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HLA typing in polymorphic light eruption
Correspondence lILA typing in actinic prurigo To the Editor: The arti~le on HLA typing in polymorphous light eruption (Lane et al. JAM ACAD DERMATOL 1991;24:570-3) totally ignored previous publications on the same topic. In February 1988, we first reported an HLA study in actinic prurigo (Bernal et a1. J AM ACAD DERMATOL 1988;18:310-2), showing an association with the alleles B40 and Cw3 that could explain the restricted ethnic distribution ofthedisease. In 1990,we reported our HLA findings in actinic prurigo among the Chimila Indians in Colombia (Bernal et a1. J AM ACAD DERMATOL 1990;22:1049-51), which demonstrated an association with the Cw4 allele. A complete description of the peculiarities of this disease among these isolates was also published (Duran et al, Int J DermatoI1989;28:228-9). Thus the current authors' hypothesis of an HLA association in actinic prurigo is supported when our results are considered. Maria M. Duran, MD, and Jaime Bernal, MD P.O. Box 90123 Bogota, Colombia
Reply To the Editor: Our article on HLA typing in actinic prurigo (AP) was published in 1990, 1 and we commented in detail on Bernal and Duran's article/ at that time. The haplotype HLA-B40, -Cw3 has long been regarded as a feature of Amerindian ancestry.l-" and we showed a significant increase in HLA-B40 and -Cw3 in Amerindians as compared with whites (p < 0.002). We stated "There was no difference ... in the frequency of either B40 alone or the B40, Cw3 haplotype between the Saskatchewan actinic prurigo patients and the Saskatchewan Indian control subjects. We were therefore unable to confirm the association of the HLA-B40, Cw3 haplotype with actinic prurigo,"! (p. 1022) as had been suggested by Bernal and Duran? in their first article. In a later publication Bernal and Duran" stated that" ... the control group [of their previous article"] was not comparable ethnically with the diseased population ... " (p. 1049) and went on to say: " ... our previous study perhaps disclosed only the Amerindian ancestry of our patients with actinic prurigo." (pp, 1050-1) We agree with these comments and therefore did not reference this article in our subsequent communications on HLA and actinic prurigo. When we wrote the article on HLA typing in polymorphous light eruption (PLE)6 in 1991, our main 6~8
objective was to show the difference between HLA typing in PLE and actinic prurigo, and we thought it unnecessary to reference Bernal and Duran's article on Chimila Indians with actinic prurigo in our succinct article, which primarily discussed PLE in whites. The article by Bernal and Duran 7 on actinic prurigo at sea level in Colombia does not discuss HLA typing. We agree with them, however, that their 1990 article' showing the significance of Cw4 in the Chimila Indians is of help in substantiating our report of the association of A24 and Cw4 in actinic prurigo in Saskatchewan Amerindians. Weare most appreciative of the pioneer work done in Colombia on actinic prurigo and have duly referred to the appropriate articles in all fivepublications on actinic prurigo from this department.
Peter R. Lane, BM, BCh, David P. Sheridan, MD, Daniel J. Hogan, MD, and Adele Moreland, MD, Royal University Hospital, Saskatoon, Canada REFERENCES 1. Sheridan DP, Lane PR, Irvine J, et al. HLA typing in actinic prurigo. J AM ACAD DERMATOL 1990;22:1019-23. 2. Bernal JE, Duran de Rueda MM, de Brigard D. Human lymphocyte antigen in actinic prurigo. JAM ACAD DERMATOL 1988;18:310-2. 3. Lawrence DN, Bodmer JG, Bodmer WF. Distribution of HLA antigens in Ticuna Indians of Brazil: results of typing a leprosy-affected family. Tissue Antigens 1980;16:152-60. 4. Vullo CM, Celis EM, Serra HM, et al. Study of HLA system in a Mantaco population: a geographically isolated American Indian tribe. Tissue Antigens 1984;23:33-40. 5. Bernal JE, Duran de Rueda MM, Ordanez CP, et al. Actinic prurigo among the Chimila Indians in Colombia: HLA studies. J AM ACAD DERMATOL 1990;22:1049-51. 6. Lane PR, Sheridan DP, Hogan DJ, et al. HLA typing in polymorphous light eruption. J AM ACAD DERMATOL 1991;24:570-3. 7. Duran de Rueda MM, Bernal JE, Ordanez CPo Actinic prurigo at sea level in Colombia. Int J Dermatol 1989;28:228-9.
lILA typing in polymorphic light eruption To the Editor: In addition to the report of Lane et a1. on HLA typing in polymorphic light eruption and their demonstrated statistical significanceof HLA group A24, Cw4 in North American Indians (J AM ACAD DERMATOL 1991;26:570-3). I report a patient from North Labrador referred to me in March 1991who had had the condition since her teenage years. Her maternal grand-
Volume 26 Number 4 April 1992
~orrespondence
mother, her mother, and one of her two children, age 5, had the same eruptionas the patient. Thispatient's HLA analysisshowed her to be part of the same groupreported by Lane et al., namely A24, 28, B51, 35, Cw4. If thesefindings are further confirmed in the Labrador Inuit, it wouldadd support to the theory of the migratory spread of this conditioneastwardfrom the BeringStrait, south through the western part of the continentto Central America and differentiateit as actinic prurigo from somewhatsimilarforms of actinic eruptiontermed polymorphous light eruption that have beenreported in Europe. J. B. Ross, MB, FRCPC Division ojDermatology Dalhousie University Halifax, Canada B3H 2Y9
us,
Reply To the Editor: Itis reassuring to have our HLA findings in actinic prurigo confirmedin an Inuit patient with actinic prurigoin Labrador, Canada. We have had numerous verbalreportsfrom clinicians that they haveseenactinic prurigoin the Cree in the James Bayarea of Northern Ontario as well as in the Inuit in the Northwest Territories. We hopethat Dr. Ross's letter will stimulate further HLA testing. Peter R. Lane, MB, FRCPC, a Daniel 1. Hogan, MD,b and David P. Sheridan, MD, a Department ofMedicine, University ofSaskatchewan, Canada,a and the Department ojDermatology and Cutaneous Surgery, University ofMiami, Florida b
Unmasking myelin proteins in neurothekeoma To the Editor: I read withgreat interest the recent article by Barnhillet al. on the cellularorigin of neurothekeoma (J AM ACAD DERMATOL 1991;25:80-8). The authors' distinction of subtypes of this tumor may sometimes be difficult on routine hematoxylin-and-eosin-stained sections, but it is valid because the cellular variant appears to be distinguishable from the myxomatous type by the failure of the cellular variant to express S-l00 protein. However, I questionthe completeness of theseauthors' inquiryintothe originof the cellularvariant ofneurothekeoma. I coauthoredan article' on a tumor bestdescribed as a cellular neurothekeoma as defined by criteria of Barnhill et al. In this study we predigested fixed tissue
659
fromthe specimenwithtrypsin beforeimmunohistochemical study using the method of Huang et al.2 The tissue was then evaluated for the presence of not only myelin basic protein but also PO and PI myelin glycoproteins with the monoclonal antibody AHMY1. 3 Immunoreactivity was detected for a protein reactive with AHMYI. Our specimen therefore appeared to be of Schwann cell origin. We concur with Barnhill et al. when they state"... technicalfactors may account for some of the differences in expression [and lack of expression]of these antigens" (p. 87) (especially myelinbasic protein and myelin glycoprotein). A follow-up study with tissue predigestion and/or the use of a more comprehensive panel of monoclonalantibodiesmay therefore provideadditionalinsight into the cellular origines) of neurothekeoma. Certainly such techniques ought to be tried to solvethe puzzle expressed by Barnhill et al. as to why cellular neurothekeomas appear to be of peripheral nerve sheath origin on light and electron microscopy yet fail to expressschwannian cell markers. Even if the bulk: of cellular neurothekeoma cells is found by unmaskingto be schwannian, I concurwith the authors that the degree of expression of cell markers by this tumor could be dependent on the "environmental condition" around it, either in vivo or caused by tissue fixation. Lack of cell marker expression could be from more usual causes as well: an unexpected cell of origin precluding the use of appropriate immunohistochemical markers and poor ontogenic differentiation within a tumor, renderinga tumor incapable of expressing certain markers. Peter J. Aronson, MD Section ofDermatology VA Medical Center Allen Park, MI48101 REFERENCES 1. Aronson PJ, Fretzin DF, Potter BS. Neurothekeoma of Gallager and Helwig (dermal nerve sheath myxoma variant). J Cutan PathoI1985;12:506-19. 2. Huang S, Minassian H, More JP. Application of immunofluorescent staining on paraffin sections improved by trypsin digestion. Lab Invest 1976;35:383-90. 3. Aso M, Hashimoto K, Hamzavi A. Immunohistochemical studies of selected skin diseases and tumors using monoclonal antibodies to neurofilament and myelin proteins. J AMACAD DERMATOL 1985;13:37-42.
Does follicular mucinosis in Hodgkin's disease represent a sign of poor prognosis? To the Editor: I wish to comment on the article by Stewart and Smoller (J AM ACAD DERMATOL 1991;24:784-5) regarding the associationof Hodgkin's disease with folli-
Reply To the Editor: Our article on HLA typing in actinic prurigo (AP) was published in 1990, 1 and we commented in detail on Bernal and Duran's article/ at that time. The haplotype HLA-B40, -Cw3 has long been regarded as a feature of Amerindian ancestry.l-" and we showed a significant increase in HLA-B40 and -Cw3 in Amerindians as compared with whites (p < 0.002). We stated "There was no difference ... in the frequency of either B40 alone or the B40, Cw3 haplotype between the Saskatchewan actinic prurigo patients and the Saskatchewan Indian control subjects. We were therefore unable to confirm the association of the HLA-B40, Cw3 haplotype with actinic prurigo,"! (p. 1022) as had been suggested by Bernal and Duran? in their first article. In a later publication Bernal and Duran" stated that" ... the control group [of their previous article"] was not comparable ethnically with the diseased population ... " (p. 1049) and went on to say: " ... our previous study perhaps disclosed only the Amerindian ancestry of our patients with actinic prurigo." (pp, 1050-1) We agree with these comments and therefore did not reference this article in our subsequent communications on HLA and actinic prurigo. When we wrote the article on HLA typing in polymorphous light eruption (PLE)6 in 1991, our main 6~8
objective was to show the difference between HLA typing in PLE and actinic prurigo, and we thought it unnecessary to reference Bernal and Duran's article on Chimila Indians with actinic prurigo in our succinct article, which primarily discussed PLE in whites. The article by Bernal and Duran 7 on actinic prurigo at sea level in Colombia does not discuss HLA typing. We agree with them, however, that their 1990 article' showing the significance of Cw4 in the Chimila Indians is of help in substantiating our report of the association of A24 and Cw4 in actinic prurigo in Saskatchewan Amerindians. Weare most appreciative of the pioneer work done in Colombia on actinic prurigo and have duly referred to the appropriate articles in all fivepublications on actinic prurigo from this department.
Peter R. Lane, BM, BCh, David P. Sheridan, MD, Daniel J. Hogan, MD, and Adele Moreland, MD, Royal University Hospital, Saskatoon, Canada REFERENCES 1. Sheridan DP, Lane PR, Irvine J, et al. HLA typing in actinic prurigo. J AM ACAD DERMATOL 1990;22:1019-23. 2. Bernal JE, Duran de Rueda MM, de Brigard D. Human lymphocyte antigen in actinic prurigo. JAM ACAD DERMATOL 1988;18:310-2. 3. Lawrence DN, Bodmer JG, Bodmer WF. Distribution of HLA antigens in Ticuna Indians of Brazil: results of typing a leprosy-affected family. Tissue Antigens 1980;16:152-60. 4. Vullo CM, Celis EM, Serra HM, et al. Study of HLA system in a Mantaco population: a geographically isolated American Indian tribe. Tissue Antigens 1984;23:33-40. 5. Bernal JE, Duran de Rueda MM, Ordanez CP, et al. Actinic prurigo among the Chimila Indians in Colombia: HLA studies. J AM ACAD DERMATOL 1990;22:1049-51. 6. Lane PR, Sheridan DP, Hogan DJ, et al. HLA typing in polymorphous light eruption. J AM ACAD DERMATOL 1991;24:570-3. 7. Duran de Rueda MM, Bernal JE, Ordanez CPo Actinic prurigo at sea level in Colombia. Int J Dermatol 1989;28:228-9.
lILA typing in polymorphic light eruption To the Editor: In addition to the report of Lane et a1. on HLA typing in polymorphic light eruption and their demonstrated statistical significanceof HLA group A24, Cw4 in North American Indians (J AM ACAD DERMATOL 1991;26:570-3). I report a patient from North Labrador referred to me in March 1991who had had the condition since her teenage years. Her maternal grand-
Volume 26 Number 4 April 1992
~orrespondence
mother, her mother, and one of her two children, age 5, had the same eruptionas the patient. Thispatient's HLA analysisshowed her to be part of the same groupreported by Lane et al., namely A24, 28, B51, 35, Cw4. If thesefindings are further confirmed in the Labrador Inuit, it wouldadd support to the theory of the migratory spread of this conditioneastwardfrom the BeringStrait, south through the western part of the continentto Central America and differentiateit as actinic prurigo from somewhatsimilarforms of actinic eruptiontermed polymorphous light eruption that have beenreported in Europe. J. B. Ross, MB, FRCPC Division ojDermatology Dalhousie University Halifax, Canada B3H 2Y9
us,
Reply To the Editor: Itis reassuring to have our HLA findings in actinic prurigo confirmedin an Inuit patient with actinic prurigoin Labrador, Canada. We have had numerous verbalreportsfrom clinicians that they haveseenactinic prurigoin the Cree in the James Bayarea of Northern Ontario as well as in the Inuit in the Northwest Territories. We hopethat Dr. Ross's letter will stimulate further HLA testing. Peter R. Lane, MB, FRCPC, a Daniel 1. Hogan, MD,b and David P. Sheridan, MD, a Department ofMedicine, University ofSaskatchewan, Canada,a and the Department ojDermatology and Cutaneous Surgery, University ofMiami, Florida b
Unmasking myelin proteins in neurothekeoma To the Editor: I read withgreat interest the recent article by Barnhillet al. on the cellularorigin of neurothekeoma (J AM ACAD DERMATOL 1991;25:80-8). The authors' distinction of subtypes of this tumor may sometimes be difficult on routine hematoxylin-and-eosin-stained sections, but it is valid because the cellular variant appears to be distinguishable from the myxomatous type by the failure of the cellular variant to express S-l00 protein. However, I questionthe completeness of theseauthors' inquiryintothe originof the cellularvariant ofneurothekeoma. I coauthoredan article' on a tumor bestdescribed as a cellular neurothekeoma as defined by criteria of Barnhill et al. In this study we predigested fixed tissue
659
fromthe specimenwithtrypsin beforeimmunohistochemical study using the method of Huang et al.2 The tissue was then evaluated for the presence of not only myelin basic protein but also PO and PI myelin glycoproteins with the monoclonal antibody AHMY1. 3 Immunoreactivity was detected for a protein reactive with AHMYI. Our specimen therefore appeared to be of Schwann cell origin. We concur with Barnhill et al. when they state"... technicalfactors may account for some of the differences in expression [and lack of expression]of these antigens" (p. 87) (especially myelinbasic protein and myelin glycoprotein). A follow-up study with tissue predigestion and/or the use of a more comprehensive panel of monoclonalantibodiesmay therefore provideadditionalinsight into the cellular origines) of neurothekeoma. Certainly such techniques ought to be tried to solvethe puzzle expressed by Barnhill et al. as to why cellular neurothekeomas appear to be of peripheral nerve sheath origin on light and electron microscopy yet fail to expressschwannian cell markers. Even if the bulk: of cellular neurothekeoma cells is found by unmaskingto be schwannian, I concurwith the authors that the degree of expression of cell markers by this tumor could be dependent on the "environmental condition" around it, either in vivo or caused by tissue fixation. Lack of cell marker expression could be from more usual causes as well: an unexpected cell of origin precluding the use of appropriate immunohistochemical markers and poor ontogenic differentiation within a tumor, renderinga tumor incapable of expressing certain markers. Peter J. Aronson, MD Section ofDermatology VA Medical Center Allen Park, MI48101 REFERENCES 1. Aronson PJ, Fretzin DF, Potter BS. Neurothekeoma of Gallager and Helwig (dermal nerve sheath myxoma variant). J Cutan PathoI1985;12:506-19. 2. Huang S, Minassian H, More JP. Application of immunofluorescent staining on paraffin sections improved by trypsin digestion. Lab Invest 1976;35:383-90. 3. Aso M, Hashimoto K, Hamzavi A. Immunohistochemical studies of selected skin diseases and tumors using monoclonal antibodies to neurofilament and myelin proteins. J AMACAD DERMATOL 1985;13:37-42.
Does follicular mucinosis in Hodgkin's disease represent a sign of poor prognosis? To the Editor: I wish to comment on the article by Stewart and Smoller (J AM ACAD DERMATOL 1991;24:784-5) regarding the associationof Hodgkin's disease with folli-