• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Dermatology 5th year, 4th lecture (Dr. Mohammad Yousif)
 

Dermatology 5th year, 4th lecture (Dr. Mohammad Yousif)

on

  • 2,192 views

The lecture has been given on May 15th, 2011 by Dr. Mohammad Yousif.

The lecture has been given on May 15th, 2011 by Dr. Mohammad Yousif.

Statistics

Views

Total Views
2,192
Views on SlideShare
2,192
Embed Views
0

Actions

Likes
1
Downloads
125
Comments
1

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel

11 of 1 previous next

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Dermatology 5th year, 4th lecture (Dr. Mohammad Yousif) Dermatology 5th year, 4th lecture (Dr. Mohammad Yousif) Presentation Transcript

    • Acne &Rosacea
      • Stem cells reside in the bulge region.
      • Differentiate into epidermis, HF, hair, sebaceous gland & duct.
      Sebaceous gland morphogenesis
    • What is the function of the sebaceous gland?
      • To produce sebum.
      • It covers the skin surface, possibly as a protectant.
      • Sebum may also have antifungal properties.
    • Acne vulgaris - Sebum composition
      • Triglycerides
      • FFAs
      • Wax esters
      • Squalene
      • Cholesterol esters
      • Cholesterol
      • 57
      • 0
      • 25
      • 15
      • 2
      • 1
      Isolated gl. (%)
      • 65
      • 0
      • 0
      • 0
      • 15
      • 20
      Epidermal lipids (%)
      • 42
      • 15
      • 25
      • 15
      • 2
      • 1
      Skin surface (%)
    •  
    •  
    •  
    •  
      • The primary defect in acne conglobata, the most severe expression of acne vulgaris, is an alteration of keratinization within the sebaceous follicle & the leakage of retained sweat into tissue surrounding plugged eccrine ducts.
    •  
    • 4 main pathologic features of acne
    • Acne P. acnes Inflammation Sebum androgen Follicular keratinization
    • Androgens (DHT) Follicular hyperkeratinization P acnes multiplication Inflammation & immune response  sebum production
    • What is a comedo?
      • A comedo is a folliculocentric collection of sebum & keratin.
      • Comedonal acne characteristically consists of both open (blackheads) & closed comedones (white-heads).
      • When the contents of a closed comedo are exposed to air, a chemical reaction occurs, imparting the black color of an open comedo.
    • Androgens Alteration of the follicular milieu Colonization with P. acnes Inflammation Sebocyte Keratinocyte Seborrhea Follicular desquamation
    • Scarring
      • 30% of patients have significant scarring.
      • Nonscarring patients.
      Holland et al. BJD 150: 72-81, 2004.
      • Scarring patients
      • Early inflammatory response, nonspecific.
      •  CD4+, langerhans cells with HLA-DR.
      • Late inflammatory response, specific with memory T-cells.
      •  CD4+, Langerhans cells.
      •  Macrophages, vascular adhesion molecules, blood vessels.
    • Scarring in acne
      • Genetically prone to scarring.
      • Whose acne has been present for a long time, even with moderate type.
      • With severe deep inflammatory acne.
      • With severe exacerbation (flare-up) with isotretinoin therapy.
      More likely to occur in patients:
    • Designing an Acne Treatment Plan
    • Mild acne Usually topical only unless!! Mainly comedones Mainly inflammatory
      • Retinoic a. 0.05% “Retin-A ® ”
      • AA 20% “Skinoren ® ”
      • Adapalene “Differen ® ”
      • AHAs/esters “Sebium AKN ® ”
      • Bpo “Panoxyl ® ”
      • Antibiotics
      • AA 20% “Skinoren ® ”
      • Adapalene “Differen ® ”
      • Zinc gluconate “Sebium AKN ® ”
      Mixed
      • Bpo + erythro “Benzamycin ® ”
      • Retinoids (T) + Antibiotics (T)
      • Skinoren ®
      • Sebium AKN ®
      Irritation
    • Moderate acne Systemic treatment Oral antibiotics Appropriate topical treatment + ? Oral isotretinoin
    • Severe acne and Resistant cases Oral isotretinoin
    • Drugs used in the treatment of acne
      • Retinoic acid 0.05%
      • Isotretinoin 0.05%
      • Adapalene
      • Azelaic acid
      Predominantly anticomedonal
      • Adapalene
      • Topical antibiotics
      Predominantly antiinflammatory Topical antibiotics Predominantly antimicrobial
      • Erythromycin
      • Clindamycin
      • Tetracycline
      • Erythromycin + Zinc
      Azelaic acid Benzoyl peroxide Benzamycin (Bp + erythromycin) I) Topical
    • Drugs used in the treatment of acne
      • Tetracycline
      • Minocycline
      • Erythromycin
      • Co-trimoxazole
      • Trimethoprim
      Antibiotics Retinoids “Isotretinoin” Steroids “Prednisolone” Hormonal regimens
      • Estrogen + prednisolone
      • Ethinyl estradiol + cyproterone acetate
      • Spironolactone
      II) Oral
    • Acne vulgaris - Treatment a) Predominantly non-inflammatory lesions:
      • Retinoic acid 0.05%
      • Azelaic acid 20%
      • Adapalene
      • Comedone extractor
      I) Mild acne: usually requires topical therapy only. b) Predominantly inflammatory lesions:
      • Benzoyl peroxide
      • Topical antibiotics: clindamycin, erythromycinor erythromycin + Zn acetate 1.2%
      • Azelaic acid 20%
      • Adapalene
    • Acne vulgaris - Treatment Systemic therapy as oral antibiotics or cyproterone acetate should be given in conjunction with appropriate topical therapy. II) Moderate to severe acne Isotretinoin III) Severe acne
    • Treatment of acne
      • Sebum production
      • Hormonal therapy
      • isotretinoin
      • P. acnes
      • Antibiotics
      • Benzoyl peroxide
      • Isotretinoin
      • Follicular hyperkeratinization
      • Topical retinoids
      • Isotretinoin
      • Inflammation
      • Antibiotics
      • Benzoyl peroxide
      • Hormonal therapy
      • Isotretinoin
    • Suppression
      • Bpo
      • Antibiotics (T)
      • Retinoids (T)
      • Sebium AKN (T)
      • Azelaic a. (T)
      • Tetracycline (S)
      • Isotretinoin
      Sebum - - - ?  - - +++ Comedones  - ++ + + - ++ P. acnes ++ ++ - + ++ ++ + Inflam. + + ?  + + + ++
    • Acne vulgaris
      • Tetracyclines (1 gm daily) better on an empty stomach. It is contraindicated in pregnancy, hepatic & renal impairement.
      • Erythromycin (1 gm daily) especially in women who might become pregnant.
      II) Systemic treatment Antibiotics
    • Systemic treatment - Antibiotics (Cont’d)
      • Clindamycin (Dalacine C ® ): 150 mg, 3 times daily. Risk of colitis.
      • Doxycycline (Vibramycin ® ): 100 mg daily.
      • Trimethoprim - sulfamethoxazole (Septrin ® ): 400-600 mg/day.
    • Systemic treatment - Antibiotics (Cont’d) Minocycline (Minocin ® ): 100 mg daily. Side effects:
      • Blue-black pigmentation & metallic taste.
      • Hypersensitivity syndrome reactions (including pulmonary eosinophilia) & serum sickness-like reactions occur within 3 ms of treatment & are characterized by fever, malaise & arthralgia.
      • Minocycline-induced systemic lupus erythematosus and hepatitis had been reported.
    •  
    • Principles of antibiotic therapy
      • Limit duration of systemic agents
      Leyden JJ. J Eur Acad dermatol Venereol, 15: 51-55, 2001. Velicer et al. JAMA, 29 (7): 827-35, 2004.
      • Antibiotic resistance.
      • Anti-inflammatory action of retinoids.
      • Breast cancer risk?
      • Use BP and BP/antibiotic combinations to minimize emergence of resistant strains.
    • Acne type Mild acne “Comedones” Initial therapy Maintenance Mild-to-moderate acne (papular / pustular) Moderate-to-severe acne (severe nodulocystic) T Adapalene or T retinoid or Bpo / T antibiotics T Adapalene + T / oral antibiotic or + Bpo antibiotic or ?? oral isotretinoin Oral isotretinoin or Cyproterone acetate T adapalene (Differin ® ) Failure Failure 3 ms Success After 3 ms success Success
    • Initial therapy Maintenance Acne type Modified from: Leyden, J Am Acad Dermatol, 2003 Oral isotretinoin or Hormonal therapy – women T. Retinoid + T./oral antibiotic or T. retinoid + BPO … antibiotic or fluid active (sebium AKN)  BPO or ?? Oral isotretinoin Failure 3 ms Failure Mild acne “ comedones” Mild-to-moderate acne (papular/pustular) Moderate-to-severe acne (severe nodulocystic) Success T. Retinoid or T. Retinoid + BPO/T. antibiotics After 3 ms success T. Retinoid &/or BPO or Fluidactive (sebium AKN) Success
    • Isotretinoin Therapeutic effects
      • Reverses comedone formation.
      • Reduces sebum levels
      • Reduces P. acnes
      • Reduces inflammation
      • Remission & cure possible
      Side effects Teratogenicity Layton AM. Am J Dermatol Treat 4: S2-S5, 1993.
      • Psychiatric
      • … .
    • Only isotretinoin
      • Miniaturizes sebaceous glands.
      • Reduces sebaceous gland output.
      • Reverses retention hyperkeratosis.
    •  
    •  
    •  
    • Isotretinoin - Side effects
      • Teratogenic: pregnancy is completely contraindicated during & for 1 month after therapy.
      Two contraceptive methods should be used
      • Effective contraception must be in use for at least 1 ms & a negative serum pregnancy test or a negative urine pregnancy test with a sensitivity of at least 50 mU/ml must be obtained within 1 wk prior to beginning therapy.
      • Contact lens use may also have to be discontinued during therapy because of discomfort or blepharoconjunctivitis.
    •  
    • What is SAPHO syndrome?
      • S ynovitis, A cne, P ustulosis, H yperostosis, & O steitis.
      • The acne associated with this syndrome is most often acne conglobata – with highly inflammatory comedones, nodules, abscesses, & draining sinuses located primarily on the trunk, which often heal with significant scarring.
    • Is there a difference between neonatal acne & infantile acne?
      • Yes
      • Neonatal acne occurs in up to 20% of newborns; it usually develops during weeks 2-4 of life.
      • It is more common in males, is relatively mild, & regresses spontaneously in most infants by age 6 ms.
      • It is thought to be due to maternal androgens & is not associated with significant scarring or an increased incidence of acne in later life.
    • Is there a difference between neonatal acne & infantile acne? (Cont’d)
      • Infantile acne usually begins between the third & sixth months of life & may persist to age 5 & rarely longer.
      • It is uncommon & occurs more often in males. It can be severe, with nodules, cysts & significant residual scarring.
    • Is there a difference between neonatal acne & infantile acne? (Cont’d)
      • Endocrine abnormalities & virilizing tumors can be associated.
      • Some studies show an increased incidence of severe acne in later life.
    • How does steroid acne differ from acne vulgaris?
      • Steroid acne has a sudden onset, the lesions are monomorphic (all lesions at the same stage of development), & comedones are absent.
      • It occurs primarily on the upper trunk, less frequently on the face, & clears when the drug is withdrawn.
    • What is Favre-Racouchot syndrome?
      • This describes the development of multiple open comedones located on the inferolateral aspect of the orbital rim in elderly patients.
      • It is associated with marked solar elastosis of the surrounding skin.
    •  
    • Regulation of sebaceous glands
      • Retinoids.
      • Androgens / estrogens.
      • Melanocortins.
      • Corticotrophin releasing hormone.
      • Insulin-like growth factors / growth hormone .
      • Peroxisome proliferator activated receptors (PPARs).
    • IGF-1
      • Insulin at high levels can interact with IGF-1 receptor.
      • IGF-1 promotes expression of enzymes responsible for androgen biosynthesis & conversion.
    • Sebum production
      • Increased sebum production in acne.
      • Micro-organisms hydrolyze triglycerides into free fatty acids.
      • Squalene, wax & triglycerides.
      • Promote bacterial clumping & colonization.
      • Increase inflammation.
      • Comedogenic.
      Kligman et al. Arch Dermatol. 102: 267-75, 1970.
    • Seb. gl. / sebum
      • Sebum comp. is unique to man
      • TGs FFAs (comedogenic)
      • linoleic a. conc.
      • Sebum related to acne and acne severity
      Lipase
    • Could acne be related to a change in skin lipid composition irrespective of the rate of sebum excretion ?
    • Squalene “ sebum” Oxidated squalene Hyperproliferation  Sebum fluidity Microcomedo Oxidation
    • Propionibacterium acnes
      • Colonizes sebaceous follicles.
      • Lipases break down sebaceous lipids into free fatty acids.
      • Produces enzymes leading to rupture of comedone walls.
      • Activate toll-like receptors.
    • Microcomedo
      • Precursor lesion of acne
      • Formation is inhibited by topical retinoids
    • Acne Excori é e
      • Sertroline (Zoloft  ) 25 mg to 50 mg
      • Takes weeks to have full impact
      • Patients do not seem to consciously admit that it helped
      • Some feel paroxetine (Paxil  ) more effective
      • Olanzapine (Zyprexa  ) 2.5 – 5.0 mg hs
    • … and consider the possibility the patient is excoriating because of demodecideosis Crotamiton or Pyrethrin Acne Excori é e
    • Acne Excori é e Use topicals! … even if you don’t think they help … it gives the patient some way to touch the face without guilt – and without picking
    • Diet & acne
      • Examined two non-westernized cultures & found no acne.
      • Hypothesis that the non-westernized diet, low in high-glycemic load carbohydrates, contributed to the absence of acne.
      Cordain et al., Arch Dermatol., 2002; 138: 1584-90.
    • Does chocolate cause acne?
      • No….
      • But, insulin & insulin-like growth factor-1 both stimulate the sebaceous gland & androgen production & insulin-like growth factor promotes keratinocyte proliferation.
    • Diet – hypothesis!
      • A diet that encourages a high insulin response chronically could promote acne by resulting in hyperinsulinemia and increased levels of IGF-1.
      • Hyperinsulinemic states as seen in some women with PCOD are associated with acne vulgaris.
      • Medications that decrease insulin resistance also improve acne in some PCOD patients.
      Diet in acne
    • Diet in acne
      • Skim milk was most highly associated with the prevalence of acne.
      • Other dairy products associated with acne included instant breakfast drinks, sherbet, cream cheese & cottage cheese.
      Adebamowo et al.
    • Diet in acne
      • Sode, french fries, chocolate candy, and pizza were not significantly associated with acne.
      Adebamowo et al.
    • Diet in acne Hypothesis Adebamowo et al.
      • Hormonal content of milk may be responsible for the association with acne.
      • Milk contains estrogens, progesterones, and androgen hormones as well as glucocorticoids and IGF-1.
    • Conclusions
      • Milk intake may influence comedogenesis through:
      • Steroid hormones: androgens, 5  -reduced steroids, other steroid hormones.
      • IGF-1 pathway.
      • Whey proteins &  -lactalbumin
      •  -lactalbumin is a potential transport protein for sex steroids & has androgenic effect on fed rats
      •  -lactalbumin undergoes pressure induced conformational change with functional alteration
    • Treatment of acne
      • Sebum production
      • Hormonal therapy
      • Sebum correction
      • isotretinoin
      • P. acnes
      • Antibiotics
      • Benzoyl peroxide
      • Isotretinoin
      • Follicular hyperkeratinization
      • Topical retinoids
      • Topical tazarotene (receptor selective)
      • Isotretinoin
      • Inflammation
      • Antibiotics
      • Benzoyl peroxide
      • Hormonal therapy
      • Isotretinoin
    • Rosacea (Acne Rosacea)
      • It is a chronic, vascular inflammatory disorder, usually limited to the center of face and characterized by persistent erythema, telangiectasia, papules and pustules.
      • Age: more between 30-50 years.
      • Sex: females are affected more.
    •  
    •  
    •  
    •  
    •  
    •  
    •  
    • Rosacea (Acne Rosacea)
      • Ocular involvement.
      • Lymphoedema.
      Complications
    • Rosacea (Acne Rosacea)
      • It affects mainly the center of the face.
      • It begins as a transient erythema with edema and telangiectasia. In most patients there are papules which are asymptomatic (in contrast with AV), and less frequently pustules but comedones and scarring are absent.
      • Rhinophyma.
      Clinically
      • The earliest sign of rosacea are facial telangiectases & persistent erythema of the central face &, less often, the neck & upper chest.
      • Most patients ultimately develop inflammatory follicular papules & pustules.
      • Comedones, if present, aren’t a 1 ry manifestation of rosacea but a result of other factors such as sun exposure (Favre-Racouchot disease).
      • In a small proportion of patients, inflammation progresses, producing large nodules, edema & tissue hyperplasia.
      • A rare persistent nonpitting edema of the central face & forehead, similar to that reported in acne patients, has also been reported.
      • Another variant, granulomatous rosacea, is characterized by multiple brown-red infiltrative papules & nodules.
      • Biopsy reveals noncaseating granulomas.
    • Rosacea (Acne Rosacea)
      • GIT disturbances.
      • Reaction to the follicular mite, Demodex follilculorum.
      • Climatic (sun).
      • Vasomotor instability.
      • Psychic factors.
      • Role of helicobacter pylori.
      • Rosacea has been reported as a manifestation of HIV infection.
      Etiology and exacerbating factors
    • Rosacea (Acne Rosacea) Avoid extremes of heat & cold, excessive sunlight, spices, hot liquids & alcohols. Treatment I) Systemic treatment
      • Tetracyclines: 250 mg 3 times daily.
      • Metronidazole (Flagyl ® ) 200 mg twice daily.
      • Isotretinoin (Accutane ® ).
    • Rosacea - Treatment (Cont’d) II) Topically
      • Bland emollient
      • Anti-acne agents
      • Topical metronidazole 0.75% gel (Metrogel ® )
      III) Plastic surgery for rhinophyma
    • Perioral dermatitis Persistent erythematous eruption of tiny papules and pustules around the mouth, nose and may be eyes. A clear zone is often seen around the vermilion border of the lips.
    •  
    • Perioral dermatitis
      • It may be due to prolonged therapy with fluorinated steroids. However, sunlight, oral contraceptive pills and fluorinated tooth paste may play a role. Many patients are heavy users of cleansers, moisturizers and make-up.
      Etiology
    • Perioral dermatitis
      • Avoid strong topical steroids.
      • Topically: hydrocortisone or non-fluorinated steroids.
      • Tetracyclines (1 g/day).
      Treatment
    •  
    •  
    • What is perioral dermatitis?
      • This common distinctive acneiform skin eruption occurs mainly in women aged 15-25 yrs, but also occurs in children.
      • Perioral dermatitis is characterized by erythema, scaling & follicular papules that occur around the mouth, nose & less frequently, the eyes.
    • What is perioral dermatitis? (Cont’d)
      • The etiology is unknown, but many patients have used mid- or high-potency steroids inappropriately. In one study, 20% of children with perioral dermatitis have a family history of rosacea.
    • What is perioral dermatitis? (Cont’d)
      • The treatment includes the cessation of all topical corticosteroids & an 8-10 wk course of a tetracycline antibiotic.
      • Tetracycline & derivatives should not be used in children under 8 yrs of age. Oral erythromycin & topical clindamycin are effective substitutes.
      • Recurrences are rare.
    •