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1. Acne conglobata 
2. Acne fulminans 
3. Neonatal acne 
4. Infantile acne 
5. Post-adolescent 
acne 
6. Acne excoriée 
7. Cosmetic / Pomade 
acne 
8. Acne Detergicans 
9. Acne mechanica 
10.Premenstrual Acne 
11.Occupational acne 
/ Chloracne 
12.Senile (solar) 
comedones 
13.Drug-induced acne 
14.Pyoderma Faciale 
15.Solid facial edema
 Conglobate: shaped in a rounded mass or 
ball 
 Severe form of inflammatory nodulocystic 
acne characterized by numerous comedones, 
large abscesses or cysts interconnecting with 
sinuses, grouped inflammatory nodules but 
without systemic manifestations. 
 Suppuration 
 on forehead, cheeks, and neck
 Occurs most frequently 
in young men 
 Follicular Occlusion Tetrad: 
I. Acne conglobata, 
II. Hiradenitis suppurva, 
III. Dissecting cellulitis of the scalp 
IV. Pilonidal cysts 
 Heals with scarring difficult to prevent 
 Treatment; oral isotretinoin for 5 months
 The association of 
1. Sterile Pyogenic Arthritis, 
2. Pyoderma gangrenosum, 
3. Acne conglobata 
 can occur in the context of an autosomal 
dominant autoinflammatory disorder 
referred to as PAPA syndrome.
 the most severe form of 
acne characterized by 
sudden onset of severely 
inflamed nodulocystic & 
suppurative acne lesions 
in association with systemic manifestations. 
 Rare form of extremely severe Teenage 
boys, chest, shoulders & back 
 Patients typically have mild to moderate 
acne prior to the onset of acne fulminans
 Rapid coalescence into painful, oozing, 
friable plaques with hemorrhagic crusts 
Rapid degeneration of nodules leaving 
ulceration can lead to significant scarring. 
 Fever, arthralgias, myalgias, 
hepatosplenomegaly, severe malaise. 
anorexia are common. Osteolytic bone 
lesions may accompany the cutaneous 
finding. 
 Ix: leukocytosis, proteinuria
 Synovitis, Acne, Pustulosis, 
Hyperostosis, and Osteomyelitis 
 Acne fulminans, acne conglobata, 
pustular psoriasis, and palmoplantar 
pustulosis 
 Chest wall is most site of 
musculoskeletal complaints
Pustules on the sole of the left foot (A) and left palm (B), 
and radioisotope scan (C) showing intense uptake by the 
sternoclavicular and first sternocostal joints.
1. Oral steroids 
2. Oral isotretinoin often with initiation of the 
latter at a low dose and/or after the acute 
inflammation subsides. 
3. Topical or intralesional corticosteroids, 
4. Oral antibiotics (limited efficacy), 
5. TNF-α inhibitors 
6. Immunosuppressives (e.g. azathioprine). 
7. Dapsone
 Postadolescent girls, reddish 
cyanotic erythema with 
abscesses and cysts 
 Distinguished from acne by 
absence of comedones, rapid 
onset, fulminant course 
and absence of acne on the 
back and chest 
 Tx; oral steroids followed 
by isotretinoin
 very common First four weeks of life 
 More than 20% of healthy newborns. 
 Facial papules or pustules typically no 
comedones. 
 Arise primarily on the cheeks and nasal 
bridge but the forehead, chin, neck and 
upper trunk can also be involved.
 The development related to hormonal 
activity in utero / An inflammatory response 
to Malassezia spp. (e.g. furfur) has been 
proposed as the etiology and will resolve 
spontaneously 1-3 months after delivery 
without evidence of scarring. 
 No treatment is required except reassurance 
for parents who may be extremely anxious 
 Tx with topical imidazoles (e.g. 
ketoconazole 2% cream).
 Cases that persist beyond 4 weeks or have 
an onset after 
 In contrast to neonatal acne, comedo 
formation is prominent and pitted scarring 
can develop. 
 Infantile acne typically resolves within 1–2 
years and remains quiescent until around 
puberty. In unusual cases, however, 
infantile-onset acne may persist into 
adolescence.
 Androgen production intrinsic to this stage 
of development including elevated levels of 
LH stimulating testicular production of 
testosterone in boys during the first 6–12 
months of life (with levels transiently 
equivalent to those during puberty) and 
elevated levels of DHEA produced by the 
infantile adrenal gland in both boys and 
girls. These androgen levels normally 
decrease substantially by 6-12 months of 
age and remain at nadir levels until 
adrenarche.
 Topical retinoids (e.g. tretinoin, 
adapalene) and benzoyl peroxide are first-line 
treatments. 
 Oral antibiotics (e.g. erythromycin, 
azithromycin) can be helpful for patients 
with a more severe inflammatory 
component, 
 Isotretinoin is occasionally required for 
recalcitrant or nodulocystic presentations
 Inflammatory acne persisting beyond 25 
years of age is most common in women, 
 Tends to flare during the week prior to 
menstruation, and typically features tender, 
deep-seated papulonodules on the lower 
third of the face, jawline and neck. 
 Approximately one-third of affected women 
have other signs of hyperandrogenism 
 Regardless of androgen levels, hormonal 
therapy is often effective.
 Papulopustular lesions week prior 
 Estrogen-dominant contraceptive pills 
will diminish
 Girls, mild acne minute or 
trivial primary lesions are 
made worse by squeezing, 
scratching, erosions and 
crusting on individual lesions. 
 Crusts, scarring, and atrophy 
 Individuals with an anxiety 
disorder, obsessive– 
compulsive disorder or 
personality disorder are 
particularly at risk
 In addition to acne Rx; 
 eliminate magnifying mirror, 
 Rx of depression; Antidepressants or 
psychotherapy
 Occurs secondary to repeated 
mechanical and frictional 
obstruction of the 
pilosebaceous outlet. 
 Well-described mechanical 
factors include rubbing by 
helmets, chin straps, 
suspenders and collars.
 Fiddler’s neck, where 
repetitive trauma from violin 
placement on the lateral neck 
results in a well-defined 
lichenified, hyperpigmented 
plaque interspersed with 
comedones. Linear & 
geometrically distributed areas 
of involvement should suggest 
acne mechanica. 
 Treatment is aimed at 
eliminating the inciting forces
 Patients wash face with comedogenic 
soaps 
 Closed comedones 
 Tx; wash only once or twice a day 
with non-comedogenic soap
 An unusual and disfiguring 
complication of AV. 
 Clinically, there is a 
distortion of the midline 
face& cheeks due to soft 
tissue swelling. 
 The woody induration may be accompanied by 
erythema. Impaired lymphatic drainage and 
fibrosis. 
 Fluctuations in severity are common, but does 
not usually resolve spontaneously.
1. Isotretinoin (0.2–1 mg/kg/day), 
alone or in combination with; 
2. Ketotifen (1–2 mg/day) or; 
3. Prednisone (10–30 mg/day), for 4–5 
months.
 Rare, females 25-40 yrs 
 Starts in spring, resolves by fall 
 Small papules on cheeks, neck, upper body 
 Comedones & pustules are sparse or absent 
 Tx; retinoic acid, abx don’t help
 Exposure to insoluble, follicle-occluding 
substances in the workplace. 
 Comedones dominate the clinical picture, with 
varying numbers of papules, pustules and cystic 
lesions distributed in exposed as well as typically 
covered areas. 
 Offending agents: 
1. Cutting oils 
2. Petroleum-based products 
3. Chlorinated aromatichydrocarbons (Chloracne) 
4. Coal tar derivatives.
 Appear after prolonged 
exposure to coal-tar 
products coal tar oils, 
 These compounds, forming 
a black plug mixed with 
dead skin cells and keratin. 
 Especially the face and arms. 
 If not treated properly, coal-tar acne can 
develop into skin cancer
 Occupational acne caused by exposure to 
chlorinated aromatic hydrocarbons, 
develops after several weeks of exposure. 
 The malar, retroauricular and mandibular 
regions of the head and neck as well as the 
axillae and scrotum, are most commonly 
afflicted with small cystic papules and 
nodules. The extremities, buttocks and 
trunk are variably involved.
 Cystic lesions can heal with significant 
scarring, and recurrent outbreaks may 
occur for many years following exposure. 
 Chloracnegens, found in electrical 
conductors and insulators, insecticides, 
fungicides, herbicides and wood 
preservatives. 
 Prevention of exposure is integral to the 
safety of at-risk employees.
 Initial management is aimed at 
vigorous removal of chemical agents 
at the time of exposure. 
 Topical or oral retinoids and oral 
antibiotics may be beneficial 
therapeutic interventions
 Closed comedones and papulopustules on 
the chin and cheeks 
 In areas of skin chronically exposed to 
follicle-occluding cosmetics 
 May take months to clear after stopping 
cosmetic product
 Blacks, males, due to greases or oils 
applied to hair. 
 Favors forehead and temples
 Acneiform eruptions are dermatoses that 
resemble acne vulgaris. 
 Lesions may be papulopustular, nodular, or 
cystic. While acne vulgaris typically consists 
of comedones, acneiform eruptions (such as 
acneiform drug eruptions) usually lack 
comedones clinically. 
 Location may be outside of the area in 
which acne vulgaris occurs. 
 Age outside the range typical of acne 
vulgaris.
 Acnelike eruptions develop as a result of; 
1.Infections. 
2.Hormonal abnormalities. 
3.Metabolic abnormalities. 
4.Genetic disorders. 
5.Drug reactions.
1.Epidermal growth factor 
receptor inhibitor-induced 
papulopustular eruption 
2.Tropical acne 
3.Radiation acne 
4.“Pseudoacne” of the 
transverse nasal crease 
5.Idiopathic facial aseptic 
granuloma 
6.Childhood flexural 
comedones 
7.Nevus comedonicus. 
8.Eruptive hair cysts. 
9.Tuberous sclerosis. 
10.Chloracne. 
11.Acneiform drug eruptions. 
12.Steroid acne. 
13.Amineptine acne. 
14.Gram-negative folliculitis. 
15.Eosinophilic pustular 
folliculitis. 
16.Pityrosporum folliculitis. 
17.Coccidioidomycosis. 
18.Secondary syphilis. 
19.Sporotrichosis. 
20.Rosacea. 
21.Perioral dermatitis. 
22.Senile (solar) comedones
 EGFR inhibitors used for the treatment of solid 
tumors, including head and neck squamous cell 
carcinoma and lung, colon and breast carcinoma. 
 The incidence of acneiform eruptions due to EGFR 
inhibitors is very high, e.g. up to 95% of patients 
treated with panitumumab. 
 Patients present with an eruption of monomorphous 
follicular pustules and papules involving the face, 
scalp and upper trunk, usually 1–3 weeks after 
beginning treatment with an EGFR inhibitor. 
 No comedonal lesions are seen either microscopically 
or clinically,
Acneiform eruptions due to epidermal growth 
factor receptor inhibitors. A,B Numerous 
monomorphous follicular pustules and crusted 
papules on the face of two patients treated with 
erlotinib
 Follicular acneiform eruption that results from 
exposure to extreme heat. 
 Markedly inflamed nodular, cystic, and 
pustular lesions on back, buttocks, & thighs 
 Face is spared 
 Young adult military 
stationed in tropics, 
furnace workers. 
 Tx; returns to a more 
moderate climate.
 Characterized by comedo-like papules 
occurring at sites of previous exposure to 
therapeutic ionizing radiation. 
 The lesions begin to appear as the acute 
phase of radiation dermatitis starts to resolve. 
 The ionizing rays induce epithelial 
metaplasia within the follicle  adherent 
hyperkeratotic plugs that are resistant to 
expression.
 The transverse nasal crease is a horizontal anatomical 
demarcation line found in the lower third of the nose 
which corresponds to the 
separation point between 
the alar cartilage and the 
triangular cartilage. 
 Milia, cysts & comedones 
can line up along this fold. 
 These acne-like lesions 
aren’t hormonally responsive 
& arise during early childhood prior to puberty. 
 Tx; consists of surgical expression as needed.
 chronic, painless, usually 
solitary nodule with an 
acneiform appearance can 
develop on the cheeks of 
young children. 
 Histopathologic evaluation 
reveals a granulomatous 
inflammatory response; dermal 
lymphohistiocytic infiltrate with 
foreign body-type giant cells. 
 They eventually resolve 
spontaneously after an average 
of 11 months without treatment
 Discrete, double-orifice comedones 
localized to the axillae & less 
commonly, the groin. 
 The majority of patients have a single 
lesion and the average age at Dx is 6 
years. 
 A small subset of cases are familial. 
 In most cases, the flexural comedones 
are discovered incidentally in patients 
presenting with other dermatologic 
concerns.
From: Childhood Flexural Comedones: A New Entity 
Arch Dermatol. 2007;143(7):909-911. doi:10.1001/archderm.143.7.909 
The left axilla showing 3 double-orifice comedones in a 4-year-old boy. 
Date of download: 9/2/2014 
Copyright © 2014 American Medical 
Association. All rights reserved. 
Figure Legend:
From: Childhood Flexural Comedones: A New Entity 
Arch Dermatol. 2007;143(7):909-911. doi:10.1001/archderm.143.7.909 
Axillary double-orifice comedo with a visible content underlying the epidermal bridge in an 8-year-old boy. 
Date of download: 9/2/2014 
Copyright © 2014 American Medical 
Association. All rights reserved. 
Figure Legend:
 Occurs in prolonged treatment with 
antibiotics for acne vulgaris or rosacea. 
 E. coli, Enterobactor, Klebsiella, Proteus. 
 Anterior nares colonized 
 Persistent papulopustular eruption, 
 These gram-negative organisms are 
typically spread to the skin of the upper 
lip, chin, and jawline. 
 Tx; isotretinoin is considered standard of 
care.
 Papulopustules with erythematous base 
 Characteristically; Clear zone around vermillion 
border. It may also include the perinasal and 
periorbital areas (periocular dermatitis). 
 Young ♀ (23-35yrs) 
 Has a superficial resemblance to rosacea
 Etiology; 
1. Topical steroids 
2. Demodex mites 
3. Contact irritants or allergens 
4. Moisturizers 
5. Cleansers 
6. Fluorinated compounds e.g. fluorinated 
toothpaste 
 Tx; d/c topical steroids or other offending agent 
- oral tetracycline 1g/d or doxycycline 
- topical pimecrolimus cream, 
- azelaic acid
 An abrupt, monomorphous eruption of 
inflammatory papules and pustules
 High-dose IV or oral corticosteroids commonly 
induce characteristic acneiform eruptions with a 
concentration of lesions on the chest and back 
 Steroid-induced acne (and rosacea) can also 
result from the inappropriate use of topical 
corticosteroids on the face. Inflamed papules and 
pustules develop on a background of erythema 
that favors the distribution of corticosteroid 
application. 
 Lesions eventually resolve following 
discontinuation of the steroid, although “steroid 
dependency” can lead to prolonged & severe 
flares post-withdrawal
1. Anabolic steroids (danazol, testosterone) 
2. Bromides 
3. Corticosteroids 
4. Corticotropin 
5. EGFR inhibitors 
6. Iodides 
7. Isoniazid 
8. Lithium 
9. Phenytoin 
10.Progestins
1. Azathioprine 
2. Barbiturates 
3. Disulfiram 
4. Halogens, other 
5. Cyclosporine 
6. Vitamins B2,6,12 
7. Psoralen + ultraviolet A (PUVA)
 Itchy, acne-like eruption and 
most often affects the trunk. 
 Tiny dome-shaped pink papules 
and small superficial pustules 
arise in crops on the upper back, 
shoulders & chest. It can 
occasionally affect other areas 
including neck, face & upper 
arms. 
 The spots may appear more 
prominent when scratched. 
 A KOH preparation of follicular 
contents reveals abundant yeast 
forms.
 AGGRAVATING FACTORS; 
I. External factors 
1. Hot, humid, sweaty environment  yeast overgrowth 
2. Wearing occlusive clothing. 
3. Sunscreens and greasy emollients. 
II. Host factors 
6. Immune deficiency. 
1. Oily skin. 
7. Medications, such as: Broad 
2. Obesity. 
3. Pregnancy. 
4. Stress or fatigue. 
5. Diabetes mellitus. 
spectrum oral antibiotics, which 
suppress skin bacteria allowing 
yeasts to proliferate. Oral 
steroids (steroid acne) OCP. 
 Tx; 1. Correct as far as possible any of the 
predisposing factors 
2. Treat yeast overgrowth (like PVC) 
3. Isotretinoin
 Arise on the face of the middle-aged 
and elderly. They affect areas 
that have been exposed to sunlight 
over a long period of time, 
particularly the cheeks, which may 
become yellow and leathery 
(solar elastosis). 
 Occur in 6% of adults older than 
50 years especially males. 
 The comedones may be open or 
closed may also be larger cysts. 
 Solar comedones are not related to 
acne vulgaris and do not usually 
become inflamed. They are 
however very persistent.
 Favre-Racouchot syndrome; usually bilaterally 
symmetrical, Solar comedones in association with 
elastosis (yellowish thickening and furrows) 
atrophy, wrinkles. It may affect the skin around the 
eyes, the temples and rarely the neck. It is thought 
to be due to a combination of sun exposure and 
heavy smoking.
 Medical: 
1. Use sun protection and 
apply oil-free sunscreen 
to exposed skin 
2. Stop smoking 
3. Wash affected areas 
twice daily with mild 
soap or cleanser and 
water 
4. Apply retinoid cream to 
affected areas at night 
5. Apply light moisturisers 
if the skin is dry 
 Surgical: require further 
treatment from time to 
time. 
1. Comedo extraction. 
If these measures are 
unhelpful, the comedones 
can often be removed by: 
2. Cautery, diathermy, 
3. Chemical peels 
4. Dermabrasion 
5. Laser (CO2)
1. To prevent the formation of new lesions. 
2. To heal existing lesions. 
3. To prevent or minimize scarring. 
4. Decrease psychological stress.
 The clinical subtype, severity, prior treatment, 
psychological impact, and presence of scarring 
should be considered for all patients with acne. 
 The treatment of acne usually involves initial 
therapy followed by long-term maintenance therapy. 
 Treatment should target as many pathophysiological 
causes as possible. 
 Use of topical or systemic antibiotic monotherapy 
may give rise to antibiotic-resistance which may 
leads to acne treatment failure & colonizing bacteria 
on skin and at remote sites, including streptococcal 
colonization of the throat.
 Use of combination therapy is more effective for the 
treatment of acne. 
 Topical retinoids used alone or as part of a 
combination therapy is considered first-line in the 
initial treatment and maintenance of all types of 
acne except for severe nodular disease, which 
requires systemic retinoid therapy. 
 Severe disease–especially scarring or trunk 
involvement–requires systemic therapy. 
 Some female patients may benefit greatly from 
hormonally targeted treatment. 
 It is essential to align the treatment regimen with 
the patient’’s goals and preferences for treatment: 
systemic versus topical, complexity of regimen.
Topical Treatments Systemic therapy 
1. Benzoyl peroxide 
2. Retinoids 
3. Antibiotics 
– Clindamycin 
– Erythromycin 
– Sodium sulfacetamide/sulfur 
4. Azelaic acid 
5. Salicylic acid 
6. Topical Dapsone 
1. Oral minocycline 
2. Oral doxycycline 
3. Oral tetracycline 
4. Oral erythromycin 
5. Oral azithromycin 
6. Oral Clindamycin 
7. Oral Sulfanomides 
8. Oral contraceptives 
9. Oral spironolactone 
10.Oral isotretinoin
1. Benzoyl peroxide 
2. Topical retinoids 
3. Topical antibacterials 
4. Azelaic acid 
5. Sodium sulfacetamide 
6. Salicyclic acid 
7. Topical dapsone
 Available as gels, creams, lotions, 
foams, washes, pads and soaps 
alone as well as in combination. 
 2.5% to 10%. 
 Potent antibacterial effect also has 
mild comedolytic properties 
 Is to introduce oxygen to the clogged parts of the 
skin pores  more oxygen is more fatal 
environment for the anaerobic bacteria. 
 Microbial resistance to benzoyl peroxide has not 
been reported.
 It is on the World Health 
Organization's List of 
Essential Medicines, a list of 
the most important 
medication needed in a 
basic health system. 
 Contact dermatitis (irritant 
> allergic)  frequency of 
application. 
 Whitening of clothing and 
bedding
 Creams, gels, liquids 
 0.01%, 0.025%, 0.04%, 0.05% 
and 0.1% 
 Cream base may be less 
irritaiting 
 1st-line therapy for mild to 
moderate inflammatory acne , 
comedonal acne, maintenance 
therapy, enhance penetration of 
other drugs.
 MOA; 
1. Normalize follicular keratinization 
2. Comedolytic  the numbers of microcomedones, 
comedones & inflammatory lesions. 
3.  FFA in the microcomedons. 
4. Anti-inflammatory; downregulating of TLR, cytokines 
5.  penetration of the other medications into the 
sebaceous follicle. 
6. It reduces the signs of aging by stimulating collagen 
production. 
7. Tretinoin also may help prevent more serious effects 
of ultraviolet radiation
 Tretinoin is photolabile so night-time application 
is recommended to prevent early degradation. 
 Adapalene to have milder comedolytic 
properties than tretinoin, it is also less irritating 
& unlike tretinoin, it is light-stable and resistant 
to oxidation by benzoyl peroxide. 
 Tazarotene synthetic retinoid, once applied, is 
converted into its active metabolite, tazarotenic 
acid. Both daily overnight application of 
tazarotene and short contact therapy regimens 
have been used and shown to be effective in the 
treatment of comedonal and inflammatory acne.
 Side effects; 
1.Local irritation 
2.Erythema, 
3.Dryness, 
4.Peeling 
5.Scaling. 
6.Pustular flare of acne occasionally occurs 
during the initial 3–4 weeks of Tx 
7. pt.’s susceptibility to sunburn.
 For their role against P. acnes. 
 creams and gels to solutions and 
pledgets 
 Erythromycin 2-3% 
 Clindamycin 1% effective 
against pustules and small 
papulopustular lesions 
 Both equally effective, combined 
with bezoyl peroxide can 
decrease resistance
 Naturally occurring 
compound found in cereal grains. 
 Cream and gel-twice daily. 
 Anti-inflammatory/ Inhibiting the 
growth of P. acnes/comedolytic 
 low adverse reactions than topical 
retinoids. 
 In addition, it may help to lighten 
postinflammatory hyperpigmentation.
 is a well-tolerated topical antibiotic 
that is thought to restrict the growth 
of P. acnes. 
 It is formulated in a 10% lotion, 
suspension, foam and cleanser, either 
alone or in combination with 5% 
sulfur. 
 Tinted formulations are also available.
 Comedolytic and mild anti-inflammatory 
agent. 
 It is also a mild chemical irritant that works 
in part by drying up active lesions. 
 Available over the counter in concentrations 
of up to 2% in numerous delivery 
formulations, including gels, creams, 
lotions, foams, solutions and washes. 
 Side effects; include erythema and 
scaling.
 Gel 5% is effective and safe as 
monotherapy and in combination with 
other topical agents in mild-to-moderate 
acne vulgaris, direct 
inhibition of leukocyte. 
 Of note, a temporary yellow–orange 
staining of the skin and hair 
occasionally occurs with concomitant 
use of topical dapsone and BPO.
 Use for 6m. or until lesions resolve. 
 MOA; 
1. Antimicrobial against P. acnes. 
2.  chemotaxis of polymorphonuclear 
leukocytes. 
3.  lipase production in P. acnes.
 Tetracycline since 1951 
 Safest and cheapest choice & good first 
choice 
 250 to 500mg QD to QID for 4 weeks or 
until lesions respond. 
 Gradual reduction in dose 
 Take on empty stomach 
 Calcium and iron decrease absorption 
 Constant or intermittent tx months to years
 Tetracycline as sole treatment will give a 
positive response in 70% 
 May take 4-6 weeks for response 
 Effects of tetracycline are obtained by the 
reduction of FFA 
 Vaginitis and perianal itching in 5% due to 
Candida albicans 
 Staining of growing teeth precludes use in 
pregnancy and children < 9 or 10 y.
 100-200mg/d 
 P. ances resistant 
to erythromycin, 
photosensitivity can 
occur 
 Gastro-Intestinal 
adverse effects
Photosensitivity from doxycycline
 More effective than 
tetracycline in AV. 
 Lipophilic derivative of 
tetracycline, greater 
penetration into the 
sebaceous follicle. 
 50 to 100mg QD or BID 
 Absorption less affected by 
milk and food 
 SE; minocycline-induced hypersensitivity 
syndrome and autoimmune reactions.
 Erythromycin; 
500mg t.i.d. 
 Azithromycin; 
250-500mg/d for 
3days 
 consider in young 
and pregnant who 
cannot use 
tetracycline.
 150-300mg t.i.d 
 works well, but can 
cause 
pseudomembranous 
colitis
 Trimethoprim/Sulfamethoxazole 
 SE; Phototoxicity, drug reactions, BM 
suppression, Scalded skin
 Worsening clinical condition correlates 
with a high minimum inhibitory 
concentration for erythromycin and 
tetracycline for P. acnes 
 Resistance lost after 2 months after 
withdrawal of antibiotic. 
 Avoid use of different oral and topical 
antibiotics at the same time
 Hormonal therapy is an established second-line 
treatment for female patients with acne. 
 work best in adult women with premenstrual 
acne. 
 Block both ovarian and adrenal production of 
androgens 
 Hormonal therapy include; 
1. Oral contraceptives 
2. Cyproterone acetate (CPA) 
3. Oral spironolactone
 Estradiol suppresses the uptake of testosterone by 
the sebaceous glands 
 Oral contraceptives containing androgenic 
progesterones may exacerbate acne. 
 Three oral contraceptives are currently FDA-approved 
for the treatment of acne, (Ortho Tri-cyclen, 
Estrostep, Yaz, Loryna and Beyaz) 
 Clinical data to support use Yasmin & Diane-35. 
 From 5th to 25th day of menstruation.
Yasmin (Ethinyl estradiol 30/drospirenone 3000) 
Drospirenone is an analog of spironolactone 
(equivalent to 25 mg) and has antiandrogenic 
and antimineralocorticoid properties.
Diane-35 (Ethinyl estradiol 
35/cyproterone acetate 2000)
 Side effects; 
1. Nausea, 
2. Vomiting, 
3. Abnormal menses, 
4. Weight gain 
5. Breast tenderness. 
6. Hypertension 
7. Thromboembolism (e.g. deep venous 
thrombosis, pulmonary embolism). 
8. Hepatotoxicity
 Progestational antiandrogen. 
 Alone orin combinationwithEED. 
 Anti-acne effects are mediated 
primarily through androgen 
receptor blockade. 
 50–100 mg daily higher doses 
may be helpful in ♀ with severe hyperandrogenism. 
 SE; 1. inhibition of ovulation & spermatogenesis 
2. Wt. gain 
3. Congenital deformities in male fetus.
 synthetic corticosteroid 
 Initiated with a low dose 
(25–50 mg/day) 
to  Side effects. 
Effective maintenance 
doses range from 
25 to 200 mg/day 
divided into 2 doses. 
 Antiandrogenic; androgen receptor blocker 
and an inhibitor of 5α-reductase. 
 for severe inflammatory acne
 Side effects; are dose-related and 
include; 
1. Potential hyperkalemia rare in young 
healthy patients. 
2. Irregular menstrual periods. 
3. Breast tenderness. 
4. Headache. 
5. Fatigue. 
6. Risk of feminization of a male fetus.
 A systemic retinoid 
 0.5 to 1 mg/kg/day 
qd or bid for 15 to 20 wks 
(taken with a fatty meal 
to  gastrointestinal 
absorption) 
 Total cumulative dose is 120-150 
mg/kg to reduce the risk of relapse. 
 Leads to a remission that may last 
months to years
 Retinoids exert their physiologic effects 
through two distinct families of nuclear 
receptors; RARs and retinoid X 
receptors (RXRs). 
 Systemic retinoids act as: 
1. Comedolytic 
2.  follicular keritization 
3. Anti-inflammatory 
4. Suppress sebum production 
5. Indirectly antimicrobial
 FOR PATIENTS WITH ACNE; 
1. Nodular or nodulocystic acne 
2. Acne conglobata 
3. Acne fulminans 
4. Severe disfiguring inflammatory acne vulgaris 
5. Acne which is resulting in scarring 
6. Moderate acne which has failed to respond to topical 
agents with oral Abc, or in ♀, hormonal Tx. 
7. Acne which relapses rapidly on discontinuing Tx. 
8. Acne which has persisted for several years, or arises 
in an individual over 25 years old 
9. When the acne has a significant adverse 
occupational, social or psychological effect.
 FOR PATIENTS SEVERELY AFFECTED BY OTHER 
FOLLICULAR CONDITIONS. THESE INCLUDE: 
1. Acne keloidalis nuchae 
2. Occupational acne/Chloracne 
3. Gram negative folliculitis 
4. Hidradenitis suppurativa 
5. Pityrosporum folliculitis 
6. Pseudofolliculitis barbae 
7. Pyoderma faciale 
8. Solid facial edema 
9. Rosacea and rhinophyma 
10. Scalp folliculitis 
11. Sebaceous hyperplasia 
12. Seborrhoea 
13. Steatocystoma multiplex
 TREATMENT FOR SCALY AND OTHER 
INFLAMMATORY SKIN CONDITIONS: 
1. Darier disease 
2. Discoid lupus erythematosus (DLE) 
3. Epidermal naevi 
4. Folliculitis decalvans 
5. Granuloma annulare 
6. Grover disease 
7. Ichthyosis 
8. Sarcoidosis 
9. Skin cancers especially when they arise in 
those with organ transplants or xeroderma 
pigmentosa
 Nasal colonization with S.aureus in 90% 
 Paradoxical worsening of acne commonly 
occur, an acne fulminans-like flare 
occasionally develops during the first few 
weeks of isotretinoin therapy for acne.
 Most patients are advised to have blood tests before 
and four weeks after treatment begins or more 
occasions during isotretinoin treatment. 
1.Pregnancy test (beta-HCG) for women and girls 
of child-bearing potential. 
2.Lipid profile (cholesterol & triglyceride levels). 
3.Liver function tests. Occasionally, isotretinoin 
may disturb liver function; this requires monitoring 
but if the reaction is mild the drug can usually be 
continued. Rarely, it causes a symptomatic 
hepatitis: the drug must then be discontinued. 
4. Blood count: this is to check for anaemia and to 
monitor white cell count and platelets.
1-Dryness of skin, conjunctiva and mucosa of the 
genitals, chapped lips (cheilitis), dry Eyes, Epistaxis 
2- Arthralgias, myalgias 
3- Mood changes, Depression & 
suicidal behavior 
4- Elevated lipids (serum triglyceride) 
5- Hepatotoxicity 
6- Abortion or Teratogenicity 
7- Nails dystrophy, paronychia, 
palmoplantar desquamation, 
8- Pseudotumor cerebri (benign intracranial HTN) 
9- Fulminans-like flare, 
10- Pyogenic granuloma 
11- Premature epiphyseal closure in children < 13 y.
 Women of childbearing age are 
urged to use 2 methods of 
contraception for 1 month 
before treatment, during 
treatment and at least 1 
month after stopping 
treatment. 
 Pregnancy test should be done 
before beginning therapy and 
monthly until therapy stops.
Drug interaction with isotretinoin 
Tetracyclines 
Vitamin-A & its 
derivatives
LESIONS SCARS 
1. Extraction of comedones 
2. Drainage of pustules and 
cysts 
3. Intralesional injection of 
corticosteroids in nodules 
& cysts 
4. Excision and unroofing of 
sinus tracts and cysts 
1. Dermabrasion 
2. Laser abrasion 
3. Chemical peels 
4. Injection of filling 
materials 
5. Excision 
6. Punch autografts
 Comedone extractor brings about 
quick resolution of comedones 
improve cosmetic appearance 
Especially beneficial for deep, 
inspissated and persistent 
comedon 
 In Isotretinoin pts 
macrocomedones present at 
week 10 to 15 of therapy 
 Nicking the surface of a closed 
comedo with an 18-gauge needle 
or a #11 blade allows easier 
expression.
 Effective in reducing inflammatory papules, 
pustules, & smaller cysts & nodule 
 Acne conglobata & acne fulminans 
 Kenalog-10 (triamcinolone 10mg/ml) 
 Diluted with NS to 5 or 2.5mg/ml 
 The maximal amount used per lesion 
should not exceed 0.1 ml. 
 The risks of corticosteroid injections; 
1. Hypopigmentation 
2. Atrophy, 
3. Telangiectasias, 
4. Needle tract scarring.
 Low-concentration are beneficial 
for the reduction of comedones. 
 The α-hydroxy acids (including 
glycolic acid), salicylic acid and 
trichloroacetic acid are the most 
common peeling agents. 
 These lipid-soluble comedolytic 
agents act by  corneocyte 
cohesion at the follicular opening 
and assist in plug extrusion. 
 Risks of chemical peels include; 
1. irritation, 
2. pigmentary alteration 
3. scarring.
 Red, Green, or Blue light: inflammatory acne 
,absorbed by P. acnes porphyrins. 
 IPL: trigger the destruction of the P. acnes. 
 PDT (photodynamic therapy) using ALA : 
induces partial destruction of the sebaceous 
glands along with the destruction of P. acnes. 
 Lasers: pulsed dye, the 1320 nm 
neodymium:YAG and especially the 1450 nm 
diode may be of therapeutic benefit for 
inflammatory acne 
 Acne vaccine 
 Metformin
1. Microdermabrasion/Dermabrasion 
2. Laser abrasion 
3. Subcision 
4. Punch autografts 
5. Injection of filling materials 
6. Chemical peels 
7. Dermaroller 
8. Full thickness surgical excision
a) CO2 laser 
b) Erbium-Yag laser.
 commonly used 
technique in the 
management of acne 
scars.
Is an option for patients with 
“ice-pick” scarring.
For discrete depressed scars 
can be temporarily 
beneficial. 
Filler substances used 
include; 
1. Hyaluronic acid, 
2. Poly-l-lactic acid, 
3. Calcium hydroxylapatite 
4. Autologous fat.
 Dermaroller is a 
cylindrical shaped drum 
with very fine needles. 
 It is a medical device 
used to stimulate skin 
cells to proliferate. 
 NEEDLE LENGTH: 1-2mm
 For; 
1. Larger hypertrophic scars, 
2. Aggregated pitted scars 
3. Sinus tracts.
References 
 Jessica San Juan Microbiology 
 Prof. Dr. Wafaa Afify 
 Bolognia 3rd ed.
Acne.cont

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Acne.cont

  • 1.
  • 2.
  • 3. 1. Acne conglobata 2. Acne fulminans 3. Neonatal acne 4. Infantile acne 5. Post-adolescent acne 6. Acne excoriée 7. Cosmetic / Pomade acne 8. Acne Detergicans 9. Acne mechanica 10.Premenstrual Acne 11.Occupational acne / Chloracne 12.Senile (solar) comedones 13.Drug-induced acne 14.Pyoderma Faciale 15.Solid facial edema
  • 4.  Conglobate: shaped in a rounded mass or ball  Severe form of inflammatory nodulocystic acne characterized by numerous comedones, large abscesses or cysts interconnecting with sinuses, grouped inflammatory nodules but without systemic manifestations.  Suppuration  on forehead, cheeks, and neck
  • 5.  Occurs most frequently in young men  Follicular Occlusion Tetrad: I. Acne conglobata, II. Hiradenitis suppurva, III. Dissecting cellulitis of the scalp IV. Pilonidal cysts  Heals with scarring difficult to prevent  Treatment; oral isotretinoin for 5 months
  • 6.
  • 7.
  • 8.
  • 9.
  • 10.  The association of 1. Sterile Pyogenic Arthritis, 2. Pyoderma gangrenosum, 3. Acne conglobata  can occur in the context of an autosomal dominant autoinflammatory disorder referred to as PAPA syndrome.
  • 11.  the most severe form of acne characterized by sudden onset of severely inflamed nodulocystic & suppurative acne lesions in association with systemic manifestations.  Rare form of extremely severe Teenage boys, chest, shoulders & back  Patients typically have mild to moderate acne prior to the onset of acne fulminans
  • 12.  Rapid coalescence into painful, oozing, friable plaques with hemorrhagic crusts Rapid degeneration of nodules leaving ulceration can lead to significant scarring.  Fever, arthralgias, myalgias, hepatosplenomegaly, severe malaise. anorexia are common. Osteolytic bone lesions may accompany the cutaneous finding.  Ix: leukocytosis, proteinuria
  • 13.
  • 14.  Synovitis, Acne, Pustulosis, Hyperostosis, and Osteomyelitis  Acne fulminans, acne conglobata, pustular psoriasis, and palmoplantar pustulosis  Chest wall is most site of musculoskeletal complaints
  • 15. Pustules on the sole of the left foot (A) and left palm (B), and radioisotope scan (C) showing intense uptake by the sternoclavicular and first sternocostal joints.
  • 16. 1. Oral steroids 2. Oral isotretinoin often with initiation of the latter at a low dose and/or after the acute inflammation subsides. 3. Topical or intralesional corticosteroids, 4. Oral antibiotics (limited efficacy), 5. TNF-α inhibitors 6. Immunosuppressives (e.g. azathioprine). 7. Dapsone
  • 17.  Postadolescent girls, reddish cyanotic erythema with abscesses and cysts  Distinguished from acne by absence of comedones, rapid onset, fulminant course and absence of acne on the back and chest  Tx; oral steroids followed by isotretinoin
  • 18.
  • 19.  very common First four weeks of life  More than 20% of healthy newborns.  Facial papules or pustules typically no comedones.  Arise primarily on the cheeks and nasal bridge but the forehead, chin, neck and upper trunk can also be involved.
  • 20.
  • 21.  The development related to hormonal activity in utero / An inflammatory response to Malassezia spp. (e.g. furfur) has been proposed as the etiology and will resolve spontaneously 1-3 months after delivery without evidence of scarring.  No treatment is required except reassurance for parents who may be extremely anxious  Tx with topical imidazoles (e.g. ketoconazole 2% cream).
  • 22.  Cases that persist beyond 4 weeks or have an onset after  In contrast to neonatal acne, comedo formation is prominent and pitted scarring can develop.  Infantile acne typically resolves within 1–2 years and remains quiescent until around puberty. In unusual cases, however, infantile-onset acne may persist into adolescence.
  • 23.  Androgen production intrinsic to this stage of development including elevated levels of LH stimulating testicular production of testosterone in boys during the first 6–12 months of life (with levels transiently equivalent to those during puberty) and elevated levels of DHEA produced by the infantile adrenal gland in both boys and girls. These androgen levels normally decrease substantially by 6-12 months of age and remain at nadir levels until adrenarche.
  • 24.
  • 25.
  • 26.  Topical retinoids (e.g. tretinoin, adapalene) and benzoyl peroxide are first-line treatments.  Oral antibiotics (e.g. erythromycin, azithromycin) can be helpful for patients with a more severe inflammatory component,  Isotretinoin is occasionally required for recalcitrant or nodulocystic presentations
  • 27.  Inflammatory acne persisting beyond 25 years of age is most common in women,  Tends to flare during the week prior to menstruation, and typically features tender, deep-seated papulonodules on the lower third of the face, jawline and neck.  Approximately one-third of affected women have other signs of hyperandrogenism  Regardless of androgen levels, hormonal therapy is often effective.
  • 28.  Papulopustular lesions week prior  Estrogen-dominant contraceptive pills will diminish
  • 29.  Girls, mild acne minute or trivial primary lesions are made worse by squeezing, scratching, erosions and crusting on individual lesions.  Crusts, scarring, and atrophy  Individuals with an anxiety disorder, obsessive– compulsive disorder or personality disorder are particularly at risk
  • 30.
  • 31.  In addition to acne Rx;  eliminate magnifying mirror,  Rx of depression; Antidepressants or psychotherapy
  • 32.  Occurs secondary to repeated mechanical and frictional obstruction of the pilosebaceous outlet.  Well-described mechanical factors include rubbing by helmets, chin straps, suspenders and collars.
  • 33.  Fiddler’s neck, where repetitive trauma from violin placement on the lateral neck results in a well-defined lichenified, hyperpigmented plaque interspersed with comedones. Linear & geometrically distributed areas of involvement should suggest acne mechanica.  Treatment is aimed at eliminating the inciting forces
  • 34.
  • 35.  Patients wash face with comedogenic soaps  Closed comedones  Tx; wash only once or twice a day with non-comedogenic soap
  • 36.  An unusual and disfiguring complication of AV.  Clinically, there is a distortion of the midline face& cheeks due to soft tissue swelling.  The woody induration may be accompanied by erythema. Impaired lymphatic drainage and fibrosis.  Fluctuations in severity are common, but does not usually resolve spontaneously.
  • 37. 1. Isotretinoin (0.2–1 mg/kg/day), alone or in combination with; 2. Ketotifen (1–2 mg/day) or; 3. Prednisone (10–30 mg/day), for 4–5 months.
  • 38.  Rare, females 25-40 yrs  Starts in spring, resolves by fall  Small papules on cheeks, neck, upper body  Comedones & pustules are sparse or absent  Tx; retinoic acid, abx don’t help
  • 39.  Exposure to insoluble, follicle-occluding substances in the workplace.  Comedones dominate the clinical picture, with varying numbers of papules, pustules and cystic lesions distributed in exposed as well as typically covered areas.  Offending agents: 1. Cutting oils 2. Petroleum-based products 3. Chlorinated aromatichydrocarbons (Chloracne) 4. Coal tar derivatives.
  • 40.
  • 41.  Appear after prolonged exposure to coal-tar products coal tar oils,  These compounds, forming a black plug mixed with dead skin cells and keratin.  Especially the face and arms.  If not treated properly, coal-tar acne can develop into skin cancer
  • 42.  Occupational acne caused by exposure to chlorinated aromatic hydrocarbons, develops after several weeks of exposure.  The malar, retroauricular and mandibular regions of the head and neck as well as the axillae and scrotum, are most commonly afflicted with small cystic papules and nodules. The extremities, buttocks and trunk are variably involved.
  • 43.  Cystic lesions can heal with significant scarring, and recurrent outbreaks may occur for many years following exposure.  Chloracnegens, found in electrical conductors and insulators, insecticides, fungicides, herbicides and wood preservatives.  Prevention of exposure is integral to the safety of at-risk employees.
  • 44.
  • 45.
  • 46.
  • 47.  Initial management is aimed at vigorous removal of chemical agents at the time of exposure.  Topical or oral retinoids and oral antibiotics may be beneficial therapeutic interventions
  • 48.  Closed comedones and papulopustules on the chin and cheeks  In areas of skin chronically exposed to follicle-occluding cosmetics  May take months to clear after stopping cosmetic product
  • 49.  Blacks, males, due to greases or oils applied to hair.  Favors forehead and temples
  • 50.
  • 51.
  • 52.  Acneiform eruptions are dermatoses that resemble acne vulgaris.  Lesions may be papulopustular, nodular, or cystic. While acne vulgaris typically consists of comedones, acneiform eruptions (such as acneiform drug eruptions) usually lack comedones clinically.  Location may be outside of the area in which acne vulgaris occurs.  Age outside the range typical of acne vulgaris.
  • 53.  Acnelike eruptions develop as a result of; 1.Infections. 2.Hormonal abnormalities. 3.Metabolic abnormalities. 4.Genetic disorders. 5.Drug reactions.
  • 54. 1.Epidermal growth factor receptor inhibitor-induced papulopustular eruption 2.Tropical acne 3.Radiation acne 4.“Pseudoacne” of the transverse nasal crease 5.Idiopathic facial aseptic granuloma 6.Childhood flexural comedones 7.Nevus comedonicus. 8.Eruptive hair cysts. 9.Tuberous sclerosis. 10.Chloracne. 11.Acneiform drug eruptions. 12.Steroid acne. 13.Amineptine acne. 14.Gram-negative folliculitis. 15.Eosinophilic pustular folliculitis. 16.Pityrosporum folliculitis. 17.Coccidioidomycosis. 18.Secondary syphilis. 19.Sporotrichosis. 20.Rosacea. 21.Perioral dermatitis. 22.Senile (solar) comedones
  • 55.  EGFR inhibitors used for the treatment of solid tumors, including head and neck squamous cell carcinoma and lung, colon and breast carcinoma.  The incidence of acneiform eruptions due to EGFR inhibitors is very high, e.g. up to 95% of patients treated with panitumumab.  Patients present with an eruption of monomorphous follicular pustules and papules involving the face, scalp and upper trunk, usually 1–3 weeks after beginning treatment with an EGFR inhibitor.  No comedonal lesions are seen either microscopically or clinically,
  • 56. Acneiform eruptions due to epidermal growth factor receptor inhibitors. A,B Numerous monomorphous follicular pustules and crusted papules on the face of two patients treated with erlotinib
  • 57.  Follicular acneiform eruption that results from exposure to extreme heat.  Markedly inflamed nodular, cystic, and pustular lesions on back, buttocks, & thighs  Face is spared  Young adult military stationed in tropics, furnace workers.  Tx; returns to a more moderate climate.
  • 58.  Characterized by comedo-like papules occurring at sites of previous exposure to therapeutic ionizing radiation.  The lesions begin to appear as the acute phase of radiation dermatitis starts to resolve.  The ionizing rays induce epithelial metaplasia within the follicle  adherent hyperkeratotic plugs that are resistant to expression.
  • 59.  The transverse nasal crease is a horizontal anatomical demarcation line found in the lower third of the nose which corresponds to the separation point between the alar cartilage and the triangular cartilage.  Milia, cysts & comedones can line up along this fold.  These acne-like lesions aren’t hormonally responsive & arise during early childhood prior to puberty.  Tx; consists of surgical expression as needed.
  • 60.  chronic, painless, usually solitary nodule with an acneiform appearance can develop on the cheeks of young children.  Histopathologic evaluation reveals a granulomatous inflammatory response; dermal lymphohistiocytic infiltrate with foreign body-type giant cells.  They eventually resolve spontaneously after an average of 11 months without treatment
  • 61.  Discrete, double-orifice comedones localized to the axillae & less commonly, the groin.  The majority of patients have a single lesion and the average age at Dx is 6 years.  A small subset of cases are familial.  In most cases, the flexural comedones are discovered incidentally in patients presenting with other dermatologic concerns.
  • 62. From: Childhood Flexural Comedones: A New Entity Arch Dermatol. 2007;143(7):909-911. doi:10.1001/archderm.143.7.909 The left axilla showing 3 double-orifice comedones in a 4-year-old boy. Date of download: 9/2/2014 Copyright © 2014 American Medical Association. All rights reserved. Figure Legend:
  • 63. From: Childhood Flexural Comedones: A New Entity Arch Dermatol. 2007;143(7):909-911. doi:10.1001/archderm.143.7.909 Axillary double-orifice comedo with a visible content underlying the epidermal bridge in an 8-year-old boy. Date of download: 9/2/2014 Copyright © 2014 American Medical Association. All rights reserved. Figure Legend:
  • 64.  Occurs in prolonged treatment with antibiotics for acne vulgaris or rosacea.  E. coli, Enterobactor, Klebsiella, Proteus.  Anterior nares colonized  Persistent papulopustular eruption,  These gram-negative organisms are typically spread to the skin of the upper lip, chin, and jawline.  Tx; isotretinoin is considered standard of care.
  • 65.
  • 66.  Papulopustules with erythematous base  Characteristically; Clear zone around vermillion border. It may also include the perinasal and periorbital areas (periocular dermatitis).  Young ♀ (23-35yrs)  Has a superficial resemblance to rosacea
  • 67.
  • 68.  Etiology; 1. Topical steroids 2. Demodex mites 3. Contact irritants or allergens 4. Moisturizers 5. Cleansers 6. Fluorinated compounds e.g. fluorinated toothpaste  Tx; d/c topical steroids or other offending agent - oral tetracycline 1g/d or doxycycline - topical pimecrolimus cream, - azelaic acid
  • 69.  An abrupt, monomorphous eruption of inflammatory papules and pustules
  • 70.  High-dose IV or oral corticosteroids commonly induce characteristic acneiform eruptions with a concentration of lesions on the chest and back  Steroid-induced acne (and rosacea) can also result from the inappropriate use of topical corticosteroids on the face. Inflamed papules and pustules develop on a background of erythema that favors the distribution of corticosteroid application.  Lesions eventually resolve following discontinuation of the steroid, although “steroid dependency” can lead to prolonged & severe flares post-withdrawal
  • 71.
  • 72. 1. Anabolic steroids (danazol, testosterone) 2. Bromides 3. Corticosteroids 4. Corticotropin 5. EGFR inhibitors 6. Iodides 7. Isoniazid 8. Lithium 9. Phenytoin 10.Progestins
  • 73. 1. Azathioprine 2. Barbiturates 3. Disulfiram 4. Halogens, other 5. Cyclosporine 6. Vitamins B2,6,12 7. Psoralen + ultraviolet A (PUVA)
  • 74.  Itchy, acne-like eruption and most often affects the trunk.  Tiny dome-shaped pink papules and small superficial pustules arise in crops on the upper back, shoulders & chest. It can occasionally affect other areas including neck, face & upper arms.  The spots may appear more prominent when scratched.  A KOH preparation of follicular contents reveals abundant yeast forms.
  • 75.  AGGRAVATING FACTORS; I. External factors 1. Hot, humid, sweaty environment  yeast overgrowth 2. Wearing occlusive clothing. 3. Sunscreens and greasy emollients. II. Host factors 6. Immune deficiency. 1. Oily skin. 7. Medications, such as: Broad 2. Obesity. 3. Pregnancy. 4. Stress or fatigue. 5. Diabetes mellitus. spectrum oral antibiotics, which suppress skin bacteria allowing yeasts to proliferate. Oral steroids (steroid acne) OCP.  Tx; 1. Correct as far as possible any of the predisposing factors 2. Treat yeast overgrowth (like PVC) 3. Isotretinoin
  • 76.  Arise on the face of the middle-aged and elderly. They affect areas that have been exposed to sunlight over a long period of time, particularly the cheeks, which may become yellow and leathery (solar elastosis).  Occur in 6% of adults older than 50 years especially males.  The comedones may be open or closed may also be larger cysts.  Solar comedones are not related to acne vulgaris and do not usually become inflamed. They are however very persistent.
  • 77.  Favre-Racouchot syndrome; usually bilaterally symmetrical, Solar comedones in association with elastosis (yellowish thickening and furrows) atrophy, wrinkles. It may affect the skin around the eyes, the temples and rarely the neck. It is thought to be due to a combination of sun exposure and heavy smoking.
  • 78.  Medical: 1. Use sun protection and apply oil-free sunscreen to exposed skin 2. Stop smoking 3. Wash affected areas twice daily with mild soap or cleanser and water 4. Apply retinoid cream to affected areas at night 5. Apply light moisturisers if the skin is dry  Surgical: require further treatment from time to time. 1. Comedo extraction. If these measures are unhelpful, the comedones can often be removed by: 2. Cautery, diathermy, 3. Chemical peels 4. Dermabrasion 5. Laser (CO2)
  • 79.
  • 80.
  • 81.
  • 82.
  • 83.
  • 84.
  • 85. 1. To prevent the formation of new lesions. 2. To heal existing lesions. 3. To prevent or minimize scarring. 4. Decrease psychological stress.
  • 86.  The clinical subtype, severity, prior treatment, psychological impact, and presence of scarring should be considered for all patients with acne.  The treatment of acne usually involves initial therapy followed by long-term maintenance therapy.  Treatment should target as many pathophysiological causes as possible.  Use of topical or systemic antibiotic monotherapy may give rise to antibiotic-resistance which may leads to acne treatment failure & colonizing bacteria on skin and at remote sites, including streptococcal colonization of the throat.
  • 87.  Use of combination therapy is more effective for the treatment of acne.  Topical retinoids used alone or as part of a combination therapy is considered first-line in the initial treatment and maintenance of all types of acne except for severe nodular disease, which requires systemic retinoid therapy.  Severe disease–especially scarring or trunk involvement–requires systemic therapy.  Some female patients may benefit greatly from hormonally targeted treatment.  It is essential to align the treatment regimen with the patient’’s goals and preferences for treatment: systemic versus topical, complexity of regimen.
  • 88.
  • 89.
  • 90.
  • 91. Topical Treatments Systemic therapy 1. Benzoyl peroxide 2. Retinoids 3. Antibiotics – Clindamycin – Erythromycin – Sodium sulfacetamide/sulfur 4. Azelaic acid 5. Salicylic acid 6. Topical Dapsone 1. Oral minocycline 2. Oral doxycycline 3. Oral tetracycline 4. Oral erythromycin 5. Oral azithromycin 6. Oral Clindamycin 7. Oral Sulfanomides 8. Oral contraceptives 9. Oral spironolactone 10.Oral isotretinoin
  • 92.
  • 93. 1. Benzoyl peroxide 2. Topical retinoids 3. Topical antibacterials 4. Azelaic acid 5. Sodium sulfacetamide 6. Salicyclic acid 7. Topical dapsone
  • 94.  Available as gels, creams, lotions, foams, washes, pads and soaps alone as well as in combination.  2.5% to 10%.  Potent antibacterial effect also has mild comedolytic properties  Is to introduce oxygen to the clogged parts of the skin pores  more oxygen is more fatal environment for the anaerobic bacteria.  Microbial resistance to benzoyl peroxide has not been reported.
  • 95.  It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.  Contact dermatitis (irritant > allergic)  frequency of application.  Whitening of clothing and bedding
  • 96.  Creams, gels, liquids  0.01%, 0.025%, 0.04%, 0.05% and 0.1%  Cream base may be less irritaiting  1st-line therapy for mild to moderate inflammatory acne , comedonal acne, maintenance therapy, enhance penetration of other drugs.
  • 97.  MOA; 1. Normalize follicular keratinization 2. Comedolytic  the numbers of microcomedones, comedones & inflammatory lesions. 3.  FFA in the microcomedons. 4. Anti-inflammatory; downregulating of TLR, cytokines 5.  penetration of the other medications into the sebaceous follicle. 6. It reduces the signs of aging by stimulating collagen production. 7. Tretinoin also may help prevent more serious effects of ultraviolet radiation
  • 98.
  • 99.  Tretinoin is photolabile so night-time application is recommended to prevent early degradation.  Adapalene to have milder comedolytic properties than tretinoin, it is also less irritating & unlike tretinoin, it is light-stable and resistant to oxidation by benzoyl peroxide.  Tazarotene synthetic retinoid, once applied, is converted into its active metabolite, tazarotenic acid. Both daily overnight application of tazarotene and short contact therapy regimens have been used and shown to be effective in the treatment of comedonal and inflammatory acne.
  • 100.  Side effects; 1.Local irritation 2.Erythema, 3.Dryness, 4.Peeling 5.Scaling. 6.Pustular flare of acne occasionally occurs during the initial 3–4 weeks of Tx 7. pt.’s susceptibility to sunburn.
  • 101.  For their role against P. acnes.  creams and gels to solutions and pledgets  Erythromycin 2-3%  Clindamycin 1% effective against pustules and small papulopustular lesions  Both equally effective, combined with bezoyl peroxide can decrease resistance
  • 102.  Naturally occurring compound found in cereal grains.  Cream and gel-twice daily.  Anti-inflammatory/ Inhibiting the growth of P. acnes/comedolytic  low adverse reactions than topical retinoids.  In addition, it may help to lighten postinflammatory hyperpigmentation.
  • 103.  is a well-tolerated topical antibiotic that is thought to restrict the growth of P. acnes.  It is formulated in a 10% lotion, suspension, foam and cleanser, either alone or in combination with 5% sulfur.  Tinted formulations are also available.
  • 104.  Comedolytic and mild anti-inflammatory agent.  It is also a mild chemical irritant that works in part by drying up active lesions.  Available over the counter in concentrations of up to 2% in numerous delivery formulations, including gels, creams, lotions, foams, solutions and washes.  Side effects; include erythema and scaling.
  • 105.  Gel 5% is effective and safe as monotherapy and in combination with other topical agents in mild-to-moderate acne vulgaris, direct inhibition of leukocyte.  Of note, a temporary yellow–orange staining of the skin and hair occasionally occurs with concomitant use of topical dapsone and BPO.
  • 106.
  • 107.  Use for 6m. or until lesions resolve.  MOA; 1. Antimicrobial against P. acnes. 2.  chemotaxis of polymorphonuclear leukocytes. 3.  lipase production in P. acnes.
  • 108.  Tetracycline since 1951  Safest and cheapest choice & good first choice  250 to 500mg QD to QID for 4 weeks or until lesions respond.  Gradual reduction in dose  Take on empty stomach  Calcium and iron decrease absorption  Constant or intermittent tx months to years
  • 109.  Tetracycline as sole treatment will give a positive response in 70%  May take 4-6 weeks for response  Effects of tetracycline are obtained by the reduction of FFA  Vaginitis and perianal itching in 5% due to Candida albicans  Staining of growing teeth precludes use in pregnancy and children < 9 or 10 y.
  • 110.  100-200mg/d  P. ances resistant to erythromycin, photosensitivity can occur  Gastro-Intestinal adverse effects
  • 112.  More effective than tetracycline in AV.  Lipophilic derivative of tetracycline, greater penetration into the sebaceous follicle.  50 to 100mg QD or BID  Absorption less affected by milk and food  SE; minocycline-induced hypersensitivity syndrome and autoimmune reactions.
  • 113.
  • 114.  Erythromycin; 500mg t.i.d.  Azithromycin; 250-500mg/d for 3days  consider in young and pregnant who cannot use tetracycline.
  • 115.  150-300mg t.i.d  works well, but can cause pseudomembranous colitis
  • 116.  Trimethoprim/Sulfamethoxazole  SE; Phototoxicity, drug reactions, BM suppression, Scalded skin
  • 117.  Worsening clinical condition correlates with a high minimum inhibitory concentration for erythromycin and tetracycline for P. acnes  Resistance lost after 2 months after withdrawal of antibiotic.  Avoid use of different oral and topical antibiotics at the same time
  • 118.  Hormonal therapy is an established second-line treatment for female patients with acne.  work best in adult women with premenstrual acne.  Block both ovarian and adrenal production of androgens  Hormonal therapy include; 1. Oral contraceptives 2. Cyproterone acetate (CPA) 3. Oral spironolactone
  • 119.  Estradiol suppresses the uptake of testosterone by the sebaceous glands  Oral contraceptives containing androgenic progesterones may exacerbate acne.  Three oral contraceptives are currently FDA-approved for the treatment of acne, (Ortho Tri-cyclen, Estrostep, Yaz, Loryna and Beyaz)  Clinical data to support use Yasmin & Diane-35.  From 5th to 25th day of menstruation.
  • 120. Yasmin (Ethinyl estradiol 30/drospirenone 3000) Drospirenone is an analog of spironolactone (equivalent to 25 mg) and has antiandrogenic and antimineralocorticoid properties.
  • 121. Diane-35 (Ethinyl estradiol 35/cyproterone acetate 2000)
  • 122.  Side effects; 1. Nausea, 2. Vomiting, 3. Abnormal menses, 4. Weight gain 5. Breast tenderness. 6. Hypertension 7. Thromboembolism (e.g. deep venous thrombosis, pulmonary embolism). 8. Hepatotoxicity
  • 123.  Progestational antiandrogen.  Alone orin combinationwithEED.  Anti-acne effects are mediated primarily through androgen receptor blockade.  50–100 mg daily higher doses may be helpful in ♀ with severe hyperandrogenism.  SE; 1. inhibition of ovulation & spermatogenesis 2. Wt. gain 3. Congenital deformities in male fetus.
  • 124.  synthetic corticosteroid  Initiated with a low dose (25–50 mg/day) to  Side effects. Effective maintenance doses range from 25 to 200 mg/day divided into 2 doses.  Antiandrogenic; androgen receptor blocker and an inhibitor of 5α-reductase.  for severe inflammatory acne
  • 125.  Side effects; are dose-related and include; 1. Potential hyperkalemia rare in young healthy patients. 2. Irregular menstrual periods. 3. Breast tenderness. 4. Headache. 5. Fatigue. 6. Risk of feminization of a male fetus.
  • 126.  A systemic retinoid  0.5 to 1 mg/kg/day qd or bid for 15 to 20 wks (taken with a fatty meal to  gastrointestinal absorption)  Total cumulative dose is 120-150 mg/kg to reduce the risk of relapse.  Leads to a remission that may last months to years
  • 127.  Retinoids exert their physiologic effects through two distinct families of nuclear receptors; RARs and retinoid X receptors (RXRs).  Systemic retinoids act as: 1. Comedolytic 2.  follicular keritization 3. Anti-inflammatory 4. Suppress sebum production 5. Indirectly antimicrobial
  • 128.  FOR PATIENTS WITH ACNE; 1. Nodular or nodulocystic acne 2. Acne conglobata 3. Acne fulminans 4. Severe disfiguring inflammatory acne vulgaris 5. Acne which is resulting in scarring 6. Moderate acne which has failed to respond to topical agents with oral Abc, or in ♀, hormonal Tx. 7. Acne which relapses rapidly on discontinuing Tx. 8. Acne which has persisted for several years, or arises in an individual over 25 years old 9. When the acne has a significant adverse occupational, social or psychological effect.
  • 129.  FOR PATIENTS SEVERELY AFFECTED BY OTHER FOLLICULAR CONDITIONS. THESE INCLUDE: 1. Acne keloidalis nuchae 2. Occupational acne/Chloracne 3. Gram negative folliculitis 4. Hidradenitis suppurativa 5. Pityrosporum folliculitis 6. Pseudofolliculitis barbae 7. Pyoderma faciale 8. Solid facial edema 9. Rosacea and rhinophyma 10. Scalp folliculitis 11. Sebaceous hyperplasia 12. Seborrhoea 13. Steatocystoma multiplex
  • 130.  TREATMENT FOR SCALY AND OTHER INFLAMMATORY SKIN CONDITIONS: 1. Darier disease 2. Discoid lupus erythematosus (DLE) 3. Epidermal naevi 4. Folliculitis decalvans 5. Granuloma annulare 6. Grover disease 7. Ichthyosis 8. Sarcoidosis 9. Skin cancers especially when they arise in those with organ transplants or xeroderma pigmentosa
  • 131.  Nasal colonization with S.aureus in 90%  Paradoxical worsening of acne commonly occur, an acne fulminans-like flare occasionally develops during the first few weeks of isotretinoin therapy for acne.
  • 132.  Most patients are advised to have blood tests before and four weeks after treatment begins or more occasions during isotretinoin treatment. 1.Pregnancy test (beta-HCG) for women and girls of child-bearing potential. 2.Lipid profile (cholesterol & triglyceride levels). 3.Liver function tests. Occasionally, isotretinoin may disturb liver function; this requires monitoring but if the reaction is mild the drug can usually be continued. Rarely, it causes a symptomatic hepatitis: the drug must then be discontinued. 4. Blood count: this is to check for anaemia and to monitor white cell count and platelets.
  • 133. 1-Dryness of skin, conjunctiva and mucosa of the genitals, chapped lips (cheilitis), dry Eyes, Epistaxis 2- Arthralgias, myalgias 3- Mood changes, Depression & suicidal behavior 4- Elevated lipids (serum triglyceride) 5- Hepatotoxicity 6- Abortion or Teratogenicity 7- Nails dystrophy, paronychia, palmoplantar desquamation, 8- Pseudotumor cerebri (benign intracranial HTN) 9- Fulminans-like flare, 10- Pyogenic granuloma 11- Premature epiphyseal closure in children < 13 y.
  • 134.
  • 135.
  • 136.  Women of childbearing age are urged to use 2 methods of contraception for 1 month before treatment, during treatment and at least 1 month after stopping treatment.  Pregnancy test should be done before beginning therapy and monthly until therapy stops.
  • 137. Drug interaction with isotretinoin Tetracyclines Vitamin-A & its derivatives
  • 138.
  • 139. LESIONS SCARS 1. Extraction of comedones 2. Drainage of pustules and cysts 3. Intralesional injection of corticosteroids in nodules & cysts 4. Excision and unroofing of sinus tracts and cysts 1. Dermabrasion 2. Laser abrasion 3. Chemical peels 4. Injection of filling materials 5. Excision 6. Punch autografts
  • 140.  Comedone extractor brings about quick resolution of comedones improve cosmetic appearance Especially beneficial for deep, inspissated and persistent comedon  In Isotretinoin pts macrocomedones present at week 10 to 15 of therapy  Nicking the surface of a closed comedo with an 18-gauge needle or a #11 blade allows easier expression.
  • 141.  Effective in reducing inflammatory papules, pustules, & smaller cysts & nodule  Acne conglobata & acne fulminans  Kenalog-10 (triamcinolone 10mg/ml)  Diluted with NS to 5 or 2.5mg/ml  The maximal amount used per lesion should not exceed 0.1 ml.  The risks of corticosteroid injections; 1. Hypopigmentation 2. Atrophy, 3. Telangiectasias, 4. Needle tract scarring.
  • 142.  Low-concentration are beneficial for the reduction of comedones.  The α-hydroxy acids (including glycolic acid), salicylic acid and trichloroacetic acid are the most common peeling agents.  These lipid-soluble comedolytic agents act by  corneocyte cohesion at the follicular opening and assist in plug extrusion.  Risks of chemical peels include; 1. irritation, 2. pigmentary alteration 3. scarring.
  • 143.
  • 144.  Red, Green, or Blue light: inflammatory acne ,absorbed by P. acnes porphyrins.  IPL: trigger the destruction of the P. acnes.  PDT (photodynamic therapy) using ALA : induces partial destruction of the sebaceous glands along with the destruction of P. acnes.  Lasers: pulsed dye, the 1320 nm neodymium:YAG and especially the 1450 nm diode may be of therapeutic benefit for inflammatory acne  Acne vaccine  Metformin
  • 145.
  • 146. 1. Microdermabrasion/Dermabrasion 2. Laser abrasion 3. Subcision 4. Punch autografts 5. Injection of filling materials 6. Chemical peels 7. Dermaroller 8. Full thickness surgical excision
  • 147.
  • 148. a) CO2 laser b) Erbium-Yag laser.
  • 149.  commonly used technique in the management of acne scars.
  • 150. Is an option for patients with “ice-pick” scarring.
  • 151. For discrete depressed scars can be temporarily beneficial. Filler substances used include; 1. Hyaluronic acid, 2. Poly-l-lactic acid, 3. Calcium hydroxylapatite 4. Autologous fat.
  • 152.
  • 153.  Dermaroller is a cylindrical shaped drum with very fine needles.  It is a medical device used to stimulate skin cells to proliferate.  NEEDLE LENGTH: 1-2mm
  • 154.  For; 1. Larger hypertrophic scars, 2. Aggregated pitted scars 3. Sinus tracts.
  • 155. References  Jessica San Juan Microbiology  Prof. Dr. Wafaa Afify  Bolognia 3rd ed.