A 1-year-old boy with papules and pustules on the cheeks

The case

A 1-year-old boy presented with recurrent red bumps and pustules on both cheeks over the past 2 months (Figure). The lesions began as small papules that gradually increased in number. His parents noted no associated fever, irritability, or other systemic symptoms. The child was otherwise healthy, with normal growth and development milestones, and had not received any new oral medications or topical products. The family also denied the use of corticosteroid creams, herbal preparations, or oils on the face.

On examination, the patient was well appearing, with normal height, weight, and head circumference for the child’s age. However, there were various erythematous papules, open and closed comedones, and pustules that were noted symmetrically on both cheeks and forehead, some with mild postinflammatory erythema. No nodules, cysts, or scarring were observed on the child. Additionally, there were no signs of virilization, hirsutism, or pubic hair. Genital examination demonstrated normal genitalia with prepubertal testes. The remainder of the physical examination was unremarkable.

Diagnosis

Infantile acne

Etiology and clinical findings

Infantile acne is a poorly understood and rare condition affecting less than 2% of infants.¹ Clinically, it has much in common with adolescent acne, and it manifests as a chronic inflammatory dermatosis. The condition is characterized by superficial inflammatory papules and pustules, comedones, and sometimes nodulocystic lesions, particularly on the cheeks, but could also appear on the forehead, chin, or nose.¹ It typically appears between aged 6 weeks and 12 months, with a male predominance.² Scarring is not common but can occur in severe cases, making early diagnosis and therapy essential to prevent complications.

Although the precise cause of infantile acne is not well established, several factors have been implicated. Increased sebaceous gland activity, possibly due to transiently elevated androgen levels from the hypothalamic-pituitary-gonadal axis activation, is considered a major contributor.¹ During the first year of life, particularly in boys, there is an upsurge of luteinizing hormone and testosterone production from the testes and fetal adrenal gland, resulting in increased sebum production and subsequent acne formation.² Genetics and family history also play a significant role, as the likelihood of infantile acne is higher in children with first-degree relatives who have been affected by acne. Other risk factors associated with persistent or severe acne include male sex and a strong hereditary predisposition.

Clinically, it presents a combination of open and closed comedones, erythematous papules, and pustules, primarily on the cheeks and often symmetrically distributed.¹ Mild postinflammatory erythema may be observed, and, in typical cases, there are no nodules, cysts, or signs of virilization, hirsutism, or pubic hair.¹ Infantile acne is usually not associated with any underlying endocrine pathology, and it is usually self-limiting, generally resolving spontaneously within the first 2 years of life.¹ Nonetheless, moderate to severe cases necessitate medical intervention to prevent scarring. Thus, physical examination should be thorough to exclude endocrine abnormalities, which are rarely associated with infantile acne and typically present with other signs such as growth acceleration or genital changes.

Differential diagnosis

The differential diagnosis of infantile acne involves careful consideration of other common pediatric skin disorders that can present similarly with papules, pustules, or facial involvement in infants. Given the overlapping clinical appearances, it is crucial to distinguish infantile acne from other inflammatory, infectious, allergic, and dermatoses of infancy (Table). The process relies on lesion morphology, distribution, patient age, associated symptoms, family history, and exposure history. Correctly identifying infantile acne avoids unnecessary treatments and ensures that more concerning conditions or mimickers are not overlooked.

Infantile acne must be differentiated from other pediatric dermatoses that share similar features but differ in etiology and clinical course. Acne vulgaris typically presents later in childhood or adolescence, often with deeper nodules and cysts.³ Periorificial dermatitis can mimic acne but lacks comedones and tends to localize around the mouth, nose, or eyes.⁴ Allergic contact dermatitis features vesicular or crusted lesions accompanied by prominent pruritus, in contrast to the nonpruritic nature of acne.⁵ Impetigo presents acutely with honey-colored crusts due to bacterial infection, while keratosis pilaris produces small follicular papules without pustules or inflammation.^6,7 Finally, endocrine or androgen excess disorders, such as congenital adrenal hyperplasia or virilizing tumors, should be suspected when acne is severe, nodulocystic, or associated with hirsutism, accelerated skeletal growth, or genital changes.⁸ Considering these distinctions allows clinicians to confidently identify benign infantile acne while maintaining vigilance for infectious or endocrine conditions that require further evaluation.

Management

Management of infantile acne is guided by disease severity, extent of involvement, and presence of comedonal vs inflammatory lesions. Most cases are mild and self-limited, requiring only gentle skin care and reassurance to the parents. Parents should be advised to avoid occlusive products, oils, and topical corticosteroids, as these may exacerbate follicular plugging and inflammation. In general, gentle cleansing with a noncomedogenic cleanser once daily is typically sufficient.

For mild to moderate inflammatory lesions, topical antimicrobial and keratolytic agents are the mainstay of therapy. Benzoyl peroxide (2.5% to 5%) is considered first-line treatment due to its bactericidal and anti-inflammatory properties and minimal risk of resistance.¹ It can be applied sparingly once daily, preferably as a low-strength, water-based formulation to minimize irritation in infants. In cases that have more pronounced pustular inflammation, topical antibiotics, such as erythromycin 2% or clindamycin 1%, can be added twice daily.¹ Combination therapy with benzoyl peroxide helps prevent Cutibacterium acnes resistance.

In older infants with persistent comedonal lesions, topical retinoids (adapalene 0.1%, tretinoin 0.025%) may be used cautiously; however, data on safety in those younger than 1 year are limited.² Systemic antibiotics are rarely indicated and reserved for extensive or refractory cases with secondary infection. Hormonal or antiandrogen therapy has no role in typical infantile acne and should be reserved for cases where endocrine abnormalities are confirmed.

It is recommended to conduct follow-ups every 4 to 6 weeks to monitor improvement and assess adverse effects or progression. Most patients respond within 2 to 3 months, with gradual resolution as androgen levels decline. Early recognition and conservative management prevent scarring and unnecessary systemic interventions.

Conclusion

Infantile acne is an uncommon but benign condition that can resemble several infectious, allergic, and endocrine disorders of infancy. Recognition of characteristic comedones and inflammatory papules in an otherwise healthy infant allows for accurate diagnosis and avoids unnecessary investigations or treatments. Most cases resolve spontaneously with gentle skin care and limited topical therapy, though severe or persistent lesions warrant endocrine evaluation. Early identification and reassurance remain central to management, preventing both overtreatment and parental anxiety.

References

1. Poole CN, McNair V. Infantile acne. In: StatPearls. StatPearls Publishing; 2023. Accessed January 5, 2026. https://www.ncbi.nlm.nih.gov/books/NBK541124/
2. Palmieri SA. Acne vulgaris in children and adolescents: what’s the cause and how to combat It. J Pediatr Pharmacol Ther. 2025;30(3):401-406. doi:10.5863/JPPT-25-01205
3. Oge’ LK, Broussard A, Marshall MD. Acne vulgaris: diagnosis and treatment. Am Fam Physician. 2019;100(8):475-484.
4. Acevedo-Fontanez LA, Sánchez-Feliciano A, Ershadi S, Reichenberg J, Eichenfield LF, Barbieri JS. Periorificial dermatitis: pathophysiology, diagnosis, and management. J Am Acad Dermatol. . 2026;94(5):1483-1492. doi:10.1016/j.jaad.2025.10.138
5. Kostner L, Anzengruber F, Guillod C, Recher M, Schmid-Grendelmeier P, Navarini AA. Allergic contact dermatitis. Immunol Allergy Clin North Am. 2017;37(1):141-152. doi:10.1016/j.iac.2016.08.014
6. Johnson MK. Impetigo. Adv Emerg Nurs J. 2020;42(4):262-269. doi:10.1097/TME.0000000000000320
7. Maghfour J, Ly S, Haidari W, Taylor SL, Feldman SR. Treatment of keratosis pilaris and its variants: a systematic review. J Dermatolog Treat. 2022;33(3):1231-1242. doi:10.1080/09546634.2020.1818678
8. Held PK, Bird IM, Heather NL. Newborn screening for congenital adrenal hyperplasia: review of factors affecting screening accuracy. Int J Neonatal Screen. 2020;6(3):67. doi:10.3390/ijns6030067