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A 65-year-old man presented with a 6-year history of itchy, oozy and scaly lesions associated with thickening and darkening of the skin over the forehead, cheeks, hands and forearms. The eczematous lesions had started insidiously 5-6 years ago initially appearing over the forehead during the start of the summer season. Photosensitivity was present in the involved area. The skin condition subsided spontaneously in the winter only to recur the following summer, became progressively longer in duration and less responsive to medication persisting even during the winter months. The body area involved also progressively increased, involving the entire face, shoulders, upper back and distal extremities.
There was no history of atopy, perfume or cosmetic use, anorexia, weight loss, subcutaneous lumps, bleeding from any site, cough, chest pain, ayurvedic or homeopathic medicine use or bladder/bowel complaints. Though, there was history of exposure to parthenium, there was no involvement of the flexures and at no time did the lesions become generalized to involve the whole body. Photosensitivity was present from the beginning.
Multiple lichenified plaques were present over the photo-exposed areas; namely the forehead, nose, malar regions, point of chin, (Fig. 1) extensor forearms, dorsum of bilateral hands and feet, shoulders and upper back. These plaques were erythematous, edematous, violaceous to gray in color showing increased skin markings and fine semi-adherent scaling. Some areas showed crusting and oozing of serous fluid. The face presented a typical leonine appearance due to the confluence of the plaques over the forehead and malar region. Depigmentation overlying these plaques (confluent to speckled) was present over the forehead, dorsum of hands and shins suggestive of superimposed lichen simplex chronicus. There was sparing of the scalp, upper eyelids, nasolabial folds, area under lower lip, submental region, ears and retroauricular region. Patient’s nails were shiny and some showed the presence of Beau’s lines. General physical and systemic examination was unremarkable.
Baseline investigation revealed eosinophilia. AEC was within normal limits. Chest X-ray showed evidence of healed pulmonary Koch’s. Skin biopsy changes were nonspecific showing acanthosis, parakeratosis, spongiosis and perivascular lymphocytic infiltrate in the dermis. Patch testing showed 3+ positivity to parthenium and fragrance mix. Phototesting could not be done due to lack of facilities.
On the basis of history and clinical examination a diagnosis of chronic actinic dermatitis was made.
Treatment and follow-up
Patient was initially started on sunscreens, topical and systemic steroids with clinical improvement. However, the lesions gradually became less responsive to treatment. Patient was then started on immunosuppressives; azathioprine and subsequently cyclosporine; but these were later withheld in view of unaffordability and side effects. Subsequently the patient was started on topical tacrolimus with marked improvement in clinical condition in the form of decreased lichenification, erythema and scaling.
Observations and discussion
The term “chronic actinic dermatitis” (CAD), coined by Hawk and Magnus in 1979, is used synonymously with the term “photosensitivity dermatitis/actinic reticuloid syndrome” coined earlier by Frain-Bell and colleagues. CAD includes four conditions: Actinic reticuloid (AR), photosensitive eczema (PE), photosensitivity dermatitis (PD) and more recently, persistent light reactivity (PLR), originally described as distinct disorders but generally accepted as variants of CAD. CAD could therefore be defined by the following criteria: A persistent eruption of eczematous character possibly associated with infiltrated papules and plaques, predominantly affecting exposed skin, although it sometimes may appear as erythroderma. CAD is a type of delayed hypersensitivity pattern. The exact mechanism is still unclear. Photobiologically, it shows a reduction in the MED to UV-B irradiation (and often also longer wavelengths) on covered skin (although tests rarely seem to be positive until a few months after the onset of the condition), with occurrence of lesions similar to those of the disease at the irradiance site. The histological appearance consists of chronic dermatitis, with or without the presence of lymphomalike changes. In this era of HIV it is interesting to note that CAD may be a presenting feature of HIV infection, usually in patients with a CD4 count of <100 cells/μL. These patients are usually otherwise asymptomatic without features of AIDS related complex (ARC). Phototesting, generally with an irradiation monochromator, is essential for a confident diagnosis of CAD, and patch and photopatch tests are essential ancillary investigations.
The diagnosis of CAD is distinct from that of Compositae dermatitis or other types of contact dermatitis and from photoallergic contact dermatitis which however can predispose to, and are associated with, the development of sensitivity to UV light, as indeed do other forms of eczema such that the patient then reacts to UV light alone in the absence of allergen. AR can be differentiated from cutaneous T-cell lymphoma, particularly the erythrodermic form, by the presence of photosensitivity and the predominance of CD8 cells in actinic reticuloid, in contrast with CD4 cells in cutaneous T-cell lymphoma, the nuclear contour index and T-cell receptor gene rearrangement studies help to establish the diagnosis.
Management essentially consists of avoidance of sunlight and of relevant associated contact allergens or photocontact allergens. The acute episode is controlled with topical and oral steroids. If the symptoms recur on tapering steroids, an adjuvant can be added. The most effective are azathioprine (50-100 mg/day) and cyclosporine (100-200 mg/day). Safer alternatives like mycophenolate mofetil (1-2 g/day) have been tried recently with good results. For patients with difficult to control disease, PUVA/UV-B therapy can be tried (tolerance induction therapy). Other drugs have been tried in CAD with variable results. These include β-carotene, hydroxychloroquine, nicotinamide, danazol and interferon-α. Retinoids have also been used with phototherapy with reasonable results. Pimecrolimus and more recently tacrolimus have been reported to be effective in treating certain patients with CAD.
The course of CAD is unpredictable. Spontaneous remission was thought to be rare. However, a recent study from Scotland using objective parameters showed that the majority of patients do improve. It was proposed that patients with AR are at increased risk for developing lymphoma, but this relationship remains controversial. Patients with erythrodermic AR, however, appear to have a shortened life expectancy.
- Hawk JLM, Magnus IA. Chronic actinic dermatitis— an idiopathic photosensitivity syndrome including actinic reticuloid and photosensitive eczema. Br J Dermatol 1979;101:24.
- Frain-Bell W, Lakshmipathi T, Rogers J, et al. The syndrome of chronic photosensitivity dermatitis and actinic reticuloid. Br J Dermatol 1974;91:617.
- Norris PG, Hawk JLM. Chronic actinic dermatitis: a unifying concept. Arch Dermatol 1990;126:376-8.
- Ramsay CA, Kobza Black A. Photosensitive eczema. Trans St Johns Hosp Dermatol Soc 1973;59:152-8.
- Wong SN, Khoo LS. Chronic actinic dermatitis as the presenting feature of HIV infection in three Chinese males. Clin Exp Dermatol 2003;28(3):265-8.
- Zak-Prelich M, Schwartz RA. Actinic reticuloid. Int J Dermatol 1999;38(5):335-42.
- Alquier-Bouffard A, et al. Chronic actinic dermatitis: treatment with topical tacrolimus (two cases). Ann Dermatol Venereol 2007;134(6-7):555-8.