Related Therapeutic strategies

Herpes simplex virus (HSV) occurs in 2 common locations: orofacial (usually due to HSV-1) and genital (usually due to HSV-2).

Read more

Seborrheic dermatitis can be limited to the scalp, but it also can involve the face and any hairy or intertriginous area and rarely can even progress to a generalized erythroderma.

Read more

Chancroid

Timothy Berger Bruce Wintroub

Saturday, January 01, 2011

The diagnosis of chancroid is usually clinical, although improved culture techniques allow isolation of the causative organism H. ducreyi. The therapeutic strategy is to eliminate the pathogenic microorganism.

Read more

Therapeutic Strategies

Chronic Cutaneous Lupus Erythematosus

Timothy Berger Bruce Wintroub

Saturday, January 01, 2011

Chronic cutaneous lupus erythematosus (LE) has several morphologic patterns. Subacute cutaneous LE (SCLE) presents with erythematous, annular, or papulosquamous lesions, which tend to heal without scarring. Discoid lupus erythematosus (DLE) causes lesions with significant hyper- and hypopigmentation and follicular plugging, and causes significant scarring. DLE may cause significant cicatricial alopecia and permanent hair loss. Both SCLE and DLE are photosensitive dermatoses. Patients with SCLE, more commonly than patients with DLE, will fulfill the criteria for the diagnosis of systemic lupus erythematosus (SLE). Due to the low prevalence of renal and central nervous system disease in chronic cutaneous LE, however, the prognosis in these patients is good. In a significant portion of patients, especially those with DLE, the skin disease will be the primary complication of their lupus erythematosus. The therapeutic strategy is to control exposure to sunlight and to suppress inflammation in an effort to prevent or minimize disfigurement.

First Steps

  1. In all patients, regardless of extent of disease, maximum photoprotection must be instituted.
  2. Local topical steroids: Prescribe a superpotent steroid cream to be applied twice daily to areas of active disease. To minimize the potential atrophogenic side effects of topical steroids administered to facial lesions, discontinue this therapy or change to a nonatrophogenic, low-potency preparation as soon as a response occurs, or after a maximum of 2 weeks.
  3. Intralesional steroids: Intralesional triamcinolone acetonide diluted 1:1 with lidocaine 1.0% (final concentration of 2.5-10 mg per mL) can be administered to active or advancing lesions. Do not perform this therapy more often than once every 3-4 weeks to minimize atrophy, and no more than 20 mg of triamcinolone should be injected at one time.

Next steps

If systemic treatment is required, the first and most beneficial alternative is antimalarials. Begin treatment with hydroxychloroquine 200 mg per day for at least 4 weeks and increase to 400 mg per day if response is slow or nonexistent. In children the dose is 6.5 mg per kg per day.

Alternative steps and work-up

  1. If the patient does not respond to hydroxychloroquine, chloroquine 250 mg per day may be used as an alternative. Chloroquine is more effective but also has a higher risk of ocular toxicity.
  2. Quinacrine 100 mg per day may be added to chloroquine or hydroxychloroquine regimens in patients failing a single antimalarial alone.
  3. Systemic steroids sometimes are effective for rapid control of severe disease or for systemic complications. An alternative therapy for long-term treatment should be instituted simultaneously (such as an antimalarial) so that the steroid course does not exceed 4-6 weeks. Systemic steroids are safe to use during pregnancy.
  4. If the response to antimalarials is unsatisfactory, isotretinoin at 0.5-2 mg per kg daily can be tried. Pregnancy prevention measures are required.
  5. Thalidomide 50-200 mg as a single nightly dose may be effective in refractory cases. Pregnancy prevention measures are required, and, in general, thalidomide should be avoided in women of childbearing potential.
  6. Dapsone 50-200 mg daily can be used alone or as an adjunct to the above treatments.
  7. Camouflage techniques are particularly helpful in patients who have developed dyspigmentation from DLE. Several lines of cosmetics are designed to mask pigmentary abnormalities.
  8. All patients with chronic cutaneous LE should have laboratory parameters checked at baseline and at yearly intervals to screen for the development of SLE.

Pitfalls

  1. Topical and intralesional steroids are potentially atrophogenic and can themselves produce pigmentary abnormalities. Prolonged or excessive usage can worsen the disfigurement in DLE.
  2. Antimalarials can produce retinal toxicity, and patients on this form of therapy should be assessed by an ophthalmologist before treatment is instituted and at 6-month intervals.
  3. Dapsone, and possibly antimalarials, can cause acute hemolysis in G6PD-deficient patients; hence, a screen for this enzyme must be obtained prior to initiation of therapy.
  4. Biologically aggressive squamous cell carcinomas can occur in old scars of DLE (as in any other cutaneous scarring process). Thus, even patients with quiescent disease need to be examined regularly for the presence of neoplastic lesions.
  5. Quinacrine can cause a lemon-yellow discoloration of the skin.
  6. Patients on isotretinoin and thalidomide should be seen monthly and evaluated for specific complications of these medications, especially psychiatric complications with isotretinoin and neuropathy with thalidomide.

Back to Therapeutic Strategies

CONTENT PROVIDED BY:
Derm101.com Logo

Disclaimer: The material above has been prepared by Derm101.com. It has not been reviewed by the DermQuest Editorial Board for its accuracy or reliability. Reference to any products, service, or other information does not constitute or imply endorsement, sponsorship, or recommendation by members of the Editorial Board.