- Email: [email protected]
Pityrosporum folliculitis during pregnancy is not pruritic folliculitis of pregnancy
1098 Letters
J AM ACAD DERMATOL DECEMBER 2005
any lesion with epidermal hyperplasia and decreased barrier function will show increased expression of VEGF. Beer further states that keloid tissue is hypoxic based on a 1982 article by Kischer.4 While keloids may be hypoxic, modern methods of tissue hypoxia have not been applied to keloids. Similarly, we have seen no evidence of microvascular occlusion in keloids, and in our experience, microvascular occlusion is always associated with distal infarction. It is difficult to propose a theory of ‘‘critical hypoxia,’’ given that fibroblasts are highly resistant to hypoxia, and that the theory of critical hypoxia has not been conclusively demonstrated for any disease state. I thus stand by our conclusion that keloids are vascular lesions, and thus amenable to antiangiogenic therapy. Jack L. Arbiser, MD, PhD Department of Dermatology Emory University School of Medicine Atlanta, Georgia REFERENCES 1. Gira AK, Brown LF, Washington CV, Cohen C, Arbiser JL. Keloids demonstrate high-level epidermal expression of vascular endothelial growth factor. J Am Acad Dermatol 2004;50:850-3. 2. Detmar M, Brown LF, Claffey KP, Yeo KT, Kocher O, Jackman RW, et al. Overexpression of vascular permeability factor/vascular endothelial growth factor and its receptors in psoriasis. J Exp Med 1994;180:1141-6. 3. Beer TW, Baldwin HC, Goddard JR, Gallagher PJ, Wright DH. Angiogenesis in pathological and surgical scars. Hum Pathol 1998;29:1273-8. 4. Kischer CW, Thies AC, Chvapil M. Perivascular myofibroblasts and micro-vascular occlusion in hypertrophic scars and keloids. Hum Pathol 1982;13:819-24. doi:10.1016/j.jaad.2005.03.019
Pityrosporum folliculitis during pregnancy is not pruritic folliculitis of pregnancy To the Editor: I read with interest the letter of Parlak et al1 in the March issue of the Journal reporting a rare case of Pityrosporum folliculitis (PF) during pregnancy. I believe that the authors’ speculation that Pityrosporum can be a cause of pruritic folliculitis of pregnancy (PFP) is not sufficiently supported by the literature and I would like to add my experience with PFP. The clinical presentation of PF differs from that of PFP. PF is a chronic, usually florid, acneiform, pruritic eruption that rarely clears spontaneously and is extremely uncommon in pregnancy (one case reported). On the contrary, PFP, which is considered by most authors a specific dermatosis of pregnancy, presents with sparse, mild, occasionally acneiform,
minimally pruritic lesions that resolve spontaneously at delivery or postpartum (approximately 30 cases reported). The authors’ claim that their case can still be PFP although it did not clear spontaneously because of the hot weather can be challenged by the fact that PFP is not known to show seasonal variation.2 With regard to treatment, a significant number of PFP cases improved with benzoyl peroxide 10%,3,4 topical steroids,4 or both, but not with ketoconazole 2% cream,4 which makes it unlikely that they could have been caused by Pityrosporum. The authors should note that cultures that were taken from pustules were negative for fungi in all PFP cases but are usually positive in PF. Furthermore, a periodic acid—Schiff (PAS) stain was consistently negative in PFP in contrast to the case of Parlak et al.1 The assumption of the authors that Pityrosporum yeasts might have been overlooked in all reported cases of PFP because serial sections were not performed can be disputed by the fact that Pityrosporum spores are readily apparent and stand out vividly on PAS-stained sections. Most dermatopathologists do not need more than two levels to identify the spores, even in hematoxylin-eosin sections. In 3 cases of PFP that I have seen, PAS-stained sections were negative (in 2/3 of cases two levels on PAS stain were examined). In addition, it is unlikely that Pityrosporum could have been missed in the original report of PFP by Zoberman and Farmer5 (6 patients) in which serial sections with hematoxylin-eosin were performed. Finally, no association with Pityrosporum species was reported in the largest series of patients with PFP.6 Detection of big loads of Pityrosporum spores in deeper parts of the hair follicle and free in the dermis, typically seen in PF, has not been reported in PFP, which is believed to be a nonmicrobial folliculitis. It has been suggested4 that PFP may be a type of steroid acne secondary to the profound hormonal changes of pregnancy. Along the same lines Parlak et al1 mention that steroid acne has shown large numbers of Pityrosporum ovale7 and attempt to find similarities between steroid acne and PF, postulating that PF and PFP could be the same entity. Nevertheless, detection of Pityrosporum yeasts was never reported in steroid acne or other acneiform eruptions during gestation. Should high levels of sex hormones during gestation favor overgrowth of Pityrosporum, then detection of Pityrosporum in biopsy specimens taken from pregnant women would be more common and cases of florid PF, such as the present, not so uncommon. Furthermore, a comedonal component, typically seen in steroid acne, is absent in both PF and PFP. Finally, even if PFP were a Pityrosporum-associated type of steroid acne, it would be debatable whether detection of
Letters 1099
J AM ACAD DERMATOL VOLUME 53, NUMBER 6
Pityrosporum (yeast overgrowth) is a primary or secondary event as several authors consider follicular occlusion to be the primary event in acneiform eruptions, including steroid acne. Based on the above one can not conclude that Pityrosporum is a possible cause of PFP. It would be of great interest to the reader if Parlak et al1 could look for Pityrosporum yeasts in a series of PFP cases that cleared spontaneously and provide us with additional data. George Kroumpouzos, MD, PhD Dermatology Clinic South Shore Medical Center Norwell, Massachusetts Department of Medicine South Shore Hospital South Weymouth, Massachusetts Reprint requests: George Kroumpouzos, MD, PhD 9 Hawthorne Pl, Suite 6D Boston, MA 02114 E-mail: [email protected] REFERENCES 1. Parlak AH, Boran C, Topc¸uoglu MA. Pityrosporum folliculitis during pregnancy: a possible cause of pruritic folliculitis of pregnancy. J Am Acad Dermatol 2005;52:528-9. 2. Kroumpouzos G, Cohen LM. Pruritic folliculitis of pregnancy. J Am Acad Dermatol 2000;43:132-4. 3. Wilkinson SM, Buckler H, Wilkinson N, O’Driscoll J, Roberts MM. Androgen levels in pruritic folliculitis of pregnancy. Clin Exp Dermatol 1995;20:234-6. 4. Holmes RC, Black MM. The specific dermatoses of pregnancy. J Am Acad Dermatol 1983;8:405-12. 5. Zoberman E, Farmer ER. Pruritic folliculitis of pregnancy. Arch Dermatol 1981;117:20-2. 6. Vaughan Jones SA, Hern S, Nelson-Piercy C, Seed PT, Black MM. A prospective study of 200 women with dermatoses of pregnancy correlating clinical findings with hormonal and immunopathological profiles. Br J Dermatol 1999;141:71-81. 7. Yu HJ, Lee SK, Son SJ, Kim YS, Yang HY, Kim JH. Steroid acne vs Pityrosporum folliculitis: the incidence of Pityrosporum ovale and the effect of antifungal drugs in steroid acne. Int J Dermatol 1998;37:772-7. doi:10.1016/j.jaad.2005.06.046
Light’s role in immunomodulation and medical therapy To the Editor: I read with interest the article by Gambichler et al1 in the April 2005 issue of the Journal. The authors review the use of narrowband UVB in skin conditions besides psoriasis. As expected, they expound on the negative biologic effects of light including photoaging, increased risk of skin cancer, and immunosuppression, yet discuss the virtues of narrowband UVB, despite the recent
finding of increased risk of basal cell carcinoma with this therapy.2 As with all things in life, the sun has both positive and negative effects. Certainly as dermatologists we have focused on the UV-induced DNA damage to keratinocytes. Moreover, we have preached total avoidance of light with photoprotective clothing, broad-brimmed hats, and sunscreens (although they have been proven to occasionally have estrogenic effects and be chemically unstable).3 However, we might be overlooking the psychologic and other medical effects of sunlight on other body cells and function. For example, with another skin cell, the melanocyte, light may induce the secretion of a wide range of signal molecules, including cytokines, melanocortin peptides, catecholamines, serotonin, and nitric oxide.4 These secretory products in turn affect keratinocytes, lymphocytes, fibroblasts, mast cells, and endothelial cells, all of which have receptors for these signal molecules. Thus, by means of melanocytes, the sun regulates the function of epidermal cells and maintains skin homeostasis. These beneficial aspects of melanocytes are contributing factors in the actions of phototherapy in the treatment of various skin disorders such as psoriasis, eczema, acne, and vitiligo. In short, the function of melanocytes in antimicrobial defense, immunomodulation, and links with the central nervous system has been somewhat ignored.4 Indeed, an appreciation of the sun’s role in melanocyte immunomodulation might explain the recent reports that high UV exposure reduces patients’ risks of developing Hodgkin’s lymphoma and non-Hodgkin’s lymphoma and increases survival from melanoma.5 More basic research into the light-induced cellular reactions, such as immunomodulation effects of melanocytes, is warranted. I query whether Gambichler et al1 and other leading dermatology colleagues might take a more moderate stance by recommending at least a minimal amount of light exposure to be in consort with optimal physical and mental health with respect to other organs, body function, and various medical disease states. Craig G. Burkhart, MD, MPH Medical University of Ohio at Toledo College of Osteopathic Medicine at Ohio University Reprint requests: Craig G. Burkhart, MD, MPH Medical University of Ohio at Toledo 5600 Monroe St, Suite 106B Sylvania, OH 43560 E-mail: [email protected]
J AM ACAD DERMATOL DECEMBER 2005
any lesion with epidermal hyperplasia and decreased barrier function will show increased expression of VEGF. Beer further states that keloid tissue is hypoxic based on a 1982 article by Kischer.4 While keloids may be hypoxic, modern methods of tissue hypoxia have not been applied to keloids. Similarly, we have seen no evidence of microvascular occlusion in keloids, and in our experience, microvascular occlusion is always associated with distal infarction. It is difficult to propose a theory of ‘‘critical hypoxia,’’ given that fibroblasts are highly resistant to hypoxia, and that the theory of critical hypoxia has not been conclusively demonstrated for any disease state. I thus stand by our conclusion that keloids are vascular lesions, and thus amenable to antiangiogenic therapy. Jack L. Arbiser, MD, PhD Department of Dermatology Emory University School of Medicine Atlanta, Georgia REFERENCES 1. Gira AK, Brown LF, Washington CV, Cohen C, Arbiser JL. Keloids demonstrate high-level epidermal expression of vascular endothelial growth factor. J Am Acad Dermatol 2004;50:850-3. 2. Detmar M, Brown LF, Claffey KP, Yeo KT, Kocher O, Jackman RW, et al. Overexpression of vascular permeability factor/vascular endothelial growth factor and its receptors in psoriasis. J Exp Med 1994;180:1141-6. 3. Beer TW, Baldwin HC, Goddard JR, Gallagher PJ, Wright DH. Angiogenesis in pathological and surgical scars. Hum Pathol 1998;29:1273-8. 4. Kischer CW, Thies AC, Chvapil M. Perivascular myofibroblasts and micro-vascular occlusion in hypertrophic scars and keloids. Hum Pathol 1982;13:819-24. doi:10.1016/j.jaad.2005.03.019
Pityrosporum folliculitis during pregnancy is not pruritic folliculitis of pregnancy To the Editor: I read with interest the letter of Parlak et al1 in the March issue of the Journal reporting a rare case of Pityrosporum folliculitis (PF) during pregnancy. I believe that the authors’ speculation that Pityrosporum can be a cause of pruritic folliculitis of pregnancy (PFP) is not sufficiently supported by the literature and I would like to add my experience with PFP. The clinical presentation of PF differs from that of PFP. PF is a chronic, usually florid, acneiform, pruritic eruption that rarely clears spontaneously and is extremely uncommon in pregnancy (one case reported). On the contrary, PFP, which is considered by most authors a specific dermatosis of pregnancy, presents with sparse, mild, occasionally acneiform,
minimally pruritic lesions that resolve spontaneously at delivery or postpartum (approximately 30 cases reported). The authors’ claim that their case can still be PFP although it did not clear spontaneously because of the hot weather can be challenged by the fact that PFP is not known to show seasonal variation.2 With regard to treatment, a significant number of PFP cases improved with benzoyl peroxide 10%,3,4 topical steroids,4 or both, but not with ketoconazole 2% cream,4 which makes it unlikely that they could have been caused by Pityrosporum. The authors should note that cultures that were taken from pustules were negative for fungi in all PFP cases but are usually positive in PF. Furthermore, a periodic acid—Schiff (PAS) stain was consistently negative in PFP in contrast to the case of Parlak et al.1 The assumption of the authors that Pityrosporum yeasts might have been overlooked in all reported cases of PFP because serial sections were not performed can be disputed by the fact that Pityrosporum spores are readily apparent and stand out vividly on PAS-stained sections. Most dermatopathologists do not need more than two levels to identify the spores, even in hematoxylin-eosin sections. In 3 cases of PFP that I have seen, PAS-stained sections were negative (in 2/3 of cases two levels on PAS stain were examined). In addition, it is unlikely that Pityrosporum could have been missed in the original report of PFP by Zoberman and Farmer5 (6 patients) in which serial sections with hematoxylin-eosin were performed. Finally, no association with Pityrosporum species was reported in the largest series of patients with PFP.6 Detection of big loads of Pityrosporum spores in deeper parts of the hair follicle and free in the dermis, typically seen in PF, has not been reported in PFP, which is believed to be a nonmicrobial folliculitis. It has been suggested4 that PFP may be a type of steroid acne secondary to the profound hormonal changes of pregnancy. Along the same lines Parlak et al1 mention that steroid acne has shown large numbers of Pityrosporum ovale7 and attempt to find similarities between steroid acne and PF, postulating that PF and PFP could be the same entity. Nevertheless, detection of Pityrosporum yeasts was never reported in steroid acne or other acneiform eruptions during gestation. Should high levels of sex hormones during gestation favor overgrowth of Pityrosporum, then detection of Pityrosporum in biopsy specimens taken from pregnant women would be more common and cases of florid PF, such as the present, not so uncommon. Furthermore, a comedonal component, typically seen in steroid acne, is absent in both PF and PFP. Finally, even if PFP were a Pityrosporum-associated type of steroid acne, it would be debatable whether detection of
Letters 1099
J AM ACAD DERMATOL VOLUME 53, NUMBER 6
Pityrosporum (yeast overgrowth) is a primary or secondary event as several authors consider follicular occlusion to be the primary event in acneiform eruptions, including steroid acne. Based on the above one can not conclude that Pityrosporum is a possible cause of PFP. It would be of great interest to the reader if Parlak et al1 could look for Pityrosporum yeasts in a series of PFP cases that cleared spontaneously and provide us with additional data. George Kroumpouzos, MD, PhD Dermatology Clinic South Shore Medical Center Norwell, Massachusetts Department of Medicine South Shore Hospital South Weymouth, Massachusetts Reprint requests: George Kroumpouzos, MD, PhD 9 Hawthorne Pl, Suite 6D Boston, MA 02114 E-mail: [email protected] REFERENCES 1. Parlak AH, Boran C, Topc¸uoglu MA. Pityrosporum folliculitis during pregnancy: a possible cause of pruritic folliculitis of pregnancy. J Am Acad Dermatol 2005;52:528-9. 2. Kroumpouzos G, Cohen LM. Pruritic folliculitis of pregnancy. J Am Acad Dermatol 2000;43:132-4. 3. Wilkinson SM, Buckler H, Wilkinson N, O’Driscoll J, Roberts MM. Androgen levels in pruritic folliculitis of pregnancy. Clin Exp Dermatol 1995;20:234-6. 4. Holmes RC, Black MM. The specific dermatoses of pregnancy. J Am Acad Dermatol 1983;8:405-12. 5. Zoberman E, Farmer ER. Pruritic folliculitis of pregnancy. Arch Dermatol 1981;117:20-2. 6. Vaughan Jones SA, Hern S, Nelson-Piercy C, Seed PT, Black MM. A prospective study of 200 women with dermatoses of pregnancy correlating clinical findings with hormonal and immunopathological profiles. Br J Dermatol 1999;141:71-81. 7. Yu HJ, Lee SK, Son SJ, Kim YS, Yang HY, Kim JH. Steroid acne vs Pityrosporum folliculitis: the incidence of Pityrosporum ovale and the effect of antifungal drugs in steroid acne. Int J Dermatol 1998;37:772-7. doi:10.1016/j.jaad.2005.06.046
Light’s role in immunomodulation and medical therapy To the Editor: I read with interest the article by Gambichler et al1 in the April 2005 issue of the Journal. The authors review the use of narrowband UVB in skin conditions besides psoriasis. As expected, they expound on the negative biologic effects of light including photoaging, increased risk of skin cancer, and immunosuppression, yet discuss the virtues of narrowband UVB, despite the recent
finding of increased risk of basal cell carcinoma with this therapy.2 As with all things in life, the sun has both positive and negative effects. Certainly as dermatologists we have focused on the UV-induced DNA damage to keratinocytes. Moreover, we have preached total avoidance of light with photoprotective clothing, broad-brimmed hats, and sunscreens (although they have been proven to occasionally have estrogenic effects and be chemically unstable).3 However, we might be overlooking the psychologic and other medical effects of sunlight on other body cells and function. For example, with another skin cell, the melanocyte, light may induce the secretion of a wide range of signal molecules, including cytokines, melanocortin peptides, catecholamines, serotonin, and nitric oxide.4 These secretory products in turn affect keratinocytes, lymphocytes, fibroblasts, mast cells, and endothelial cells, all of which have receptors for these signal molecules. Thus, by means of melanocytes, the sun regulates the function of epidermal cells and maintains skin homeostasis. These beneficial aspects of melanocytes are contributing factors in the actions of phototherapy in the treatment of various skin disorders such as psoriasis, eczema, acne, and vitiligo. In short, the function of melanocytes in antimicrobial defense, immunomodulation, and links with the central nervous system has been somewhat ignored.4 Indeed, an appreciation of the sun’s role in melanocyte immunomodulation might explain the recent reports that high UV exposure reduces patients’ risks of developing Hodgkin’s lymphoma and non-Hodgkin’s lymphoma and increases survival from melanoma.5 More basic research into the light-induced cellular reactions, such as immunomodulation effects of melanocytes, is warranted. I query whether Gambichler et al1 and other leading dermatology colleagues might take a more moderate stance by recommending at least a minimal amount of light exposure to be in consort with optimal physical and mental health with respect to other organs, body function, and various medical disease states. Craig G. Burkhart, MD, MPH Medical University of Ohio at Toledo College of Osteopathic Medicine at Ohio University Reprint requests: Craig G. Burkhart, MD, MPH Medical University of Ohio at Toledo 5600 Monroe St, Suite 106B Sylvania, OH 43560 E-mail: [email protected]