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Puva puede alterar los linfocitos circulantes o intradrmicos y su funcin

inmunolgica o al provocar cambios en los vasos de la superficie cutnea

tanto in vivo como in vitro.
The exact mechanism of UVB for phototherapeutic utility for PL is unknown,
and yet the immunomodulating effects of UV radiation do serve an
important function. Both BB-UVB phototherapy (290320 nm) (1214),
psoralen plus UVA (320400 nm) photochemotherapy (18, 19) and UVA-1
(340400 nm) (21) have been reported previously as effective treatments
for PLEVA and PLC. All of these therapies modulate the inflammatory and
immunologic activities of the skin through unique photobiologic mechanisms
of action that are different from each other (22). NB-UVB is about five to 10fold less potent than BB-UVB for erythema induction, hyperplasia, edema,
sunburn cell formation and Langerhans cell depletion from the skin. By
contrast, NB-UVB appears to have relatively more suppressive effects than
BB-UVB on systemic immune response, including lymphoproliferation (22
24). Interestingly, Ozawa et al. (25) have demonstrated that NB-UVB causes
greater depletion of T cells in inflammated skin lesions than BB-UVB, and
has direct cytotoxic actions on T cells infiltrating skin lesions. Their in vivo
results have been paralleled by in vitro experiments Table 3. Results of UVB
phototherapy in PL compared with the literature Study Disease subtype and
number of patients Type of UVB phototherapy Number of treatments or
weeks (mean) Total cumulative dose (J/cm2 , mean) Clinic response and
follow up LeVine (12) PLK (11) BB-UVB 29 (1059) 9.24 (0.80637.077) CR in
all patients Follow-up data are not stated Tham (13) PLEVA (1) PLC (17) BBUVB 33.2 (1577) 0.20.5 mW/cm2 Cumulative dose is not reported CR %
82.4 NR; 3 patients Relapse in two patients within 6 months2 years) Tay et
al. (14) PLEVA (3) PLC (2) BB-UVB 11 weeks 4.2 CR in all patients Relapse in
two patients within 79 months Pasic et al. (15) PLEVA (3) PLC (6) NB-UVB
19 (1424) 6.5 (3.02311.8) PR: 3 PLC: CR: 3 PLC (33.3%) NR: 3 PLEVA
Follow-up data are not stated Pavlotsky et al. (16) PLEVA (10) PLC (3)
Overlap (1) BB-UVB 11 weeks 3.6 CR: 93.3% Relapse free: 71% (mean follow
up 58 months) PLEVA (10) PLC (2) Overlap (3) NB-UVB 9 weeks 15 CR:
92.9% Relapse free: 75% (mean follow up 34 months) Khachemoune and
Blyumin (17) PLK (1) NB-UVB 20 NS Relapse free: 100% (at follow up 1 year)
This study PLEVA (23) NB-UVB 33.85 (3053) 16.3 (8.243) CR: 65.2%
Relapse free 86% (at follow up 612 months) PR: 34.8% PLK (8) NB-UVB 32.4
(2560) 13.7 (7.127.1) CR: 87.5% Relapse free: 71.4% (at follow up 612
months) PR: 12.5% Clinical diagnosis. CR, complete response; PR, partial
response; NR, no response; PLEVA, pityriasis lichenoides et varioliformis
acuta; PLC, pityriasis lichenoides chronica; NS, not stated; NB-UVB,
narrowband UVB; BB-UVB, broadband UVB. 131 r 2008 The Authors Journal
compilation r 2008 Blackwell Munksgaard Photodermatology,
Photoimmunology & Photomedicine 24, 128133 Phototherapy for pityriasis
lichenoides where exposure of T cells to moderate doses of NB-UVB induced
rapid apoptosis. The greater capacity of NB-UVB in depletion of dermal T
cells is probably related to the somewhat deeper penetration of this
wavelength in dermis compared with BB-UVB and the ability to administer a
higher dosage with NB-UVB sources because of its less burning potency (22
25). Recent studies have demonstrated that UVB suppresses the
alloactivating and antigen-presenting capacity of epidermal Langerhans

cells and enhances (or modulates) interleukin-1 (IL-1), IL-6, IL-8, IL-10, IL-12
and tumor necrosis factor a production by human keratinocytes (26). The
modulation of circulating cytokines accounts for systemic NB-UVB-induced
immunosuppression in human subjects (22, 26). Intercellular adhesion
molecule 1 (ICAM-1) is observed on cells in inflammatory skin diseases
(including PLEVA) that can cause pruritus (2729). UVB irradiation has been
found to suppress the expression of ICAM-1 in cultured human keratinocytes
(29). UVB has been reported to decrease the release of histamine from mast
cells. UVB phototherapy given two to three times a week for 4 weeks
decreased the itch response of the skin when histamine was injected, or
when a mast cell degranulator, compound (48/80), was injected (30). Duthie
et al. (31) concluded that UVB light possibly suppresses the function of
neoplastic clonal T-cell populations in the skin and so serves as an immune
up-regulator. These UVB-induced alterations may partly account for its
immunotherapeutic role in preventing the progression of the disease.