Revista Paulista de Pediatria · 4 authors, 1 centre
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This case series of seven infants with severe intestinal insufficiency found that 57.1% developed hypothyroidism, likely due to iodine deficiency from prolonged exclusive parenteral nutrition without iodine supplementation. Thyroid dysfunction was successfully treated with levothyroxine via gastric or rectal routes. The findings highlight the need for mandatory thyroid screening in children receiving long-term parenteral nutrition without iodine.
**Background:** Severe intestinal insufficiency in infants often requires prolonged exclusive parenteral nutrition (PN). In Brazil, PN solutions do not contain iodine, an essential trace element for thyroid hormone synthesis. Iodine deficiency can lead to hypothyroidism, but data on thyroid function in this population are limited. This study aimed to describe thyroid function status in infants with severe intestinal dysfunction.
**Methods:** A retrospective study was conducted at the Neonatal Intensive Care Center-2 (CTIN-2), Instituto da Criança e do Adolescente, Hospital das Clínicas, Universidade de São Paulo, Brazil. All newborns and infants with severe intestinal dysfunction hospitalized between 2015 and 2020 were included. Data collected included gestational age, birth weight, underlying pathology, hospital stay, presence of thyroid dysfunction, age at onset, initial and maximum levothyroxine dose, administration route, and outcome. Thyroid dysfunction screening involved monthly free T4 and TSH measurements.
**Key Results:** Of 914 hospitalizations during the study period, seven children (0.76%) developed severe intestinal insufficiency. Underlying pathologies included vanishing gastroschisis (42.9%), Berdon syndrome (28.5%), apple peel syndrome (14.3%), and OIES syndrome (14.3%). Mean gestational age was 33.3±1.6 weeks, mean birth weight was 2,113.9±370.9 g, median hospitalization was 420 days (range 37–690), and mortality was 42.9%. Short bowel syndrome (loss of >80% of small intestine) was present in 71.4% of cases. Cholestasis (direct bilirubin >2 mg/dL) occurred in 42.9%.
Four of seven cases (57.1%) presented thyroid dysfunction (hypothyroidism) based on altered free T4 and TSH levels. Cases 2, 3, 6, and 7 had abnormal values: minimum free T4 ranged from 0.42 to 0.87 ng/dL and maximum TSH ranged from 5.50 to 169.10 mIU/mL. Cases 1 and 4 had normal values; case 5 had a mildly elevated TSH not confirmed on repeat testing. Age at onset of thyroid dysfunction ranged from 27 to 114 days of life. Initial levothyroxine doses were 25–50 μg/day, with therapeutic doses of 25–100 μg/day. Two children received levothyroxine via gastric route and two via rectal route; all achieved normal thyroid function within 15–30 days. None had abnormal neonatal screening for hypothyroidism.
**Clinical Implications:** This case series demonstrates a high prevalence (57.1%) of hypothyroidism in infants with severe intestinal insufficiency receiving exclusive PN without iodine, consistent with iodine deficiency as the likely etiology. The rate exceeds the previously reported 33% risk in similar populations. Prematurity (all cases were <37 weeks) may further increase vulnerability. The study confirms that both gastric and rectal levothyroxine administration can effectively normalize thyroid function in these patients. The authors recommend mandatory periodic screening for thyroid dysfunction (free T4 and TSH) in children on prolonged PN without iodine, consistent with ESPGHAN guidelines. Key limitations include the small sample size, single-center design, and inability to measure serum or urinary iodine levels. The long-term question of whether thyroid function normalizes after intestinal recovery and enteral iodine intake remains unanswered.