# Growth Failure and Non-thyroidal Illness in an Infant

**Authors:** Shunsuke Shimazaki, Miu Kishimura, Junichi Sato

PMC · DOI: 10.7759/cureus.102664 · Cureus · 2026-01-30

## TL;DR

A malnourished infant showed non-thyroidal illness and low IGF-1, but recovered after proper feeding, highlighting the link between nutrition, thyroid function, and growth.

## Contribution

This case provides insights into the interrelationship between malnutrition, thyroid function, and growth regulation in infants.

## Key findings

- The infant exhibited non-thyroidal illness and low IGF-1 due to malnutrition, not pituitary or thyroid disease.
- Nutritional rehabilitation restored growth and normalized thyroid and IGF-1 levels.
- Low IGF-1 reflects GH resistance and reduced insulin and leptin signaling in malnourished infants.

## Abstract

Reports incorporating pituitary function testing in infants with non-thyroidal illness (NTI) are rare. Here, we describe the case of an infant (a 1-year-3-month-old boy) with failure to thrive secondary to inappropriate feeding practices. The infant developed NTI and reduced IGF-1 levels. He exhibited markedly impaired growth velocity, with low free triiodothyronine (T3), free thyroxine (T4), and insulin-like growth factor 1 (IGF-1) levels despite normal thyroid-stimulating hormone (TSH) levels and intact anterior pituitary responses on stimulation testing.

Neuroimaging revealed no structural abnormalities. Upon nutritional rehabilitation with age-appropriate caloric intake, he exhibited catch-up growth and normalization of thyroid function and IGF-1 levels. This case demonstrates that NTI and low IGF-1 levels may occur in infants with malnutrition. The pathophysiology of NTI involves inflammatory cytokine-mediated alterations, suppression of hypothalamic-pituitary-thyroid axis regulation, and hypoleptinemia during starvation. Low IGF-1 levels reflect growth hormone (GH) resistance, mediated by fibroblast growth factor 21, and reduced insulin and leptin signaling. This case highlights the necessity of evaluating the nutritional and clinical background when assessing endocrine abnormalities to avoid misdiagnosing intrinsic pituitary or thyroid disease. Prompt nutritional intervention is critical for restoring growth and endocrine homeostasis. This case provides insights into the interrelationship between malnutrition, thyroid function, and growth regulation during early childhood.

## Linked entities

- **Proteins:** IGF1 (insulin like growth factor 1), PIN (insulin precursor), lepa (leptin a)

## Full-text entities

- **Genes:** Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, GHR (growth hormone receptor) [NCBI Gene 2690] {aka GHBP, GHIP}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891] {aka LEM6, PGC-1(alpha), PGC-1alpha, PGC-1v, PGC1, PGC1A}, TRH (thyrotropin releasing hormone) [NCBI Gene 7200] {aka Pro-TRH, TRF}, GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, FGF21 (fibroblast growth factor 21) [NCBI Gene 26291], GNRH1 (gonadotropin releasing hormone 1) [NCBI Gene 2796] {aka GNRH, GRH, LHRH, LNRH}, POMC (proopiomelanocortin) [NCBI Gene 5443] {aka ACTH, CLIP, LPH, MSH, NPP, OBAIRH}, GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}
- **Diseases:** inflammatory (MESH:D007249), trauma (MESH:D014947), cow's milk allergy (MESH:D016269), starvation (MESH:D013217), caloric insufficiency (MESH:D000309), malignancy (MESH:D009369), diabetes mellitus (MESH:D003920), Growth Failure (MESH:D051437), edema (MESH:D004487), liver cirrhosis (MESH:D008103), weight gain (MESH:D015430), vomiting (MESH:D014839), nutritional disturbance (MESH:D009748), systemic diseases (MESH:D034721), pituitary hypoplasia (MESH:D010900), GH resistance (MESH:D046150), psychomotor developmental delay (MESH:D011596), malnutrition (MESH:D044342), endocrine abnormalities (MESH:D004700), ESS (MESH:D005067), failure to thrive (MESH:D005183), cardiac murmur (MESH:D006337), asphyxia (MESH:D001237), abdominal mass (MESH:D000007), thyroid abnormalities (MESH:D013959), respiratory abnormalities (MESH:D015619), anorexia nervosa (MESH:D000856), goiter (MESH:D006042), sepsis (MESH:D018805)
- **Chemicals:** BE (MESH:D001608), N (MESH:D009584), cortisol (MESH:D006854), Base excess (-), T4 (MESH:D013974), Bicarbonate (MESH:D001639), lipid (MESH:D008055), T3 (MESH:D014284)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12951800/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12951800/full.md

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Source: https://tomesphere.com/paper/PMC12951800