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Abstract

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The diagnosis of acne is usually easy, but there are some pitfalls to be avoided. ‘Keloid acne of the neck’ and beard folliculitis are not acnes in the usual sense: both are inflammatory and fibrous reactions of the hair follicles and frizzy hair; no retentional lesions, blackheads and microcysts – are visible. Gram negative folliculitis classically occurs in acneic male subjects who have undergone extensive treatment with general antibiotics or local antiseptics, but ‘de novo’ cases do exist. On black skin, this condition is not exceptional, it occurs in both sexes and usually takes the nodular form. The diagnosis should be considered if there is any aggravation of acne which is resistant to classic treatment, with painful nodules on the cheeks. Treatment is based on appropriate antibiotherapy for several weeks and possibly, in a second phase, on Isotretinoin. Pityrosporum folliculitis occurs mainly on the trunk. More frequent in men than in women, it is chiefly observed in subjects living in a hot, humid climate. Demodicidosis is manifested by outbreaks of papular or papulopustular lesions of the face. On black skin the principal differential diagnosis is acne. The presence of numerous parasites is necessary for diagnosis. Clinically speaking, an important sign is when the eyelids are affected. Ivermectin is effective. Acneiform dermatitis may be induced by depigmenting preparations containing powerful dermocorticoids. It is therefore important, in cases of very inflammatory acne, to look for the other clinical signs of voluntary depigmentation. In countries where it is endemic, lepromatous leprosy should be considered. Other common dermatitis may simulate acne or else be associated with it, such as eruptive hidradenoma or molluscum contagiosum. Analysis of the different elementary lesions and the absence of retentional lesions generally enable a diagnosis to be established.

Acne is very frequent among Africans. In France, patients with a black skin who are of African and West Indian origin have acne as their first reason for consultation with a doctor (29%).1 Acne is a chronic inflammatory disease of the pilosebaceous follicle. It affects 80% of adolescents. Acne affecting black skin is mainly of inflammatory type. The earliness of the inflammatory reaction may sometimes make the retentional lesions less visible – this has been histologically demonstrated. The papulopustules are predominant. The nodules are not frequent and, if present, they can be associated with keloid scars. The simultaneous findings of inflammatory lesions (i.e., papules and pustules) and retentional lesions (i.e., open and closed comedos), is mandatory for making an accurate diagnosis of acne. On black skin, postinflammatory pigmentations are constant, often predominant, and frequently the main reason for consultation, ahead of acne. Patients with pigmented skin therefore often associate the severity of their acne with the visibility of hyper pigmentation, as this may constitute a significant social handicap for them.2,3 The diagnosis of acne is usually easy, but certain traps need to be avoided.

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Figure 1  Demodex folliculitis

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Figure 2  Pityrosporum folliculitis

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Figure 3  Gram negative folliculitis

Acne keloidalis nuchae acne and pseudo folliculitis barbae are not acne in the true sense of the word: they are both inflammatory processes of the hair follicles from the scalp or from frizzy hair followed by fibrous, reactions. Chronic inflammatory lesions result in hypertrophic scars, especially on the nape of the neck. There are no visible retentional lesions, open and closed comedos. These two diseases are easily differentiated from acne.4

Acne may be mistaken for gram-negative folliculitis caused by pityrosporum yeast and demodex mite.

Gram-negative folliculitis usually occurs in male patients suffering from acne, undergoing long-term treatment with systemic antibiotics or topical antiseptics, although there are some “de novo” cases. Two varieties have been described: type I, characterized by superficial pustules around the mouth and nostrils and type II, which is uncommon, and is defined by inflammatory and painful nodules on the cheeks. The germs found most often are Klebsiella, Escherichia coli, Enterobacter; Proteus is found in the nodular forms. On black skin, this disorder is not unusual, often occurs in both genders, and usually as the nodular variety. If acne becomes more severe and resistant to regular treatment and includes painful nodules on the cheeks, this diagnosis must be considered. Treatment is based on antibiotics, adapted to the responsible germ over several weeks and, secondarily, isotretinoin, if necessary.5,6

Pityrosporum folliculitis is found mainly on the trunk. It is characterized by follicular papules and pustules on the skin, which are often itchy. This is more common in men than women, and is mainly encountered in people living in hot, humid climates. The absence of comedos and the monomorphic appearance suggest the diagnosis. Mycological investigation reveals the presence of Malassezia in 90% of cases. Topical, and possibly systemic, imidazoles are the usual treatment although there are frequent relapses.7

Signs of demodex folliculitis are outbreaks of papular or papulopustular lesions on the face but there are no comedos. In black skin, the main differential diagnosis is acne and not rosacea. In black patients, rosacea is not common and erythema, which does not affect black skin, loses its semiological value. Clinically, the diagnosis must be considered if there is an acneiform, itchy skin rash, with no retentional lesions. An important sign is the fact that the papules often affects the eyelids. By simply scraping the papules and spreading out the material on a slide, one is able to display the demodex mites and these parasites can be quantified. The presence of a large number of mites, establishes the diagnosis. Treatment with metronidazole or other topical antiparasitic medication is disappointing but systemic ivermectin is effective.8

Corticosteroids induced “acne” is a type of acneiform dermatitis, which may be induced by depigmenting preparations containing powerful dermocorticoids. As these preparations are frequently used by African people as lighteners or for attempts to remove post-acne pigmentation, this may lead to a vicious circle, which is a source of diagnostic and therapeutic confusion. It is therefore important, in front of a very inflammatory acne, to look for other clinical signs of skin bleaching (stretch marks or striae, strips of pigmentation on the hands, etc.) to be able to recommend appropriate treatment.9

The other so-called types of drug-based “acne” (corticoids, isoniazid, lithium, halogens, antineoplastic drugs, etc.) must be investigated for a monomorphous papulopustular outbreak, without comedos. These are not neoplastic drugs acne but actually folliculitis caused by medication.

Hidradenitis suppurativa (HS) of the face and back may be mistaken for nodular acne. The classic appearance is that of suppurative or relapsing nodules and abscesses in areas where the apocrine glands are located. Face and back involvment must be recognized; it is most frequently associated with classic localisations, although it may be isolated. HS of the face and back is characterized by the presence of draining sinuses, painful coalescent nodules and rounded depressed scars and sometimes rope like hypertrophic scars. There may be open comedos. This aspect suggests severe acne; thus treatment with isotretinoin is prescribed, usually leading to worsening. Treatment with a combination of rifampicin and clindamycin for 10 weeks is effective; maintenance treatment with doxycycline is necessary.10

Nodular lepromatous leprosy on the face is frequently diagnosed in countries where this is endemic.

Other common dermatoses may mimic acne or be associated with it, such as eruptive hidradenomas or molluscum contagiosum.

As it is very common for acne to affect black skin, this diagnosis must not be made for any inflammatory dermatosis of the face and back. The analysis of clinical features and absence of comedos and their clinical evolution development generally allow the diagnosis to be established.

References

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  2. Abstract
  3. References