a 39-year - old man visited our clinic with a 2-week history of whitening of the eyelashes of his left lower lid .
the patient reported that this started with 1 to 2 lashes on the central part of his eyelid and that adjacent eyelashes subsequently became involved over the next few days .
otherwise the patient was in excellent health with no significant medical history ; he had no known drug allergies and was on no chronic medications .
there was no associated family history of vitiligo , poliosis , or autoimmune disorders such as vkh or sarcoidosis . on examination , a pigmented skin nevus , approximately 4 mm in diameter ,
was noted above a patch of white eyelashes on the central aspect of the left lower eyelid ( fig .
1 ) . according to the patient , the nevus had existed and remains unchanged since childhood .
no other abnormalities of the eyelid were noted and there was no vitiligo or signs of periocular inflammation .
his visual acuity was 20/20 in both eyes and there were no significant findings in the anterior segment or fundus .
serological tests for autoimmunity ( antinuclear , antimitochondrial , and antismooth muscle antibodies ) were negative and human leukocyte antigen ( hla ) typing failed to demonstrate types hla - dr4 or dw53
excisional biopsy of the central eyelid , including the pigmented nevus and white eyelashes , was performed .
on histopathologic examination , the nevus cells appeared unremarkable and showed no evidence of malignancy .
marked deficiency of melanocytes in the hair follicles was visible as compared with the normal overlying epidermis ( fig .
2 ) . infiltration of inflammatory cells , including lymphocytes and macrophages , was observed in the dermis ( fig . 3 ,
the majorities of halo nevi are acquired compound melanocytic nevi and appear in childhood and early adolescence . the site of predilection is the trunk and the back , especially when there are multiple lesions . patients with halo melanocytic nevi usually seek medical attention when their pigmented lesions develop a rim of depigmentation . over time ,
i , the central nevus remains brown in color or its pigment can disappear leading to a pink - colored papule ( stage ii )
. then the central papule disappears , leading to a circular area of depigmentation ( stage iii ) .
finally , the depigmented area may repigment ( stage iv ) , leaving no trace of its existence .
the underlying pathophysiology of the halo phenomenon is not well understood , but may possibly be the result of an immune response leading to nevus cell destruction .
some authors suggest an autoimmune response directed against antigenic changes of dysplastic nevi while others regard it as an autoimmune phenomenon against melanocytes , as occurs in vitiligo .
however , cellular and antibody - mediated immune mechanisms seem to be heavily involved in both theories and it is now well accepted that the inflammatory response is predominantly lymphocytic in nature , often with the addition of a small number of melanophages .
there are four histologic forms of halo nevi described : ( a ) inflammatory halo nevus , ( b ) noninflammatory nevus , ( c ) halo nevus without halo or halo nevus phenomenon , and ( d ) halo dermatitis around a melanocytic nevus ( mayerson 's nevus ) .
a halo nevus without the halo phenomenon is very rare and can only be diagnosed by histology .
.   described spontaneous regression of congenital nevi without the development of the halo phenomenon .
sotiriadis et al .   reported one case of a halo nevus without the halo phenomenon which developed on the trunk of a 5-year - old girl .
they reported pathologic findings of a thin epidermis with marked orthokeratotic hyperkeratosis and dense lymphocytic infiltration intermingled with melanocytes ; these findings were consistent with the diagnosis of a halo nevus . a t - cell - mediated autoimmune response leading to melanocyte destruction with resultant poliosis and associated halo nevi in vkh disease
however , our case exhibited no evidence of autoimmune disease and no halo phenomenon or vitiligo . in our case only histopathologic findings , such as infiltration of lymphocytes and melanophages , suggested the regression phase of the melanocytic halo nevus .
total loss of melanocytes in eyelash follicles may be an isolated sign of the halo phenomenon without depigmentation of the skin . despite an in - depth review of the literature
. the only reports of halo nevi of the eyelids were accompanied by vitiligo , not poliosis . also , a case of poliosis with a conjunctival melanoma has been described .
one possible , though very unlikely , explanation for the presence of poliosis without skin depigmentation occurring in this case may be a predilection of melanin - rich hair follicles for immunologic reactivity .
it is not possible for us to state with certainty why this may have occurred in the setting of a halo nevus undergoing regression , although it is very likely that the inflammation resulted from an exaggerated cell - mediated immune response . in conclusion
, we herein present a case of a halo nevus with poliosis of the eyelashes as the only sign of the halo phenomenon .
further analysis is needed to elucidate the mechanism of spontaneous regression of a halo nevus without depigmentation .
 a 39-year - old man with poliosis of his lower eyelid lashes visited our clinic . 
 he reported that his symptoms began with a few central lashes and then spread along the adjacent lashes during the ensuing 2 weeks . 
 a pigmented nevus , approximately 4 mm in diameter , was identified just above the white lashes without surrounding skin depigmentation . 
 no specific findings were identified with regard to the patient 's general health or serologic and radiologic testing . 
 excisional biopsy of the pigmented nevus was performed . 
 on histopathologic examination , infiltration of the dermis by numerous lymphocytes and melanophages was observed . 
 the poliosis was ultimately diagnosed as a presenting sign of the halo phenomenon in the regressive stage of a melanocytic nevus . 