Discussion:
While CLP may exhibit spontaneous improvement over time, systemic
treatments are required for several patients due to persistent of
itching and cosmetic issues, especially in a generalized pattern.
Numerous modalities of treatment for CLP were used as corticosteroids
(topical and systemic), retinoids, MTX, azathioprine, cyclosporine,
phototherapy, and biologics. However, there are no formal care
guidelines based on facts yet.11
In the current study, among NB-UVB group, 36.7% of patients showed
complete response to treatment and 26.6% of patients had partial
response to treatment.
It has been found that the clinical efficiency of NB-UVB in a
retrospective study among 20 patients for the treatment of widespread
CLP was 55% patients (full responses) and 20% patients (partial
responses).10
A retrospective study examined the efficiency of UVB for the treatment
of generalized CLP in 50 patients. According to their findings, 70% of
the patients achieved a full response, 85% of those were still in
remission. The authors deduced that NB-UVB is a safe and effective
alternative line for treatment of generalized LP.12
Also, it has been reported that treatment of 16 generalized traditional
therapy resistant CLP patients with NB-UVB 3 times weekly achieved a
full response in 68.75% patients and partial response in 12.5%
patients. The authors found that an increased number of sessions were
correlated with a substantial increase in the overall
response.13
While for the MTX group, 50% of patients showed partial response to
treatment and 30% of patients showed complete response. In agreement
with our findings, MTX therapy was effective for complete clearance of
the lesions of CLP in more than 90% of the patients.8
According to our knowledge, this was the first study that evaluated the
effect of MTX on the serum levels of TNF-α among CLP patients. In the
current study, there was a statistically significant difference between
the two treatment groups in the median TNF-α level after treatment.
Furthermore, the median level of TNF-α decreased significantly after
treatment in the MTX group. The median TNF-α was increased
insignificantly after treatment in the NB-UVB group. Also, the level of
TNF-α in the MTX group decreased significantly after treatment by 41%
in response to treatment, compared with only 0.8% in the NB-UVB group,
that suggests the molecular action of MTX on inflammatory diseases by
inhibiting cytokine production induced by T cell
activation.14
In the current study, in the NB-UVB group; for pairwise comparisons,
patients with complete response had 2% changes vs. 22% change in cases
with partial response and this was statistically insignificant. Unlike,
patients with partial response had 22% changes vs. -25% changes in
cases with no response and this was a statistically significant.
Likewise, patients with complete response had 2% change vs. -25%
change in cases with no response and this was statistical significant.
This may be explained by the effect of NB-UVB in the production of
anti-inflammatory cytokines and alternations in the expression of
adhesion molecules that inhibit TNF-α mediated
inflammation.6
In the MTX group; for pairwise comparisons, patients with complete
response showed 68% decrease in the level of TNF-α compared with 29%
decrease in cases with partial response and this was statistically
significant. Moreover, patients with complete response showed 68%
decrease in the level of TNF-α compared with 22% decrease in cases with
no response and this was statistically significant. Contradictory,
patients with partial response showed 29% decrease in the level of
TNF-α compared with 22% decrease in cases with no response and this was
statistically insignificant. However, it has been found that serum
levels of TNF-α were found to be significantly increased in patients
with CLP 5, and MTX was an effective therapy for
patients with CLP 8,9, there is no previous study
assessed the effect of MTX in the reduction of TNF-α level in patients
with CLP.
The significant increase in serum TNF-α level in patients with CLP may
be caused by local and systemic productions of the TNF-α by several cell
types. TNF-α may be secreted by lymphocytes (T and B), macrophages,
natural killer cells, langerhans cells, monocytes, mast cells,
fibroblasts, endothelial cells, and keratinocytes.15The significant efficacy of MTX in the reduction of serum TNF-α level in
patients with CLP may be related to its ability to suppress replication
and function of lymphocytes (T and B), inhibition of chemotaxis,
suppression of monocyte ⁄macrophage stimulation, and inhibition of
histamine release from basophils.11
Anyway, these findings need further evidences on several comprehensive
large-sized multicenter clinical studies and to be more evidenced by
further assessments of the non-lesional and lesional tissue expressions
of TNF-α before and after NB-UVB phototherapy and MTX therapy in
patients with CLP.
This study concluded that NB-UVB phototherapy and MTX therapy were
clinically effective in the treatment of patients with CLP. MTX therapy
was more efficient in the reduction of TNF-α level than NB-UVB
phototherapy in patients with LP. TNF-α could be an essential cytokine
in the pathogenesis of CLP.