Acne in children – Neonatal acne, Infantile acne, Mid-childhood acne and Preadolescent acne

INTRODUCTION

Acne is one of the most common diseases affecting the pediatric population and a frequent chief complaint for office visits for both pediatricians and dermatologists. While it is primarily a skin disorder of adolescents, acne is also a less studied, but equally important, condition faced by children who have not yet reached puberty. This special group of acne patients may be categorized into the following four clinical entities on the basis of the time of onset and clinical features: neonatal, infantile, mid-childhood, and preadolescent acne. The clinical presentation, pathophysiology, differential diagnosis, workup, and treatment of each of these types of acne differ to varying degrees and will therefore be addressed on an individual basis.

NEONATAL ACNE

Clinical Presentation

Neonatal acne, also known as acne neonatorum, presents between the time of birth and approximately the first four to six weeks of life. It has been estimated that neonatal acne affects as many as 20% of newborns (1). “Neonatal acne” may actually be a term used for a heterogeneous set of conditions presenting with papules and pustules, as well as true early acne presenting with comedones. The condition “neonatal cephalic pustulosis” (NCP) has been described as a more distinct entity of superficial pustules without comedones, which may involve the forehead, cheeks, chin, neck, scalp, chest, and back (2,3).

Table 1    Acne in the Younger Patient

Acne type                                                                               Age range

Neonatal acne                                                                            0 6 wk

Infantile acne                                                                             0 1 yr

Mid childhood acne                                                                  1 8 yr

Preadolescent acne                                                                    8 12 yr

Pathophysiology

The pathophysiology of acneiform eruptions in the newborn is only partially understood. Studies have implicated Pityrosporum spp., formerly known as Malassezia (M. sympodalis and M. globosa), as a cause of NCP. Some, but not all, neonates with acne are either smear- or culture-positive for a member of the species (2 5). For children with positive smears or cultures, it is likely that the papulopustular lesions are a result of inflammatory reaction to the Pityrosporum spp. in the skin.

Both NCP and true acne in neonates may be influenced by a combination of several factors: excess sebum production and hormonal effects on neonatal sebocytes (2,6,7). Neonates have enlarged sebocytes and have an excess of sebum excretion (8). Newborns even excrete more sebum compared with older infants, perhaps due, in part, to placental hormonal transmission from mother to newborn (6,8). One study compared sebum excretion rates (SER) in mothers prenatally, mothers and their neonates immediately after birth, and mothers and their infants between weeks 5 and 12 of age (9). A significant correlation was found between the presence of high maternal SER perinatally and high neonatal SER immediately after birth, whereas infant SER between weeks 5 and 12 was found to be significantly lower compared with the neonatal postpartum SER.

Differential Diagnosis and Evaluation

The presentation of acne in the neonate is similar to that of a number of skin diseases that may appear during the first month of life, including, but not limited to, NCP, transient neonatal pustular melanosis, erythema toxicum neonatorum, and bacterial or Candida infection. Similar to neonatal acne, and perhaps synonymous with it, NCP presents during the first weeks of life with erythematous papules and pustules on the face and neck. Smears obtained from pustules may contain Malassezia spp. on microscopic examination (5). In the literature, the distinction between NCP and neonatal acne is controversial and unclear. Transient neonatal pustular melanosis can present at delivery or within the first day of life, with pustules on the chin, neck, or trunk, usually in darker-skinned babies. In approximately 24 hours, the pustules will rupture and leave behind light brown macules with a faint white rim of scale.

Occasionally, the baby is born with lesions already transformed into the brown, macular stage. Erythema toxicum neonatorum presents primarily in the first week of life, most often in the first 48 to 72 hours but usually not at delivery. It begins with an erythematous macule that develops a central papule or pustule. Lesions are located primarily on the trunk, face, or extremities and resolve without treatment. The diagnosis may be confirmed with observation of eosinophils in a Gram stain or Tzanck smear of a pustule (10). Signs and symptoms in the newborn that suggest that the pustules may be associated with a significant infection including fever in the mother or infant, skin lesions on the mother during the perinatal period, fussiness, feeding difficulties, or other signs of illness in the newborn, should prompt culture of the pustules for organisms, including bacteria, viruses, and fungi, further infectious disease work-up and medical therapy as appropriate should be undertaken. This is particularly important if the distribution of the lesions is atypical for neonatal acne or other benign transient neonatal pustular disorders.

Treatment

Most neonatal acne is self-limited, lasting from a few days to several weeks. Given this short-lived course, many clinicians elect to reassure parents that neonatal acne will resolve on its own, without scarring, and elect not to treat with any medication (11). If families prefer treatment, a short course of topical azoles, such as 2% ketoconazole cream, is often sufficient to reduce Pityrosporum colonization and may improve NCP (5). Some infants with true comedonal and inflammatory acne presenting in the neonatal period may have a prolonged course, overlapping with infantile acne, and may be treated with topical acne therapies, including retinoids, antibiotics, benzoyl peroxide, and combination therapies, rarely requiring systemic therapies.

INFANTILE ACNE

Clinical Presentation

Infantile acne may start in the first month of life or later and can persist for months to years, usually resolves by 24 months of age. It is a relatively rare condition and presents more often in boys than in girls. There may be inflammatory papules, pustules, cysts, and/or nodules, and, unlike in neonatal acne, comedones are usually present. Lesions present on the cheeks primarily but can also be found on the forehead, chin, and trunk. A rare subset of infants with acne have refractory, inflammatory cysts, draining sinuses, and nodules findings more commonly associated with adolescent acne(12). It is believed that the presence of infantile acne, regardless of severity, may predict more severe adolescent acne compared with teenagers who did not have acne as infants (13).

Pathophysiology

The pathogenesis of infantile acne is better understood than that of neonatal acne. It is thought to arise because of increased adrenal androgen [dehy-droepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS)] production by the fetal adrenal gland, the inner zone of the adrenal corre-sponding to the later zona reticularis (14). This is the androgen-secreting portion of the adrenal, which shrinks after the first year of life and then reappears during adrenarche, usually around ages eight or nine years in girls and boys, respectively. Adrenal androgens stimulate sebaceous glands and, in turn, infants have been shown to have increased sebum production during this period (8). Over the first six months of age, this production of adrenal androgens gradually decreases, as infantile acne shows signs of improvement. In infant boys, during the first six months of life, the testes have been shown to produce androgen levels similar to that of mid-pubertal boys and there appears to be a related increase in the amount of infantile acne in boys compared with girls (15).

Differential Diagnosis and Evaluation

The differential diagnosis of infantile acne is broad and includes periorificial dermatitis, cutaneous infections, seborrhea, and acne secondary to hormonal abnormalities. For the majority of infantile acne cases, clinical findings are typical and no workup is necessary. The exception is hormone abnormality related infantile acne, whose workup will be discussed later in this section.

The most common conditions mistaken for acne in infants can often be differentiated on the basis of clinical findings. Periorificial dermatitis lacks open and closed comedones and, instead, exhibits inflammatory papules, often with erythema and scale, distributed around the eyes, nose, and mouth, but sparing the oral commissure. It responds to topical antimicrobials, including topical erythromycin and metronidazole, and can be exacerbated, or induced, by, high-potency topical steroid use. Acneiform-like lesions associated with infectious etiologies also lack comedones and are usually pustular, more focally distributed, and may or may not be accompanied by systemic signs such as fever. Culture and/or smear and microscopic examination of pustule contents will usually diagnose the responsible organisms. Most frequent are Staphylococcus aureus and Candida albicans. Seborrhea can exhibit papules and pustules mimicking acne, but its distribution will favor the scalp, ear, nasolabial folds, eyebrows, and sternum, and lesions may coalesce into plaques accompanied by a greasy, yellow scale. Miliaria pustulosa is a rare cause of infantile pustules in circumstances of excessive heat and or occlusion. Eosinophilic pustular folliculitis is rarely seen on the face but often affects the scalp.

Acne can be the presenting sign infants with hormonal abnormalities. Careful evaluation of the infant should include assesment of linear growth pattern, testicular size, and for pubic or axillary hair. These patients tend to have acne that is severe, persistent, and/or refractory to treatment; it is recommended, therefore, that infants presenting with these acne features undergo endocrine laboratory testing to rule out several rare endocrine diseases. See section “Pre-adolescent Acne: Differential Diagnosis and Evaluation” for recommended laboratory testing.

Treatment

The basic treatment modalities used for infantile acne are similar to conventional acne medications used for teenagers. Medications include topical benzoyl peroxide, retinoids, antibiotics, and combinations of these. For more severe cases requiring oral antibiotic therapy, oral erythromycin can be used. For most cases of infantile acne requiring topical retinoid treatment, milder-strength retinoids such as adapalene or low-potency tretinoin are tolerated best. If irritation is excessive, every-other-day application can be attempted, coupled with liberal moisturizer use. Tetracyclines are contraindicated in this age range because of risk of permanent tooth discoloration. While erythromycin is less effective, its safety profile makes it the oral antibiotic of choice in this population. For cases with erythromycin-resistance, clindamycin and trimethoprim-sulfamethoxazole are alternatives.

Infantile acne is rarely severe enough to warrant consideration of isotretinoin, and the FDA has only approved its use in children aged 12 years and older. However, for severe, scarring infantile acne, aggressive therapy may be needed. There are reports of successful, off-label treatment with isotretinoin(12,15 22). Isotretinoin may occur at dosages ranging from 0.5 to 2 mg/kg/day in toddlers, with treatment duration varying from 5 to 14 months (12,15 22). In addition to requiring off-label usage, the administration of iso-tretinoin in infants is further complicated by its lack of availability in a liquid or suspension formulation. The drug capsules need to be split and given to children, often in manners requiring some ingenuity. Furthermore, once split, clinicians, pharmacists, and families must also be careful of the high light and oxygen lability of the drug. To overcome these difficulties, one reported clinical pearl is to freeze the isotretinoin capsules, then split them in halves, thirds, or quarters as needed to get the appropriate dose, and place them in a chocolate or a candy bar (12).

Table 2

Use of Isotretinoin in Infants

Author

Refs

Age (mo)

Sex
Burket and Storrs

22

18

F
Arbegast et al.

21

20

M
Horne et al.

20

20

M
Mengesha et al.

19

20

F
Mengesha et al.

19

37

F
Cunliffe et al.

15

M
Sarazin et al.

18

20

F
Barnes et al.

12

14

F
Barnes et al.

12

13

F
Torrelo et al.

17

10

M
Hello, M et al.

(16)

9

M
Hello, M et al.

(16)

16

M

MID-CHILDHOOD

Clinical Presentation

The mid-childhood acne category encompasses children presenting with acne beyond roughly one year and before eight years of age. This is the rarest time period in which to encounter a child with acne, probably because there is vir-tually no adrenal or gonadal source of androgen in this developmental period. The morphology of acne during this period includes open and closed comedones, inflammatory papules, pustules, cysts, and nodules. Distribution is primarily on the face, and less often on the chest and back. Scarring and postinflammatory dyspigmentation can be observed.

Pathophysiology

When present, the pathophysiology of mid-childhood acne is often similar to that of preadolescent acne, to be discussed in section “Preadolescent Acne: Patho-physiology.” However, since the adrenal glands normally produce relatively little androgen during this period, mid-childhood acne may be commonly caused by an underlying endocrine abnormality (23).

Differential Diagnosis and Evaluation

There should be strong consideration of an underlying endocrine disorder in mid-childhood acne, and a workup is usually warranted. The most likely causes are congenital adrenal hyperplasia, malignant adrenal or gonadal tumors, true precocious puberty, premature adrenarchy, and polycystic ovary syndrome (PCOS). Evaluation may include a radiologic assessment of bone age, plotting of the child’s growth over time (looking for unexpected crossing of percentiles on the growth chart), or abnormal hormone levels, such as high levels of the androgens, testosterone, and DHEAS.

Table 2     Guide for Evaluation of Mid childhood Acne

Bone age. Accelerated with androgen excess. Delayed in Cushing’s syndrome Growth chart

. Height crossing percentiles upward in androgen excess

. Weight crossing percentiles upward and height downward in Cushing’s syndrome Hormone levels

. High levels of androgens such as free testosterone and DHEAS in tumors and PCOS

. High levels of 17 a hydroxyprogesterone in CAH

Abbreviations: DHEAS, dehydroepiandrosterone sulfate; PCOS, polycystic ovary syndrome; CAH, congenital adrenal hyperplasia.

For a discussion of complete laboratory workup recommendations, see section “Preadolescent Acne: Differential Diagnosis and Evaluation.”

Treatment

Treatment is generally very similar to that used for teenagers and adults with acne. The one therapeutic difference is the limitation of use of the tetracycline family of oral antibiotics to children of at least eight years of age when tooth enamel is permanently laid down. Instead, oral erythromycin may be utilized, or antibiotics less commonly used for acne such as trimethoprim-sulfa.

Appropriate indications for the use of isotretinoin in young children include severe, scarring acne, and acne unresponsive to conventional therapy. Family history of severe acne and psychosocial dysfunction may be considered as well. The dosage by weight is similar to that used for young adults. Several concerns regarding potential side effects of isotretinoin in young children have been raised, including the effects of isotretinoin on bone growth, the risk of depression, the potential for relapse upon isotretinoin completion, and a potential increased risk of onset of inflammatory bowel disease (IBD). While the issue of bone growth is particularly important in children because of the risk of premature closure of the epiphyses with isotretinoin (24), this has been reported in cases of high-dose, long-term isotretinoin use for disorders of keratinization, and no strong evidence suggests this to be a problem when using conventional dosages for the treatment of acne (25). A loss of bone density with the use of isotretinoin for cystic acne has also been shown in an older male popu-lation, while no specific changes in bone density were noted in a population of adolescents in a prospective study (26,27). There are also rare reports of diffuse idiopathic skeletal hyperostosis (DISH) with isotretinoin use, which most commonly affects the anterior spine; however, these reports are rare, and there is insufficient evidence to support routine radiologic screening for this condition in patients treated with isotretinoin for acne (27).

There have been concerns regarding isotretinoin use and IBD stemming from reports of presentation of IBD after use of isotretinoin (28). Given the high rates of development of IBD in the population age groups generally treated with istotretinoin, and conflicting epidemiologic data, it remains uncertain if reports of IBD associated with isotretinoin are chance associations or if a biological relationship is plausible (28 30). The concerns about efficacy and relapse in pre-pubertal children treated with isotretinoin are also unique. While isotretinoin is generally quite effective in this age group, studies have stated that younger age of isotretinoin is a risk factor for more frequent need for further courses of isotretinoin therapy as compared with its use in older patients. This may be due to continued hormonal stimulation in an adolescent pattern that predisposes to acne in this age group. Careful selection of patients and close postisotretinoin follow-up are warranted.

PREADOLESCENT ACNE

Clinical Presentation

What is most unique about preadolescent acne compared with conventional adolescent acne is its distribution on the face lesions generally occur on the forehead, nose, medial cheeks, and chin, and the trunk is usually unaffected or last to be affected. The primary morphology is usually comedonal in early lesions. Inflammatory papules and pustules usually present later and are relatively fewer in number. One distinctive feature of preadolescent acne is the presence of open comedones in the ear, which is often mistaken by parents for poor hygiene/dirt and scrubbed excessively. There may be significant progres-sion in a subgroup of these individuals from noninflammatory comedonal acne to severe, inflammatory disease with scarring.

Pathophysiology

In children from 8 to 12 years, it has been suggested that acne may represent a presenting sign of puberty sometimes appearing first prior to the development of pubic hair and breasts in girls and pubic hair and testicular enlargement in boys (31,32). The appearance of circulating serum androgens coincides with the onset of sebum production and presentation of acne in boys and girls. These androgens are derived from the adrenal glands, ovaries, and testes. Clinically, adrenarche is the term describing adrenal androgen maturation, and gonadarche is ovarian or tes-ticular maturation. In girls, the prevalence and severity of acne have been associated with early pubertal maturation. In particular, early onset of significant numbers of comedones in females is predictive of the development of severe, inflammatory acne as a teenager (31,33). Increased severity of acne is also associated with earlier onset of menarche. In girls who will eventually develop more severe acne, mean levels of DHEAS and total and free testosterone levels are higher even four years before menarche, although they may still be within the “normal” range (31).

Prepubertal acne is correlated with early and increased sebum output and increased numbers of skin follicles producing acne. With increasing age and pubertal status, the number of sebum-secreting follicles, area of sebum production on the skin, and density of Propionibacterium acnes increase in children who have acne (34). In age-matched individuals who did not develop acne, sebaceous gland activity and P. acnes counts on the skin did not increase with advancing age. It has been suggested, therefore, that the onset of sebum secretion and the expansion of P. acnes flora on the skin occur earlier in children with acne compared with those who do not develop acne. In contrast, P. acnes counts obtained from the nares increased proportionate to age, regardless of the status of the acne.

Additional factors thought to play a role in the onset of preadolescent acne include family history of acne and low weight at birth (35,36). Preadolescents with acne often report at least one first relative with a history of acne (35). Additionally, demographic studies on preadolescents with acne have shown a possible association between low birth weight and an increased likelihood of preadolescent acne (36). While explanations for this association are limited, one suggestion is that there may be a correlation between low birth weight and later findings of insulin resistance and PCOS also known to be related to acne. Further studies are needed to delineate a more detailed causal relationship.

Differential Diagnosis and Evaluation

The differential diagnosis of prepubescent acne includes, but is not limited to, keratosis pilaris, miliaria, drug-induced acne, pediatric rosacea, periorificial dermatitis, sarcoidosis, and cutaneous lupus. Hormone dysregulation due to a variety of etiologies must be considered. When evidence of hormonal irregu-larities is found on clinical and/or laboratory workup, the more common and concerning etiologies include premature adrenarche, Cushing’s disease or syn-drome, late-onset congenital adrenal hyperplasia, benign or malignant neoplasms of the gonads or adrenal glands, or true central precocious puberty.

If there is any suspicion of hormonal dysregulation in a preadolescent with acne, it is suggested that a hormonal workup be considered. In particular, children with persistent acne despite treatment, severe acne, and/or clinical evidence of virilization should undergo a more thorough evaluation. It has been recommended that the child’s height and weight be plotted on a growth chart, the physician perform a complete physical examination looking, in par-ticular, for signs of virilization such as hirsutism, clitoromegaly, androgenetic alopecia, increased muscle mass, and deepening of the voice, and an assessment be made of his or her Tanner stage of development. Bone age should be determined with radiologic imaging of the left hand and wrist. Laboratory evaluation may include total and free serum testosterone levels, dehydroepi-androsterone sulfate (DHEAS), A-4 adrostenedione, leutinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, and 17-oc hydroxyprogesterone. If congenital adrenal hyperplasia is suspected, ACTH (Cortrosyn®) stimulation testing with a full range of the androgenic steroids, which are precursors to cortisol, should be measured. If abnormalities are noted, evaluation by a pedi-atric or gynecologic endocrinologist should be sought.

Treatment

Treatment of preadolescent acne is similar to that of adolescents and adults. From a behavioral perspective, it is important to address the child’s own thoughts about his or her acne. In many cases, particularly with only comedonal lesions without an inflammatory component, the child may be unconcerned about the appearance of the acne. Occasionally, there is conflict between the child and parent about treatment. Postponing treatment until the child is more motivated is a valid option as long as there is little risk of scarring. Good skin care practices can be discussed, such as avoiding rigorous facial scrubbing and resisting the urge to “pimple-pop.” A basic discussion of acne pathogenesis is often helpful. In particular, discussing the lack of good evidence for a role of dirt or of food in the pathogenesis of acne can help alleviate the tension between parent and child.

If medical intervention is desired, it is best to start with the mildest agents possible while still providing therapeutic efficacy. Benzoyl peroxide may be used for as a first-line agent it is inexpensive, easy to apply, and available in many formulations (including washes, gels, and pads), and has a long track record of efficacy and safety when used as monotherapy for mild acne (37). From a pathogenic perspective, it also has excellent antimicrobial effects and has minimal tendency to induce antibiotic resistance in the acne-causing organism, P. acnes (38,39), as compared to some topical antibiotics. Warnings should be given about bleaching of clothing, towels, and linen, and for leave-on products often nighttime application may be most practical. Topical retinoids remain the cornerstone of treatment for significant comedonal acne and have significant effect on inflammatory lesions (40). Families should be counseled on the proper application of a pea-sized amount to the entire acne-prone areas rather than spot treatment of individual lesions.

To avoid excessive dryness of the skin, appli-cations may be initiated several times a week or every other day combined with a noncomedogenic gentle moisturizing agent containing sunscreen. If this is tol-erated, slow titration up to daily application is better tolerated. Topical retinoids may be used combined with benzoyl peroxide and/or with topical antibiotics if a multifaceted regimen approach is warranted, and topical retinoid/antibiotic combinations may be utilized. Clindamycin and erythromycin solutions or gels have long been used for cases of mild acne vulgaris. However, with emerging antibiotic resistance patters of P. acnes, it is now recommended that they be used in stabilized combination products with benzoyl peroxide (41). In patients unable to tolerate or are allergic to benzoyl peroxide, topical clindamycin or dapsone may be viable alternatives.

Systemic acne treatment, such as antibiotics, isotretinoin, and ocasionally hormonal therapy, antiandrogens, can be added to the patient’s regimen for more severe acne. For children of ages eight and above, after their dental enamel has been laid down, drugs of the tetracycline family (tetracycline, doxycycline, or minocycline) are safe options. Similar to treatment of adolescent and adult acne, many practitioners will initiate treatment of moderate to severe acne in this age group with oral antibiotics, in combination with topical benzoyl peroxide and topical retinoids. Hormonal therapy, including estrogen-containing oral contra-ceptives, is not indicated in girls prior to menarche but can be a very useful adjuvant when more conventional treatment fails. For oral medication, it is also important to determine whether the patient is able to swallow pills; otherwise, liquid preparations, crushed tablets, or sprinkling of capsule contents on food are alternatives to be considered.

Recently, it has been recommended to limit the duration of oral antibiotics to three months (42), in consideration of preadolescents being early in what is commonly a multi-year course of acne, and to minimize bacterial resistance. The rationale behind this recommendation is twofold; first, preadolescents may only be at the cusp of many years of acne, and safeguarding of oral antibiotics and systemic retinoid for later use is best. Additionally, long-term antibiotic use may not be prudent with the emerging concerns about bacterial resistance to antibiotics. Recommended oral antibiotics for preteens (eight years and above) are doxycycline, minocycline and tetracycline. They are no longer contra-indicated by this age because tooth formation, including enamel deposition, is complete and no longer affected by the tetracycline family. If the patient has a tetracycline allergy, other options include erythromycin, clindamycin, trimethoprim-sulfamethoxazole, cephalexin, or amoxicillin. However, these medications are not routinely used for acne and are secondary alternatives because of poorer efficacy, risks of antibiotic resistance, and other associated side effects. It is prudent to restrict use of these drugs because not only P. acnes but other microbial flora may develop drug resistance and thus effect drug efficacy for other indications.

When isotretinoin is used in preadolescent acne, the dosage and risk of side effects are similar to those described for mid-childhood acne. It is important to recognize that an additional issue in this age group is the variability of pubertal status, and the need for pregnancy prevention counseling in menarchal girls, and the use of the iPLEDGE program, legally required in the United States. The risk of depression has been proposed as a concern for any individual treated with isotretinoin. Acne itself can be a severe psychosocial stressor and a potential trigger for depression, especially in young people, and successful treatment of acne has been shown to improve depression (43,44). While the increased risk for depression and suicide in patients taking isotretinoin remains controversial, patients and families must be made aware of this concern and be vigilant for signs of mood change (43 45).

An additional treatment option for nodular acne lesions is intralesional injection of low-potency corticosteroids (46). The risks of this procedure are steroid-induced atrophy of the skin, the rare possibility of systemic absorption with subse-quent adrenal suppression, and the fear of injections of many children. To minimize these risks, it is recommended to use low concentrations of steroid, such as tri-amcinolone acetonide 2 mg/mL at low volumes, perform careful and slow injections, and employ standard pediatric techniques to reassure and secure the patient.

How medications are used is important in successful treatment of acne in the young. Studies have shown adherence at all ages to be only 65%, with a negative correlation with age (47). Additionally, many children are unmotivated to treat their acne and are, instead, brought to the office for treatment under duress by their parents. Others have problems adhering to complicated, multidrug regimens, which often take several weeks or months to show signs of efficacy. Therefore, it is often important to simplify the acne therapy as much as possible. Once-daily treatment, even if it means alternating therapies every other day, may be superior to twice-a-day dosing. The formulation of the product may also be important, such as using pumps or pads versus liquids and creams. Additionally, what might be important to each child can vary significantly some are concerned more with hyper-pigmentation or scarring, whereas others may be more concerned about the texture and smell of products in the treatment regimen. Speaking directly to the patient rather than through the parent and allowing the child to feel that he or she is in partnership with his physician and has some control over the acne regimen is helpful for successful therapy in this age group.

SUMMARY

Acne in the younger patient presents unique challenges. While neonatal acne appears to have a pathophysiology and a morphology that may be unrelated to acne at all, infantile, mid-childhood, and preadolescent acne share in being potential markers for underlying hormonal abnormalities. Once underlying endocrine etiologies are ruled out, however, the basic management principles for these types of acne are similar to those used for older teenagers and adults. These include topical antimicrobials and retinoids, systemic antibiotics, isotretinoin, and hormonal therapy. However, it is vital to employ a pediatric approach to the selection and delivery of acne care in young children to ensure successful therapy and satisfied patients and their families.

REFERENCES

1. Jansen T, Burgdorf WH, Plewig G. Pathogenesis and treatment of acne in childhood. Pediatr Dermatol 1997; 14:17 21.

2. Bergman JN, Eichenfield LF. Neonatal acne and cephalic pustulosis: is Malassezia the whole story? Arch Dermatol 2002; 138:255 256.

3. Niamba P, Weill FX, Sarlangue J, et al. Is common neonatal cephalic pustulosis (neonatal acne) triggered by Malassezia sympodialis? Arch Dermatol 1998; 134:995 998.

4. Ayhan M, Sancak B, Karaduman A, et al. Colonization of neonate skin by Malas sezia species relationship with neonatal cephalic pustulosis. J Am Acad Dermatol 2007; 57:1012 1018.

5. Rapelanoro R, Mortureux P, Coupie B, et al. Neonatal Malassezia furfur pustulosis. Arch Dermatol 1996; 132:190 193.

6. Antoniou C, Dessinioti C, Stratigos AJ, et al. Clinical and therapeutic approach to childhood acne: an update. Pediatr Dermatol 2009; 26:373 380.

7. Lucky AW. A review of infantile and pediatric acne. Dermatology 1998; 196:95 97.

8. Agache P, Blanc D, Barrand C, et al. Sebum levels during the first year of life. Br J Dermatol 1980; 103:643 649.

9. Henderson CA, Taylor J, Cunliffe WJ. Sebum excretion rates in mothers and neo nates. Br J Dermatol 2000; 142:110 111.

10. Morgan AJ, Steen CJ, Schwartz RA, et al. Erythema toxicum neonatorum revisited. Cutis 2009; 83:13 16.

11. Kaminer MS, Gilchrest BA. The many faces of acne. J Am Acad Dermatol 1995; 32: S6 S14.

12. Barnes CJ, Eichenfield LF, Lee J, et al. A practical approach for the use of oral isotretinoin for infantile acne. Pediatr Dermatol 2005; 22:166 169.

13. Herane MI, Ando I. Acne in infancy and acne genetics. Dermatology 2003; 206:24 28.

14. Cantatore Francis JL, Glick SA. Childhood acne: evaluation and management. Dermatol Ther 2006; 19:202 209.

15. Cunliffe WJ, Baron SE, Coulson IH. A clinical and therapeutic study of 29 patients with infantile acne. Br J Dermatol 2001; 145:463 466.

16. Hello M, Prey S, Leaute Labreze C, et al. Infantile acne: a retrospective study of 16 cases. Pediatr Dermatol 2008; 25:434 438.

17. Torrelo A, Pastor MA, Zambrano A. Severe acne infantum successfully treated with isotretinoin. Pediatr Dermatol 2005; 22:357 359.

18. Sarazin F, Dompmartin A, Nivot S, et al. Treatment of an infantile acne with oral isotretinoin. Eur J Dermatol 2004; 14:71 72.

19. Mengesha YM, Hansen RC. Toddler age nodulocystic acne. J Pediatr 1999; 134:644 648.

20. Horne HL, Carmichael AJ. Juvenile nodulocystic acne responding to systemic isotretinoin. Br J Dermatol 1997; 136:796 797.

21. Arbegast KD, Braddock SW, Lamberty LF, et al. Treatment of infantile cystic acne with oral isotretinoin: a case report. Pediatr Dermatol 1991; 8:166 169.

22. Burket JM, Storrs FJ. Nodulocystic acne occurring in a kindred of steatocystoma. Arch Dermatol 1987; 123:432 433.

23. Lucky AW. Hormonal correlates of acne and hirsutism. Am J Med 1995; 16: 89S 94S.

24. DiGiovanna JJ. Isotretinoin effects on bone. J Am Acad Dermatol 2001; 45: S176 S182.

25. Milstone LM, McGuire J, Ablow RC. Premature epiphyseal closure in a child receiving oral 13 cis retinoic acid. J Am Acad Dermatol 1982; 7:663 666.

26. Leachman SA, Insogna KL, Katz L, et al. Bone densities in patients receiving isotretinoin for cystic acne. Arch Dermatol 1999; 135:961 965.

27. DiGiovanna JJ, Langman CB, Tschen EH, et al. Effect of a single course of isotretinoin therapy on bone mineral density in adolescent patients with severe, recalcitrant, nodular acne. J Am Acad Dermatol 2004; 51:709 717.

28. Reddy D, Siegel CA, Sands BE, et al. Possible association between isotretinoin and inflammatory bowel disease. Am J Gastroenterol 2006; 101:1569 1573.

29. Bernstein CN, Nugent Z, Longobardi T, et al. Isotretinoin is not associated with inflammatory bowel disease: a population based case control study. Am J Gastro enterol 2009; 104:2774 2778.

30. Crockett SD, Gulati A, Sandler RS, et al. A causal association between isotretinoin and inflammatory bowel disease has yet to be established. Am J Gastroenterol 2009; 104:2397 2393.

31. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in premenarchal girls. An early sign of puberty associated with rising levels of dehydroepiandrosterone. Arch Dermatol 1994; 130:308 314.

32. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in early adolescent boys. Correlations with pubertal maturation and age. Arch Dermatol 1991; 127:210 216.

33. Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five year longitudinal study. J Pediatr 1997; 130:30 39.

34. Mourelatos K, Eady EA, Cunliffe WJ, et al. Temporal changes in sebum excretion and propionibacterial colonization in preadolescent children with and without acne. Br J Dermatol 2007; 156:22 31.

35. Ballanger F, Baudry P, N’Guyen JM, et al. Heredity: a prognostic factor for acne. Dermatology 2006; 212:145 149.

36. Pandolfi C, Zugaro A, Lattanzio F, et al. Low birth weight and later development of insulin resistance and biochemical/clinical features of polycystic ovary syndrome. Metabolism 2008; 57:999 1004.

37. Gollnick H, Schramm M. Topical therapy in acne. J Eur Acad Dermatol 1998; 11(suppl 1):S8 S12; discussion S28 S29.

38. Leyden JJ, Wortzman M, Baldwin EK. Antibiotic resistant Propionibacterium acnes suppressed by a benzoyl peroxide cleanser 6%. Cutis 2008; 82:417 421.

39. Bojar RA, Cunliffe WJ, Holland KT. The short term treatment of acne vulgaris with benzoyl peroxide: effects on the surface and follicular cutaneous microflora. Br J Dermatol 1995; 132:204 208.

40. Krakowski AC, Eichenfield LF. Pediatric acne: clinical presentations, evaluation, and management. J Drugs Dermatol 2007; 6:589 593.

41. Mills O, Thornsberry C, Cardin CW, et al. Bacterial resistance and therapeutic outcome following three months of topical acne therapy with 2% erythromycin gel versus its vehicle. Acta Derm Venereol 2002; 82:260 265.

42. Dre´no B, Bettoli V, Ochsendorf F, et al. European recommendations on the use of oral antibiotics for acne; European Expert Group on Oral Antibiotics in Acne. Eur J Dermatol 2004; 14:391 399.

43. Marqueling AL, Zane LT. Depression and suicidal behavior in acne patients treated with isotretinoin: a systematic review. Semin Cutan Med Surg 2007; 26:210 220.

44. Azoulay L, Blais L, Koren G, et al. Isotretinoin and the risk of depression in patients with acne vulgaris: a case crossover study. J Clin Psychiatry 2008; 69:526 532.

45. Jacobs DG, Deutsch NL, Brewer M. Suicide, depression, and isotretinoin: is there a causal link? J Am Acad Dermatol 2001; 45:S168 S175.

46. Levine RM, Rasmussen JE. Intralesional corticosteroids in the treatment of nodulocystic acne. Arch Dermatol 1983; 119:480 481.

47. Zaghloul SS, Cunliffe WJ, Goodfield MJ. Objective assessment of compliance with treatments in acne. Br J Dermatol 2005; 152:1015 1021.

Jean-Paul Marat

Many tips are based on recent research, while others were known in ancient times. But they have all been proven to be effective. So keep this website close at hand and make the advice it offers a part of your daily life.