Acquired Immunodeficiency Syndrome; what can skin tell?

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Acquired Immunodeficiency Syndrome; what can skin tell?

Acquired Immunodeficiency Syndrome; what can skin tell?

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  • 1. Acquired Immunodeficiency Syndrome; what skin can tell? Almansouri Daifallah MD
  • 2. AIDS – Acquired Immunodeficiency Syndrome – An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive T-lymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections.
  • 3. -One of the commonest AIDS manifestation 90%
  • 4. -One of the earlist signs
  • 5. - Prognostic marker
  • 6. Objectives
  • 7. Classification of skin diseases in AIDS 1- The disease itself; malignancy (6%). – A) AIDS-defining cutaneous cancers e.g. KS (5%), BCNHL. – B) non-AIDS-defining cutaneous cancers e.g. SCC(anal), BCC, melanoma ( bad prognosis) HPV tumor (anal or cervical). 2- Oppurtunistic infection; viral, bact, fungal, parasitic.
  • 8. Skin condition reflects AIDS progression • Early stage; morbilliform eruption, condylomata acuminata and verrucae. • The immune system is compormised; recurrent varicella zoster, treatment-resistant seborrheic dermatitis, numerous hyperkeratotic warts, and oral hairy leukoplakia. • Late stage; 73% have CMV and HSV • Advanced; Leishmaniasis and miliary TB, PPE, Photosensitivity
  • 9. 34% has KAPOSI sarcoma • Difinition; KSHV/HHV8 induced prolifiration of endothelials > chronic inflammation > angiogenesis. • DP: prolifration of infected endothelial cells and presence of immune cells. • 3 sites; skin, lymphnodes, and viscera. • Homosexual men; majority. • Pink>palpable>brown> painful. • Recover immunity> KAPOSI remission.
  • 10. KAPOSI SA
  • 11. Opportunistic infection: viral 1- Herpesviridae: A) HSV> peri-oral/anal ulcer (necrosis), B) HZV > typical + atypical. C) CMV > commonest cause of perineal ulcer. Tx: acyclovir. 2- EBV: hairy leukoplakia (non-malignant). 3- HPV-66: recurrent, widely spreaded warts. 4- MC: papule ē umbilication. Tx: imiquimod is curative. NB. perineal ulcer/CMV infection > bad overall patient prognosis.
  • 12. Herpitic ulcers
  • 13. MC
  • 14. CMV perineal ulcer
  • 15. Fungal infection • Superficial: oral/viginal* candidiasis. Tx: oral azole. • Deep: cryptococcosis (cellulitis, ulcers), histoplasmosis, blastomycos is. NB:. *viginal candidiasis is commonest AIDS presentation in US.
  • 16. Bacterial infection 1 - M avium-intracellulare complex (MAC): MOSTLY disseminated from else where. 2 - Syphlis: coinfection, ?diagnosis, presentation; typ vs atypical. 3 - Staph. aureus is the commonest (impetigo, cellulitis), also MRSA is higher in HIV.
  • 17. Parasitic 1 - Scabies: hyperkeratotic, scaly maculopapular eruptions or crusted plaques. 2 - leshminiasis: atypical disseminated.
  • 18. Papulosquamous Dermatoses • • • • Seborrheic dermatitis: 83% Tx: SA, coal tar, Tacrolimus, Xerosis: 4.5% Tx: emollients. Psoriasis: trigger or bad prognosis. ichthyosis: new onset+ HIV+ Drug abuse = human lymphotropic virus II > profound helper T-cell depletion. • Pruritic papular eruption (PPE): 81% have advanced HIV. – Tx: steroids, UV-B, PUVA, and pentoxifylline
  • 19. Hair and nails • Alopecia; HIV itself or indinavir. • Onychomycosis: common. • Nail pegmentation: HIV itself or Zidovudine
  • 20. Drug eruption • SJS/TEN: higher rate than general papulation - reported for: Fluconazole, Clindamycin and other antibiotics, Phenobarbital, Chlormezanone • Trimethoprim-sulfamethoxazole for Pneumocystis: mostly results in morbilliform eruption.
  • 21. Home message • Rull out AIDS in any pt ē resistant, generalised or atypical fungal infection. • Examine AIDS patient always for drug eruption. • 
Staph. A is commenest bacterial infection. • Vaginal candidiasis is commonest presentation. • Kaposi sa is commonest malignancy and improved when immunity recovered.
  • 22. NIH guidlines http://aidsinfo.nih.gov/guidelines
  • 23. 2013WHO guidlines http://apps.who.int/iris/bitstream/ 10665/94334/1/9789241506168_en g.pdf
  • 24. Thank you • This presentation is on my slideshare.net/daveallah
  • 25. References