The British journal of dermatology
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Case Reports
A case of linear IgA bullous dermatosis with IgA anti-type VII collagen autoantibodies.
In this study we present a patient with the sublamina densa type of linear IgA bullous dermatosis (LABD), with IgA autoantibodies reactive with the 290-kDa type VII collagen (the epidermolysis bullosa acquisita (EBA) antigen) and with immunoblotting of normal human dermal extracts. The clinical and histological features of the present case were compatible with those of LABD but quite different from those of EBA. ⋯ These results indicate that, whereas EBA antibodies react with the NC1 domain of type VII collagen, the epitope in this case is different from that of EBA (and is most likely on the central triple helical domain). This difference may be responsible for the clinical presentation in this patient being distinct from that of EBA.
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Comparative Study
Down-regulation of Langerhans cell protein kinase C-beta isoenzyme expression in inflammatory and hyperplastic dermatoses.
The family of protein kinase C (PKC) isoenzymes plays a fundamental part in signal transduction, and thereby regulates important cellular functions, including growth, differentiation, cytokine production and adhesion molecule expression. In lesional psoriatic skin, Ca(2+)-dependent PKC activity, PKC-beta protein and epidermal Langerhans cell (LC) PKC-beta immunostaining are significantly decreased, indicating activation and subsequent down-regulation of PKC. Whether these changes occur in other inflammatory/hyperplastic dermatoses is, however, unknown. ⋯ These data indicate that: (i) down-regulation of LC PKC-beta occurs in a variety of inflammatory and hyperplastic skin disorders, and is not unique to psoriasis, and (ii) the pattern of epidermal LC PKC-beta and CD1a expression varies among the diseases studied. In mice, PKC activation induces LC migration. Thus, down-regulation of epidermal LC PKC-beta associated with reduced CD1a+ epidermal LCs in allergic and irritant contact dermatitis suggests that PKC-beta may transduce the signal for migration of LCs from human epidermis.
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Comparative Study Clinical Trial
Narrow-band UVB (TL-01) phototherapy: an effective preventative treatment for the photodermatoses.
Twenty patients with photodermatoses [actinic prurigo (n = 6), hydroa vacciniforme (n = 4), idiopathic solar urticaria (n = 1), amiodarone-induced photosensitivity (n = 1) and a range of cutaneous porphyrias (n = 8)] were treated with a 'hardening' course of narrow-band ultraviolet B (TL-01) phototherapy in springtime. The response to phototherapy was monitored subjectively, by interviewing patients after the summer, and objectively by monochromator phototesting, before and after phototherapy. ⋯ Adverse effects included erythema (seven patients), pruritus (five) and provocation of the eruption (four). We now routinely consider narrow-band UVB phototherapy for problem photodermatoses.
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Clinical Trial Controlled Clinical Trial
Pretreatment of photoaged forearm skin with topical tretinoin accelerates healing of full-thickness wounds.
Pretreatment of skin with all-trans retinoic acid (tretinoin) has been shown to enhance wound healing. Previous studies have mainly used animal models to demonstrate this effect. We wanted to determine whether pretreatment could promote wound healing in severely photoaged dorsal forearm skin. ⋯ On the tretinoin-treated side, the wound areas were 35-37% smaller on days 1 and 4, and 47-50% smaller on days 6, 8, 11, compared with the controls. Clinically and histologically, reepithelialization occurred more rapidly. Thus tretinoin dramatically accelerated wound healing in photodamaged skin.