Plaque, cutaneous

Topical and oral bexarotene are approved for early-stage (patch and plaque) cutaneous T-cell lymphoma that is refractory to at least one other therapy. Oral bexarotene is also approved for refractory cases of advanced disease however, the best response has been noted in early disease. 

Mastocytomas and diffuse cutaneous mastocytosis are further manifestations of cutaneous mastocytosis (CM) [9]. Solitary mastocytomas are common in children. Most are present at birth or develop in infancy. These lesions are flat or mildly elevated, well demarcated, solitary yellowish red-brown plaques or nodules, typically 2-5 cm in diameter. Diffuse cutaneous mastocytosis is a rare disorder characterized by diffuse mast cell infiltration of large areas of the skin that presents in infants in the first year of life. Severe edema and leathery indurations of the skin leads to accentuation of skin folds (pseudo-lichenified skin) and a peau-dbrange-like appearance. Systemic complications include hypotension and gastrointestinal hemorrhage. Infants and young children with considerable mast cell infiltration of the skin sometimes exhibit blister formation in the first 3 years of life. MPCM and other forms of CM have been classified in a consensus nomenclature (table 1) [10]. 

Alefacept (Amevive) is a dimeric fusion protein that binds to CD2 on T cells to inhibit cutaneous T-cell activation and proliferation. It also produces a dose-dependent decrease in circulating total lymphocytes. Alefacept is approved for treatment of moderate to severe plaque psoriasis and is also effective for treatment of psoriatic arthritis. Significant response is usually achieved after about 3 months of therapy. The recommended dose is 15 mg intramuscularly once weekly for 12 weeks. Adverse effects are mild and include pharyngitis, flu-like symptoms, chills, dizziness, nausea, headache, injection site pain and inflammation, and nonspecific infection. 

PUVA is most useful for the treatment of severe psoriasis. Early (patch and plaque) stage cutaneous T-cell lymphoma (CTCL) also responds to PUVA therapy. In addition, patients in advanced stages of CTCL have been treated with a modification of PUVA known as extracorporeal photopheresis. In this therapy, blood from a CTCL patient who has taken psoralen is exposed to UVA light and returned to the patient. Lymphocytes are altered or destroyed by the treatment, and theoretically, the return of these abnormal cells triggers an immune response directed against certain lymphocyte surface antigens. The effectiveness of this modality appears to be variable. 

That atherosclerotic plaques may regress has been amply demonstrated in experimental animals [65] and more recently in humans [66]. Similarly, both human cutaneous and tendinus xanthomas may undergo regression with specific treatment regimens [67], At least four mechanisms appear essential in plaque regression ... 

The diagnosis of xanthelasma is made based on the clinical presentation of the cutaneous lesions.They are oval or elongated yellowish plaques occurring just beneath the skin. There is no concomitant inflammation or pain, but they may be of cosmetic concern. 

A 57-year-old man developed the typical cutaneous erosions and plaques of Sweet s syndrome after taking celecoxib 100 mg bd for 1 week for bursitis. Celecoxib was withdrawn and the mucocutaneous lesions began to clear. However, the bursitis recurred and he restarted celecoxib. The cutaneous lesions worsened dramatically. After withdrawal of celecoxib for the second time the lesions cleared completely. 

Injection-site reactions are common after subcutaneous injection of interferon beta-lb, and are more frequent than with any other available interferons. In a multicenter placebo-controUed trial, 65% of patients receiving interferon beta-lb had reactions at the injection site compared with 6% in the placebo group (2). In contrast, only 5% of those who received interferon beta-la had injection site reactions (3). The clinical features of injection site reactions to interferon beta-lb mostly consist of benign inflammatory reactions, but they can sometimes be more severe, with sclerotic dermal plaques, painful erythematous nodules, and deep cutaneous ulcers with skin necrosis (SEDA-21,... 

Acute febrile neutrophilic dermatosis (Sweet s syndrome) can occur in patients with acute promyelocytic leukemia given a retinoid. Sweet s syndrome is characterized by five cardinal features fever, neutrophilia, multiple raised painful asymmetric erythematous cutaneous plaques, dermal infiltrates consisting of mature neutrophils, and a rapid response to glucocorticoid therapy. In up to 10-20% of cases it precedes or coincides with a diagnosis of malignancy, most commonly acute myelogenous leukemia. In cases associated with tretinoin the symptoms come on at 7-34 days and the skin lesions are seen on the face, limbs, and back. 

A fixed eruption is an unusual hypersensitivity reaction, characterized by one or more well demarcated erythematous plaques, that recur at the same cutaneous (or mucosal) site or sites each time exposure to the offending agent occurs. The sizes of the lesions vary from a few millimeters to as much as 20 centimeters in diameter. Almost any drug that is ingested, injected, inhaled, or inserted into the body can trigger this skin reaction. 

Topical ALA application and subsequent exposure to polychromatic or laser light was used effectively to treat plaque-stage cutaneous T-cell lymphoma [68,69,94a]. However, the apparent clinical cure was not confirmed histologically [94b] (Table 8). 

Lublin-Tannenbaum T, Katzenelson E, El-ad B, Katz E. Correlation between cutaneous reaction in vaccinees immunized against smallpox and antibody titer determined by plaque neutralization test and ELISA. Viral Immunology. 1990 3 (1) 19-25. 

Psoriasis is an inflammatory skin disease characterized by red, scaly, raised plaques. Usually, the psoriasis lesions are several centimeters in diameter and separated by normal-appearing skin [239, 240]. Psoriasis involves a chronic cutaneous pathologic process, driven by interactions between infiltrating leukocytes (Tcells, dendritic cells, macrophages, neutrophils), cytokines, chemokines and keratinocytes, the cells from the epidermis. The disease is initiated or exacerbated by infections, physical and/or emotional stress, antigenic stimuli and various medications (e.g., lithium, P-block-ers [241, 243]). Psoriatic plaques can revert back to symptomless skin spontaneously or after treatment vdth selective immune-targeted agents [239, 240, 242-244]. 

In all these studies, either serum antibody or the plaque-forming response was tested with the exception of IgE, which was tested by a passive cutaneous anaphylaxis test. In none of the experiments was an attempt made to delineate the cell types that may be stimulated by the retinoid. Therefore, we do not know presently whether the drug acts on B cells, T cells, antigen-presenting cells or other cell types. Three different retinoids were employed and it is not known whether any one in particular may be superior to the others for immunostimula-tion because no comparative studies have been done. 

Similarly, four patients with previously treatment-resistant mycosis fungoides (cutaneous T cell lymphoma) responded well to oral isotretinoin, 2-3 mg/kg/ day, with production of prolonged partial remission (Kessler et al., 1983). Tumors and plaques underwent near complete clearing. The skin lesions of cutaneous T cell lymphoma are characterized by epidermal infiltration with atypical mononuclear cells, mainly helper T cells but lower than normal numbers of killer T cells. In this regard, retinoic acid has been shown to enhance antigen-specific cytotoxic T cell activity (Dennett and Lotan, 1978), suggesting one immune mechanism by which retinoids could affect mycosis fungoides. 

A 73-year-old woman developed weakness and ei hematous plaques on the trunk and limbs after taking propafenone for 2 months. She had a neutropenia with a predominance of immature cells in the bone marrow. Skin biopsy was compatible with subacute cutaneous lupus erythematosus. After withdrawal of all drugs there was complete clinical and analytical recovery. Her medications were then sequentially re-introduced, with the exception of propafenone. After 6 months she remained asymptomatic. 

A 32-year-old woman presented with a pruritic eruption 2 weeks after commencing escitalopram. The eruption had spread from her trunk to the extremities. On examination, there were multiple inflammatory papules around hair follicles, some of which had coalesced to form plaques on her chest, shoulders, back and buttocks. There were some pustules evident on the upper aspect of her chest. Biopsy specimen of a papule from her upper back revealed follicular plugging and a mild to moderate lymphocytic infiltrate. With the cessation of escitalopram, the eruption remitted spontaneously over several weeks, however when another SSRI was started and an acneiform eruption occurred. Changing the class of antidepressant again resulted in remission, with no further cutaneous effects. 

PUVA is a psoralen+UV-A treatment for eczema, psoriasis, graft-versus-host disease, vitiligo, mycosis fungoides, large-plaque parapsoriasis and cutaneous T-cell lymphoma. The psoralen is applied or taken orally to sensitise the skin, and then the skin is exposed to UV A. The psoralens allow a relatively lower dose of UV A to be used. When they are combined with exposure to UV A in PUVA, they are highly effective at clearing psoriasis and vitiligo. 

Skin A 73-year-old woman, with a 30-year history of subacute cutaneous lupus erythematosus presented with an acute flare of her disease, characterised by erythematous, annular and scaly plaques over her trunk and limbs. She had been in remission, and off-treatment for 4 years. One week before, she had been started on therapy with naproxen for arthritis in combination with omeprazole for gastrointestinal protection. Both drugs were discontinued by the patient because of her acute disease flare. Her symptoms resolved after 2 months of oral treatment with prednisolone. Three months later flie patient presented again with another sudden-onset flare of subacute cutaneous lupus erythematosus involving her face, trunk, arms, buttocks and thighs. Two weeks earlier, she had been restarted on naproxen plus omeprazole. On this occasion, the patient was treated with oral prednisolone (40 mg) and hydroxychloroquine (200 mg) twice daily. Mycophenolate mofetil (500 mg twice daily) was introduced 1 week later because of her further deterioration. In the meantime, omeprazole was discontinued. These actions were followed by a dramatic improvement of the subacute cutaneous lupus erythematosus within 5 weeks [53 ]. 

Popa AM, VaUa K, Radharkrishnan L, Cuellar S, Vfllano JL. Bevadzumab-induced oral mucositis in background of cutaneous plaque-type... 

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