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Palmoplantar pustular lesions in mycosis fungoides
Volume 25 Number 4 October 1991
Corresponde~e
733
REFERENCES
his works in which he has not bothered. to mention him-
1. Bandmann HJ, Dohn W. Epicutantestung. Munchen: Bergamnn Verlag, 1967. 2. Machackova J, et ai. Epikutanni.testy: expozice alergemi 24 a 48 bodin. Srovmivaci studie. Cs Dermatol (In press.) 3. Kalimo K, Lammintausta K. 24 and 48 hour allergen exposure in patch testing. Comparative study with 11 common contact allergens and NiCli. Contact Dermatitis 1984; 10;25-9.
self.
There is much evidence in John Hunter's own writings to prove that he repeatedly and deliberately inoculated patients with venereal matter. There is good reason to as~ sume, therefore, that Hunter performed the crucial experiment on some person other than himself. E. S. Benjamin, MD Cape Town. South Africa
Dermatology and the history of ideas To the Editor: In the August 1990 issue of the JOURNAL (1990;23:311-5) John Wolf in his commentary states: " ... ill-fated self-experimentation of John Hunter ... he inoculated his penis with pus from a patient suffering from gonorrhea ... he died of syphilitic heart disease in 1793." (p. 314)
However, a contrary view was expressed by Qvist1: "There is no evidence to show that John Hunter ever suffered from venereal disease and there are good reasons to believe that this inoculation experiment was performed not on himself but on some other individual." The allegations that John Hunter suffered from venereal disease and that he inoculated himself with the disease can be refuted by consideration of his autopsy findings, the clinical features of his illness, and Hunter's own description of the inoculation experiment. John Hunter's autopsy was performed. by Everard Home and showed. advanced generalized atherosclerosis with calcified coronary arteries and ossified carotid and vertebral arteries. Prof. J. L. Turk states that in his opinion "there is no evidence in the autopsy report ofany pathological changes that might have been caused by syphilis and that there is no doubt that Hunter died as a result of coronary artery disease of atheromatous origin."l (p. 46) The clinical features of John Hunter's illness were myocardial and cerebral ischemia. In Everard Home's opinion John Hunter suffered from angina for the last 20 years of his life. The inoculation experiment is recorded in detail in his famous treatise but a careful study of this workshows that the actual subject of the experiment is never identified. Experiments made to ascertain the Progress and Ef· fects of the Veneral Poison: "... Two punctures were made on the penis with a lancet dipped in venereal matter from a gonorrhoea... " Hunter did not state that he inoculated himself. He simply stated that two punctures were made. The complete absence of the first person in the description of the experiment is striking and important because Hunter's works abound in the use of the personal pronoun. There are few pages in all his works in which he has not used it. Nearly all his observations were personal. Itis remarkable that this experiment, supposed by so many to have been performed on himself, should be just the one section in aU
REFERENCE 1. Qvist G. John Hunter 1728-1793. London: William Heinemann, 1981:43, 45-50.
Palmoplantar pustular lesions in mycosis fungoides To the Editor: We have read with interest the briefcommunication by Moreno et at, "Palmoplantar Pustulosis as a Manifestation of Cutaneous T Cell Lymphoma (MycosisFungoides)" (JAM ACADDBRMATOL 1990;23:7589). The authors reported. a case of mycosis fungoides (MF) with palmoplantar pustular lesions; the biopsy specimen revealed the characteristic histopathologic features of MF. They mentioned that there was no prior report of pustular cases of MF showing involvement of palms and soles. However, we have previously reported similar pustular lesions in a 4S-year-old Japanese man. l Our patient was unique in that there was a monoclonal neoplastic proliferation of CDS T cells instead of CD4 T cells that are commonly found in MF. Moreover, the MF in our case was aggressive like other reported cases of the suppressor T cell type of MF2 ; it showed a fulminant clinical course including the involvement of the central nervous system after the development of the palmar pustular lesions. Therefore of interest to us in relation to the unique paImoplantar pustular lesions of MF is the T cell subset of the neoplastic cells in the case of Moreno et ai. as well as the detail of the later clinical course; it was simply stated that the patient died 3 months later of Pseudomonas aeruginosa sepsis, a unusual infection that occurs mostly in patients with debilitated clinical conditions. Hachiro Tagami, MD Setsuya Aiba, MD Kyoko Ohkouchi. MD Department ofDermatology, Tohoku University School ofMedicine, Sendai, Japan
REFERENCES 1. Ohkouchi K, Aiba S, Tagami H. OKT8-reactive cell mycosis fungoides. Arch DermatoI 1986;122:20-3.
Journal of the American Academy of Dermatology
734 Correspondence 2. Buechiner SA, Winkelmann RK, Banks PM. T cells and Tcell subsets in mycosis fungoides and parapsoriasis. Arch Dermatol 1984;120:897-905.
The pathogenesis of Sweet's syndrome To the Editor: Wakefield et al. are to be commended for their excellent review ofcolony-stimulating factors (J AM ACAD DERMATOL 1990;23:903-12). In their discussion of both adverse effects and colony-stimulating factors in dermatology, they refer to the development of Sweet's syndrome in a patient with hairy cell leukemia treated with granulocytecolony-stirnulating factor (G-CSF).1 As mentioned by the authors, the diagnosis of Sweet's syndrome in this patient had not been confirmed by a Iesional skin biopsy; we have previously addressed this issue and contest the diagnosis of Sweet's syndrome in this patient. 2 Actually, the case report reveals that the patient had a skin biopsy-proven leukocytoclastic vasculitis before receiving G-CSF and had enlargement of existing lesions and similar-appearing new lesions after receiving G-CSF therapy. I Cutaneous leukocytoclastic vasculitis has been observed in several patients with hairy cell leukemia. 3 Hence, treatment of the patient of Glaspy et a1. 1 with G-CSF probably exacerbated her underlying hairy cell leukemia-related leukocytoclastic vasculitis; therefore, on the basis of the available information, her skin lesions did ~ot represent either malignancy-associated Sweet's syn4rpme or G-CSF-induced Sweet's syndrome. Colony-stimulating factors may participate, directly or indirectly, in the origin ofseveral dermatologic conditions.
We have previously suggested the possibility that the pathogenesis ofSweet's syndrome may be secondary to an inappropriate secretion of one or more of the endogenous cytokines. 4 GoingS has also postulated that a cytokine may contribute to the etiology of Sweet's syndrome. The pathophysiologic response to,some of these proteins (such as G-CSF and interleukin 1 or epidermal cell thymocyteactivating factor) would account for the clinicopathologic changes observed in this condition: fever, leukocytosis, and neutrophilic dermal infiltrate. This intriguing hypothesis remains to be confirmed.
Philip R. Cohen, MD, q and Razelle Kurzrock, MD,b Department of Dermatology, The University of Texas Medical School at Houston,c' and Department of Clinical Immunology and Biological Therapy, M. D. Anderson Cancer Center,b Houston, Texas b REFERENCES 1. Glaspy JA, Baldwin Ge, Robertson PA, et al. Therapy for neutropenia in hairy cell leukemia with recombinant human granulocyte colony-stimulating factor. Ann Intern Med 1988;109:789-95. 2. Cohen PR, Kurzrock R. Diagnosing the Sweet syndrome [Letter]. Ann InternMed 1989;110:573-4. 3. Spann CR, Callen JP, Yam LT, et al. Cutaneous leukocytoclastic vasculitis complicating hairy cell leukemia (leukemic reticuloendotheliosis). Arch Dermatol1986;122:1057-9. 4. Cohen PR, Talpaz M, Kurzrock R. Malignancy-associated Sweet's syndrome: review of the world literature. J Clin Oncoll988;6:1887-97. 5. Going J1. Is the pathogenesis of Sweet's syndrome mediated by interleukin I? [Letter] Br J Dermato11987;116:282-3.
BOUND VOLUMES AVAILABLE TO SUBSCRIBERS Bound volumes of the JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY are available to subscribers (only) for the 1991 issues from the Publisher at a cost of $60.00 for domestic, $82.20 for Canadian, and $78.00 for international for volume 24 (January-June) and volume 25 (July-December). Shipping charges are included. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 60 days after publication of the last issue in the volume. The binding is durable buckram with the journal name, volume number, and year stamped in gold on the spine. Payment must accompany all orders. Contact Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318. USA: phone (800) 325-4177, ext. 4351.
Subscriptions must be in force to qualify. Bound volumes are /lot available in place of a regular journal subscription.
Corresponde~e
733
REFERENCES
his works in which he has not bothered. to mention him-
1. Bandmann HJ, Dohn W. Epicutantestung. Munchen: Bergamnn Verlag, 1967. 2. Machackova J, et ai. Epikutanni.testy: expozice alergemi 24 a 48 bodin. Srovmivaci studie. Cs Dermatol (In press.) 3. Kalimo K, Lammintausta K. 24 and 48 hour allergen exposure in patch testing. Comparative study with 11 common contact allergens and NiCli. Contact Dermatitis 1984; 10;25-9.
self.
There is much evidence in John Hunter's own writings to prove that he repeatedly and deliberately inoculated patients with venereal matter. There is good reason to as~ sume, therefore, that Hunter performed the crucial experiment on some person other than himself. E. S. Benjamin, MD Cape Town. South Africa
Dermatology and the history of ideas To the Editor: In the August 1990 issue of the JOURNAL (1990;23:311-5) John Wolf in his commentary states: " ... ill-fated self-experimentation of John Hunter ... he inoculated his penis with pus from a patient suffering from gonorrhea ... he died of syphilitic heart disease in 1793." (p. 314)
However, a contrary view was expressed by Qvist1: "There is no evidence to show that John Hunter ever suffered from venereal disease and there are good reasons to believe that this inoculation experiment was performed not on himself but on some other individual." The allegations that John Hunter suffered from venereal disease and that he inoculated himself with the disease can be refuted by consideration of his autopsy findings, the clinical features of his illness, and Hunter's own description of the inoculation experiment. John Hunter's autopsy was performed. by Everard Home and showed. advanced generalized atherosclerosis with calcified coronary arteries and ossified carotid and vertebral arteries. Prof. J. L. Turk states that in his opinion "there is no evidence in the autopsy report ofany pathological changes that might have been caused by syphilis and that there is no doubt that Hunter died as a result of coronary artery disease of atheromatous origin."l (p. 46) The clinical features of John Hunter's illness were myocardial and cerebral ischemia. In Everard Home's opinion John Hunter suffered from angina for the last 20 years of his life. The inoculation experiment is recorded in detail in his famous treatise but a careful study of this workshows that the actual subject of the experiment is never identified. Experiments made to ascertain the Progress and Ef· fects of the Veneral Poison: "... Two punctures were made on the penis with a lancet dipped in venereal matter from a gonorrhoea... " Hunter did not state that he inoculated himself. He simply stated that two punctures were made. The complete absence of the first person in the description of the experiment is striking and important because Hunter's works abound in the use of the personal pronoun. There are few pages in all his works in which he has not used it. Nearly all his observations were personal. Itis remarkable that this experiment, supposed by so many to have been performed on himself, should be just the one section in aU
REFERENCE 1. Qvist G. John Hunter 1728-1793. London: William Heinemann, 1981:43, 45-50.
Palmoplantar pustular lesions in mycosis fungoides To the Editor: We have read with interest the briefcommunication by Moreno et at, "Palmoplantar Pustulosis as a Manifestation of Cutaneous T Cell Lymphoma (MycosisFungoides)" (JAM ACADDBRMATOL 1990;23:7589). The authors reported. a case of mycosis fungoides (MF) with palmoplantar pustular lesions; the biopsy specimen revealed the characteristic histopathologic features of MF. They mentioned that there was no prior report of pustular cases of MF showing involvement of palms and soles. However, we have previously reported similar pustular lesions in a 4S-year-old Japanese man. l Our patient was unique in that there was a monoclonal neoplastic proliferation of CDS T cells instead of CD4 T cells that are commonly found in MF. Moreover, the MF in our case was aggressive like other reported cases of the suppressor T cell type of MF2 ; it showed a fulminant clinical course including the involvement of the central nervous system after the development of the palmar pustular lesions. Therefore of interest to us in relation to the unique paImoplantar pustular lesions of MF is the T cell subset of the neoplastic cells in the case of Moreno et ai. as well as the detail of the later clinical course; it was simply stated that the patient died 3 months later of Pseudomonas aeruginosa sepsis, a unusual infection that occurs mostly in patients with debilitated clinical conditions. Hachiro Tagami, MD Setsuya Aiba, MD Kyoko Ohkouchi. MD Department ofDermatology, Tohoku University School ofMedicine, Sendai, Japan
REFERENCES 1. Ohkouchi K, Aiba S, Tagami H. OKT8-reactive cell mycosis fungoides. Arch DermatoI 1986;122:20-3.
Journal of the American Academy of Dermatology
734 Correspondence 2. Buechiner SA, Winkelmann RK, Banks PM. T cells and Tcell subsets in mycosis fungoides and parapsoriasis. Arch Dermatol 1984;120:897-905.
The pathogenesis of Sweet's syndrome To the Editor: Wakefield et al. are to be commended for their excellent review ofcolony-stimulating factors (J AM ACAD DERMATOL 1990;23:903-12). In their discussion of both adverse effects and colony-stimulating factors in dermatology, they refer to the development of Sweet's syndrome in a patient with hairy cell leukemia treated with granulocytecolony-stirnulating factor (G-CSF).1 As mentioned by the authors, the diagnosis of Sweet's syndrome in this patient had not been confirmed by a Iesional skin biopsy; we have previously addressed this issue and contest the diagnosis of Sweet's syndrome in this patient. 2 Actually, the case report reveals that the patient had a skin biopsy-proven leukocytoclastic vasculitis before receiving G-CSF and had enlargement of existing lesions and similar-appearing new lesions after receiving G-CSF therapy. I Cutaneous leukocytoclastic vasculitis has been observed in several patients with hairy cell leukemia. 3 Hence, treatment of the patient of Glaspy et a1. 1 with G-CSF probably exacerbated her underlying hairy cell leukemia-related leukocytoclastic vasculitis; therefore, on the basis of the available information, her skin lesions did ~ot represent either malignancy-associated Sweet's syn4rpme or G-CSF-induced Sweet's syndrome. Colony-stimulating factors may participate, directly or indirectly, in the origin ofseveral dermatologic conditions.
We have previously suggested the possibility that the pathogenesis ofSweet's syndrome may be secondary to an inappropriate secretion of one or more of the endogenous cytokines. 4 GoingS has also postulated that a cytokine may contribute to the etiology of Sweet's syndrome. The pathophysiologic response to,some of these proteins (such as G-CSF and interleukin 1 or epidermal cell thymocyteactivating factor) would account for the clinicopathologic changes observed in this condition: fever, leukocytosis, and neutrophilic dermal infiltrate. This intriguing hypothesis remains to be confirmed.
Philip R. Cohen, MD, q and Razelle Kurzrock, MD,b Department of Dermatology, The University of Texas Medical School at Houston,c' and Department of Clinical Immunology and Biological Therapy, M. D. Anderson Cancer Center,b Houston, Texas b REFERENCES 1. Glaspy JA, Baldwin Ge, Robertson PA, et al. Therapy for neutropenia in hairy cell leukemia with recombinant human granulocyte colony-stimulating factor. Ann Intern Med 1988;109:789-95. 2. Cohen PR, Kurzrock R. Diagnosing the Sweet syndrome [Letter]. Ann InternMed 1989;110:573-4. 3. Spann CR, Callen JP, Yam LT, et al. Cutaneous leukocytoclastic vasculitis complicating hairy cell leukemia (leukemic reticuloendotheliosis). Arch Dermatol1986;122:1057-9. 4. Cohen PR, Talpaz M, Kurzrock R. Malignancy-associated Sweet's syndrome: review of the world literature. J Clin Oncoll988;6:1887-97. 5. Going J1. Is the pathogenesis of Sweet's syndrome mediated by interleukin I? [Letter] Br J Dermato11987;116:282-3.
BOUND VOLUMES AVAILABLE TO SUBSCRIBERS Bound volumes of the JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY are available to subscribers (only) for the 1991 issues from the Publisher at a cost of $60.00 for domestic, $82.20 for Canadian, and $78.00 for international for volume 24 (January-June) and volume 25 (July-December). Shipping charges are included. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 60 days after publication of the last issue in the volume. The binding is durable buckram with the journal name, volume number, and year stamped in gold on the spine. Payment must accompany all orders. Contact Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318. USA: phone (800) 325-4177, ext. 4351.
Subscriptions must be in force to qualify. Bound volumes are /lot available in place of a regular journal subscription.