o ther dermatoses r rosenstock n.
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o ther dermatoses R:Rosenstock

o ther dermatoses R:Rosenstock

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o ther dermatoses R:Rosenstock

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  1. other dermatosesR:Rosenstock ByM.H.DavariMD ShahidSadoughi University of medical sciences

  2. Work-related health problems as reported by UK occupational physicians during 1996 Problem Musculoskeletal Dermatological Respiratory Hearing loss Other Percentage 45.3 23.4 9.2 8.7 13.9 Thirty percent of occupational injury and 40% of occupational disease are dermatologic P.M

  3. Occupational acne 1. Oil acne (folliculitis) • Pathogenesis: hair follicle is particularly susceptible to irritation from lipids • plugging of the follicle (comedo formation) or • induce an inflammatory reaction by rupture of the follicular wall (folliculitis) • Petroleum distillates, cutting oils, pitch, and tar • Clinical course: dorsae of the hands and forearms • Diagnosis: • area of involvement • history

  4. Age: any age • Prevention: • Protective clothing • Mandatory daily laundering of work clothes • Treatment: similar to those for routine acne • Oral antibiotics (tetracycline and erythromycin) • Topical antibiotics (clindamycin; erythromycin) • Refractory Comedones long-term topical retinoids

  5. Acne vulgaris • Persons at risk:workers in fast food restaurants, actors, actresses, models, and cosmeticians • Age: peak 11-20 yrs • Pathogenesis: in addition to oil, Friction, heat, and sweating • Clinical course: face, neck, upper chest and back • Diagnosis: history of exposure • Treatment and prognosis: like oil acnea

  6. Viktor Yushchenko, the Ukranian President who was supposedly assassinated by the KGB with dioxin poisoning.

  7. chloracne • Sensitive indicator of systemic exposure to specific polyaromatic hydrocarbons • Persons at risk include workers: hydrocarbonbased pesticides and herbicides, electrical workers exposed to older polychlorinated biphenyl (PCB) • Pathogenesis: follicular level of the agent may be of greatest importance • Clinical course: pale yellow (straw) cyst + comedo • inflammatory papules and pustules of acne vulgaris are not evident • postauricular folds, the malar crescent, and the genitalia. • The nose typically is spared • onset within 2w–2m • regress over a 4–6m (1-2 yr)

  8. Non-cutaneous findings: Hepatomegaly, Hepatic porphyria, Peripheral neuropathy • TCDD causing chloracne at the lowest concentrations • Diagnosis: • history of exposure (suggest) • Serum levels of suspect compounds and metabolites should be obtained (confirmation of exposure) (GC/MS) • Biopsy cause loss of follicular sebaceous glands (DDX: actinic elastoticcomedones)

  9. Treatment: • Difficult • Oral antibiotics, topical retinoic acid, and oral isotretinoin • Cyst formation prevent by early retinoid therapy • Prevention: • Even minute exposures must be avoided • shower facilities • Use disposable clothing for workers • Routinely monitor for plant contamination using wipe samples • Routinely educate and monitor workers.

  10. Pigmentary disorders • 1. Hyperpigmentation • Types: • Exogenous pigment deposition • Deposition in skin systemically • Photoeruptions (more common) • PIH (more common) Or by wood lamp examination: • Epidermal? • Dermal • Mix • Workers at risk: heavy metals, organic nitrogen compounds and dyes

  11. Hyperpigmentation: nitro compounds and dyes that stain skin

  12. Hyperpigmentation: metals that may be systemically or locally deposited in skin • Clinical course: • The most striking form of dyspigmentationis argyriadue to systemic deposition ofsilver. • Pigmentation from heavy metal toxicity exacerbated by exposure to the sun • PIH occurs at the sites of skin injury • Diagnosis: • History & examination • Wood lamp examination • Biopsy

  13. Prevention: • Sun screen • Protective clothes (exposure to organic dye-like component) • Treatment: • Tattoos and systemic heavy metal toxicity may be irreversible • PIH: may persist for months (dark skin) • Retinoic acid • Hydroquinone

  14. 2. Hypopigmentation: • PIH • Cutaneous injury, from inflammation or trauma • Leukodermia • Hydroquinone or derivatives of alkyl phenols and catechols • Workers at risk: rubber workers, photographic developers, hospital housekeepers, printers, and workers in the oil, paint and plastics industries • Pathogenesis: • direct cytotoxic effect on melanocytes • formation of antigens, which activate lymphocytes • Diagnosis : wood lamp • Treatment: • long-term PUVA • allograft

  15. Picture of a phototoxic drug reaction

  16. Photodermatoses • UVA: aging, occupational dermatosis • UVB: sun burn • UVA,B,C: carcinogen • Outdoor occupations Phototoxic: Nonimmunologic, reactive O2, improve immediately with avoidance Photo allergic: type IV imune reaction, substance convert to hapten, Not improve immediately with avoidance

  17. Phototoxic agents • Some common plants containing furocoumarins

  18. Picture of photoallergic and phototoxic dermatides

  19. Contact photodermatitis

  20. Diagnosis: • History of sun exposure • Typical photodistribution • Exposure to photoactive substances • biopsy may be helpful to exclude other causes of photosensitivity (lupus erythematosus, medications) • Prevention: • Sunscreens: (SPF) rating of #15 or better ,(which is less effective in preventing UVA) • Use of protective clothing • EPA (enviromental protection agency)


  22. Treatment: • open-wet dressings • bland emollients • Rarely systemic steroids for severe cases. • Prognosis: • Workers with clinical signs of chronic sun exposure are at risk for cutaneous malignancies and should be followed closely

  23. ERYTHEMA AB IGNE • The area usually is regional corresponding to the site of repeated applications of heat • Workers exposed to furnaces, such as cooks, stokers, glass blowers, and kiln operators • Clinical course: • Early: • vasodilation (livedoreticularis) • Later: • Poikiloderma(epidermal atrophy, telangiectasia, and pigment alteration) • SCC and Merkel cell carcinomas occur in the poikilodermatous area

  24. Diagnosis: • The local nature of the condition, along with a history of exposure to heat, is suggestive • Biopsy: exclude other conditions associated with livedoreticularis • Prevention: • Repeated exposure avoided • Education of workers at risk is the key to prevention. • Treatment • Cessation of exposure in early changes. • permanent change: monitored for future development of skin carcinoma

  25. MILIARIA • Bakers, foundry workers, cooks, coke oven operators, and workers with similar exposure to excessive heat that causes sweating • blockage of the sweat ducts • Trunk: most commonly affected location, especially the chest, back, submammary, and axillary areas • Clinical lesions are on a spectrum encompasssing clear vesicles • if the blockage is in the superficial epidermis (miliariacrystallina) • macules or papules if the blockage is in the lower epidermis (miliariarubra) or • flesh-colored to pale white papules if the obstruction is in the dermis (miliariaprofunda).

  26. Symptoms usually are absent with miliariacrystallina, while miliariarubra and miliariaprofunda may be pruritic or painful • May lead to inadequate body thermoregulation with accompanying heat exhaustion • Pathogenesis: • Sweating and maceration cause plugging of the eccrine sweat duct with ductal keratin. Microbial organisms may invade the macerated keratin and cause further plugging of the duct • Diagnosis: • clinical picture, symptoms, and the history of onset after excessive heat exposure and sweating.

  27. Prevention: • exposures should be avoided • Hexachlorophene soap decrease bacterial population. • Maceration of the skin should be avoided by frequent clothing changes when sweating is profuse. • Treatment and prognosis • Removal • A period of a week or more should elapse before re-exposure of the individual to the hot environment is attempted, particularly if the eruption is severe enough to cause a decrease in systemic heat tolerance.

  28. OCCUPATIONAL ACRO-OSTEOLYSIS AND SCLERODERMA • Cleaners of vinyl chloride polymerization reactor tanks • Raynaud’s phenomenon • Osteolyticbone changes • sclerodermia • Silicadust have been reported to be at risk for developing: • Raynaud’s phenomenon • Scleroderma • organic solvents has also been associated with: • systemic sclerosis

  29. Diagnosis: • Patients presenting with Raynaud’s phenomenon without a history of vibration exposure should be questioned regarding exposure to vinyl chloride, silica, organic solvents, and epoxy resins • Prevention • Workers cleaning polymerization reactor tanks of vinyl chloride need complete skin and respiratory protection. • Respiratory protection also is critical in those workers exposed to silica. • All workers with Raynaud’s phenomenon, whether or not the condition is job related, should have protection of their hands from cold weather • Treatment and prognosis • Acro-osteolysisstabilize after withdrawal from vinyl chloride monomer exposure • Scleroderma of any cause, however, tends to be progressive.