgG+ for CD. After the newborn had positive PCR for T cruzi and IgG+ antibodies to CD, the paediatrics service consulted the pharmacy service regarding the possibility of a pharmaceutical compounding preparation (PCP) for paediatric dosing of benznidazole. The dosage regimen, according to WHO criteria, was 5–10 mg/kg/day of benznidazole for 60 days, divided into two daily doses. 4 PCP were found from available benznidazole tablets (Abarax): 2 oral suspensions (PCP1, PCP2), capsules and envelopes. PCP1 (benznidazole 1%) contained polysorbate-80, sodium carboxymethylcellulose, acesulfame potassium, methylparaben, propylparaben, banana and strawberry flavour, sunset yellow colourant and distilled water. PCP2 (benznidazole 10 mg/mL) needed sorbitol, sodium carboxymethylcellulose, citric acid and simple syrup. Capsules required an additional carrier diluent and the last PCP only needed Abarax tablets, containing excipients such as corn starch and lactose. The liquid PCP were discarded because these contained sorbitol, acesulfame potassium and/or parabens, opting for the development of envolopes for the newborn and the ease of weekly dosage adjustment based on patient weight. The start dosage was 8.2 mg (3260 g body weight; week 1) and the end dose was 24 mg (4980 g; week 7). After treatment with benznidazole, a progressive decrease in antibody titres was observed, with confirmation of cure at approximately 2 months and negativisation PCR with normal blood count and biochemistry. A review was conducted in the ophthalmology service (11 weeks after initiation of treatment) to assess treatment toxicity, not apparently objectifying alterations in the fundus, although noting that it was difficult to assess the potential toxicity of benznidazole with minimum reliability.

Conclusion Benznidazole was effective and well tolerated, although careful monitoring was necessary. PCP allows the pharmacist to individualise treatment when commercial presentations are not available.

No conflict of interest

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