Acne and Acneiform

2 Dermatoses

Acne vulgaris is a follicular disorder affecting tances produced by Propionibacterium acnes seep
susceptible pilosebaceous follicles, primarily of into dermis and attract neutrophils and activate
the face, neck, and upper trunk and characteri- complement.
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matory lesions. It is one of the most common CLINICAL FEATURES
dermatoses affecting the teenage population. The comedones, open or closed, are the patho-
Boys have a peak incidence between ages of genic lesions of acne (Figs 2.1A and B). Papules,
16 and 19 years and girls between ages of 14 pustules, nodules, and cysts (Fig. 2.2) may also
and 16 years. Both sexes are equally affected. appear during the course of the disease. The
Most cases of acne subside completely within a lesions are localized to the face, neck, back,
few years of their onset but a small percentage anterior chest, and extremities. The open come-
continue to remain active. done, also called blackhead, has a widely dilated
Acne vulgaris is a dermatosis of unknown RULÀFHÀOOHGZLWKNHUDWLQOLSLGVDQGRUJDQLVPV
etiology. However, many factors are incrimina- Melanin imparts black color to the lesion.
ted in its pathogenesis and aggravation. Andro- The closed comedone, a whitehead, is a
genic stimulation at puberty is believed to VPDOO ÁHVK FRORUHG SDSXOH WKDW KDV RQO\ D
increase the activity of sebaceous glands and microscopic opening, which prevents its con-
sebum production. A change in the process of tents from escaping. Continued production
keratinization of the sebaceous follicle may pro- of sebum and keratin, leads to rupture of the
duce an increased adherence of the horn cells follicular wall, releasing the contents into
resulting in retention hyperkeratosis. Free fatty WKH GHUPLV DQG LQLWLDWLQJ DQ LQÁDPPDWRU\
acids in the surface lipids are also suspected to UHVSRQVH 7KLV LQÁDPPDWLRQ LQ WKH GHUPLV LV
be comedogenic. Bacterial colonization of the responsible for the papules, pustules, cysts,
sebaceous follicle may also contribute in the and nodules.
pathogenesis of acne. Propionibacterium acnes,
Staphylococcus epidermidis, and Pityrosporum DIAGNOSIS
ovale colonize the follicle and produce lipases. There are no diagnostic tests for acne vulgaris.
These lipases hydrolyse the sebum triglycerides Diagnosis is clinical. However, lesions of acne
to free fatty acids, which contribute to follicular vulgaris need to be differentiated from acnei-
hyperkeratosis. Also biologically active subs- form dermatoses.
 Acne and Acneiform Dermatoses 13

A B
Figures 2.1A and B: Acne vulgaris—comedons
Neonatal acne: It is characterized by the
formation of comedones in a newborn. The
lesions are localized to the nose and adjacent
areas of cheeks. It is due to stimulation of the
sebaceous glands by maternal hormones. It
clears spontaneously.
Drug acne: Prolonged application of topical
steroids especially on the face, systemic corti-
costeroids, adrenocorticoids, iodides, bromides,
lithium, and isoniazid may result in acne. The
lesions consist of small papules and pustules
localized mainly on the trunk.
Occupational acne: Several industrial com-
pounds like tar derivatives, cutting oils, chlori-
nated hydrocarbons may cause acne. The lesions
DUH LQÁDPPDWRU\ DQG SUHVHQW DV FRPHGRQHV
papules, pustules, large nodules, and cysts.
Figure 2.2: Acne vulgaris—cystic acne They tend to involve areas covered by clothing
 14 Textbook of Clinical Dermatology

permitting intimate contact between the offen- (grade III). Small, red bumps (nodules) or
ding chemical and skin. Face is usually spared. pustules are its salient clinical manifestations,
Tropical acne: This develops in tropical climate spreading across the nose, cheeks, forehead
and is localized to trunk and buttocks. It re- and chin. Hyperglandular subtypes may
sembles acne conglobata and presents as deep, lead to different forms of phyma, of which
ODUJHLQÁDPPDWRU\QRGXOHV rhinophyma is the most frequent.
Acne cosmetica: Certain cosmetics induce acnei- Moreover, in view of the natural history of
form eruption and are responsible for persistent the disease National Rosacea Society Expert
low grade close comedones on the face. Committee on CODVVLÀFDWLRQ DQG Staging of
Pomade acne: The pomade applied to the scalp rosacea had taken cognizance of subtypes and
may spill to the forehead and cause acne. It is variants of rosacea and their characteristics,
frequently seen in black males. The lesions are and had made certain recommendations, the
multiple, closely packed, closed comedones. briefs of which are replicated in Table 2.1. The
Rosacea/ Acne rosacea: Rosacea/acne rosacea clinical features are more or less similar to those
is a well-conceived fascinating overture. It described (vide supra), with the only addition
is a common facial dermatosis, which may of granulomatous rosacea.
have deleterious effects on the patient’s The condition seems to be a reaction
psychosocial interactions. It is a disease of pattern, and is heralded by remissions and
the middle age, more prevalent in skin type exacerbation. The diagnosis in the current
I and II, than those in darker skin type. It is, SDWLHQW FRQIRUPHG WR LQÁDPPDWRU\ JUDGH ,,,
therefore, worthwhile to emphasize that the rosacea, and had ventured through the well-
entity is recognized to occur in phases, and recognized phases. The microscopic pathology
may pass through distinct phases namely was complementary, and was characterized by
pre-rosacea (grade 1), vascular rosacea (grade dilation of the hair follicle(s), dense perivascular
,,DQG,QÁDPPDWRU\URVDFHDJUDGH,,,3UH DQGSHULIROOLFXODUO\PSKRKLVWLRF\WLFLQÀOWUDWH
URVDFHD JUDGH  LV LGHQWLÀHG E\ D VLPSOH and lymphocytic exocytosis and edema, in
WHQGHQF\WREOXVKÁXVKZKLFKPD\SURJUHVV the follicular epithelium in addition to focal
to a persistent redness in the central portion epithelioid cell granulomas. The preceding
of the face, occupying the nose in particular. FKDQJHV DUH ODUJHO\ FRQÀQHG WR WKH XSSHU
The redness of the face is an outcome of dermis, while lower dermis is relatively
dilation of blood vessels approximating the free. Nevertheless, it is imperative to take
skin surface. The progression of this phase stock of the other clinical conditions which
may trespass into vascular rosacea (grade II). may simulate rosacea/acne rosacea; acne
The latter may develope small blood vessels vulgaris, erysipelas, seborrhoeic -and contact
on the nose and cheeks swell and become eczema as well as systemic diseases like lupus
apparent resulting in telangiectasia. Also the erythematosus, dermatomyositis, scleroderma,
skin may become overtly sensitive. It may sarcoidosis, leukemia, and lupus miliaris
also have an accompaniment of oily skin and disseminatus faciei. Although the precise
dandruff. The continuation of the disease may pathogenesis and pathophysiology 3 of the
XOWLPDWHO\ UHVXOW LQ LQÁDPPDWRU\ URVDFHD condition is only speculative yet destruction of
 Acne and Acneiform Dermatoses 15
Table 2.1: Subtype s and variants of rosacea and their characteristics
Subtype Characteristics
Erythematotelangiectatic Flushing and persistent central facial erythema with or without telangiectasia.
Papulopustular Persistent central facial erythema with transient, central facial papules or pustules
or both.
Phymatous Thickening of skin, irregular surface nodularities and enlargement. May occur on the
nose, chin, forehead, cheeks, or ears.
Ocular Foreign body sensation in the eyes, burning or stinging, dryness, itching, ocular
photosensitivity, blurred vision, telangiectasia of the sclera or other parts of the eye,
or periorbital edema.
Variants granulomatous 1RQLQÀDPPDWRU\KDUGEURZQ\HOORZRUUHGFXWDQHRXV

Table 2.2: Systemic therapy for acne vulgaris

Drugs Trade name Dosage Duration of therapy Other information
1. Antibiotics
a. Tetracycline Hostacycline 250 mg four times a 4–5 weeks Prolonged use may
day initially. result in gram-negative
Maintenance with Several months folliculitis.
250–500 mg daily. Also predisposes to
monilial vaginitis.
b. Erythromycin Erythrocin 250 mg four times a 4–5 weeks Estolate salt may cause
day initially. cholestatic jaundice.
Maintenance with Several months
250–500 mg daily.
c. Doxycycline Nudoxy 100–200 mg daily 4–5 weeks
initially followed by
maintenance dose Several months
of 50–100 mg daily.
d. Minocycline 50-100 mg twice a day. Several months High incidence of CNS
side-effects.
e. Clindamycin 150 mg thrice a day. A few weeks to Pseudomembranous
months colitis.
2. Estrogens
Ethinyl 100 µg once a day. A few months To be used only in
estradiol females over 16 years
with recalcitrant, severe,
pustulocystic acne.
3. Retinoids
Isotretinoin Accutane 1 mg per kg per day 15-20 weeks and if To be used only in severe
    IRUIDFLDOOHVLRQV UHTXLUHGDVHFRQG GLV¿JXULQJF\VWLFDFQH
2 mg per kg per day course after two Not to be used in
for truncal acne. months. pregnancy.
Contraception advised
during the treatment.
 16 Textbook of Clinical Dermatology

the dermal vessels and connective tissue seem In moderately severe cases, topical retinoids
to be accountable for the development of a DUH DGYLVHG 7UHWLQRLQ  SHUFHQW FUHDP
FKURQLFLQÁDPPDWLRQ7KLVPD\LQWXUQOHDGWR (Retino-A, Eudyna) may be used. These pre-
the phenotype of the various grades of rosacea. parations are applied once daily to all areas
except around the eyes. They should be applied
Treatment on dried skin. Erythema and peeling are the
The treatment of acne vulgaris may consist of effects of therapy. Patient should be cautioned
topical therapy, systemic therapy, or a combina- about the initial exacerbation of the lesions and
tion of both. also advised to protect the skin from sunlight.
Topical therapy alone is indicated for mild Keratolytics like sulfur, resorcinol, and
to moderate lesions, and it may consist of the D-hydroxy acids are irritants and are thus avoided.
following: Systemic therapy: The details of systemic the-
For mild lesions, consisting of only comedo- rapy are displayed in Table 2.2.
nes, bacteriostatic agents are indicated. These
are as follows: RECOMMENDED READING
‡ %HQ]R\O SHUR[LGH³ SHUFHQW JHO SHUQR[ 1. Buxton PK. ABC of dermatology: Acne and rosa-
cea. Br Med J
gel) 2. Drake LA. American Academy of Dermatology.
‡ 7RSLFDODQWLELRWLFV Guidelines for care of acne vulgaris. J Am Acad
– Erythromycin 2 percent lotion (acnesol) Dermatol. 1990;22:676-680.
and 3 percent cream (acnicin) 3. Kligman AM. An overview of acne. J Invest Derma-
tol 1974; 6: 268-287.
– Clindamycin phosphate 1 percent lotion 4. Leyden JT. Retinoids and acne. J Am Acad Derma-
(cleocin) tol. 1988; 19:164.
– Tetracycline hydrochloride lotion.   6KDOLWD$5$FQHUHYLVWHGDUFKDermatol 1994;130:
363.
Benzoyl peroxide is administered for come-   6DUGDQD.*DUJ9.6HKJDO91HWDO(IÀFDF\RI
dones, while the papular and pustular lesions À[HGORZGRVHLVRWUHWLQRLQPJDOWHUQDWHGD\V
respond to topical antibiotics. Clindamycin and with topical clindamycin gel in moderately severe
erythromycin are equally effective. They not acne vulgaris. J Eur Acad Dermatol Venereol. (In
Press).
RQO\DUHEDFWHULRVWDWLFEXWDOVRVXSUHVVLQÁDP 7. Sehgal V, Sharma S, Sardana K. Rosacea/acne ro-
mation. They are applied twice daily and cause VDFHDHIÀFDF\RIFRPELQDWLRQWKHUDS\RID]LWKUR-
mild dryness and erythema. mycin and topical 0.1% tacrolimus ointment. J Eur
Acad Dermatol Venereol. 2008; 22:1366-368.