SEBACEOUS GLANDS DISORDERS

Prof

IHAB YOUNIS

SEBACEOUS GLANDS

• Found on all areas of the skin except for the palms, soles, and dorsa of the feet

• They are holocrine glands, i.e., their secretion is formed by complete cell destruction

• Most sebaceous

glands have their

ducts opening into

hair follicles

(pilosebaceous

apparatus)

• Free sebaceous glands (not associated with hair follicles) open directly to the surface of the skin, e.g., Meibomian glands of the eyelids, Tyson's glands of the prepuce, and free glands in the female genitalia and in the areola of nipples

Hormonal control

• Sebaceous gland development is an early event in puberty, and the prime hormonal stimulus for this glandular development is androgen

• Although the sebaceous glands are very small throughout the prepubertal period, they are large at the time of birth, probably as a result of androgen stimulation in utero, and acne may be seen in the neonatal period

• Sebum production is low in children

• Testicular androgen maintains sebum production at a higher level in men than women where androgens are produced by the adrenals and ovaries

• In women sebum production decreases significantly after the age of 50

• In both sexes, estrogen administration decreases the size of the sebaceous glands and the production of sebum

• Sebum is composed of triglycerides and free fatty acids, wax esters, squalene, and cholesterol

• Sebum controls moisture loss from the epidermis. The water-holding power of cornified epithelium depends on the presence of lipids

• Sebum also protects against fungal and bacterial infections of the skin due to its contents of free fatty acids. Ringworm of scalp becomes rare after puberty

Composition and function

ACNE VULGARIS

Etymology

• The word acne comes from the Greek word "akme“ which means the highest point. It was misspelled by the 6th century author, Aëtius, into “acne”

Etiology

• Sex prevalence: -It starts earlier in girls than boys due to

earlier onset of puberty -It is more common in males than in

females during adolescence but more common in women than in men during adulthood

• Age prevalence:

- It may be present in the first few weeks of life when a newborn is still under the influence of maternal hormones and when the androgen-producing portion of the adrenal gland is disproportionately large. This neonatal acne resolves spontaneously

- Some degree of acne affects 95% of 16-years old boys and girls but only 20% of sufferers need medical help

-Adolescent acne usually begins prior to the onset of puberty, when the adrenal gland begins to produce and release more androgen hormone

-Acne resolves slowly between the age of 20-25

-As many as 80% of patients have some degree of acne by the age of 40 but only 1% of males and 5% of females have significant lesions

• Genetic factors

-Acne was present in 45% of boys with a history of affection of one or both parents compared to 8% of boys without affected parents

-Acne is more common in whites than in blacks

• Four key factors are responsible for the development of an acne lesion:

1- Comedone formation (comedogenesis) 2- Excess sebum 3- Presence & activity of Propionibacterium

acnes 4- Inflammation

1 -Comedone formation(comedogenesis)

The exact underlying cause is not known, 3 theories exist:

i.Androgen hormones

- Comedones begin to appear around adrenarche

- The degree of comedonal acne in prepubertal girls correlates with circulating levels of DHEA-S -Androgen hormone receptors are present in the portion of the follicle where the comedone forms

- Sebaceous activity is predominantly dependent on androgens, thus, abnormally high levels of sebum secretion could result from high overall androgen production, or increased availability of free androgen, because of a deficiency in sex-hormone-binding globulin (SHBG)

- Most men and women with acne have normal circulating levels of androgen hormones, thus an end-organ hyperresponsiveness to androgen hormones has been hypothesized

ii- Changes in lipid composition(see later)

iii- Inflammation(see later)

2 -Excess sebum(seborrhea)

• Excess sebum may dilute the normal epidermal lipids resulting in diminished concentrations of linoleic acid. This relative decrease in linoleic acid may be what initiates comedone formation

3 -P. acnes

• P. acnes is a microaerophilic organism

• It has not been shown to be present in microcomedo, but its presence in later lesions is almost certain

• P. acnes stimulates inflammation by producing proinflammatory mediators that diffuse through the follicle wall

• Recent studies have shown that P. acnes binds to the toll-like receptor (receptors that recognize abnormal organisms) on monocytes leading to the production of multiple proinflammatory cytokines, including IL-12, IL-8, and tumor necrosis factor

• Hypersensitivity to P. acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not

4 -Inflammation

• Interleukin–1–alpha has been used in a tissue model to induce follicular epidermal hyperproliferation and comedone formation

• Prior to duct rupture mediators of inflammation diffuse though the follicular duct into the dermis causing a type IV (cellular) immune response

• Later, the duct ruptures causing a macrophage giant cell foreign-body reaction

• P.acnes is the source of antigen to which the reaction is produced

• Toll receptors regulate the production of cytokines which contribute to the production of inflammation in acne

• Toll receptors look at P.acnes as abnormal as it is not often present in follicles from subjects without acne

Clinically

• Lesions are distributed over the areas rich in sebaceous glands

• The face may be the only involved skin surface, but the chest, the back, and the upper arms are often involved

Types:

1- Comedonal acne :

-Blackheads(open comedones):result when a pore is partially blocked, allowing some of the trapped sebum , bacteria & dead keratinocytes to

slowly drain to the

surface. The black

color is due to the

presence of melanin

- Whiteheads(closed comedones):result when a pore is completely blocked. Whiteheads are normally quicker in life cycle than

blackheads

Sandpaper white comedones:• Numerous(as many as 500)• Very small • Most often found on the forehead• Feel rough to the touch

Macrocomedones:• Greater than 1mm in diameter• Black or white

2- Mild inflammatory acne is characterized

by painful inflammatory papules and comedones

3- Moderate inflammatory acne has

comedones,inflammatory papules, and

pustules & greater numbers of lesions

4- Nodular acne is characterized by

comedones, inflammatory lesions, and

large nodules

(the term nodulocystic acne is

incorrect as acne cysts are

not true cysts as they are

NOT lined by epithelium).

Scarring is often evident

5-Acne conglobata:

• Characterized by large numbers of deep nodules that frequently fuse to form multiple draining sinuses

on the face and trunk

• It commonly heals

with scarring

• It may last up to the

age of 50 years

6- Acne fulminans:

• It is an uncommon, immunologically induced, systemic disease in which the offending antigen is P. acnes

• Patients are young males, who quite suddenly develop extensive inflammatory lesions, especially on the trunk• Usually associated with fever,

leukocytosis, arthralgia, inflammatory bone lesions, and transient glomerulonephritis

Scarring in acne

• Scarring occurs in up to 90% but socially noticed scars occur in only 22% of cases

• Common scars are the ‘Ice picks’ scars commonly found on the cheeks

• Hypertrophic scars and keloids can occur less commonly

• 1

Classification of Acne Severity

I-Mild: < 20 comedones, or < 15 inflammatory lesions, or < 30

total lesionsII-Moderate 20 to 100 comedones, or 15 to 50 inflammatory lesions,

or 30 to 125 total lesionsIII-Severe

> 5 cysts, or total comedo count > 100, or total inflammatory count > 50, or > 125 total lesions

Factors affecting acne

1-Diet• A wealth of folklore has blamed acne on

certain foods, in particular chocolate and pork fat, but scientific proof is lacking

2-Premenstrual flaring• Flare occurs in up to70% of women 2-7

days before menstruation• Possibly it is due to a change of hydration

of pilosebaceous epithelium

3-Sweating

• Excerbation occurs in up to 15% of cases living in hot humid environment

• Ductal hydration may be responsible

4-UV

• There is no scientific evidence that sunlight improves acne

• UV radiation may enhance the comedogenicity of sebum

5-Other factors:

• Studies show conflicting results concerning the effect of stress and smoking on acne

Histopathology

• Comedo development starts as an expanding mass of lipid-impregnated keratinous material, resulting in thinning and ballooning-out of the follicular wall

• At the same time, the sebaceous glandsbegin to atrophy and are replaced by undifferentiated epithelial cells

•Open comedo has a patulous orifice &keratinous material arranged in a lamellar compact fashion

•Closed comedo has a narrow distended orifice &keratinous material is not compact

• The initial event appears to be escape of lipid through an edematous comedo wall, with the development of a cellular reaction in the adjacent dermis. Once completerupture has occurred, the entire contents of the comedo are extruded into the dermis

• Inflammatory reaction is much greater, and giant cells are common. Withinthe inflammatory infiltrate, P. acnes may be observed free and within polymorphs

• Depending upon the site and extent ofinflammation, these ruptured lesions may appear as a pustule, a nodule, oras a nodule surmounted by a pustule

Pustule following rupture of a sebaceous follicle. The original walls of the follicle can be seen at the follicular orifice. New strands of epithelial cells are migrating from the epidermis to encapsulate the inflammatory mass, making the inflammatory material appear to be within the follicle

Nodule from a ruptured closed comedo. In the upper portion of the lesion there is lamellar keratinous material from the comedo. Below this, necrotic material is being encapsulated by new epithelial cells. Multinucleated giant cells are present in the inflammatory infiltrate inthe dermis

Treatment

• Treatment should be directed toward the known pathogenic factors involved in acne i.e. follicular hyperproliferation, excess sebum, P. acnes, and inflammation

• The grade and the severity of the acne

help in determining which of the following

treatments, alone or in combination, is

most appropriate

A-Topical treatments

1-Topical retinoids

They are• Comedolytic • Aanti-inflammatory• They cause epidermal differentiation and, thus,

normalize follicular hyperproliferation and hyperkeratinization

• They may be used alone or in combination with other acne medications

• Because irritation, redness and peeling are common, they are used once daily by night and exposure time is increased gradually

• Four generations of topical retinoids are available:

-1st generation:Tretinoin (Retin-A, Acnefree 0.025%, 0.05%, and 0.1% creams. Also available as 0.01% and 0.025% gels )

-2nd generation:Isotretinoin (Isotrex 0.05% gel )

-3rd generation:Adapalene gel, 0.1%

-4th generation:Tazarotene(Zarotex 0.05% and 0.1% cream and gel )

• The use of mild, nondrying cleansers and noncomedogenic moisturizers may help reduce irritation• Alternate-day dosing may be used if irritation persists• In general, the order of irritancy increases

as one progresses from the use of cream preparations to gels to the solution

• Topical retinoids have been associated with sun sensitivity. Instruct patients about sun protection

2-Topical antibiotics

• Mainly used for their role against P. acnes• They may also have anti-inflammatory

properties• Topical antibiotics are not comedolytic• Bacterial resistance (up to 58%)

developed to many of these agents. The development of resistance is lessened if topical antibiotics are used in combination with benzoyl peroxide

Commonly prescribed topical antibiotics include:

• Erythromycin(acnebiotic,Acne zincomycin)

• Clindamycin (dalacine T)

• They are available in a variety of topical agents

• They may be applied once or twice a day

• Gels and solutions may be more irritating than creams or lotions

3 -Benzoyl peroxide(Panoxyl, Akneroxid cream and gel)

• Effective against P. acnes• Bacterial resistance to benzoyl peroxide has

not been reported• It is available in a variety of topical

forms(Akneroxide,Panoxyl lotions & creams)• Used once or twice a day• May cause a true allergic contact dermatitis.

More often, an irritant contact dermatitis develops especially if used with tretinoin or when accompanied by aggressive washing

4-Azelaic acid(Skinoren,Azaderm 20% cream)

• It is found naturally in wheat, and it is produced by Malassezia furfur

• It is bactericidal, keratolytic and antiinflammatory

• The cream is applied to the area affected once daily, then if tolerated twice-daily after thoroughly cleansing the skin

• Some improvement should be seen after one month of using azelaic acid cream. Further improvement should occur with maximum results after six months' continuous use

• It helps reduce pigmentation, so it's useful for darker skinned patients whose acne spots leave persistent brown marks

B- Systemic Treatment

I-Systemic Antibiotics

1-Tetracyclines

• They decrease the concentration of free fatty acids in sebum. Their level is an indication of the metabolic activity of the organism and its secretion of other proinflammatory products

• They may act through direct suppression of the number of P. acnes, but part of its action may also be due to its anti-inflammatory activity

• Interactions:

-Bioavailability ↓ with antacids containing Al, Ca, Mg, Fe, Bism

-Can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy

-Can increase effects of anticoagulants• Their use during tooth development (last half of

pregnancy through age 8 y) can cause permanent yellow-brown staining of teeth; also, tetracyclines have been reported to inhibit skeletal growth in the fetus

A-Tetracycline HCl(Tetracid 250 mg cap)

• It is usually given initially in a dose of 1000 mg/day(divided). The dose is often decreased as improvement occurs and may be continued at a level of 250 mg/day for a minimum of 6 months

• Tetracycline should be taken on an empty stomach to promote absorption

B- Doxymycine 100mg cap (Vibramycine,

doxymycine,Tolexine)

• Aappears to be more effective than tetracycline, and drug resistance is less likely to occur

• Dose: 50 to 100 mg twice daily• The major disadvantage of its use is that

it can produce photosensitivity reactions, and patients should be switched to another antibiotic, if possible, during the summer months

C- Minocycline(minocine 50 mg tab)

• Minocycline is given in divided dosages at a level of 100 mg/day to 200 mg/day.

• Patients on minocycline should be monitored carefully as the drug can cause blue-black pigmentation, especially in the acne scars, as well as the hard palate, alveolar ridge, and anterior shins

2- Macrolides:Erythromycine(erythrocine 500

tab), Azithromycin(Zithromax 250 tab,azrolid 500 tab)

• Erythromycine is the only safe antibiotic to administer to pregnant women or children

• Dose 1000 mg/day orally (divided) on empty stomach

• There is increasing evidence of the development of erythromycin-resistant strains of P. acnes Therefore, it is wise to limit the use of oral erythromycin to those cases where tetracyclines are contraindicated (pregnancy&young children)

• Azithromycin (500 mg 3 times weekly), can give 80% clearance in 12 weeks

3-Clindamycine (Dalacine c,Clindacine,150 mg cap)

• Oral clindamycin has been used in the past, but because of the potential of pseudomembranous colitis, it is now rarely used for acne

4-Trimethoprim-sulfamethoxazole

(Sutrim,Septazole tab)

• Although effective in acne, the potential for side effects is great. So, they should be used only in patients with severe acne who do not respond to other antibiotics

• If they are used, the patient must be monitored for potential hematologic suppression approximately monthly

II-Hormonal therapy

1-Contraceptive pills

• Two oral contraceptives are currently FDA approved for the treatment of acne: Cilest (norgestimate 250 µg + ethinyl estradiol 35 µg) and Estrostep (ethinyl estradiol 20 to 35 µg + norethindrone acetate1 mg )

• They increase SHBG, resulting in a decrease in circulating free testosterone

• Estrogen supresses sebaceous gland leading to decreasing sebum production by 25%

• Used in unresponsive cases in young women after more conventional regimens have failed

• Improvement occurs after 2-4 months , but relapses may occur if treatment is discontinued

• Side effects include nausea, vomiting, abnormal menses, weight gain, and breast tenderness

• Rare but more serious complications include thrombophlebitis, pulmonary embolism, and hypertension

2-Spironolactone(Aldactone,25,100 mg tab)

• Blocks the binding of androgens to androgen receptors

• Good candidates for this drug are individuals with a premenstrual flare-up of their acne, acne onset after the age of 25, oily skin, coexistent hirsutism, and acne that has a predilection for the chin and mandible

• Start patients on 50 to 100 mg/day taken with meals. If no clinical response is seen in 1 to 3 months, adjust the dose up to 200 mg/day if necessary. Once maintenance has been achieved, try to lower the dose to the lowest effective daily dose

• Menstrual irregularities and breast tenderness are common side effects

• The drug should not be used during pregnancy, because it may block the normal development of male genitalia

• It alters potassium excretion (usually only at higher doses and in only 10% of patients). Serum electrolytes should be monitored during initial institution of therapy. Nausea, vomiting, and anorexia are also common

3- Cyproterone acetate (Diane:Cyproterone acetate 2mg and

Ethinylestradiol 35mcg tab)

• Blocks the androgen receptors • Given as one tab/day starting from the first

day of menstruation for 21 days• The drug is then stopped for 7 days during

which a small amount of menstrual blood is seen

• Acne usually improves by 40-50% by the third cycle and by 80-90% by the ninth cycle

4- Prednisone (Hostacorten 5 mg tab)

• Useful in female patients, with severe acne unresponsive to conventional therapy, who suffer from adrenal gland overproduction of androgens

• 2.5 to 7.5 mg, administered at night • For individuals with an acute acne flare,

Prednisone can also be used in a dose of 20 mg/day for 1 week before an important occasion such as a wedding

III- Isotretinoin (Roaccutane;Netlook,

10,20,30 mg cap)

•

• The use of the oral retinoid, isotretinoin, has revolutionized the management of severe treatment-resistant acne

• The remarkable aspects of isotretinoin therapy is that the response rate may be as high as 90% with one to two courses and the longevity of the remission, which lasts for months to years in the great majority of patients

• It causes normalization of epidermal differentiation, depresses sebum excretion by 70%,it is anti-inflammatory, and even reduces the presence of P acnes

Six months later

• Indications for treatment with isotretinoin include:

1-Less than 50% improvement after 6 months of oral and topical therapy

2- scarring

3-Associated psychological distress

4-Acne that relapses quickly once conventional therapy is discontinued

• The initial dose of isotretinoin is 0.5 to 1.0 mg/kg of the patient's body weight. Many of the problems with this drug come from starting at too high a dose

• For the first month, a patient may be started at 20 mg daily. This allows for monitoring of any adverse effects

• The daily dose may be increased each month by an additional 20 mg (e.g., 20 mg first month, 40 mg second month, 60 mg third month, etc) to a dose of approx.1 mg/kg

• Because back and chest lesions respond less than facial lesions, dosages as high as 2 mg/kg per day may be necessary

• There appears to be no advantage to single versus divided dose, but isotretinoin absorption is enhanced by taking it with meals

• Patients with severe acne, particularly those with granulomatous lesions, will often develop marked flares of their disease when isotretinoin is started. Therefore, the initial dosing should be low, even below 0.5 mg/kg per day. These patients often need pre-treatment for 1 to 2 weeks with prednisone (40 to 60 mg per day), which may have to be continued for the first 2 weeks of therapy

• Clinical results can be obtained with dosages as low as 0.1 mg/kg per day. However, with such dosages, the incidence of relapses after therapy is greater

• Isotretinoin is usually given for 20 weeks, but the length of the course of treatment is not absolute; in patients who have not shown an adequate response, therapy can be extended, if necessary

• Some improvement is usually seen for 1 to 2 months after isotretinoin is discontinued, so that total clearing is not a necessary endpoint for determining when to discontinue therapy

• Because the skin will often continue to clear after drug administration has been stopped, at least a 2-month waiting period and preferably a 6-month period is advised before one commits a patient to a second course of therapy

• In a 10-year follow-up study, 61% of patients were free from acne

• Of those who relapsed, 23% required a second course

• Ninety-six percent had relapsed within 3 years of therapy

• Truncal acne had a higher relapse rate• Patients given a cumulative dose of 120

mg/kg overall were less likely to relapse

• Using isotretinoin during pregnancy resulted in spontaneous abortion or birth defects in 83% of cases, so it should be given only to cases not responding to other therapy

• Furthermore, women who are of childbearing age must be fully informed of the risk of pregnancy. The patient must either avoid sexual exposure totally or should employ two highly effective contraception techniques such as the use of an oral contraceptive and condoms with a spermicidal jelly

• Contraception must be started at least 1 month before isotretinoin therapy

• The patient must have a negative serum pregnancy test at the time when therapy is decided upon and on the second or third day of the next menstrual period or 11 days after the last unprotected intercourse in a woman who is amenorrheic

• Contraception should continue throughout the course of isotretinoin and for 1 month after stopping treatment

• The pregnancy test should be repeated monthly to maintain patient awareness

• Because the drug is not mutagenic, there is no risk to a fetus conceived by a male who is taking isotretinoin

• Cheilitis of varying degrees is found in almost all cases

• Other side effects that are likely to be seen in over 50 % of patients are dryness of the mucous membranes, xerosis, conjunctivitis, and pruritus

• Less frequent side effects include bone and joint pain; thinning of hair; headache; palmoplantar desquamation; and nausea and vomiting

• Laboratory abnormalities include elevations in triglycerides, ESR, platelet count, liver function tests, and white blood cells in the urine and decreases in red blood cell parameters, white cell counts, and high-density lipoprotein levels

• The elevation of triglycerides, which is dose-related, is of particular concern because it is often accompanied by a decrease in the high-density lipoprotein levels, which may increase the risk of coronary artery disease

• Associated mood changes and depression have been reported during treatment. Although the cause is not clear, patients should be informed of this potential effect

• The patient is considered at high risk for abnormal healing and development of excessive granulation tissue following procedures. Many dermatologists delay elective procedures, such as dermabrasion or laser resurfacing, for up to a year after completion of therapy. Other procedures to be avoided during therapy include tattoos, piercings, leg waxing, and other epilation procedures

Therapeutic decisions

• Comedonal Acne: Topical tretinoin or adapalene(less irritant) is the treatment of choice. Starting with a lower concentration of the cream (available as 0.025, 0.05, and 0.1%) or gel (available as 0.01 and 0.025%) and increasing the concentration if local irritation does not occur. Topical azelaic acid has some comedolytic activity. It is less potent than tretinoin but may be useful in patients who cannot tolerate topical tretinoin or other retinoids

• Mild Inflammatory Acne :Most patients have a response after two to four weeks of twice-daily application of a topical antibiotic, topical benzoyl peroxide, or the combination of benzoyl peroxide and erythromycin. Treatment should be continued until no new lesions develop and then should be slowly discontinued

-The combination of a topical retinoid applied once daily and either a topical or a systemic antibiotic is the best approach. The choice between topical and systemic antibiotic therapy usually depends on the extent of skin involvement and the severity of the inflammation

- Benzoyl peroxide plus erythromycin are the most effective topical antimicrobial therapies

- Usually four to six weeks are needed to reduce P. acnes and to curtail the formation of new inflammatory lesions

•Moderate inflammatory acne:

- Patients treated with an oral antibiotic may also be given topical antibiotics, particularly when the dose of the oral drug is reduced. In general, the dose of an antibiotic should not be reduced before two to four months. Long-term control requires the suppression of P. acnes for prolonged periods

• Nodular acne:

-Systemic isotretinoin is the treatment of choice, particularly those who have scarring

-An alternative to systemic isotretinoin in women with persistent acne that is unresponsive to therapy with antibiotics and topical tretinoin is therapy with estrogen or an antiandrogen

- For patients with larger inflammatory lesions, local injection of a corticosteroid is effective

• Acne conglobata: Oral isotretinoin is the treatment of choice in

patients with this type of acne; in some, systemic corticosteroid therapy may be given before or concomitantly with isotretinoin

• Acne fulminans:

Oral corticosteroids are the therapy of choice

C-Physical modalities

1-Chemical PeelsLight chemical peels of glycolic acid and other chemical agents are used to loosen blackheads and decrease acne papules

2-Comedo Extraction

• Used primarily in patients who do not respond to comedolytic agents

• Patient is treated first with a topical retinoid for 3 to 4 weeks

• This procedure is done using the comedo extractor and should only be performed by a dermatologist as inaccurate placement of the comedo extractor

may serve only to push the inflammatory material further into the skin

• The removal of open comedones does not materially influence the course of the disease because these lesions do not become inflammatory,but they are removed for cosmetic purposes

• In contrast, closed comedones should be removed to prevent their rupture. The material contained within the comedo can be removed only after the orifice is gently enlarged with a no. 25 needle or other suitable sharply pointed instrument

3-Laser:.Nd:YAG, diode, and Er:glass lasers show promise in the treatment of inflammatory acne and clinical improvement in acne scars. Treatments are typically performed monthly for 4 to 6 months. Pulsed dye lasers can be used to minimize erythema of active acne lesions and acne scars

4-Photodynamic therapy: Significant clearence for at least 20 weeks was reported

5-Ultraviolet light : Exposure to sunlight or UVB sunlamps may be moderately effective in some patients

6-Cryosurgery:Freezing with liquid nitrogen will hasten resolution of old nodules(>7 days)

6-Intralesional Steroids Injection

• Intralesional steroid injection either by the use of an insulin syringe or by the Dermojet, usually dramatically decreases the size of deep nodular lesions

• The injection of 0.05 to 0.25 mL per lesion of a triamcinolone acetonide suspension (2.5 to 10 mg/mL) is recommended as the anti-inflammatory agent. It is often has to be repeated every 2 to 3 weeks

• Most lesions, particularly early ones, will flatten and disappear within 48 hours of injection

D-Treatment of scars

1-Laser skin resurfacing: Ablative CO2/Er:YAG laser skin resurfacing can improve the appearance of acne scars of all types but requires significant post-operative wound care and recovery time

2-Dermabrasion using high-speed diamond buffing drills can remove small and superficial scars and sometimes deep scars

3-Fat transfer and injection of filler substances can be used to elevate acne scars

General points

• Soaps, detergents, and astringents can remove sebum from the surface of the skin but do not alter sebum production and are of no therapeutic value. In fact, vigorous scrubbing can aggravate acne by promoting the development of inflammatory lesions

• Dietary restrictions have no role in therapy• The patient should be advised against

picking, pinching or squeezing noninflammatory or inflamed lesions, which can aggravate the acne and cause scarring

Acne variants

1-Acne excoriée

• Occurs predominantly in females

• Some primary inflammatory acne lesions may be present, and in other patients no lesions can be found

• Patients play with the skin to exacerbate even the smallest lesions. There is often some personality or psychological problem

• There are no active acne lesions, only scratch marks, sores and scars.

All the inflammatory

lesions and

comedones

have been

removed by

picking or

squeezing

• Treatment is with 1g/day of tetracycline for months and advice not to pick the spots

• Topical treatment tends to irritate the skin and aggravate the problem

• In the group with virtually no acne spots, pimozide (2mg twice a day) and appropriate psychotherapeutic procedures may help

2-Drug-induced acne/acneiform eruptions

• Folliculitis may appear following administration of glucocorticoids or corticotropin or prolonged use of topical steroids. A similar eruption can occur due to iodides and bromides(e.g. sedatives, expectorants) and INH. Androgens including anabolic steroids and gonadotrophins, may precipitate acne, especially in athletes who take illegal performance-enhancing drugs

• It differs from acne vulgaris in the type of lesions observed and its distribution:

1-The lesions are usually all in the same stage of development, consisting of small pustules and red papules. Postinflammatory hyper-pigmentation may occur,

but comedones, cysts, and scarring are unusual 2-In contrast to acne vulgaris, they appear mainly on the trunk, shoulders, and upper arms,with lesser involvement of the face

3-Externally induced acne

• A-Cosmetic acne:• Cosmetic companies are testing their

compounds adequately for comedogenicity before marketing. Consequently, with the exception of very greasy, occlusive products, cosmetics are infrequent etiologic agents for acne

• Occurs as folliculitis in the perioral area of mature females, especially those who had acne as adolescents and have used cosmetics for a long time

• The area to which the cosmetic was applied is studded with closed and open comedones and some papules& pustules

• Treatment with

topical retinoids or

benzoyl peroxide is

usually successful

B-Pomade acne:• Pomades are greasy preparations used to

'defrizz' curly Negroid hair. The rash is similar to cosmetic acne but consists of non-inflamed lesions around the forehead and other areas where

greasy pomades may

extend onto the hairless

skin• Treatment is with topical

retinoids

C-Oil and Tar acne:

• Acne from these agents tends to be quite inflammatory with large comedones, papules, pustules, large nodules, and true cysts. Tar acne is often accompanied by hyperpigmentation

• The lesions are not restricted to the face and, in fact, are more common on covered areas where intimate contact with clothing saturated with the offending compound is maintained

D-Chloracne• It is caused by exposure to halogenated

aromatic hydrocarbons, which are most often found in fungicides, insecticides, herbicides and wood preservatives

• It is the most common skin sign of dioxin poisoning (formed as a by-product of the manufacture, molding, or burning of organic chemicals and plastics that contain chlorine)

• There are open and closed comedones with uninflamed nodules and cysts• Lesions are most often seen on the cheeks, behind the ears, in the axilla and in the groins

• Topical therapy with retinoids worth a trial

• Long-term oral antibiotic therapy may be needed for the inflammatory lesions

• Gentle cautery under local anaesthetic cream (EMLA applied for 90min under polythene occlusion) produces excellent results

E-Mechanical acne:• Acne occurs at the site of physical trauma, e.g. by occluding the skin with adhesive tape or continuous friction with a belt or a violin in violin players• Treatment is the same as for other forms of acne, plus removal of the cause

4- Infantile and juvenile acne• Presents as facial acne at around 3-24

months, and may last up to 5 years of age• Mainly affects males• The lesions are more localized than in adults and particularly affect the cheeks. All acne lesions can be found• Patients may develop significant acne as teenagers

• May result from excess androgen due to transplacental stimulation of the adrenal gland, as most sufferers have elevated plasma adrenal androgen

• Treatment consists of oral erythromycin (125mg three times a day) for 6 months, and topical therapy (preferably benzoyl peroxide, erythromycin or retinoids) is essential until lesions have totally disappeared

ROSACEA

Etiology

• The etiology of rosacea is unknown

• Several factors may play a role in its development

1-Vasculature

• Increased blood flow and increased numbers of blood vessels that are closer to the surface of the face skin are thought to be responsible for the redness and flushing associated with rosacea

• Furthermore, vasodilatation, the normal response to hyperthermia, is thought to be exaggerated in rosacea patients

2-Climatic exposures

• Exposure to solar irradiation damages cutaneous blood vessels and dermal connective tissue. This may explain why rosacea predominately affects the facial convexities and has a tendency to flare in the spring and summer

• However, other studies suggest the contrary, i.e. most patients' symptoms do not worsen in the sunlight and do not flare with an acute exposure to ultraviolet light

3-Dermal matrix degeneration

• There is:

- damage to the blood vessels endothelium leading to leaking of serum proteins, inflammatory mediators, and metabolic waste

- degeneration of the dermal matrix leading to poor tissue support of cutaneous vessels

• However, it is not known which process starts first leading to subsequent occurrence of the other

4-Chemicals and ingested agents

• Most evidence does not support that dietary factors (e.g. spicy foods and hot drinks) play a main role in the pathogenesis

• Certain medications such as the antiarrhythmic amiodarone (Cordarone) , topical steroids, nasal steroids, and high doses of vitamins B-6 and B-12 may cause flares

5-Microbial organisms

• Demodex species (mites that normally inhabit human hair follicles) may play a role in the pathogenesis of rosacea

• Demodex prefers skin regions

that are affected in rosacea,

such as the nose and cheeks

• Conflicting evidence exists regarding the role of demodex in rosacea:

-Some studies showed an immune response of helper-inducer T cell infiltrates surrounding the Demodex antigens

-Others showed that Demodex is found in large numbers of healthy individuals without rosacea

• All ages can be affected, including pediatric patients. Peak incidence occurs in the fourth to seventh decades

• More than 10% of the general population in USA exhibits dermatologic characteristics of rosacea; of these, up to 60% experience ocular complications

• Rosacea occurs much more commonly in fair-skinned white patients

• In races with increased skin pigmentation it may be underreported, rather than less prevalent

• Females are affected with rosacea twice as often as males

• However, disease manifestations, especially rhinophyma, are frequently more severe in males than in females

Clinically

• Four clinical types of rosacea exist:

1-Erythematotelangiectatic type

• Central facial flushing, often accompanied by burning or stinging• The redness usually spares the periocular skin• These patients usually have skin with a

fine texture

•The erythematous areas of the face at times appear

rough with scale

likely due to

chronic,

low-grade

dermatitis

• Frequent triggers to flushing include acutely felt emotional stress, hot drinks, alcohol, spicy foods, exercise, cold or hot weather, and hot baths and showers. These patients also report that the burning or stinging is exacerbated when topical agents are applied.

2-Papulopustular rosacea• It is the classic presentation of rosacea• Patients are middle aged &predominately

present with a red central portion of their face containing small erythematous papules surmounted by pinpoint pustules• Telangiectasias may be present but may be difficult to distinguish from the erythematous background

3-Phymatous rosacea• There are marked skin thickenings and

irregular surface nodularities of

the nose, chin, forehead,

one or both ears,

and/or the eyelids

4-Ocular rosacea• Ocular manifestations may precede the

cutaneous signs by years. Yet, frequently they develop concurrently with dermatologic manifestations

• They include blepharitis,

conjunctivitis, inflammation

of the meibomian glands, and conjunctival telangiectasias. Patients may describe eye stinging or burning, dryness, irritation with light, or foreign body sensation

Histopathology• Dilatation of upper and mid-dermal vessels

and lymphatics with perivascular and perifollicular

lymphohistio-

cytic infiltrate

is generally

present in all

cases

• Reflecting the clinical presentation, various other pathologic changes can be seen from case to case,

including neutrophils

accumulation,

resulting in a

superficial pustule

• Granulomatous infiltrates, with epithelioid histiocytes forming a tuberculoid pattern are reported to occur

in about 10% of all

cases, and caseation

necrosis has been

identified in about

10% of these patients

Treatment

I-General measures• Where possible, reduce factors causing

facial flushing• Avoid oil-based facial creams• Never apply a topical steroid• Use light oil-free facial sunscreens• Keep your face cool: minimize your exposure

to hot or spicy foods, alcohol, hot showers and baths and warm rooms.

II-Oral antibiotics

• Several courses are often needed from time to time as the antibiotics do not cure the disorder

1-Tetracyclines• Tetracycline 250 mg PO qd to 500 mg PO

tid or Doxymycine

• Prescribed for 6 to 12 weeks, the duration and dose depending on the severity

2-Metronidazole (Flagyl,Flagycure 250 mg)

• Aactive against various anaerobic bacteria and protozoa

• Beneficial against papules and pustules of rosacea

• Topical applications are helpful for mild disease and as an adjuvant to systemic therapy

• Dose: 200 mg PO bid Topical: Wash affected area and apply a thin film to affected area bid

• May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine

• Usually safe in pregnancy but benefits must outweigh the risks

• Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy

3-Erythromycin (Erythrocine)

• Can be used when tetracyclines are not tolerated or are contraindicated

• Dose: 500 mg PO bid

4-Clindamycin (DalacineT 10 mg/ml sol)

• Effective against mild-to-moderate papulopustular rosacea• Dose : Apply to affected area qd

5-Azithromycin (Zithromax)

• Dose 500 mg PO on day 1, followed by 250 mg PO qd for next 4 days

• Interactions : Toxicity increases with coadministration of fluconazole and pimozide

• May increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin

• Usually safe in pregnancy but benefits must outweigh the risks

III-Isotretinoin (Ro-ccutane,Netlook,10,20,30 mg cap)

• Recent research showed a role of vascular endothelial growth factors (VEGF) in rosacea

• Retinoids appear to modulate the expression of VEGFs in the skin; this may explain the therapeutic benefit of isotretinoin in the treatment of rosacea

• May be helpful for recalcitrant disease, but recurrence is common

• Dose: 0.5-1 mg/kg/d PO divided bid for 4 months

• InteractionsToxicity may occur with vitamin A coadministration; pseudotumor cerebri or papilledema may occur when coadministered with tetracyclines; isotretinoin may reduce plasma levels of carbamazepine and contraceptive efficacy

• PregnancyX - Contraindicated in pregnancy

1 month after oral isotretinoin

Treatment of erythema

• Oral and topical antibiotics are often ineffective in the treatment of erythema and flushing. Low-dose clonidine (Catapres; 0.05 mg twice daily) may be effective in controlling flushing, especially in women who are postmenopausal

• A nonselective beta blocker (such as long-acting propranolol [Inderal], 80 to 240 mg daily, and nadolol [Corgard], 40 to 80 mg daily) may also be used

Treatment of telangectasia• Treatment with a pulsed dye laser may be

effective in advanced cases and if performed by an experienced physician, laser therapy usually has no complications

• Temporary hyperpigmentation of treated areas may occur in 5 to 20 percent of patients.

Treatment of rhinophyma • The initial stages of rhinophyma may

respond to antibiotic treatment, but more advanced cases must be treated with surgery

• A number of techniques have been advocated, including dermabrasion, cryosurgery, and excision of hypertrophic tissue by electrosurgery or with a laser

PERIORAL DERMATITIS

Etiology

• An underlying cause cannot be detected in all patients

• Topical steroids:Many patients abuse topical steroid preparations. No clear correlation exists between the risk of POD and strength of the steroid or the duration of the abuse

• Cosmetics: Fluorinated toothpaste; skin care ointments and creams, especially those with a petrolatum or paraffin base are suggested to be causative factors

• Physical factors: UV light, heat, and wind worsen POD

• Microbiologic factors: Fusiform spirilla bacteria, Candida species, and other fungi have been cultured from lesions. Their presence has no clear clinical relevance

• Miscellaneous factors: Hormonal factors are suspected because of an observed premenstrual deterioration. Oral contra-ceptives may be a factor

• The incidence is estimated to be 0.5-1% in industrialized countries

• The incidence seems to be lower in less developed countries, but no statistics are available

• Women account for an estimated 90% of the cases

• Perioral dermatitis can occur in children, but the vast majority of patients are aged 20-45 years

Clinically

• Skin lesions occur as grouped follicular reddish papules, papulovesicles, and papulopustules on an erythematous base

• They are located in the perioral area, nasolabial fold, and lateral portions of the lower eyelids

• Symptoms consist of a sensation of burning and tension but itching is rare

• Histologic findings are similar to those of rosacea

Treatment

• The patient should be advised that remission might not occur for weeks, despite correct treatment

• In every case, an initial worsening of the symptoms may occur with treatment, especially if topical steroids are withdrawn. The patient should be made aware of this complication. In cases of preceding long-term abuse of topical steroids, steroid weaning with low-dose 0.1-0.5% hydrocortisone cream can be tried initially

• Zero-therapy is based on the idea that by ceasing use of all topical medications and cosmetics, the underlying causative factor for POD is eliminated. This form of therapy is appropriate in very compliant patients. This therapeutic option is often limited because of the patient's tendency to overtreat his or her condition

• In severe forms of POD, systemic treatment with antiacne drugs is required

• In unresponsive and granulomatous forms, oral isotretinoin may be considered

• In cases with minor presentations, as well as in children and pregnant women, individualized topical therapy is generally recommended

• Pimecrolimus cream significantly reduced the Severity Index compared with vehicle in a randomized, double-blind study

STEATOCYSTOMA MULTIPLEX

Etiology

• It is a rare familial disorder of the pilosebaceous unit that has an autosomal dominant transmission

• Both sexes are equally affected

• Cysts present during adolescence and early adulthood. SM is a lifelong condition

Clinically• Cysts are concentrated in areas with high No. of sebaceous glands (upper torso, proximal extremities) but can present anywhere on the skin (ie, face,groin)• The involved area becomes studded with deep,

flesh-to-yellow colored, superficial, dermal papules

• Some lesions may become inflamed, and erythema may surround them

• When a cyst spontaneously ruptures to the skin surface or is incised and drained intentionally, the contents appear as an odorless creamy or oily fluid

Histopathology• Cysts are located in the mid dermis• The cyst wall is lined by squamous

epithelium with a toothed surface• Walls contain flattened lobules of sebaceous

glands among the epithelial cells• Each cyst is attached to overlying normal epidermis by thin strands of undiffer- entiated epithelial cells• The cystic space contains keratin, vellous hair, sebum etc

Treatment

• The patient may desire intervention for cosmetic reasons

• Unfortunately, isotretinoin (despite known effects of decreasing sebaceous gland activity) has shown inconsistent results, according to the literature. In at least 1 patient, isotretinoin appeared to worsen the condition, which necessitated cessation of the drug

Surgical Care

• Aspiration: Individual cyst contents can be aspirated through an 18-gauge needle, but the effect is only temporary

• This technique is thought to be the treatment of choice for facial lesions because the scarring associated with excisional approaches is avoided

• Surgical excision: Excision of all cysts on a patient is not feasible because of the large numbers of cysts usually present

• However, excision of some of

the larger lesions can be per-

formed using a small surgical

punch or a sharp-tipped cautery

point to puncture the cyst wall.

The cyst's contents then can be

expressed prior to everting the

cyst lining with forceps to des-

troy it by electrodesiccation The

wound heals by 2ry intension

• Carbon dioxide laser: At least 1 published report exists of the successful treatment of SM using a carbon dioxide laser