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Granuloma annulare perforans in herpes zoster scars
Journal of the American Academy of Dermatology Volume 29, Number 5, Part 2
der angiomas. The lesions of eruptive pseudoangiomatosis can be differentiated from telangiectases by the presence ofendothelial cells that protrude into the vessel lumen. In spider angiomas there are centrally located dilated arterioles with thin branches, without prominence of the endothelial lining. Clinically, eruptive pseudoangiomatosis must be differentiated from bacillary angiomatosis, bartonellosis, and pyogenic granuloma. In all three of these disorders the skin lesions are generally larger and last considerably longer than the 7- to IO-day duration that we observed in our patients. Spontaneous resolution does not occur. The occurrence of multiple pyogenic granulomas is relatively rare. 3 Histologically, eruptive pseudoangiomatosis shares with bacillary angiomatosis and bartonellosis the presence of a prominent endothelial lining. 4 However, eruptive pseudoangiomatosis shows no blood vessel proliferation, inflammatory infiltrate with neutrophils, or granular deposits that represent clustered bacilli. Pyogenic granuloma is characterized by a dome-shaped proliferation of small blood
Prose et al. vessels lined by oval endothelial cells. An epidermal collarette and a variable degree of mixed inflammatory infiltrate may be present. Although the data of Cherryet aLI implicated an enterovirus, the evidence linking the cutaneous lesions to a systemic viral infection in our patients was circumstantiaL It appears most likely that eruptive pseudoangiomatosis is a viral exanthem. However, it may be an unusual cutaneous reaction pattern to several different organisms.
REFERENCES 1. Cherry JD, Bobinski JE, Horvath FL, et al. Acute heman-
gioma-like lesions associated with ECHO viral infections. Pediatrics 1969;44:498-502. 2. Ghadially FN. Ultrastructural pathology of the cell. Stoneham, Mass.: Butterworth-Heinemann, 1975:424-8. 3. Dillman AM, Miller RC, Hansen RC. Multiple pyogenic granulomata in childhood. Pediatr DermatoI1991;8:28-31. 4. LeBoit PE, Berger TG, Egbert BM, et al. Bacillary angiomatosis: the histopathology and differential diagnosis of a pseudoneoplastic infection in patients with human immunodeficiency virus disease. Am J Surg Pathol 1989;13:90920.
Granuloma annulare perforans in herpes zoster scars Dieter Krahl, MD, Wolfgang Hartschuh, MD, and Wolfgang Tilgen, MD
Heidelberg, Germany Granuloma annulare perforans limited to a thoracic dermatome that was previously involved by herpes zoster occurred in a 51-year-old woman who also had Lennert's lymphoma. Of the various local granulomatous infiltrates described after herpes zoster, granuloma annulare perforans is unique, although ordinary granuloma annulare has been described in a few patients. A high incidence of specific and nonspecific reaction patterns in herpes zoster scars has been described in patients with malignant lymphoma. In contrast to previous patients, all of whom had chronic lymphatic leukemia, our patient had Lennert's lymphoma. (J AM ACAD DERMATOL 1993;29:859-62.) Several variants of granuloma annulare (GA) can be distinguished clinically and histopathologically, including the lichenoid, infiltrated, plaquelike, tu-
From the Universitals-Hautklinik, Ruprecht-Karls-University. Reprint requests: Dicter Krahl, MD, Universitats-Haulklinik, Vossslr. 2, D-6911S Heidelberg, Germany. Copyright ® 1993 by the American Academy of Dermatology, Inc. 0190.9622/93 $1.00 +.10 16/4/48998
berous, subcutaneous, and perforating types with limited, disseminated, or generalized distribution. 1 The chief histologic patterns are the palisading granuloma and the interstitial form. A rare epithelioid nodule type also occurs. Combinations of these patterns frequently occur within individual lesions and in the same patient. Perforating granuloma annulare (PGA) shows transepidermal elimination of degenerated collagen from the center of palisading granuloma type lesions.
859
860 Krahl et al.
Journal of the American Academy of Dermatology November 1993
Fig. 1. Granuloma annulare perforans in area of previous herpes zoster.
Fig. 3. Granuloma annulare with its transepidermal elimination site. (Hematoxylin-eosin stain; XIO.)
Fig. 2. Close-up of partly crusted, pseudopustular papules.
Fig. 4. Degenerated connective tissue in contact with epidermal undersurface. (Hematoxylin-eosin stain; X25.)
Herpes zoster may be followed locally by other skin diseases such as psoriasis, 2 morphea, 3 HIV-associated Kaposi's sarcoma, 4 and leukemic infiltrates. 5 ,6 Granulomatous reactions that can develop in herpes zoster scars are pseudolymphoma,7, 8 sarcoidal reaction,9, 10 and granuloma annulare. Granuloma annulare has been described in eight patients thus far. ll - 17 We describe for the first time a patient who had the perforating variant of GA after herpes zoster.
moderately severe neuralgia. No signs of severe necrosis or dissemination were found. She was known to have a lymphoepithelioid cellular lymphoma (Lennert's lymphoma) that was in remission after multiple courses of chemotherapy. The patient was treated with oral acyclovir and 1 month later the zoster had cleared, leaving superficial scars. Four months later new lesions appeared in the same region (Figs. I and 2). We observed numerous pseudopustular, yellow, 2 mm papules on an erythematous base that were limited to the right T 3 dermatome. The lesions were more closely aggregated in the dorsal region. Some of the papules were crateriform and crusted. This became more marked in subsequent weeks.
CASE REPORT A 5I -year-old woman had herpes zoster that was limited to her right T 3 dermatome and accompanied by
Journal of the American Academy of Dermatology Volume 29, Number 5, Part 2
A biopsy specimen revealed a necrobiotic focus in the papillary dermis that was in contact with an epidermal erosion covered by a scale crust. The degenerated collagen was surrounded by a radially arranged palisading granuloma that contained numerous histiocytic giant cells in addition to lymphocytes (Figs. 3 and 4). Mucin deposition and lack of elastic fibers were demonstrated in the necrobiotic focus by alcian blue and elastic tissue stains, respectively. Around the palisading granuloma interstitial histiocytic infiltration with mucin deposition could be seen. Results of immunohistochemical studies showed marking of cellular infiltrates, mostly for CD3 (pan-T), COlI, and CDw14 (monocytes). T lymphocytes were mostly of the CD4-positive subset. A diagnosis of PGA was made. Treatment with topical corticosteroids led to partial regression of the lesions, leaving slightly depressed scars.
DISCUSSION
The previously described cases of GA after herpes zoster have not been of the perforating variant. Some problems with differential diagnosis were initially raised in the case of our patient with PGA. The pseudopustular appearance of her papules was clinically suggestive of a herpes zoster relapse, which could have been a possible consequence of immunosuppression by the malignant lymphoma and chemotherapy. We also considered subcorneal pustular dermatosis of Sneddon-Wilkinson, 18 tuberculosis,19 and pustular psoriasis. 2 It was also necessary to exclude a cutaneous manifestation of her Lennert's lymphoma. Localization of malignant lymphomatous infiltrates in herpes zoster scars has been reported. 5, 6 However, each of these possibilities could be eliminated by the histologic and immunochemical findings. The perforating form of GA is classed among the perforating diseases. 20, 21 As a consequence of transepidermal elimination it is the only variant of GA that resolves with scarring. Perforation and transepidermal elimination appear to result from the superficial location of degenerated connective tissue. 22, 23 Furthermore, the epidermis in scars of herpes zoster is atrophic and may be "penetrated" more easily. In contrast to some other perforating disorders, for example, reactive perforating collagenosis or elastosis perforans serpiginosa, formation of hyperplasticlips of the adjacent epidermis or of an eliminating channel is not a regular feature of GAP.22,23 This finding corresponds to our own observations, but other authors 20,24 have reported more prominent reactions of the epidermis or even
Krahl et al. 861 transfo1licular elimination. 25 Perforation in GA appears to occur only in the palisading granulomatype tissue reaction with well-demarcated homogeneous degenerated material and not in the diffuse interstitial type. 20-24, 26 Serial sectioning is required for reliable identification of the transepidermal elimination site. 2o, 23, 26, 27 The occurrence of GA after a viral infection (varicella, herpes zoster, or warts 28 ) or immunization (tuberculin skin testing29 ) has been interpreted as a consequence of persisting antigenic material or tissue antigen alteration by microbes, which elicits a delayed (type IV) immune response. 11 In accordance with previous results 30 the immunohistochemical findings in our case demonstrated T lymphocytes, mostly T helper cells, as the predominating cell population. The predilection of GA and several other granulomatous reactions, as well as malignant lymphoma infiltrates, for areas previously involved by herpes zoster may be interpreted as Koebner's phenomenon. 6, 12,15 All patients with lymphoma who have either nonspecific or specific infiltrates in their zoster (or varicella 31 ) scars had chronic lymphatic leukemia. 5, 6, 8, 17,31 Our patient is the first with Lennert's lymphoma. REFERENCES 1. Kresbach H. Variationsbreite des Granuloma anulare. In: Braun-Falco 0, Schill WB, eds. Fortschritte der praktischen Dermatologie und Venerologie; vol II. Berlin: Springer, 1987:216-22. 2. Bohnstedt RM. Herpes zoster als isomorpher Reizeffekt bei Psoriasis. Z Haut Geschlechtskr 1957;22:202-6. 3. Zimmermann H. Zoster als Priimorbid einer zirkumskripten Sklerodermie. Dermatol Wochenschr 1964;150: 112-6. 4. Niedt GW, Prioleau PG. Kaposi's sarcoma occurring in a dermatome previously involved by herpes zoster. J AM ACAD DERMATOL 1988;18:448-51. 5. Aberer W, Zonzits E, Soyer HP, et a1. Postzosterische spezifische Hautinfiltrate bei chronischer Iyrnphatischer Leukiimie. Hautarzt 1990;41:455-7. 6. Raab W. Herpes zoster als isomorpher Reizeffekt bei chronisch lymphatischer Leukiimie. Arch Klin Exp DermatoI1984;218:215-21. 7. SanchezJL, Mendez lA, Palacio R. Cutaneous pseudolymphoma at the site of resolving herpes zoster. Arch DermatoI1981;117:377. 8. WolffHH, Wendt V, Winzer M. Cutaneous pseudolymphoma at the site of prior herpes zoster eruption. Arch Dermatol Res 1987;279:52-4. 9. Bisaccia E, Scarborough DA, Carr RD. Cutaneous sarcoid granuloma formation in herpes zoster scars. Arch DermatoI1983;119:788-9. 10. Wright AL, Cotton DWK, Winfield AD. Granuloma formation in herpes zoster scars. Dermatologica 1989;179: 45-6.
Krahl et al. 11. Friedman S, Fox B, Albert H. Granuloma anulare arising in herpes zoster scars. J AMAcADDERMATOL 1986;14:76470. 12. Guill MA, Goette DK. Granuloma annulare at sites of healing herpes zoster. Arch DermatoI1978;1l:1383. 13. Hayakawa K, Mizukawa Y, Shiohara T, et al. Granuloma annulare arising after herpes zoster [Letter]. Int J DermatoI1992;31:745-6. 14. Kleber R, Landthaler M, Burg G. Postzosterisches Granuloma anulare. Hautarzt 1989;40:110-11. 15. Packer RH, Fie1dsJP, King LE Jr. Granuloma annulare in herpes zoster scars. Cutis 1984;34:177-9. 16. Shideler SJ, Richards M. Granuloma annulare arising after herpes zoster [Letter]. JAM ACAD DERMATOL 1986; 15:1049-50. 17. Zanolli MD, Powell BC, McCalmont T, et al. Granuloma annulare and disseminated herpes zoster. Int J Oermatol 1992;31 :55-7. 18. Kohl PK, Hartschuh W, Tilgen W, et al. Pyoderma gangrenosum followed by subcorneal pustular dermatosis in a patient with IgA paraproteinemia. J AM ACAD DERMATOL 1991 ;24:325-8. 19. Civatte P. Les formes tuberculo-ulcereuses et tuberculogommeuses du granuloma annulaire. Ann Dermatol Syphiligr 1952;79:387-97. 20. Duncan WC, Smith JD, Knox JM. Generalized perforating granuloma annulare. Arch OermatoI1973;108:570-2.
Journal of the American Academy of Dermatology November 1993
21. Levi L, Sala G, Galbiati G. Granuloma anulare perforans: zwei klinisch verschiedenartige Verlaufsformen. Hautarzt 1986;37:23-7. 22. Delaney T J, Gold SC, Leppard B. Disseminated perforating granuloma annulare. Br J Dermatol 1973;89:523-6. 23. Owens OW, Freeman RG. Perforating granuloma annulare. Arch Dermatol 1971 ;103:64-7. 24. Gattlen JM, Delacretaz J. Le granulome annulaire perforant. Dermatologica 1975;151:368-75. 25. Bardach RG. Granuloma annulare with transfollicular perforation. J Cutan Pathol 1977;4:99-104. 26. Izumi AK. Generalized perforating granuloma annulare. Arch Dermatol 1973;108:708-9. 27. Samlaska CP, Sandberg GD, Maggio KL, et al. Generalized perforating granuloma annulare. J AM ACAD DERMATOL 1992;27:319-22. 28. Ward WHo Warts and granuloma anulare. Br Med J 1956;2:1484-6. 29. Beer WE, Jares EW. Granuloma anulare following tuberculin heaf tests. Trans St Johns Hosp Dermatol Soc 1966;52:68-70. 30. Buechner SA, Winkelmann RK, Banks PM. Identification of T-cell subpopulations in granuloma anulare. Arch DermatoI1983;119:125-8. 31. Fischer G, Jaworski R. Granuloma formation in herpes zoster scars [Letter]. J AM ACAD DERMATOL 1987;16: 1261-3.
In utero acute graft-versus-host disease in a neonate with severe combined immunodeficiency Guylaine Alain, MD,a Charles Carrier, MD,b Louis Beaumier, MD,b Jean Bernard, MD,c Martin Lemay, MD,d and Aubert Lavoie, MD e Montreal and Sainte-Fay, Quebec, Canada We describe a male neonate with severe combined immunodeficiency who at birth had acute graft-versus-host disease (GVHD) as a result of maternal-fetal transfusion during pregnancy. Several clinical signs helped establish this diagnosis. Findings of a skin biopsy specimen confirmed the diagnosis of acute GVHD. Immunologic evaluation disclosed an absence ofT and B lymphocytes. Acute GVHD in severe combined immunodeficiency most often occurs during the first weeks of life; intrauterine occurrence is unusual. (J AM ACAD DERMATOL 1993;29:862-5.)
From the Universite de Montreal" and the Department of Pediatrics and Neonato1ogy,h Department of Dermatology,C Department of Anatomo-Pathology,d and Department of Immunology-Allergy,C Le Centre Hospitalier de l'Universite Laval. Reprint requests: Aubert Lavoie, MD, Departement d'ImmunologieAllergie, Le Centre Hospitalier de l'Universite Laval, Local 1210, Suinte-Foy, Quebec, Canada G1V 4G2. Copyright © ]993 by the American Academy of Dermatology, Inc. 0190-9622/93 $1.00 +.10 16/4/49349
862
Severe combined immunodeficiency (SCID) represents a heterogeneous group of genetic disorders characterized by severe impairment of cellular and humoral immunity.l It is linked to the X chromosome in a high percentage of cases. 2, 3 There is also an autosomal recessive form; SCID may also be caused by a genetic deficiency in adenosine deaminase or purine-nucleoside phosphorylase. 4
der angiomas. The lesions of eruptive pseudoangiomatosis can be differentiated from telangiectases by the presence ofendothelial cells that protrude into the vessel lumen. In spider angiomas there are centrally located dilated arterioles with thin branches, without prominence of the endothelial lining. Clinically, eruptive pseudoangiomatosis must be differentiated from bacillary angiomatosis, bartonellosis, and pyogenic granuloma. In all three of these disorders the skin lesions are generally larger and last considerably longer than the 7- to IO-day duration that we observed in our patients. Spontaneous resolution does not occur. The occurrence of multiple pyogenic granulomas is relatively rare. 3 Histologically, eruptive pseudoangiomatosis shares with bacillary angiomatosis and bartonellosis the presence of a prominent endothelial lining. 4 However, eruptive pseudoangiomatosis shows no blood vessel proliferation, inflammatory infiltrate with neutrophils, or granular deposits that represent clustered bacilli. Pyogenic granuloma is characterized by a dome-shaped proliferation of small blood
Prose et al. vessels lined by oval endothelial cells. An epidermal collarette and a variable degree of mixed inflammatory infiltrate may be present. Although the data of Cherryet aLI implicated an enterovirus, the evidence linking the cutaneous lesions to a systemic viral infection in our patients was circumstantiaL It appears most likely that eruptive pseudoangiomatosis is a viral exanthem. However, it may be an unusual cutaneous reaction pattern to several different organisms.
REFERENCES 1. Cherry JD, Bobinski JE, Horvath FL, et al. Acute heman-
gioma-like lesions associated with ECHO viral infections. Pediatrics 1969;44:498-502. 2. Ghadially FN. Ultrastructural pathology of the cell. Stoneham, Mass.: Butterworth-Heinemann, 1975:424-8. 3. Dillman AM, Miller RC, Hansen RC. Multiple pyogenic granulomata in childhood. Pediatr DermatoI1991;8:28-31. 4. LeBoit PE, Berger TG, Egbert BM, et al. Bacillary angiomatosis: the histopathology and differential diagnosis of a pseudoneoplastic infection in patients with human immunodeficiency virus disease. Am J Surg Pathol 1989;13:90920.
Granuloma annulare perforans in herpes zoster scars Dieter Krahl, MD, Wolfgang Hartschuh, MD, and Wolfgang Tilgen, MD
Heidelberg, Germany Granuloma annulare perforans limited to a thoracic dermatome that was previously involved by herpes zoster occurred in a 51-year-old woman who also had Lennert's lymphoma. Of the various local granulomatous infiltrates described after herpes zoster, granuloma annulare perforans is unique, although ordinary granuloma annulare has been described in a few patients. A high incidence of specific and nonspecific reaction patterns in herpes zoster scars has been described in patients with malignant lymphoma. In contrast to previous patients, all of whom had chronic lymphatic leukemia, our patient had Lennert's lymphoma. (J AM ACAD DERMATOL 1993;29:859-62.) Several variants of granuloma annulare (GA) can be distinguished clinically and histopathologically, including the lichenoid, infiltrated, plaquelike, tu-
From the Universitals-Hautklinik, Ruprecht-Karls-University. Reprint requests: Dicter Krahl, MD, Universitats-Haulklinik, Vossslr. 2, D-6911S Heidelberg, Germany. Copyright ® 1993 by the American Academy of Dermatology, Inc. 0190.9622/93 $1.00 +.10 16/4/48998
berous, subcutaneous, and perforating types with limited, disseminated, or generalized distribution. 1 The chief histologic patterns are the palisading granuloma and the interstitial form. A rare epithelioid nodule type also occurs. Combinations of these patterns frequently occur within individual lesions and in the same patient. Perforating granuloma annulare (PGA) shows transepidermal elimination of degenerated collagen from the center of palisading granuloma type lesions.
859
860 Krahl et al.
Journal of the American Academy of Dermatology November 1993
Fig. 1. Granuloma annulare perforans in area of previous herpes zoster.
Fig. 3. Granuloma annulare with its transepidermal elimination site. (Hematoxylin-eosin stain; XIO.)
Fig. 2. Close-up of partly crusted, pseudopustular papules.
Fig. 4. Degenerated connective tissue in contact with epidermal undersurface. (Hematoxylin-eosin stain; X25.)
Herpes zoster may be followed locally by other skin diseases such as psoriasis, 2 morphea, 3 HIV-associated Kaposi's sarcoma, 4 and leukemic infiltrates. 5 ,6 Granulomatous reactions that can develop in herpes zoster scars are pseudolymphoma,7, 8 sarcoidal reaction,9, 10 and granuloma annulare. Granuloma annulare has been described in eight patients thus far. ll - 17 We describe for the first time a patient who had the perforating variant of GA after herpes zoster.
moderately severe neuralgia. No signs of severe necrosis or dissemination were found. She was known to have a lymphoepithelioid cellular lymphoma (Lennert's lymphoma) that was in remission after multiple courses of chemotherapy. The patient was treated with oral acyclovir and 1 month later the zoster had cleared, leaving superficial scars. Four months later new lesions appeared in the same region (Figs. I and 2). We observed numerous pseudopustular, yellow, 2 mm papules on an erythematous base that were limited to the right T 3 dermatome. The lesions were more closely aggregated in the dorsal region. Some of the papules were crateriform and crusted. This became more marked in subsequent weeks.
CASE REPORT A 5I -year-old woman had herpes zoster that was limited to her right T 3 dermatome and accompanied by
Journal of the American Academy of Dermatology Volume 29, Number 5, Part 2
A biopsy specimen revealed a necrobiotic focus in the papillary dermis that was in contact with an epidermal erosion covered by a scale crust. The degenerated collagen was surrounded by a radially arranged palisading granuloma that contained numerous histiocytic giant cells in addition to lymphocytes (Figs. 3 and 4). Mucin deposition and lack of elastic fibers were demonstrated in the necrobiotic focus by alcian blue and elastic tissue stains, respectively. Around the palisading granuloma interstitial histiocytic infiltration with mucin deposition could be seen. Results of immunohistochemical studies showed marking of cellular infiltrates, mostly for CD3 (pan-T), COlI, and CDw14 (monocytes). T lymphocytes were mostly of the CD4-positive subset. A diagnosis of PGA was made. Treatment with topical corticosteroids led to partial regression of the lesions, leaving slightly depressed scars.
DISCUSSION
The previously described cases of GA after herpes zoster have not been of the perforating variant. Some problems with differential diagnosis were initially raised in the case of our patient with PGA. The pseudopustular appearance of her papules was clinically suggestive of a herpes zoster relapse, which could have been a possible consequence of immunosuppression by the malignant lymphoma and chemotherapy. We also considered subcorneal pustular dermatosis of Sneddon-Wilkinson, 18 tuberculosis,19 and pustular psoriasis. 2 It was also necessary to exclude a cutaneous manifestation of her Lennert's lymphoma. Localization of malignant lymphomatous infiltrates in herpes zoster scars has been reported. 5, 6 However, each of these possibilities could be eliminated by the histologic and immunochemical findings. The perforating form of GA is classed among the perforating diseases. 20, 21 As a consequence of transepidermal elimination it is the only variant of GA that resolves with scarring. Perforation and transepidermal elimination appear to result from the superficial location of degenerated connective tissue. 22, 23 Furthermore, the epidermis in scars of herpes zoster is atrophic and may be "penetrated" more easily. In contrast to some other perforating disorders, for example, reactive perforating collagenosis or elastosis perforans serpiginosa, formation of hyperplasticlips of the adjacent epidermis or of an eliminating channel is not a regular feature of GAP.22,23 This finding corresponds to our own observations, but other authors 20,24 have reported more prominent reactions of the epidermis or even
Krahl et al. 861 transfo1licular elimination. 25 Perforation in GA appears to occur only in the palisading granulomatype tissue reaction with well-demarcated homogeneous degenerated material and not in the diffuse interstitial type. 20-24, 26 Serial sectioning is required for reliable identification of the transepidermal elimination site. 2o, 23, 26, 27 The occurrence of GA after a viral infection (varicella, herpes zoster, or warts 28 ) or immunization (tuberculin skin testing29 ) has been interpreted as a consequence of persisting antigenic material or tissue antigen alteration by microbes, which elicits a delayed (type IV) immune response. 11 In accordance with previous results 30 the immunohistochemical findings in our case demonstrated T lymphocytes, mostly T helper cells, as the predominating cell population. The predilection of GA and several other granulomatous reactions, as well as malignant lymphoma infiltrates, for areas previously involved by herpes zoster may be interpreted as Koebner's phenomenon. 6, 12,15 All patients with lymphoma who have either nonspecific or specific infiltrates in their zoster (or varicella 31 ) scars had chronic lymphatic leukemia. 5, 6, 8, 17,31 Our patient is the first with Lennert's lymphoma. REFERENCES 1. Kresbach H. Variationsbreite des Granuloma anulare. In: Braun-Falco 0, Schill WB, eds. Fortschritte der praktischen Dermatologie und Venerologie; vol II. Berlin: Springer, 1987:216-22. 2. Bohnstedt RM. Herpes zoster als isomorpher Reizeffekt bei Psoriasis. Z Haut Geschlechtskr 1957;22:202-6. 3. Zimmermann H. Zoster als Priimorbid einer zirkumskripten Sklerodermie. Dermatol Wochenschr 1964;150: 112-6. 4. Niedt GW, Prioleau PG. Kaposi's sarcoma occurring in a dermatome previously involved by herpes zoster. J AM ACAD DERMATOL 1988;18:448-51. 5. Aberer W, Zonzits E, Soyer HP, et a1. Postzosterische spezifische Hautinfiltrate bei chronischer Iyrnphatischer Leukiimie. Hautarzt 1990;41:455-7. 6. Raab W. Herpes zoster als isomorpher Reizeffekt bei chronisch lymphatischer Leukiimie. Arch Klin Exp DermatoI1984;218:215-21. 7. SanchezJL, Mendez lA, Palacio R. Cutaneous pseudolymphoma at the site of resolving herpes zoster. Arch DermatoI1981;117:377. 8. WolffHH, Wendt V, Winzer M. Cutaneous pseudolymphoma at the site of prior herpes zoster eruption. Arch Dermatol Res 1987;279:52-4. 9. Bisaccia E, Scarborough DA, Carr RD. Cutaneous sarcoid granuloma formation in herpes zoster scars. Arch DermatoI1983;119:788-9. 10. Wright AL, Cotton DWK, Winfield AD. Granuloma formation in herpes zoster scars. Dermatologica 1989;179: 45-6.
Krahl et al. 11. Friedman S, Fox B, Albert H. Granuloma anulare arising in herpes zoster scars. J AMAcADDERMATOL 1986;14:76470. 12. Guill MA, Goette DK. Granuloma annulare at sites of healing herpes zoster. Arch DermatoI1978;1l:1383. 13. Hayakawa K, Mizukawa Y, Shiohara T, et al. Granuloma annulare arising after herpes zoster [Letter]. Int J DermatoI1992;31:745-6. 14. Kleber R, Landthaler M, Burg G. Postzosterisches Granuloma anulare. Hautarzt 1989;40:110-11. 15. Packer RH, Fie1dsJP, King LE Jr. Granuloma annulare in herpes zoster scars. Cutis 1984;34:177-9. 16. Shideler SJ, Richards M. Granuloma annulare arising after herpes zoster [Letter]. JAM ACAD DERMATOL 1986; 15:1049-50. 17. Zanolli MD, Powell BC, McCalmont T, et al. Granuloma annulare and disseminated herpes zoster. Int J Oermatol 1992;31 :55-7. 18. Kohl PK, Hartschuh W, Tilgen W, et al. Pyoderma gangrenosum followed by subcorneal pustular dermatosis in a patient with IgA paraproteinemia. J AM ACAD DERMATOL 1991 ;24:325-8. 19. Civatte P. Les formes tuberculo-ulcereuses et tuberculogommeuses du granuloma annulaire. Ann Dermatol Syphiligr 1952;79:387-97. 20. Duncan WC, Smith JD, Knox JM. Generalized perforating granuloma annulare. Arch OermatoI1973;108:570-2.
Journal of the American Academy of Dermatology November 1993
21. Levi L, Sala G, Galbiati G. Granuloma anulare perforans: zwei klinisch verschiedenartige Verlaufsformen. Hautarzt 1986;37:23-7. 22. Delaney T J, Gold SC, Leppard B. Disseminated perforating granuloma annulare. Br J Dermatol 1973;89:523-6. 23. Owens OW, Freeman RG. Perforating granuloma annulare. Arch Dermatol 1971 ;103:64-7. 24. Gattlen JM, Delacretaz J. Le granulome annulaire perforant. Dermatologica 1975;151:368-75. 25. Bardach RG. Granuloma annulare with transfollicular perforation. J Cutan Pathol 1977;4:99-104. 26. Izumi AK. Generalized perforating granuloma annulare. Arch Dermatol 1973;108:708-9. 27. Samlaska CP, Sandberg GD, Maggio KL, et al. Generalized perforating granuloma annulare. J AM ACAD DERMATOL 1992;27:319-22. 28. Ward WHo Warts and granuloma anulare. Br Med J 1956;2:1484-6. 29. Beer WE, Jares EW. Granuloma anulare following tuberculin heaf tests. Trans St Johns Hosp Dermatol Soc 1966;52:68-70. 30. Buechner SA, Winkelmann RK, Banks PM. Identification of T-cell subpopulations in granuloma anulare. Arch DermatoI1983;119:125-8. 31. Fischer G, Jaworski R. Granuloma formation in herpes zoster scars [Letter]. J AM ACAD DERMATOL 1987;16: 1261-3.
In utero acute graft-versus-host disease in a neonate with severe combined immunodeficiency Guylaine Alain, MD,a Charles Carrier, MD,b Louis Beaumier, MD,b Jean Bernard, MD,c Martin Lemay, MD,d and Aubert Lavoie, MD e Montreal and Sainte-Fay, Quebec, Canada We describe a male neonate with severe combined immunodeficiency who at birth had acute graft-versus-host disease (GVHD) as a result of maternal-fetal transfusion during pregnancy. Several clinical signs helped establish this diagnosis. Findings of a skin biopsy specimen confirmed the diagnosis of acute GVHD. Immunologic evaluation disclosed an absence ofT and B lymphocytes. Acute GVHD in severe combined immunodeficiency most often occurs during the first weeks of life; intrauterine occurrence is unusual. (J AM ACAD DERMATOL 1993;29:862-5.)
From the Universite de Montreal" and the Department of Pediatrics and Neonato1ogy,h Department of Dermatology,C Department of Anatomo-Pathology,d and Department of Immunology-Allergy,C Le Centre Hospitalier de l'Universite Laval. Reprint requests: Aubert Lavoie, MD, Departement d'ImmunologieAllergie, Le Centre Hospitalier de l'Universite Laval, Local 1210, Suinte-Foy, Quebec, Canada G1V 4G2. Copyright © ]993 by the American Academy of Dermatology, Inc. 0190-9622/93 $1.00 +.10 16/4/49349
862
Severe combined immunodeficiency (SCID) represents a heterogeneous group of genetic disorders characterized by severe impairment of cellular and humoral immunity.l It is linked to the X chromosome in a high percentage of cases. 2, 3 There is also an autosomal recessive form; SCID may also be caused by a genetic deficiency in adenosine deaminase or purine-nucleoside phosphorylase. 4