Volume 25 Number 6, Part 1 December 1991 REFERENCE 1. Elbaum D.1. Comparison of the stability of topical isotretinoin and topical tretinoin and their efficacy in acne. J AM ACAD DERMATOL 1988;19:486-91.
Halogenoderma and monoclonal gammopathy
To the Editor: We were interested in the two cases of vegetating iododerma in patients with an underlying monoclonal gammopathy reported by Soria et al. (J AM ACAD DERMATOL 1990;22:418-22). We observed a woman with acute bromoderma who had a monoclonal gammopathy. For 1 month, a 55-year-old woman took oral bromo galactogluconate (Calcibronat, Sandoz Laboratories) (2.7 gmjday) for nervousness. Fifteen days after the beginning of this treatment, papulopustular lesions appeared on the limbs, then on the trunk and the face. They evolved to crusted nodules. She did not stop treatment and waited for 2 more weeks before seeking medical attention. On admission, her serum bromidelevelwas 11 mmolfL (normal 3.10 mmolfL) and the urinaryJevel was 4.25 mmoljday. Serum urea nitrogen and creatinine levels were normal. The serum electrophoresis disclosed an abnormal protein migrating between the f3- and 'Y-globulin. Serum immunoelectrophoresis showed a IgG-K monoclonal protein. No Bence Jones protein was found. Bone marrow aspiration and complete x-ray skeletal examination were normal. A skin biopsy specimen revealed acanthosis and papillomatosis and a dense dermal inflammatory infiltration with neutrophils and eosinophils. Skin lesions healed with minimal scarring after cessation of bromine treatment and with treatment with clobetasol propionate cream. Bromine belongs to the halogen group that includes iodine, fluorine, and chlorine. Each may induce cutaneous toxicity. 1-3 The pathogenesis ofbromoderma is unknown. The significance of an associated gammopathy remains unclear. The monoclonal protein did not induce any significant renal impairment that could interfere with halide elimination in Soria's cases or in ours. Iododerma and bromoderma may mimic a neutrophilic dermatosis such as pyoderma gangrenosum both clinically and histologically.4 Moreover, neutrophilic dermatosis, especially pyoderma gangrenosum, are frequently associated with a monoclonal gammopathy.5 To assess further the frequency and the role of monoclonal gammopathy in halogenoderma, serum immunoelectrophoresis should be performed in every case. Florence Cordoliani, MD, Michel Rybojad, MD, Patrice Morel, MD, and Antoine Puissant, MD, Service de Dermatologie, H8pital Saint-Louis, Paris, France
Correspondence
1099
REFERENCES 1. Fitzpatrick TB. Bromodenna. Arch Dermatol 1964;90; 236-7. 2. Blasik LG, Spencer SK. Fluoroderma. Arch Dermatol 1979;115:1334-5. 3. Rycroft RJG. Acne of external chemical origin. In: Rook A, Wilkinson DS, Ebling FJG, et al. Textbook of dermatology. London: Blackwell, 1986:573-5. 4. David M, Ingber A, SandbankM, et al. Bromoderma caused by carbromal hydroxyzine hydroxychloride. Biomed Pharmaco11983;37:298-300. 5. Schwaerge SM, Bergfeld WF, Senitzer D, et al. Pyoderma gangrenosum: a review. J AM ACAD DERMATOL 1988; 18:559-68. Reply
To the Editor: The patient described with bromoderma and monoclonal gammopathy is noteworthy. We are not aware of a similar previous case, I so it represents a new expanding example of the association between halogenoderma and monoclonal gammopathy. We agree with Cordoliani et al. that halogenoderma may mimic a neutrophilic dermatosis such as pyoderma gangrenosum (PG), on a clinicopathologic basis and in its association with monoclonal gammopathy. Furthermore, iodide is a known cause of PG exacerbation2 and PO has been reported after administration of iodine-containing radiographic contrast. 3 The role of monoclonal gammopathy in the pathogenesis of halagenoderma is unknown, but it should be investigated in each patient with this kind of eruption as in neutrophilic dermatoses such as PG4 and subcorneal pustular dermatosis. 5 Caridad Soria, MD,a Francisco Allegue, MD,aAgustin Espana, MD,a Antonio Rocamora, MD,b Antonio Harto, MD,a and Antonio Ledo, MD, a Departments ofDermatology a and Pathology,b Hospital Rambny Cajal, Madrid, Spain
REFERENCES 1. Soria C, Munoz Zato E, Espana A. Halogenodermias. Piel 1990;5:17-22. 2. Newel LM,Malkinson FD. Commentary: pyoderma gangrenosum. Arch Derll1atoI1982;118:769-73. 3. Mahod JM, Sneddon lB. Pyoderma gangrenosum complicating non-Hodgkin's lymphoma. Br J Dermatol 1980; 102:223"5. 4. Powell FC, Schroeter AL, Su WPD, et al. Pyoderma gangrenosum and monoclonal gammopathy. Arch Dermatol 1983;119:468-72. 5. Kasha EE, Epinette WW. Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) in association with a monoclonal IgA gammopathy. J AM ACAD DERMATOL 1988; 19:854-8.
Halogenoderma and monoclonal gammopathy
To the Editor: We were interested in the two cases of vegetating iododerma in patients with an underlying monoclonal gammopathy reported by Soria et al. (J AM ACAD DERMATOL 1990;22:418-22). We observed a woman with acute bromoderma who had a monoclonal gammopathy. For 1 month, a 55-year-old woman took oral bromo galactogluconate (Calcibronat, Sandoz Laboratories) (2.7 gmjday) for nervousness. Fifteen days after the beginning of this treatment, papulopustular lesions appeared on the limbs, then on the trunk and the face. They evolved to crusted nodules. She did not stop treatment and waited for 2 more weeks before seeking medical attention. On admission, her serum bromidelevelwas 11 mmolfL (normal 3.10 mmolfL) and the urinaryJevel was 4.25 mmoljday. Serum urea nitrogen and creatinine levels were normal. The serum electrophoresis disclosed an abnormal protein migrating between the f3- and 'Y-globulin. Serum immunoelectrophoresis showed a IgG-K monoclonal protein. No Bence Jones protein was found. Bone marrow aspiration and complete x-ray skeletal examination were normal. A skin biopsy specimen revealed acanthosis and papillomatosis and a dense dermal inflammatory infiltration with neutrophils and eosinophils. Skin lesions healed with minimal scarring after cessation of bromine treatment and with treatment with clobetasol propionate cream. Bromine belongs to the halogen group that includes iodine, fluorine, and chlorine. Each may induce cutaneous toxicity. 1-3 The pathogenesis ofbromoderma is unknown. The significance of an associated gammopathy remains unclear. The monoclonal protein did not induce any significant renal impairment that could interfere with halide elimination in Soria's cases or in ours. Iododerma and bromoderma may mimic a neutrophilic dermatosis such as pyoderma gangrenosum both clinically and histologically.4 Moreover, neutrophilic dermatosis, especially pyoderma gangrenosum, are frequently associated with a monoclonal gammopathy.5 To assess further the frequency and the role of monoclonal gammopathy in halogenoderma, serum immunoelectrophoresis should be performed in every case. Florence Cordoliani, MD, Michel Rybojad, MD, Patrice Morel, MD, and Antoine Puissant, MD, Service de Dermatologie, H8pital Saint-Louis, Paris, France
Correspondence
1099
REFERENCES 1. Fitzpatrick TB. Bromodenna. Arch Dermatol 1964;90; 236-7. 2. Blasik LG, Spencer SK. Fluoroderma. Arch Dermatol 1979;115:1334-5. 3. Rycroft RJG. Acne of external chemical origin. In: Rook A, Wilkinson DS, Ebling FJG, et al. Textbook of dermatology. London: Blackwell, 1986:573-5. 4. David M, Ingber A, SandbankM, et al. Bromoderma caused by carbromal hydroxyzine hydroxychloride. Biomed Pharmaco11983;37:298-300. 5. Schwaerge SM, Bergfeld WF, Senitzer D, et al. Pyoderma gangrenosum: a review. J AM ACAD DERMATOL 1988; 18:559-68. Reply
To the Editor: The patient described with bromoderma and monoclonal gammopathy is noteworthy. We are not aware of a similar previous case, I so it represents a new expanding example of the association between halogenoderma and monoclonal gammopathy. We agree with Cordoliani et al. that halogenoderma may mimic a neutrophilic dermatosis such as pyoderma gangrenosum (PG), on a clinicopathologic basis and in its association with monoclonal gammopathy. Furthermore, iodide is a known cause of PG exacerbation2 and PO has been reported after administration of iodine-containing radiographic contrast. 3 The role of monoclonal gammopathy in the pathogenesis of halagenoderma is unknown, but it should be investigated in each patient with this kind of eruption as in neutrophilic dermatoses such as PG4 and subcorneal pustular dermatosis. 5 Caridad Soria, MD,a Francisco Allegue, MD,aAgustin Espana, MD,a Antonio Rocamora, MD,b Antonio Harto, MD,a and Antonio Ledo, MD, a Departments ofDermatology a and Pathology,b Hospital Rambny Cajal, Madrid, Spain
REFERENCES 1. Soria C, Munoz Zato E, Espana A. Halogenodermias. Piel 1990;5:17-22. 2. Newel LM,Malkinson FD. Commentary: pyoderma gangrenosum. Arch Derll1atoI1982;118:769-73. 3. Mahod JM, Sneddon lB. Pyoderma gangrenosum complicating non-Hodgkin's lymphoma. Br J Dermatol 1980; 102:223"5. 4. Powell FC, Schroeter AL, Su WPD, et al. Pyoderma gangrenosum and monoclonal gammopathy. Arch Dermatol 1983;119:468-72. 5. Kasha EE, Epinette WW. Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) in association with a monoclonal IgA gammopathy. J AM ACAD DERMATOL 1988; 19:854-8.
