445
higher in persons exposed to silica dust than in the nonexposed male population (3). This is the first case report of LAC and anticardiolipin antibodies associated with silica-associated systemic sclerosis. Patients with silica-associated systemic sclerosis have been shown to have clinical, immunological and serological features indistinguishable from those patients with idiopathic systemic sclerosis (4). Therefore, it is no wonder that LAC, previously reported in idiopathic systemic scleroderma (5-7), may be present in silica-associated systemic sclerosis. Silica is phagocyted by macrophages that release interleukin 1 (IL-1) (9). IL-1 acts on helper T-cells and monocytes that liberate IL-2 and IL-6 (3,10). These cytokines may co-stimulate B-cells that are responsible for immunoglobulin production. As silica is chemically inert and cannot be digested, after the death of macrophage, silica is again exposed for ingestion and the phagocytic process starts again. We conclude that the presence of LAC and anticardiolipin antibodies completes the commonly agreed upon manifestations of silica-induced scleroderma. J.M. DURAND, M.F. AILLAUD*, G. KAPLANSKI, P. LEFEVRE, M.C. ALESSI*, I. JUHAN-VAGUE*, J. SOUBEYRAND. Department of Internal Medicine, CHU Sainte Marguerite, Marseille; Department of Haematology, CHU Timone, Marseille, France. REFERENCES 1. 2. 3. 4.
5. 6. 7.
8. 9.
Bramwell,B. Diffuse scleroderma : its frequency, its occurence in stone masons, its treatment by fibrolys in elevations of temperature due to fibrolysininjections. Edinburgh Med J, 1914, 12, 387. Devulder, B., Plouvier, B., Martin, JC, Lenoir, L. L'association scl6rodermie-silicoseou syndrome d'Erasmus. Presse M6d. 1977, 6, 2877-9. Haustein, U.F., Ziegler, V., Herrmann, K., Mehlhorn, J., Schmidt, C. Silica-induced scleroderma. J Am Acad Dermatol 1990, 22, 444-8. Rustin, M.H.A., Bull, H.A., Ziegler, V., Melhlhorn, J., Haustein, U.F., Maddison, P.J., James, J., Dowd, P.M. Silica-associated systemic sclerosis is clinically, serologically and immunologicallyindistinguishable from idiopathic systemic sclerosis. Br J Dermatol 1990, 123, 725-34. Masi,A.T. Classification of systemic sclerosis (scleroderma): relationship of cutaneous subgroup in early disease to outcome and serologic reactivity. J Rheumatol 1988, 15, 894-8. Albert, J., Ekoue, J.M., Cunningham, M., Humair L. Circulating anticoagulantin CREST syndrome.Br J Rheumatol, 1984, 23 : 20-3. Guillevin, L., Leroux, G., Berdah, J. Anticoagulant lupique et thromboses au cours de la scl6rodermie. Ann M6d Interne, 1987, 138, 144. Saveuse,H., Rouveix, E., Roussi, J., Dorra M. Scl6rodermie et anticoagulant circulant de type antiprothrombinase. Ann M6d Interne 1988, 139:230. Heppleston, A.G., Styles, F.S. Activity of a macrophage factor in collagen formation by silica. Nature 1967, 214, 521-2.
10. Wong, C.G., Clark, S.C. Multiple actions of interleukin-6 within a cytokine network. Immunol Today 1988, 9, 137-41. BONE AIDS
MANIFESTATIONS
ASSOCIATED
WITH
To the Editor: AIDS patients have a high incidence of non-Hodgkin's B-cell lymphoma (NHL). If the most common extranodal lymphoma sites are bone marrow (1) there are usually no clinical symptoms or X-ray changes. A 50-year-old homosexual Caucasian man had been seropositive for the human immunodeficiency virus (HIV) since 1985 (Centers for Disease Control, group 2). In December 1990, he complained of headaches. A skull X-ray showed multiple lytic lesions mimicking multiple myeloma. There was no other bone lesion. Biopsy of a lytic lesion revealed large cells NHL. Major laboratory findings were : white blood count 3.4 109/1, CD4 210/ mm 3. The osteomedullary biopsy and myelogram were normal. The patient was treated with chemotherapy (MACOP-B regimen) and a complete remission was obtained (with no relapse at 14 months). Bone manifestations associated with AIDS have mostly been limited to case reports. Recently, Sabbagh and colleagues in a retrospective study have observed six cases on 1400 AIDS cases between 1981 and 1990 (2). Three types of manifestations were observed : malignant lymphoma, infectious osteomyelitis and reflex sympathetic dystrophy syndrome secondary to central nervous system involvement. In the literature, several authors described cases of bone marrow involvement as initial sites of NHL in patients with high risk of AIDS but there was no mention of radiological changes (2). In NHL, lytic bone lesions mimicking multiple myeloma remain exceptional (3). These are related to the production of osteoclast activating factor by tumour cells (3). These factors are responsible for excessive osteoclastic resorption. So, bone involvement by NHL with osteolytic lesions mimicking multiple myeloma can be the first sign of AIDS and should alert the clinician to the possibility of HIV infection essentially in young patients.
B. TAILLAN, G. GARNIER, E. FERRARI, E. DRAI, P. D U J A R D I N Department of Internal Medicine, H6pital de Cimiez, BP179, 06003 Nice cedex 1, France. REFERENCES 1. Kaplan, L.D., Abrams, D.I., Feigall, E. et al. AIDS-associated nonHodgkin's lymphoma in San Francisco, JAMA 1989, 261, 219-24. 2. Sabbagh,M., Meyer, O., De Bandt, M. et al. Bone manifestations associated with the acquired immunodeficiency syndrome (AIDS). Ann Med Interne 1992, 143, 50-56. 3. Rossi, J.F., Bataille, R., Chappard, D., Alexandre, C., Janbon, C. B cells malignancies presenting with unusual bone involvement and mimicking multiple myeloma : Study of nine cases. Am J Med 1987, 83, 10-16.
higher in persons exposed to silica dust than in the nonexposed male population (3). This is the first case report of LAC and anticardiolipin antibodies associated with silica-associated systemic sclerosis. Patients with silica-associated systemic sclerosis have been shown to have clinical, immunological and serological features indistinguishable from those patients with idiopathic systemic sclerosis (4). Therefore, it is no wonder that LAC, previously reported in idiopathic systemic scleroderma (5-7), may be present in silica-associated systemic sclerosis. Silica is phagocyted by macrophages that release interleukin 1 (IL-1) (9). IL-1 acts on helper T-cells and monocytes that liberate IL-2 and IL-6 (3,10). These cytokines may co-stimulate B-cells that are responsible for immunoglobulin production. As silica is chemically inert and cannot be digested, after the death of macrophage, silica is again exposed for ingestion and the phagocytic process starts again. We conclude that the presence of LAC and anticardiolipin antibodies completes the commonly agreed upon manifestations of silica-induced scleroderma. J.M. DURAND, M.F. AILLAUD*, G. KAPLANSKI, P. LEFEVRE, M.C. ALESSI*, I. JUHAN-VAGUE*, J. SOUBEYRAND. Department of Internal Medicine, CHU Sainte Marguerite, Marseille; Department of Haematology, CHU Timone, Marseille, France. REFERENCES 1. 2. 3. 4.
5. 6. 7.
8. 9.
Bramwell,B. Diffuse scleroderma : its frequency, its occurence in stone masons, its treatment by fibrolys in elevations of temperature due to fibrolysininjections. Edinburgh Med J, 1914, 12, 387. Devulder, B., Plouvier, B., Martin, JC, Lenoir, L. L'association scl6rodermie-silicoseou syndrome d'Erasmus. Presse M6d. 1977, 6, 2877-9. Haustein, U.F., Ziegler, V., Herrmann, K., Mehlhorn, J., Schmidt, C. Silica-induced scleroderma. J Am Acad Dermatol 1990, 22, 444-8. Rustin, M.H.A., Bull, H.A., Ziegler, V., Melhlhorn, J., Haustein, U.F., Maddison, P.J., James, J., Dowd, P.M. Silica-associated systemic sclerosis is clinically, serologically and immunologicallyindistinguishable from idiopathic systemic sclerosis. Br J Dermatol 1990, 123, 725-34. Masi,A.T. Classification of systemic sclerosis (scleroderma): relationship of cutaneous subgroup in early disease to outcome and serologic reactivity. J Rheumatol 1988, 15, 894-8. Albert, J., Ekoue, J.M., Cunningham, M., Humair L. Circulating anticoagulantin CREST syndrome.Br J Rheumatol, 1984, 23 : 20-3. Guillevin, L., Leroux, G., Berdah, J. Anticoagulant lupique et thromboses au cours de la scl6rodermie. Ann M6d Interne, 1987, 138, 144. Saveuse,H., Rouveix, E., Roussi, J., Dorra M. Scl6rodermie et anticoagulant circulant de type antiprothrombinase. Ann M6d Interne 1988, 139:230. Heppleston, A.G., Styles, F.S. Activity of a macrophage factor in collagen formation by silica. Nature 1967, 214, 521-2.
10. Wong, C.G., Clark, S.C. Multiple actions of interleukin-6 within a cytokine network. Immunol Today 1988, 9, 137-41. BONE AIDS
MANIFESTATIONS
ASSOCIATED
WITH
To the Editor: AIDS patients have a high incidence of non-Hodgkin's B-cell lymphoma (NHL). If the most common extranodal lymphoma sites are bone marrow (1) there are usually no clinical symptoms or X-ray changes. A 50-year-old homosexual Caucasian man had been seropositive for the human immunodeficiency virus (HIV) since 1985 (Centers for Disease Control, group 2). In December 1990, he complained of headaches. A skull X-ray showed multiple lytic lesions mimicking multiple myeloma. There was no other bone lesion. Biopsy of a lytic lesion revealed large cells NHL. Major laboratory findings were : white blood count 3.4 109/1, CD4 210/ mm 3. The osteomedullary biopsy and myelogram were normal. The patient was treated with chemotherapy (MACOP-B regimen) and a complete remission was obtained (with no relapse at 14 months). Bone manifestations associated with AIDS have mostly been limited to case reports. Recently, Sabbagh and colleagues in a retrospective study have observed six cases on 1400 AIDS cases between 1981 and 1990 (2). Three types of manifestations were observed : malignant lymphoma, infectious osteomyelitis and reflex sympathetic dystrophy syndrome secondary to central nervous system involvement. In the literature, several authors described cases of bone marrow involvement as initial sites of NHL in patients with high risk of AIDS but there was no mention of radiological changes (2). In NHL, lytic bone lesions mimicking multiple myeloma remain exceptional (3). These are related to the production of osteoclast activating factor by tumour cells (3). These factors are responsible for excessive osteoclastic resorption. So, bone involvement by NHL with osteolytic lesions mimicking multiple myeloma can be the first sign of AIDS and should alert the clinician to the possibility of HIV infection essentially in young patients.
B. TAILLAN, G. GARNIER, E. FERRARI, E. DRAI, P. D U J A R D I N Department of Internal Medicine, H6pital de Cimiez, BP179, 06003 Nice cedex 1, France. REFERENCES 1. Kaplan, L.D., Abrams, D.I., Feigall, E. et al. AIDS-associated nonHodgkin's lymphoma in San Francisco, JAMA 1989, 261, 219-24. 2. Sabbagh,M., Meyer, O., De Bandt, M. et al. Bone manifestations associated with the acquired immunodeficiency syndrome (AIDS). Ann Med Interne 1992, 143, 50-56. 3. Rossi, J.F., Bataille, R., Chappard, D., Alexandre, C., Janbon, C. B cells malignancies presenting with unusual bone involvement and mimicking multiple myeloma : Study of nine cases. Am J Med 1987, 83, 10-16.
