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bullous lupus erythematosus ( ble ) is a rare subset of systemic lupus erythematosus ( sle ) .
there have been few studies addressing hypopigmented lesions in lupus erythematosus ( le ) . in this study
, we would like to introduce a rare case of sle , and show immunohistochemical and ultrastructural findings of the vitiliginous lesions following erosive erythema .
a 57-year - old male patient had noticed itchy erythema on the frontal chest in may 2011 , and thereafter experienced disease enlargement and partial crust formation . since no clinical effect of 10 mg / day of oral prednisolone was observed , he was referred to our hospital on july 7 , 2011 . in terms of the clinical findings at the first visit ,
symmetric red papules and centrifugal erythema , surrounded by an annular erosive crust , were distributed on the upper extremities and trunk in line with the seborrheic region .
the center of the erythematous lesions in the skin tended to be notably resolved ( fig .
although his skin disease was initially suspected to be a bullous disease , neither anti - desmoglein 1/3 nor anti - bp 180 antibodies were detected .
laboratory tests revealed cytopenia ( wbc , 10,470/l ; neu , 72.6% ; lymph , 13.0% ; mono , 14.0% ; eosino , 0.1% ; baso , 0.3% ; rbc , 3.85  10/l ; hb , 12.7 g / dl ; ht , 38.5% ; platelet , 180  10/l ) , ana ( 1/320 , homogeneous + speckled pattern ) , positive anti - sm antibodies , anti - rnp , anti - cardiolipin antibodies , and low c3 and c4 levels .
metal patch and photo tests were negative , and no internal malignancy was detected by whole - body imaging .
a biopsy of the erythematous lesion showed individual apoptotic keratinocytes and liquefaction with partial cleft formation on the epidermis , and lymphocytes predominantly infiltrated in the upper dermis and perivascular area ( fig .
the direct immunofluorescence findings of the uninvolved lesion were granular deposition of igg and igm in the basal membrane .
these laboratory and histological findings led to a final diagnosis of ble type i. in an immunohistochemical analysis for immunocompetent cells , cd8 cells , instead of cd4 cells , and hla - dr - activating t cells were found to have densely infiltrated into the epidermis of the erythematous lesion .
the cd68 macrophages densely infiltrated into the upper dermis , and there was a slight infiltration of il-17a cells and foxp3 cells ( fig . 2a 
h ) . an increased dose of oral prednisolone was effective not only for spiking fever , cytopenia and hypocomplement level , but also crusted bullae and fused erythema ( fig .
instead , annular incomplete hypopigmentation tracing the crusted lesions was noted 1 month later ( fig .
our histological observations of the hypopigmented lesion showed a decrease , but not total absence , of melanosomes and melanocytes detected by masson - fontana ( fig .
in addition , an ultrastructural analysis of a hypopigmented lesion revealed attenuated melanin production , with the presence of immature melanosomes in the remaining melanocytes , whereas no disturbance of melanin transfer to adjacent keratinocytes was noted ( fig .
ble is a rare variant of sle , with an incidence of less than 0.2 cases per million per year , and represents only 23% of the cases of autoimmune subepidermal bullous dermatoses .
clinically , ble is characterized by a disseminated vesiculobullous skin rash that may or may not be limited to areas exposed to light . although it is considered to be an acquired bullous disease caused by anti - type vii collagen antibodies , the same as epidermolysis bullosa acquisita , the bullous lesions in ble usually remit without scar formation , which is common in cases of epidermolysis bullosa acquisita . since antibodies such as anti - desmoglein 1/3 antibodies and anti - bp 180 antibodies were not detected , the present case of ble was diagnosed according to the diagnostic criteria .
a histopathological examination revealed subepidermal blisters with neutrophilic microabscesses in the dermal papillae , perivascular inflammatory infiltration composed of lymphomononuclear cells , and in some cases , leukocytoclastic vasculitis .
our case also showed individual apoptotic keratinocytes , liquefaction with a partial cleft on the epidermis and lymphocytes predominantly infiltrating into the upper dermis and perivascular area . in our case
franca and de souza   reviewed the histological features of 12 patients with depigmented or hypopigmented lesions in 220 patients with cutaneous le , and the most common histological findings were summarized as : cellular infiltration ( 75% ) , hyperkeratosis ( 66.7% ) , thinning and flattening of the epidermis ( 58.3% ) and lower number of melanocytes compared to normal skin .
we observed similar histological findings in our case , including apoptotic keratinocytes , atrophy of the epidermis and superficial lymphocytic infiltration in the dermis and a decreased number of melanocytes . for a more detailed observation
, we carried out the immunohistochemical and ultrastructural analyses for both the erythematous and subsequent hypopigmented lesions .
for the immunohistochemical analysis , cd8 cells ( instead of cd4 cells ) and hla - dr - activating t cells were found to have densely infiltrated into the epidermis of the erythematous lesion . there was a decrease in the number of cd1a
langerhans cells . while the cd68 macrophages densely infiltrated the upper dermis , there was a slight infiltration of il-17a cells and foxp3 cells .
liquefaction , degeneration and dense infiltration of cd8 t cells into the epidermis were detected , possibly resulting in hypopigmentation accompanied by le . whereas the cd8 t cells were densely found in the affected lesions , the il-17a cells and foxp3 regulatory t cells were sparsely present
moreover , we detected a large number of th17 cells infiltrating in the depigmented lesions compared to the uninvolved skin in nonsegmental vitiligo patients [ 6 , 7 ] .
with regard to ultrastructural findings , while melanosome production in melanocytes was attenuated , adjacent keratinocytes took over a significant number of mature melanosomes , indicating that there were decreases in both the melanocyte and melanosome number without impaired melanosome transfer to keratinocytes . taking into consideration both these immune responses and the lupus condition , we considered the following process to be involved in the pathogenesis of the annular hypopigmentation ; cytotoxic t cells penetrated into the epidermis followed by melanocyte destruction .
thereafter , pigment incontinentia followed by the recruitment of numerous cd68 melanophages in the upper dermis induced activation of melanin - specific antigen presentation , resulting in positive loop cellular immunity . the cd8 cytotoxic cell - related immune response
was thus induced , and melanocyte were attacked , leading to basal membrane degeneration , which may have played a major role in the hypopigmentation associated with le .
early induction of systemic prednisolone treatment may have led to lesion improvement owing to the sufficient inhibition of this vicious disease cycle .
we experienced a case of le associated with annular hypopigmentation . we suppose that a cd8 cytotoxic cell - related immune response in addition to basal membrane degeneration may play a major role in the development of hypopigmentation associated with le .
early administration of effective treatment may be important for restoration of the pigmentation . although annular hypopigmentation is generally regarded as secondary hypopigmentation after local inflammation , annular hypopigmentation following ble also occurs in some patients .
we believe that using a detailed morphological and hematological analysis in additional patient samples will help to elucidate the exact mechanism(s ) underlying the development of hypopigmentation in patients with ble .
a 57-year - old male had been suffering from an itchy map - shaped symmetrical erosive erythema with a crust that was attached to his upper arm and buttock , and occasionally he suffered from spiking fever . 
 laboratory examinations showed neither anti - desmoglein 1/3 antibodies nor anti - bp 180 antibodies , and he fulfilled the criteria for a diagnosis of systemic lupus erythematosus ( sle ) . 
 histologically , there was eosinophilic necrosis of keratinocytes , liquefaction and degradation with severe lymphocyte infiltration into the epidermis and subepidermal blister formation , suggestive of a variant of sle , bullous lupus erythematosus ( ble ) . 
 one month after remission of ble , peculiar annular hypopigmentation appeared on the peripheral borders . 
 an immunohistochemical analysis showed a decrease in melan a - positive melanocytes and concomitant pigment incontinentia , with dense infiltration of cd8 + t cells and il-17a+ th17 cells . 
 an ultrastructural analysis revealed a decrease , but not a complete disappearance , of both melanocytes and melanosomes , and no impairment in melanosomal transfer . in this case report 
 , we would like to introduce the development of annular depigmentation complicated with ble , and discuss the effects of lupus condition on melanocyte damage based on immunohistological and electromicroscopic findings of those vitiliginous lesions .