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Subacute cutaneous lupus erythematosus associated with cilazapril
Rampen FHJ, Fleuren BAM, de Boo TM, Leemens WAJG. Prevalence of common "acquired" nevocytic nevi and dysplastic nevi is not related to ultraviolet exposure. J Am Acad Dermatol 1988; 18:
1
679-83. 2
Hughes BR, Cunliffe WJ, Bailey CC. Excess benign melanocytic naevi after chemotherapy for malignancy in childhood. BMJ 1989; 299: 88-91. de Wit
PEJ, de Vaan GAM, De Boo TM, Lemmens WAJG, Rampen FHJ. Prevalence of naevocytic naevi after chemotherapy for
3
childhood cancer. Med Pediatr Oncol 1990; 18: 336-38. Nelemans PJ, Rampen FHJ, Groenendal H, Kiemeney LALM, Ruiter DJ, Verbeek ALM. Swimming and the risk of cutaneous melanoma. Melanoma Res 1994; 4: 281-86.
4
Delay in onset of malaria with mefloquine
prophylaxis SiR-With increasing use of mefloquine prophylaxis in British residents travelling abroad, it is of concern to note
breakthrough falciparum malaria occurring in patients returning from East and West Africa.1,2 It seems that the pattern of presentation is different in individuals on mefloquine prophylaxis compared with travellers on chloroquine and proguanil prophylaxis. In a review of 112 non-immune patients on chloroquine and proguanil prophylaxis who presented to the Hospital for Tropical Diseases with falciparum malaria, the mean (SD) interval from arrival in the UK to diagnosis was 14-03 (13-2) days. In 1994, 6 non-immune men presented to the hospital with falciparum malaria despite taking mefloquine prophylaxis. The mean interval between return to the UK and diagnosis was 43-8 days (range 14-79 days). Their countries of infection were The Gambia (in 3), Tanzania (2), and Sudan. Length of visit ranged from 7-31 days. Ringwald and colleagues report 4 cases of mefloquine prophylaxis failure in French travellers to Africa.’ The mean interval between return from Africa and presentation with malaria was 31.55 days. Raccurt et al also report clinical symptoms appearing between 2 and 30 days in 16 French travellers who contracted falciparum malaria in West Africa despite mefloquine prophylaxis.2 In half of these cases the diagnosis was delayed for more than a week after the onset of fever.
Mefloquine appears to delay the onset of falciparum malaria in returned travellers and considering malaria in the differential diagnosis of a febrile patient months after travel remains the important message. JH
Day, *R H Behrens
Hospital for Tropical Diseases, London NW1 4PE, 1
2
UK
Ringwald P, Bartczak S, Le Bras J, et al. Failure of anti-malarial prophylaxis with mefloquine in Africa. Trans R Soc Trop Med Hyg 1990; 84: 348-49. Raccurt CP, Dumestre-Toulet V, Abraham E, Le Bras E, Brachet-Liermain A, Ripert C. Failure of falciparum malaria prophylaxis by mefloquine in travelers from West Africa. Am J Med Hyg 1991; 45: 319-24.
Subacute cutaneous lupus associated with cilazapril SiR-We
report
a
Trop
erythematosus
of subacute cutaneous lupus associated with cilazapril therapy for
case
erythematosus (SCLE) hypertension. A previously healthy 64-year-old white woman started taking captopril 50 mg daily in January, 1994, because of hypertension. 1 month later, symptomless skin lesions appeared on her face, upper trunk, and extensor surfaces of her arms. These lesions had persisted for 5 months when she visited her family physician, who immediately withdrew captopril. Within 2 weeks her cutaneous lesions disappeared, 398
but cilazapril 5 mg daily was then prescribed. 2 weeks later, she noticed a facial rash, similar to previously described, that worsened with sun exposure and lasted over 5 months. She was then referred to our dermatology unit. She had no other complaints and was still taking cilazapril. General physical examination was normal. Skin examination revealed fine scaling erythematous papules over her forehead and cheeks; appendages and mucous membranes were normal. A skin biopsy specimen from a lesion confirmed the diagnosis of SCLE. Direct immunofluorescence showed IgG deposition at the dermoepidermal junction; no other deposits of immunoglobulins or complement were found. Erythrocyte sedimentation rate was 39 mm/h. Complete blood cell and differential counts, blood biochemistry, serum proteins, standard coagulation tests, and urinalysis were normal. Her antinuclear antibody titre was 1/40 and anti-Ro/skinsensitising antibodies (SSA) were positive. Anti-DNA, anti-
Sm, anti-ribonucleoprotein, anti-histones, anti-cardiolipin antibodies, and rheumatoid factor were negative. HLA DR3 was found. Her skin lesions cleared within 2 weeks of stopping cilazapril. 6 months later, the patient remained free from cutaneous lesions, whereas positive antiRo antibodies still persisted. SCLE is a subset of lupus erythematosus’ characterised by photosensitivity and erythematous nonscarring, papulosquamous eruption on sun-exposed areas, with histology consistent with lupus erythematosus. Other distinctive findings include the frequent presence of antiRo/SSA antibodies, and an increased frequency of human histocompatibility antigen HLA DR3. SCLE has been associated with other rheumatic diseases, such as rheumatoid arthritis and Sjogren’s syndrome, and with drugs’ including thiazides, but many other compounds have also been incriminated. 1,2 In most of these patients, skin lesions resolved after discontinuation of treatment. Several cutaneous reactions to angiotensin-converting enzyme (ACE) inhibitors have been documented including maculopapular and urticarial eruptions, lichenoid dermatitis, bullous diseases, pityriasis-rosea-like rash, SchonleinHenoch purpura, and psoriasis. Most of these cutaneous adverse effects have been related to captopril. Moreover, captopril has been reported to induce an eruption that clinically suggested SCLE but with histopathology that showed lichenoid features.3 The development of antinuclear antibodies in up to 15% of healthy patients after captopril or enalapril administration is also recognised.4 However, captopril-induced systemic lupus erythematosus syndrome is considered exceptional. In our patient, it is unlikely that ACE inhibitors were directly involved in antinuclear antibody and anti-Ro antibody production because the skin eruption rapidly resolved when antihypertensive drugs were discontinued with no further symptoms whereas antibodies remain. Therefore, we speculate that ACE inhibitors might stimulate anti-Ro/SSA antibodies to produce SCLE in genetically predisposed individuals (expressing HLA DR3).
phenotype
*M L Fernández-Díaz, P Herranz, M C Suárez-Marrero, J Borbujo, R Manzano, M Casado Servicio de
1 2
3 4 5
Dermatología, Hospital
La Paz, P° Castellana 261, 28046 Madrid,
Spain
Sontheimer RD. Subacute cutaneous lupus erythematosus: a decade’s perspective. Med Clin North Am 1989; 73: 1073-90. Reed BR, Huff JC, Jones SK, Orton PW, Lee LA, Norris DA. Subacute cutaneous lupus erythematosus associated with hydrochlorothiazide therapy. Ann Intern Med 1985; 103: 49-51. Patri P, Nigro A, Rebora A. Lupus erythematosus-like eruption from captopril. Acta Derm Venerol (Stockh) 1985; 65: 447-48. Schwartz D, Pines A, Averbuch M, Levo Y. Enalapril-induced antinuclear antibodies. Lancet 1990; 336: 187. Pelayo M, Vargas V, González A, Vallano A, Esteban R, Guardia J. Drug-induced lupus-like reaction to captopril. Ann Pharmacother 1993; 27: 1542.
1
679-83. 2
Hughes BR, Cunliffe WJ, Bailey CC. Excess benign melanocytic naevi after chemotherapy for malignancy in childhood. BMJ 1989; 299: 88-91. de Wit
PEJ, de Vaan GAM, De Boo TM, Lemmens WAJG, Rampen FHJ. Prevalence of naevocytic naevi after chemotherapy for
3
childhood cancer. Med Pediatr Oncol 1990; 18: 336-38. Nelemans PJ, Rampen FHJ, Groenendal H, Kiemeney LALM, Ruiter DJ, Verbeek ALM. Swimming and the risk of cutaneous melanoma. Melanoma Res 1994; 4: 281-86.
4
Delay in onset of malaria with mefloquine
prophylaxis SiR-With increasing use of mefloquine prophylaxis in British residents travelling abroad, it is of concern to note
breakthrough falciparum malaria occurring in patients returning from East and West Africa.1,2 It seems that the pattern of presentation is different in individuals on mefloquine prophylaxis compared with travellers on chloroquine and proguanil prophylaxis. In a review of 112 non-immune patients on chloroquine and proguanil prophylaxis who presented to the Hospital for Tropical Diseases with falciparum malaria, the mean (SD) interval from arrival in the UK to diagnosis was 14-03 (13-2) days. In 1994, 6 non-immune men presented to the hospital with falciparum malaria despite taking mefloquine prophylaxis. The mean interval between return to the UK and diagnosis was 43-8 days (range 14-79 days). Their countries of infection were The Gambia (in 3), Tanzania (2), and Sudan. Length of visit ranged from 7-31 days. Ringwald and colleagues report 4 cases of mefloquine prophylaxis failure in French travellers to Africa.’ The mean interval between return from Africa and presentation with malaria was 31.55 days. Raccurt et al also report clinical symptoms appearing between 2 and 30 days in 16 French travellers who contracted falciparum malaria in West Africa despite mefloquine prophylaxis.2 In half of these cases the diagnosis was delayed for more than a week after the onset of fever.
Mefloquine appears to delay the onset of falciparum malaria in returned travellers and considering malaria in the differential diagnosis of a febrile patient months after travel remains the important message. JH
Day, *R H Behrens
Hospital for Tropical Diseases, London NW1 4PE, 1
2
UK
Ringwald P, Bartczak S, Le Bras J, et al. Failure of anti-malarial prophylaxis with mefloquine in Africa. Trans R Soc Trop Med Hyg 1990; 84: 348-49. Raccurt CP, Dumestre-Toulet V, Abraham E, Le Bras E, Brachet-Liermain A, Ripert C. Failure of falciparum malaria prophylaxis by mefloquine in travelers from West Africa. Am J Med Hyg 1991; 45: 319-24.
Subacute cutaneous lupus associated with cilazapril SiR-We
report
a
Trop
erythematosus
of subacute cutaneous lupus associated with cilazapril therapy for
case
erythematosus (SCLE) hypertension. A previously healthy 64-year-old white woman started taking captopril 50 mg daily in January, 1994, because of hypertension. 1 month later, symptomless skin lesions appeared on her face, upper trunk, and extensor surfaces of her arms. These lesions had persisted for 5 months when she visited her family physician, who immediately withdrew captopril. Within 2 weeks her cutaneous lesions disappeared, 398
but cilazapril 5 mg daily was then prescribed. 2 weeks later, she noticed a facial rash, similar to previously described, that worsened with sun exposure and lasted over 5 months. She was then referred to our dermatology unit. She had no other complaints and was still taking cilazapril. General physical examination was normal. Skin examination revealed fine scaling erythematous papules over her forehead and cheeks; appendages and mucous membranes were normal. A skin biopsy specimen from a lesion confirmed the diagnosis of SCLE. Direct immunofluorescence showed IgG deposition at the dermoepidermal junction; no other deposits of immunoglobulins or complement were found. Erythrocyte sedimentation rate was 39 mm/h. Complete blood cell and differential counts, blood biochemistry, serum proteins, standard coagulation tests, and urinalysis were normal. Her antinuclear antibody titre was 1/40 and anti-Ro/skinsensitising antibodies (SSA) were positive. Anti-DNA, anti-
Sm, anti-ribonucleoprotein, anti-histones, anti-cardiolipin antibodies, and rheumatoid factor were negative. HLA DR3 was found. Her skin lesions cleared within 2 weeks of stopping cilazapril. 6 months later, the patient remained free from cutaneous lesions, whereas positive antiRo antibodies still persisted. SCLE is a subset of lupus erythematosus’ characterised by photosensitivity and erythematous nonscarring, papulosquamous eruption on sun-exposed areas, with histology consistent with lupus erythematosus. Other distinctive findings include the frequent presence of antiRo/SSA antibodies, and an increased frequency of human histocompatibility antigen HLA DR3. SCLE has been associated with other rheumatic diseases, such as rheumatoid arthritis and Sjogren’s syndrome, and with drugs’ including thiazides, but many other compounds have also been incriminated. 1,2 In most of these patients, skin lesions resolved after discontinuation of treatment. Several cutaneous reactions to angiotensin-converting enzyme (ACE) inhibitors have been documented including maculopapular and urticarial eruptions, lichenoid dermatitis, bullous diseases, pityriasis-rosea-like rash, SchonleinHenoch purpura, and psoriasis. Most of these cutaneous adverse effects have been related to captopril. Moreover, captopril has been reported to induce an eruption that clinically suggested SCLE but with histopathology that showed lichenoid features.3 The development of antinuclear antibodies in up to 15% of healthy patients after captopril or enalapril administration is also recognised.4 However, captopril-induced systemic lupus erythematosus syndrome is considered exceptional. In our patient, it is unlikely that ACE inhibitors were directly involved in antinuclear antibody and anti-Ro antibody production because the skin eruption rapidly resolved when antihypertensive drugs were discontinued with no further symptoms whereas antibodies remain. Therefore, we speculate that ACE inhibitors might stimulate anti-Ro/SSA antibodies to produce SCLE in genetically predisposed individuals (expressing HLA DR3).
phenotype
*M L Fernández-Díaz, P Herranz, M C Suárez-Marrero, J Borbujo, R Manzano, M Casado Servicio de
1 2
3 4 5
Dermatología, Hospital
La Paz, P° Castellana 261, 28046 Madrid,
Spain
Sontheimer RD. Subacute cutaneous lupus erythematosus: a decade’s perspective. Med Clin North Am 1989; 73: 1073-90. Reed BR, Huff JC, Jones SK, Orton PW, Lee LA, Norris DA. Subacute cutaneous lupus erythematosus associated with hydrochlorothiazide therapy. Ann Intern Med 1985; 103: 49-51. Patri P, Nigro A, Rebora A. Lupus erythematosus-like eruption from captopril. Acta Derm Venerol (Stockh) 1985; 65: 447-48. Schwartz D, Pines A, Averbuch M, Levo Y. Enalapril-induced antinuclear antibodies. Lancet 1990; 336: 187. Pelayo M, Vargas V, González A, Vallano A, Esteban R, Guardia J. Drug-induced lupus-like reaction to captopril. Ann Pharmacother 1993; 27: 1542.