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who found only one weakly positive ANA among 147 pregnant patients tested. In the study by Polishuk and coworkers (1) human fetal thyroid was utilized as antigen for immunofluorescent ANA determinations whereas Hess and Baum (2) used rat liver sections. The disparity in results has not been subsequently resolved to our knowledge. As part of a current study investigating the incidence of ANA among patients with idiopathic recurrent fetal wastage we have evaluated the incidence of ANA in a control population of 97 normal pregnant women. Human spleen imprints were utilized as antigen (3) and undiluted sera studied for presence of ANA. Fluorescence of nuclei (FANA) was graded from 0 to 4 plus. Two plus or greater was considered positive. Antibodies to DNA were evaluated using a hemagglutination technique (4) in all patients with positive findings for ANA. Sera from pregnant women were obtained during the first trimester of pregnancy at the time of their first prenatal visit. Four (4.1%) of these patients had positive ANA. This figure is similar to that observed by Svec and Veit ( 5 ) who noted ANA in 4.3% of 70 normal nonpregnant younger women utilizing a comparable FANA technique. The FANA immunofluorescent pattern was homogeneous in all cases. No difference in age or number of pregnancies could be appreciated between pregnant women with or without ANA. Anti-DNA antibodies were absent in all patients. These results concur with the findings of Hess and Baum (2) and suggest that there is no increased incidence of antinuclear antibodies during at least the first trimester of pregnancy. The disparate findings of Polishuk et a1 (1) may be related to their having tested women on several occasions during pregnancy. The authors do not state whether most tests were positive late in pregnancy. It is also possible that some of the differences in the incidence of ANA in various studies arise from the use of different nuclear antigen substrates or from variations in definition of what level of ANA constitutes a significantly positive result. Our studies related to the incidence of ANA in patients with recurrent fetal wastage are currently in progress. STEPHENC. HINKLE,MD IRWINR. MERKATZ,MD MICHAELT. GYVES, MD BENO MICHEL,MD ROLANDW. MOSKOWITZ, MD Case Western Reserve University Cleveland, Ohio
REFERENCES 1. Polishuk WZ, Beyth Y, Izak G : Antinuclear factor and LE
cells in pregnant women. Lancet 2:270, 1971 2. Hess EV, Baum J: Antinuclear factor and LE cells in pregnant women. Lancet 2:871, 1971 3. Svec KH: The use of human spleen imprints for routine testing for serum antinuclear factors by immunofluorescence. Am J Clin Pathol47:432439, 1967 4. DeBoer DC, Moskowitz RW, Michel B: Skin basement membrane immunofluorescence in rheumatoid arthritis. Arthritis Rheum 20:653-656, 1977 5. Svec KH, Veit BC: Age-related antinuclear factors: immunologic characteristics and associated clinical aspects. Arthritis Rheum 10:509-5 16, 1967
Giant cell arteritis in an elderly black woman To the Editor: In a recent review of the manifestations of giant cell arteritis, Healey and Wilske stated: “The predilection of giant cell arteritis and polymyalgia rheumatics for Caucasians is striking. No documented case has been reported in any other race” (1). A similar statement was also made in a previous letter in the New England Journal of Medicine which these two investigators co-authored with Terasaki (2). Since these publications appeared, there have been three reports of giant cell inflammation of the temporal artery in elderly black women (3-5). In addition, a Pima American Indian has been described with clinical polymyalgia rheumatica, but in whom a temporal artery biopsy was negative for giant cell arteritis (6). To our knowledge, there have been no reports of temporal giant cell arteritis in black men. We were stimulated by these reports to review the patients at our institution with temporal arteritis over the last 5 years. We found 3 persons with biopsy proven giant cell arteritis of the temporal artery: a black woman, a white woman, and a Mexican man. The black woman was 73 years old and complained of throbbing, bitemporal headaches and numerous episodes of diplopia which abruptly began 2 weeks before admission. A biopsy of a temporal artery showed an arteritis, with giant cells in the media and disruption of the internal elastic membrane. Additional laboratory data included a sedimentation rate of 58 mm/hour (Wintrobe method), and negative results for antinuclear antibody, rheumatoid factor, and VDRL. The patient’s symptoms responded well to prednisone in an initial dose of 60 mg daily, and she has since been asymptomatic.
203
This case illustrates that giant cell arteritis can occur in nonwhites. Hence, this disease should definitely be considered in any person, regardless of race, when the clinical symptoms and physical findings suggest it. DONALD T. KING,MD JAMESF. FREED,MD Harbor General Hospital Torrance, Calfornia 90509 REFERENCES 1. Healey LA, Wilske KR: Manifestations of giant cell arteri-
tis. Med Clin North Am 61:261-270, 1977 2. Terasaki PI, Healey LA, Wilske KR: Distribution of HLA haplotypes in polymyalgia rheumatica. N Engl J Med 295:905, 1976 3. Goodman LJ, Layfer LF, Banner BF: Polymyalgia rheumatic and giant-cell arteritis in a black woman. N Engl J Med 298:113, 1978 4. Dirnant J, Farmer PM, Sobol N: Giant cell arteritis in a black person. Arthritis Rheum 21:391-393, 1978 5 . Ballou SP, Khan MA, Kushner I: Giant-cell arteritis in a black patient. Ann Intern Med 88:659-660, 1978 6. Jacobs RC: Polyrnyalgia rheumatica in an American Indian. Arthritis Rheum 20: 1429, 1977
Coexistence of ankylosing spondyli tis and rheumatoid arthritis in a single family To the Editor: In the past several years increasing attention has been paid to the occurrence of ankylosing spondylitis (AS) and rheumatoid arthritis (RA) in the same individual (1-4). In none of the cases reported in the literature so far has either condition been observed to be present in other family members. We have observed a family in which one member was found to have AS and RA, and both conditions were seen separately in other members of the family. HLA typing studies revealed positivity for B27 in all members affected with a rheumatic condition and in 50% of the first degree relatives. The index patient is a 53-year-old white male painter followed at the Rheumatic Disease Unit (RDU) of the Royal Victoria Hospital. He was first seen at the RDU in September 1973 because of pain and stiffness of neck and lower back. Examination revealed a decreased chest expansion, tenderness, pain on motion, and decreased range of motion of the entire spine. Tenderness was also elicited on pressure of the sacroi-
liac joints. The diagnosis of ankylosing spondylitis was made clinically. X-ray examination showed bilateral sacroiliitis and spondylitic involvement of the entire spine consistent with the diagnosis of AS. HLA typing revealed positivity for B27. Butazolidin 100 mg three times daily was begun. Because of the extraordinary family history of AS, the pedigree was included in the familial study of ankylosing spondylitis that we were conducting at the time (Family JO, Ref. 5). However, shortly after we first saw this patient in our clinic, he developed morning stiffness and a peripheral symmetrical polyarthritis which involved small and large joints. By the end of 1974 he had developed typical manifestations of classic rheumatoid arthritis. Rheumatoid nodules were present, and synovial thickening of wrists, metacarpophalangeal, and proximal interphalangeal joints with bilateral ulnar deviation deformities developed. Rheumatoid factor became positive shortly after the onset of polyarthritis in both synovial fluid and serum. Antinuclear factor was negative. No other significant serologic abnormalities were noted. Biopsy of one of the subcutaneous nodules was consistent with the diagnosis of rheumatoid nodule. X-ray revealed erosive changes on proximal interphalangeal and wrist joints. From the time the patient developed polyarthritis, therapeutic management became very difficult. Aspirin in full doses was given in conjunction with Butazolidin and physical therapy. Because of poor response, gold therapy was begun but had to be discontinued after the patient had received 1 gm because of skin rash and proteinuria. At the beginning of 1975, prednisone 10 mg and azathioprine 100 mg daily were begun. In spite of the medication, the patient’s condition continued to deteriorate. On 200 mg azathioprine he showed improvement, but active synovitis persists. Twenty members were studied. Ankylosing spondylitis was found in one of his siblings (a 46-yearold female) and RA in two others (a 56-year-old female and a 36-year-old male). By history it was concluded that the proband’s deceased maternal grandfather had also had AS. All affected members were B27 positive, as well as 50% of his first degree relatives. This patient illustrates some of the clinical aspects of the concomitant presentation of AS and RA, already reviewed by Good et a1 (4). From the clinical presentation of our patient and the reports in the literature, a pattern is emerging regarding the characteristics of the clinical association of AS and RA. The patient is usually male with a long history of back pain. The ankylos-
who found only one weakly positive ANA among 147 pregnant patients tested. In the study by Polishuk and coworkers (1) human fetal thyroid was utilized as antigen for immunofluorescent ANA determinations whereas Hess and Baum (2) used rat liver sections. The disparity in results has not been subsequently resolved to our knowledge. As part of a current study investigating the incidence of ANA among patients with idiopathic recurrent fetal wastage we have evaluated the incidence of ANA in a control population of 97 normal pregnant women. Human spleen imprints were utilized as antigen (3) and undiluted sera studied for presence of ANA. Fluorescence of nuclei (FANA) was graded from 0 to 4 plus. Two plus or greater was considered positive. Antibodies to DNA were evaluated using a hemagglutination technique (4) in all patients with positive findings for ANA. Sera from pregnant women were obtained during the first trimester of pregnancy at the time of their first prenatal visit. Four (4.1%) of these patients had positive ANA. This figure is similar to that observed by Svec and Veit ( 5 ) who noted ANA in 4.3% of 70 normal nonpregnant younger women utilizing a comparable FANA technique. The FANA immunofluorescent pattern was homogeneous in all cases. No difference in age or number of pregnancies could be appreciated between pregnant women with or without ANA. Anti-DNA antibodies were absent in all patients. These results concur with the findings of Hess and Baum (2) and suggest that there is no increased incidence of antinuclear antibodies during at least the first trimester of pregnancy. The disparate findings of Polishuk et a1 (1) may be related to their having tested women on several occasions during pregnancy. The authors do not state whether most tests were positive late in pregnancy. It is also possible that some of the differences in the incidence of ANA in various studies arise from the use of different nuclear antigen substrates or from variations in definition of what level of ANA constitutes a significantly positive result. Our studies related to the incidence of ANA in patients with recurrent fetal wastage are currently in progress. STEPHENC. HINKLE,MD IRWINR. MERKATZ,MD MICHAELT. GYVES, MD BENO MICHEL,MD ROLANDW. MOSKOWITZ, MD Case Western Reserve University Cleveland, Ohio
REFERENCES 1. Polishuk WZ, Beyth Y, Izak G : Antinuclear factor and LE
cells in pregnant women. Lancet 2:270, 1971 2. Hess EV, Baum J: Antinuclear factor and LE cells in pregnant women. Lancet 2:871, 1971 3. Svec KH: The use of human spleen imprints for routine testing for serum antinuclear factors by immunofluorescence. Am J Clin Pathol47:432439, 1967 4. DeBoer DC, Moskowitz RW, Michel B: Skin basement membrane immunofluorescence in rheumatoid arthritis. Arthritis Rheum 20:653-656, 1977 5. Svec KH, Veit BC: Age-related antinuclear factors: immunologic characteristics and associated clinical aspects. Arthritis Rheum 10:509-5 16, 1967
Giant cell arteritis in an elderly black woman To the Editor: In a recent review of the manifestations of giant cell arteritis, Healey and Wilske stated: “The predilection of giant cell arteritis and polymyalgia rheumatics for Caucasians is striking. No documented case has been reported in any other race” (1). A similar statement was also made in a previous letter in the New England Journal of Medicine which these two investigators co-authored with Terasaki (2). Since these publications appeared, there have been three reports of giant cell inflammation of the temporal artery in elderly black women (3-5). In addition, a Pima American Indian has been described with clinical polymyalgia rheumatica, but in whom a temporal artery biopsy was negative for giant cell arteritis (6). To our knowledge, there have been no reports of temporal giant cell arteritis in black men. We were stimulated by these reports to review the patients at our institution with temporal arteritis over the last 5 years. We found 3 persons with biopsy proven giant cell arteritis of the temporal artery: a black woman, a white woman, and a Mexican man. The black woman was 73 years old and complained of throbbing, bitemporal headaches and numerous episodes of diplopia which abruptly began 2 weeks before admission. A biopsy of a temporal artery showed an arteritis, with giant cells in the media and disruption of the internal elastic membrane. Additional laboratory data included a sedimentation rate of 58 mm/hour (Wintrobe method), and negative results for antinuclear antibody, rheumatoid factor, and VDRL. The patient’s symptoms responded well to prednisone in an initial dose of 60 mg daily, and she has since been asymptomatic.
203
This case illustrates that giant cell arteritis can occur in nonwhites. Hence, this disease should definitely be considered in any person, regardless of race, when the clinical symptoms and physical findings suggest it. DONALD T. KING,MD JAMESF. FREED,MD Harbor General Hospital Torrance, Calfornia 90509 REFERENCES 1. Healey LA, Wilske KR: Manifestations of giant cell arteri-
tis. Med Clin North Am 61:261-270, 1977 2. Terasaki PI, Healey LA, Wilske KR: Distribution of HLA haplotypes in polymyalgia rheumatica. N Engl J Med 295:905, 1976 3. Goodman LJ, Layfer LF, Banner BF: Polymyalgia rheumatic and giant-cell arteritis in a black woman. N Engl J Med 298:113, 1978 4. Dirnant J, Farmer PM, Sobol N: Giant cell arteritis in a black person. Arthritis Rheum 21:391-393, 1978 5 . Ballou SP, Khan MA, Kushner I: Giant-cell arteritis in a black patient. Ann Intern Med 88:659-660, 1978 6. Jacobs RC: Polyrnyalgia rheumatica in an American Indian. Arthritis Rheum 20: 1429, 1977
Coexistence of ankylosing spondyli tis and rheumatoid arthritis in a single family To the Editor: In the past several years increasing attention has been paid to the occurrence of ankylosing spondylitis (AS) and rheumatoid arthritis (RA) in the same individual (1-4). In none of the cases reported in the literature so far has either condition been observed to be present in other family members. We have observed a family in which one member was found to have AS and RA, and both conditions were seen separately in other members of the family. HLA typing studies revealed positivity for B27 in all members affected with a rheumatic condition and in 50% of the first degree relatives. The index patient is a 53-year-old white male painter followed at the Rheumatic Disease Unit (RDU) of the Royal Victoria Hospital. He was first seen at the RDU in September 1973 because of pain and stiffness of neck and lower back. Examination revealed a decreased chest expansion, tenderness, pain on motion, and decreased range of motion of the entire spine. Tenderness was also elicited on pressure of the sacroi-
liac joints. The diagnosis of ankylosing spondylitis was made clinically. X-ray examination showed bilateral sacroiliitis and spondylitic involvement of the entire spine consistent with the diagnosis of AS. HLA typing revealed positivity for B27. Butazolidin 100 mg three times daily was begun. Because of the extraordinary family history of AS, the pedigree was included in the familial study of ankylosing spondylitis that we were conducting at the time (Family JO, Ref. 5). However, shortly after we first saw this patient in our clinic, he developed morning stiffness and a peripheral symmetrical polyarthritis which involved small and large joints. By the end of 1974 he had developed typical manifestations of classic rheumatoid arthritis. Rheumatoid nodules were present, and synovial thickening of wrists, metacarpophalangeal, and proximal interphalangeal joints with bilateral ulnar deviation deformities developed. Rheumatoid factor became positive shortly after the onset of polyarthritis in both synovial fluid and serum. Antinuclear factor was negative. No other significant serologic abnormalities were noted. Biopsy of one of the subcutaneous nodules was consistent with the diagnosis of rheumatoid nodule. X-ray revealed erosive changes on proximal interphalangeal and wrist joints. From the time the patient developed polyarthritis, therapeutic management became very difficult. Aspirin in full doses was given in conjunction with Butazolidin and physical therapy. Because of poor response, gold therapy was begun but had to be discontinued after the patient had received 1 gm because of skin rash and proteinuria. At the beginning of 1975, prednisone 10 mg and azathioprine 100 mg daily were begun. In spite of the medication, the patient’s condition continued to deteriorate. On 200 mg azathioprine he showed improvement, but active synovitis persists. Twenty members were studied. Ankylosing spondylitis was found in one of his siblings (a 46-yearold female) and RA in two others (a 56-year-old female and a 36-year-old male). By history it was concluded that the proband’s deceased maternal grandfather had also had AS. All affected members were B27 positive, as well as 50% of his first degree relatives. This patient illustrates some of the clinical aspects of the concomitant presentation of AS and RA, already reviewed by Good et a1 (4). From the clinical presentation of our patient and the reports in the literature, a pattern is emerging regarding the characteristics of the clinical association of AS and RA. The patient is usually male with a long history of back pain. The ankylos-
