204
ing spondylitis seems to occur first in a mild to severe form. Rheumatoid arthritis usually develops during the third or fourth decade of life, and its clinical course is independent of the AS. As far as is known, the presence of B27 does not modify the manifestations of RA on these patients with AS or in the relatives.
L. R. ESPINOZA, MD Section of Rheumatology College of Medicine University of South Florida Tampa, Florida 33612 F. B. DOVE,MD C. KIRKOSTERLAND, MD Rheumatic Disease Unit Royal Victoria Hospital Montreal, P.Q. H3A-IAI Canada REFERENCES I . Rosenthal SH, Lidsky MD, Sharp JT: Arthritis with nodules following ankylosing spondylitis. JAMA 206:28932894, 1968 2. Luthra HS, Ferguson RH, Conn DL: Coexistence of ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum 19:lII-1l4, 1976 3. Fallet GH, Mason M, Berry H, et al: Rheumatoid arthritis and ankylosing spondylitis occurring together. Br Med J 1:804-807. 1976 4. Good AE, Hyla JF, Rapp R: Ankylosing spondylitis with rheumatoid arthritis and subcutaneous nodules. Arthritis Rheum 20:1434-1437, 1977 5. Espinoza LR, Oh JH, Kinsella, TD, Stacey CH, Osterland CK, Dove FB: Ankylosing spondylitis: familial studies and HLA-27 antigen distribution. J Rheumatol 1:254-258, 1974
Relapsing polychondritis To the Editor: Current recommendations in rheumatology texts for treatment of relapsing polychondritis include systemic corticosteroids (1-3). We wish to report a case of relapsing polychondritis in which systemic corticosteroids were ineffective and the response to Avlosulfon (dapsone) appeared unequivocal. Mrs. C. O., a 37-year-old white female, was seen in the dermatology clinic on June 5, 1977 with a swollen, painful, and red right ear. Initially she had been treated with 2 intramuscular 80 mg doses of Depo-
Medrol 1 week apart and later with Velosef for 1 week with no improvement. Her medical history was of interest because in 1976 she had developed a red, swollen, and tender nose which resolved spontaneously. In February of 1977 a diagnosis of “inflammation of the cartilage of the ribs” was made because of bilateral parasternal pain and tenderness; resolution was spontaneous. The patient denied any history of fever, symptoms of rheumatoid or collagen vascular disease, or cardiovascular symptoms. Results of a physical examination were normal other than marked redness, swelling, and tenderness of the right ear except for the lobe. Laboratory evaluation showed a white blood cell count of 14,700 with 72% polymorphonuclear leukocytes. The erythrocyte sedimentation rate was 43, and fluorescent antinuclear antibody test was negative. Rheumatoid factor was not done. The patient was given Avlosulfon 100 mg twice daily. When seen again on July 18, 1977, the patient reported improvement in the ear after 4 days and no symptoms after 1 week of dapsone. She was seen again on August 15 at which time her ear appeared almost normal, and she had a normal erythrocyte sedimentation rate. The dapsone was discontinued on October 5 with no recurrence of symptoms since. One other patient with relapsing polychondritis has been reported as responding to dapsone (4). The mechanism of response to dapsone in an inflammatory state such as relapsing polychondritis may be inhibition of lysosomal enzymes (5). Considering the significant undesirable side effects of steroids, the relatively infrequent side effects of dapsone, and the frequent ineffectiveness of steroids in relapsing polychondritis, we think a trial of dapsone is warranted, either initially or when systemic corticosteroids have failed to establish control of the inflammatory symptoms. Because polychondritis is rare and unpredictable in its course, the response to dapsone may be difficult to establish, but perhaps further individual case reports will allow assessment of its effectiveness in this disease.
JAMESR. CARPENTER, MD W. L. MACAULAY, MD Departments of Rheumatology and Dermatology Fargo Clinic Fargo, North Dakota
205
REFERENCES 1. Pearson CM: Relapsing polychondritis, Arthritis and Al-
lied Conditions. Eighth edition. Edited by JL Hollander and DJ McCarty, Jr. Philadelphia, Lea & Febiger, 1971, pp 866-873 2. Mannik M, Gilliland BC: Miscellaneous arthritides and ex-
traarticular rheumatism, Harrison’s Principles of Internal Medicine. Eighth edition. Edited by GW Thorn, et al. New York, McGraw-Hill, 1977, pp 2077-2080 3. Christian CL: Diseases with which arthritis is frequently associated, Textbook of Medicine. Fourteenth edition. Edited by PB Beeson and W McDermott. Philadelphia, Saunders, 1975, pp 154-155 4. Martin J, Roenigk HH, Lynch W, Tingwald FR: Relapsing polychondritis treated with dapsone. Arch Dermatol 112:1272-1274, 1976 5 . Barranco VP: Inhibition of lysosomal enzymes by dapsone. Arch Dermatol 110563-566, 1974
Hemoflagellate kinetoplasts and the diagnosis of SLE To the Editor: Recently, Aarden et a1 described an immunofluorescent method capable of detecting antibodies to dsDNA by using the kinetoplast of the flagellate, Cri-
thidia luciliae as a substrate (1). The kinetoplast of these organisms is a modified mitochondrion containing a localized concentration of dsDNA, which has been shown by others to be exclusively double stranded DNA (2,3). By use of well characterized sera specific for dsDNA, the observations of Aarden et a1 were further confirmed by several investigators ( 4 4 . Since in several developing countries Trypanosoma organisms are used as substrate for the diagnosis of Chagas’ disease, we have compared the Crithidia method with two other hemoflagellates, namely Trypanosoma and Leishmania. The organisms were maintained in Roithman’s nondefined liquid media at room temperature. To perform the test the organisms were air dried on glass slides and fixed in 95% ethanol to serve as a substrate. Lupus sera were serially diluted until the highest reactive titer. In Figures 1 to 3 we present the indirect immunofluorescence preparation of SLE patients with high levels of antibodies to DNA using as organisms Crithidia, Trypanosoma, and Leishmania, respectively. Strong staining of the kinetoplasts is evident with Crithidia whereas with the two other preparations the staining is less evident since the kinetoplast lies close to the nuclei and both appear equally fluorescent, which is not the case with Crithidia luciliae.
Figure 1. Crithidia organisms incubated with lupus sera and stained with fluorescein labeled antihuman IgG. Note the strong staining of the kinetoplasts when compared to the nuclei (X IOOO).
ing spondylitis seems to occur first in a mild to severe form. Rheumatoid arthritis usually develops during the third or fourth decade of life, and its clinical course is independent of the AS. As far as is known, the presence of B27 does not modify the manifestations of RA on these patients with AS or in the relatives.
L. R. ESPINOZA, MD Section of Rheumatology College of Medicine University of South Florida Tampa, Florida 33612 F. B. DOVE,MD C. KIRKOSTERLAND, MD Rheumatic Disease Unit Royal Victoria Hospital Montreal, P.Q. H3A-IAI Canada REFERENCES I . Rosenthal SH, Lidsky MD, Sharp JT: Arthritis with nodules following ankylosing spondylitis. JAMA 206:28932894, 1968 2. Luthra HS, Ferguson RH, Conn DL: Coexistence of ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum 19:lII-1l4, 1976 3. Fallet GH, Mason M, Berry H, et al: Rheumatoid arthritis and ankylosing spondylitis occurring together. Br Med J 1:804-807. 1976 4. Good AE, Hyla JF, Rapp R: Ankylosing spondylitis with rheumatoid arthritis and subcutaneous nodules. Arthritis Rheum 20:1434-1437, 1977 5. Espinoza LR, Oh JH, Kinsella, TD, Stacey CH, Osterland CK, Dove FB: Ankylosing spondylitis: familial studies and HLA-27 antigen distribution. J Rheumatol 1:254-258, 1974
Relapsing polychondritis To the Editor: Current recommendations in rheumatology texts for treatment of relapsing polychondritis include systemic corticosteroids (1-3). We wish to report a case of relapsing polychondritis in which systemic corticosteroids were ineffective and the response to Avlosulfon (dapsone) appeared unequivocal. Mrs. C. O., a 37-year-old white female, was seen in the dermatology clinic on June 5, 1977 with a swollen, painful, and red right ear. Initially she had been treated with 2 intramuscular 80 mg doses of Depo-
Medrol 1 week apart and later with Velosef for 1 week with no improvement. Her medical history was of interest because in 1976 she had developed a red, swollen, and tender nose which resolved spontaneously. In February of 1977 a diagnosis of “inflammation of the cartilage of the ribs” was made because of bilateral parasternal pain and tenderness; resolution was spontaneous. The patient denied any history of fever, symptoms of rheumatoid or collagen vascular disease, or cardiovascular symptoms. Results of a physical examination were normal other than marked redness, swelling, and tenderness of the right ear except for the lobe. Laboratory evaluation showed a white blood cell count of 14,700 with 72% polymorphonuclear leukocytes. The erythrocyte sedimentation rate was 43, and fluorescent antinuclear antibody test was negative. Rheumatoid factor was not done. The patient was given Avlosulfon 100 mg twice daily. When seen again on July 18, 1977, the patient reported improvement in the ear after 4 days and no symptoms after 1 week of dapsone. She was seen again on August 15 at which time her ear appeared almost normal, and she had a normal erythrocyte sedimentation rate. The dapsone was discontinued on October 5 with no recurrence of symptoms since. One other patient with relapsing polychondritis has been reported as responding to dapsone (4). The mechanism of response to dapsone in an inflammatory state such as relapsing polychondritis may be inhibition of lysosomal enzymes (5). Considering the significant undesirable side effects of steroids, the relatively infrequent side effects of dapsone, and the frequent ineffectiveness of steroids in relapsing polychondritis, we think a trial of dapsone is warranted, either initially or when systemic corticosteroids have failed to establish control of the inflammatory symptoms. Because polychondritis is rare and unpredictable in its course, the response to dapsone may be difficult to establish, but perhaps further individual case reports will allow assessment of its effectiveness in this disease.
JAMESR. CARPENTER, MD W. L. MACAULAY, MD Departments of Rheumatology and Dermatology Fargo Clinic Fargo, North Dakota
205
REFERENCES 1. Pearson CM: Relapsing polychondritis, Arthritis and Al-
lied Conditions. Eighth edition. Edited by JL Hollander and DJ McCarty, Jr. Philadelphia, Lea & Febiger, 1971, pp 866-873 2. Mannik M, Gilliland BC: Miscellaneous arthritides and ex-
traarticular rheumatism, Harrison’s Principles of Internal Medicine. Eighth edition. Edited by GW Thorn, et al. New York, McGraw-Hill, 1977, pp 2077-2080 3. Christian CL: Diseases with which arthritis is frequently associated, Textbook of Medicine. Fourteenth edition. Edited by PB Beeson and W McDermott. Philadelphia, Saunders, 1975, pp 154-155 4. Martin J, Roenigk HH, Lynch W, Tingwald FR: Relapsing polychondritis treated with dapsone. Arch Dermatol 112:1272-1274, 1976 5 . Barranco VP: Inhibition of lysosomal enzymes by dapsone. Arch Dermatol 110563-566, 1974
Hemoflagellate kinetoplasts and the diagnosis of SLE To the Editor: Recently, Aarden et a1 described an immunofluorescent method capable of detecting antibodies to dsDNA by using the kinetoplast of the flagellate, Cri-
thidia luciliae as a substrate (1). The kinetoplast of these organisms is a modified mitochondrion containing a localized concentration of dsDNA, which has been shown by others to be exclusively double stranded DNA (2,3). By use of well characterized sera specific for dsDNA, the observations of Aarden et a1 were further confirmed by several investigators ( 4 4 . Since in several developing countries Trypanosoma organisms are used as substrate for the diagnosis of Chagas’ disease, we have compared the Crithidia method with two other hemoflagellates, namely Trypanosoma and Leishmania. The organisms were maintained in Roithman’s nondefined liquid media at room temperature. To perform the test the organisms were air dried on glass slides and fixed in 95% ethanol to serve as a substrate. Lupus sera were serially diluted until the highest reactive titer. In Figures 1 to 3 we present the indirect immunofluorescence preparation of SLE patients with high levels of antibodies to DNA using as organisms Crithidia, Trypanosoma, and Leishmania, respectively. Strong staining of the kinetoplasts is evident with Crithidia whereas with the two other preparations the staining is less evident since the kinetoplast lies close to the nuclei and both appear equally fluorescent, which is not the case with Crithidia luciliae.
Figure 1. Crithidia organisms incubated with lupus sera and stained with fluorescein labeled antihuman IgG. Note the strong staining of the kinetoplasts when compared to the nuclei (X IOOO).
