790
BRITISH JOURNAL OF RHEUMATOLOGY VOL. XXXI NO. 11 TABLE I EFFICACY OF EXTRACORPOREAL PHOTOTHERAPY (DAYS 1-50)
Patient 1
Symptom
Day:
1
20 50
Patient 2 1
20 50
No of tender joints 13 5 6 13 3 12 2 7 15 6 No of swollen joints Visual analogue scale (mm) 100 50 50 50 20 300 180 300 240 0 Morning stiffness (mins) 15 7 11 15 6 Ritchie index 101 54 118 63 45 C-reactive protein (mg/1)
11 14 75 30 16 69
Patient 3 1 13 15 50 30 20 7
[2] using a different schedule and technique. In view of the excellent tolerance and efficacy further controlled studies are warranted. P. HlLLIQUIN*
'Service de Rhumatologie A, Hdpital Cochin, Paris; tPoste de Transfusion Sanguine, Hotel-Dieu et Hdpital Cochin, Paris, France. Accepted 2 July 1992 1. Edelson R, Berger C, Gasparro F, et al. Treatment of cutaneous T cell lymphoma by extracorporeal photochemotherapy. N EnglJMed 1987;316:297-303. 2. Malawista SE, Trock DH, Edelson RL. Treatment of rheumatoid arthritis by extra corporeal photochemotherapy: A pilot study. Arthritis Rheum 1991;34:646-54. 3. Andreu G, Boccaccio C, Lecrubier C, et al. Ultra violet irradiation of platelet concentrates: feasibility in transfusion practice. Transfusion 1990;30:401-6. 4. BoccacioC, Garcia I, Klaren i,etal. Ultra violet irradiation of platelet concentrates: in vitro and in vivo preclinical evaluation. Transfus Sci 1990;ll:141-7. 5. Gasparro F, Dell'Amico R, Goldminz D, Simmons E, Weingold D. Molecular aspects of extracorporeal chemotherapy. Yale J Bio! Med 1989;62:579-93. Chloroquine-induced Vitiligo in a Patient with Juvenile Onset Rheumatoid Arthritis SIR—We describe a 29-year-old black male with seropositive rheumatoid arthritis (RA) since the age of 14 years. He was treated with non-steroidal anti-inflammatory drugs (NSAIDs) and analgesics and remained relatively asymptomatic until the age of 25, when his disease became active. He was maintained on increased doses of NSAIDs until 2 years later (age 27), when a diseasemodifying agent had to be added to achieve better control. Roentgenograms at this stage revealed significant erosive disease at the metacarpophalangeal, proximal interphalangeal and carpal joints. Initial laboratory investigations demonstrated the following values: sheep cell agglutination test titre 1:64; latex agglutination test titre 1:320; antinuclear factor titre 1:10; erythrocyte sedimentation rate 76 mm/h (Westergren); C-reactive protein 8.2mg/dl; plasma viscosity 2.2 cp; circulating immune complexes 39%. The patient showed a gratifying response to the addition of chloroquine and was maintained on this drug and NSAIDs until 2 years later (age 29), when he developed areas of facial depigmentation. There was no past-dermatological history of note. His chloroquine was stopped and on follow up a month later no improvement was noted. He was subsequently referred to the dermatologists who confirmed the diagnosis of vitiligo. The morphology of the skin lesions was such that skin scrapings or skin biopsy were felt not to be indicated. The patient was started on vitamin C (100 mg/day) as placebo. On review
0 3 0 0 4 5
3 2 0 15 4 20
1
20 50
13 5 5 16 6 4 60 32 30 180 15 30 17 6 7 129 77 83
Patient 5 1
20 50
15 1 4 18 8 11 80 23 30 180 45 45 22 8 13 89 43 52
Patient 6 1
20 50
Patient 7 1
20 50
20 1 17 2 1 10 0 9 14 5 90 30 70 20 5 180 30 150 150 0 30 2 23 20 6 250 71 145 10 5
1 7 10 30 6 94
2 months later there was a dramatic improvement with virtually no trace of the vitiligo present. The patient did not use any topical treatment during the period. His arthritis remained inactive during this time. Vitiligo is a common skin disorder and has been associated with certain autoimmune diseases but not RA [1-3]. Chloroquine, a disease-modifying agent used in the treatment of RA, is known to cause hyperpigmentation secondary to sun exposure. Various dermatological reactions have been reported with chloroquine, including macular, urticarial, lichenoid and purpuric skin eruptions; photosensitivity and erythema multiforme [4, 5]. Bleaching of the skin has not been reported in the English literature. The most conspicuous side-effect of chloroquine is a depigmentation (bleaching) of the hair. This bleaching is reversible on drug withdrawal [6]. However, bleaching of the skin has not been described: on the contrary chloroquine is a well-documented cause of skin hyperpigmentation [4—8]. Idiopathic vitiligo is a common skin condition characterized by asymptomatic, variously sized or shaped, single or multiple patches of depigmentation. It has been reported in association with certain autoimmune diseases, particularly thyroid disease, pernicious anaemia, Addison's disease and diabetes mellitus [1-3]. The diagnosis of vitiligo can be confirmed histologically, but the clinical appearances are sometimes considered pathognomonic. Biopsy has the added advantage of demonstrating melanocytes preserved in the hair follicles, which may help in prognostication. However, the face is not aesthetically a suitable site for biopsy. Fungal infections and post-inflammatory hypopigmentation should always be considered in the differential diagnosis. These were not considered to be relevant in our patient at the time. Apart from two case reports [9,10] describing cases in which RA and vitiligo co-existed, a literature search revealed no clear association between these two diseases. Alarcon-Segovia [9] described a case of repigmentation of vitiligo with penicillamine therapy for RA and Collen et al. [10] described a case of hitherto unreported primary ovarian failure, juvenile arthritis and vitiligo. Without rechallenging the patient with the chloroquine we can only postulate that the vitiligo was caused by the drug. While we accept that our case does not prove the relationship between vitiligo and chloroquine, the circumstantial evidence is highly suggestive that the association is more than coincidental. This is the first report of such a side-effect in association with chloroquine. The vitiligo could have been secondary to the underlying autoimmune disease but, to the best of our knowledge, an association between vitiligo and RA has not been previously described. Similarly we can only postulate that the improvement in the vitiligo was a result of the chloroquine withdrawal and not due to the natural history of the skin disease or due to the treatment with the placebo.
Downloaded from http://rheumatology.oxfordjournals.org/ at University of Otago on July 27, 2015
C. J. MENKES,* G. ANDREU,! F. HESHMATI,!
20 50
Patient 4
LETTERS TO THE EDITOR L. A. GONGGRYP, A. A. KALLA
Department of Medicine, Rheumatic Diseases Unit, University of Cape Town, South Africa Accepted 17 July 1992
Juvenile Arthritis and Coeliac Disease SIR—We read with interest the case report: Oligoarthritis—a Presenting Feature of Occult Coeliac Disease [9]. We now report a case of arthritis and coeliac disease affecting a child. Our patient a 21-year-old Caucasian woman, first presented at 2.5 years of age with symmetrical polyarthritis affecting elbows, wrists, fingers and knees. There was fever but not the characteristic pattern of Still's disease, there was no rash. She had had diarrhoea from the age of 8 months, this was attributed to gluten intolerance and treated by dietary restriction; it subsided progressively and disappeared by 3 years of age. Four months before the onset of arthritis, she had had 'enteritis' treated by antibiotics. Her grandfather had iritis and lumbar pain. On physical examination, apart from the prominent arthritis, there was a polylymphoadenopathy and a moderate enlargement of the spleen. Laboratory tests revealed an increased erythrocyte sedimentation rate; rheumatoid factors were negative, as were anti-nuclear antibodies. A diagnosis of chronic juvenile arthritis was made, and she was treated with aspirin and gold salts. This, treatment had only moderate success in controlling arthritis. Seven years later, she was referred to our Rheumatology Department for local treatment with osmic acid for chronic bilateral synovitis of the knee. X-rays showed small erosions of both carpal and metacarpophalangeal joints. Her height was 117 cm (2 SD below normal) and she weighed 16.5 kg (3 SD below normal). Apart from a moderate increase of lipid content in the faeces (4.5 g compared to a norm of 2 g) with the presence of soaps, no other malabsorption feature (anaemia, hypoproteinemia, hypocalcaemia, hypokaliemia, evidence of osteomalacia) was detectable, HLA B27 was positive. Between 1980 and 1987, she had some painful crises, and remained on anti-inflammatory symptomatic treatment. In 1987, when she was 16 years of age, the statoponderal delay was still present and the possibility of occult coeliac disease was raised, a jejunal biopsy was performed which demonstrated villous atrophy. A glutenfree diet was then commenced.
There was a spectacular recovery in height and weight (respectively, 14 cm and 10 kg) within 2 years; a complete disappearance of the arthritis and an improvement in enteric histology was confirmed after 1 year of treatment. The patient has carried on with the diet and has no articular complaint apart from minimal painless hydarthrosis of the left knee. A few years ago, osteo-articular manifestations of this intestinal disorder were thought to be extremely rare [7, 8], and mainly due to the depletion of calcium, potassium and magnesium [6-9] or to metabolic bone disease (osteomalacia and/or osteoporosis) [5, 7-9]. It now seems obvious that a diagnosis of malabsorption syndrome should have been suspected earlier. In chronic juvenile arthritis, there can be a growth disturbance but weight is infrequently impaired. The age of onset is unusual, since the early 1980s after Prier et al. [1] and Addelizi et al. [10], some cases [ 2 , 4 , 5 , 9 ] concerning adults, have been published, the youngest patient was 15 years of age [6]. Our patient did not have either of the two major features of malabsorption present in occult coeliac disease of the adult, osteomalacia and anaemia [6-8]. The intestinal manifestations largely preceded the articular ones, and were considered as cured in the absence of diarrhoea. The presence of H L A B27, although not usual, was present in two of the six patients studied by Bourne [5]; one of them had radiological sacro-iliitis, which until now has not presented in our patient. Even though the etiology of the disease may be questionable, the therapeutic proof of gluten withdrawal, is reliable evidence. M. SIMOES, B. AMOR
Rheumatology Department, Hdpital Cochin, 27, ruedu Fg Saint Jacques, 75674 Paris Cedex 14, France Accepted 15 July 1992 1. Prier A, Le Quintrec Y, Camus JP, Gendre JP, Bradel P. Polyarthrites inflammatoires associees a une atrophie villositaire du grele. Rev Rhum 1980;47:661-5. 2. Gendre JP, Luboinski J, Prier A, Camus JP, Le Quintrec Y. Anomalies de la muqueuse jejunale et polyarthrite rhumatoide: 30 cas. Gastroenterol Clin Biol 1982;6:772-5. 3. Alcalay M. Les manifestations articulaires des maladies inflammatoires chroniques de 1'intestin. Gastroenterol Clin Biol 1982;6:755-8. 4. Parke AL, Fagan DA, Chadwick VS, Hughes GR. Coeliac disease and rheumatoid arthritis. Ann Rheum Dis 1984; 43:378-80. 5. Bourne JT, Kumar P, Huskisson EC, Mageed R, Unsworth DJ, Wojtulewski JA. Arthritis and coeliac disease. Ann Rheum Db 1985;44:592-8. 6. Pinals RS. Arthritis associated with gluten sensitive enteropathy. / Rheumatol 1986;13:201-3. 7. Bouhnik Y, Rambaud JC. Manifestations systfmiques associees a la maladie coeliaque de l'adulte. Gastroenterol Clin Biol 1991;15:28-33. 8. Bouhnik Y, Prost A, Rambaud JC. Les manifestations syst£miques des ente'rocolopathies chroniques. In: Kahn MF, Ed. Les maladies systtmiques. 3 ed. Paris: Flammarion/Me'decine-sciences, 1991. 9. Chakravarty K, Scott DGI. Oligoarthritis. A presenting feature of occult coeliac disease. Br J Rheumatol 1992; 31:348-50. 10. Addelizzi RA, Pecora AA, Chiesa JC. Coeliac disease: case report with an associated arthropathy. Am J Gastroenterol 1983;I2:475-93.
Gouty Arthropathy and Synovial Uric Acid SIR—In western societies acute gout is most common in the first metatarsophalangeal (MTP), the ankle and the knee joint [1,2]. There are no inherent physiological or
Downloaded from http://rheumatology.oxfordjournals.org/ at University of Otago on July 27, 2015
1. Nordlund JJ, Lerner AB. Vitiligo. Arch Dermatol 1982; 118:5-8. 2. Dawber RPR. Clinical associations of vitiligo. Postgrad Med J 1970;46:276-7. 3. Burns-Cox CJ, Pearson JEG. Addison's disease, vitiligo and multiple autoantibodies. Postgrad Med J 1972;48:115-17. 4. Wade A (ed). Martindale. The extra pharmacopoeia, 27th edn London: Pharmaceutical Press, 1977;343-8. 5. Dukes MNG (ed). Meyler's side effects of drugs, 11th edn, Amsterdam: Elsevier, 1988;584. 6. Robins AH (ed). Biological perspectives on human pigmentation. Cambridge: Cambridge University Press, 1991 ;136-7. 7. Levontine A, Almeyda J. Drug induced changes in pigmentation. Br J Rheumatol 1973;89:105-12. 8. Levy H. Chloroquine induced pigmentation. S Afr Med J 1982;62:735-7. 9. Alarcon-Segovia D. Repigmentation of vitiligo under penicillamine treatment for rheumatoid arthritis. Arch Dermatol 1982;118:962. 10. Collen RJ, et al. Primary ovarian failure, juvenile rheumatoid arthritis and vitiligo. Am J Dis Child 1979;133:548-600.
791
BRITISH JOURNAL OF RHEUMATOLOGY VOL. XXXI NO. 11 TABLE I EFFICACY OF EXTRACORPOREAL PHOTOTHERAPY (DAYS 1-50)
Patient 1
Symptom
Day:
1
20 50
Patient 2 1
20 50
No of tender joints 13 5 6 13 3 12 2 7 15 6 No of swollen joints Visual analogue scale (mm) 100 50 50 50 20 300 180 300 240 0 Morning stiffness (mins) 15 7 11 15 6 Ritchie index 101 54 118 63 45 C-reactive protein (mg/1)
11 14 75 30 16 69
Patient 3 1 13 15 50 30 20 7
[2] using a different schedule and technique. In view of the excellent tolerance and efficacy further controlled studies are warranted. P. HlLLIQUIN*
'Service de Rhumatologie A, Hdpital Cochin, Paris; tPoste de Transfusion Sanguine, Hotel-Dieu et Hdpital Cochin, Paris, France. Accepted 2 July 1992 1. Edelson R, Berger C, Gasparro F, et al. Treatment of cutaneous T cell lymphoma by extracorporeal photochemotherapy. N EnglJMed 1987;316:297-303. 2. Malawista SE, Trock DH, Edelson RL. Treatment of rheumatoid arthritis by extra corporeal photochemotherapy: A pilot study. Arthritis Rheum 1991;34:646-54. 3. Andreu G, Boccaccio C, Lecrubier C, et al. Ultra violet irradiation of platelet concentrates: feasibility in transfusion practice. Transfusion 1990;30:401-6. 4. BoccacioC, Garcia I, Klaren i,etal. Ultra violet irradiation of platelet concentrates: in vitro and in vivo preclinical evaluation. Transfus Sci 1990;ll:141-7. 5. Gasparro F, Dell'Amico R, Goldminz D, Simmons E, Weingold D. Molecular aspects of extracorporeal chemotherapy. Yale J Bio! Med 1989;62:579-93. Chloroquine-induced Vitiligo in a Patient with Juvenile Onset Rheumatoid Arthritis SIR—We describe a 29-year-old black male with seropositive rheumatoid arthritis (RA) since the age of 14 years. He was treated with non-steroidal anti-inflammatory drugs (NSAIDs) and analgesics and remained relatively asymptomatic until the age of 25, when his disease became active. He was maintained on increased doses of NSAIDs until 2 years later (age 27), when a diseasemodifying agent had to be added to achieve better control. Roentgenograms at this stage revealed significant erosive disease at the metacarpophalangeal, proximal interphalangeal and carpal joints. Initial laboratory investigations demonstrated the following values: sheep cell agglutination test titre 1:64; latex agglutination test titre 1:320; antinuclear factor titre 1:10; erythrocyte sedimentation rate 76 mm/h (Westergren); C-reactive protein 8.2mg/dl; plasma viscosity 2.2 cp; circulating immune complexes 39%. The patient showed a gratifying response to the addition of chloroquine and was maintained on this drug and NSAIDs until 2 years later (age 29), when he developed areas of facial depigmentation. There was no past-dermatological history of note. His chloroquine was stopped and on follow up a month later no improvement was noted. He was subsequently referred to the dermatologists who confirmed the diagnosis of vitiligo. The morphology of the skin lesions was such that skin scrapings or skin biopsy were felt not to be indicated. The patient was started on vitamin C (100 mg/day) as placebo. On review
0 3 0 0 4 5
3 2 0 15 4 20
1
20 50
13 5 5 16 6 4 60 32 30 180 15 30 17 6 7 129 77 83
Patient 5 1
20 50
15 1 4 18 8 11 80 23 30 180 45 45 22 8 13 89 43 52
Patient 6 1
20 50
Patient 7 1
20 50
20 1 17 2 1 10 0 9 14 5 90 30 70 20 5 180 30 150 150 0 30 2 23 20 6 250 71 145 10 5
1 7 10 30 6 94
2 months later there was a dramatic improvement with virtually no trace of the vitiligo present. The patient did not use any topical treatment during the period. His arthritis remained inactive during this time. Vitiligo is a common skin disorder and has been associated with certain autoimmune diseases but not RA [1-3]. Chloroquine, a disease-modifying agent used in the treatment of RA, is known to cause hyperpigmentation secondary to sun exposure. Various dermatological reactions have been reported with chloroquine, including macular, urticarial, lichenoid and purpuric skin eruptions; photosensitivity and erythema multiforme [4, 5]. Bleaching of the skin has not been reported in the English literature. The most conspicuous side-effect of chloroquine is a depigmentation (bleaching) of the hair. This bleaching is reversible on drug withdrawal [6]. However, bleaching of the skin has not been described: on the contrary chloroquine is a well-documented cause of skin hyperpigmentation [4—8]. Idiopathic vitiligo is a common skin condition characterized by asymptomatic, variously sized or shaped, single or multiple patches of depigmentation. It has been reported in association with certain autoimmune diseases, particularly thyroid disease, pernicious anaemia, Addison's disease and diabetes mellitus [1-3]. The diagnosis of vitiligo can be confirmed histologically, but the clinical appearances are sometimes considered pathognomonic. Biopsy has the added advantage of demonstrating melanocytes preserved in the hair follicles, which may help in prognostication. However, the face is not aesthetically a suitable site for biopsy. Fungal infections and post-inflammatory hypopigmentation should always be considered in the differential diagnosis. These were not considered to be relevant in our patient at the time. Apart from two case reports [9,10] describing cases in which RA and vitiligo co-existed, a literature search revealed no clear association between these two diseases. Alarcon-Segovia [9] described a case of repigmentation of vitiligo with penicillamine therapy for RA and Collen et al. [10] described a case of hitherto unreported primary ovarian failure, juvenile arthritis and vitiligo. Without rechallenging the patient with the chloroquine we can only postulate that the vitiligo was caused by the drug. While we accept that our case does not prove the relationship between vitiligo and chloroquine, the circumstantial evidence is highly suggestive that the association is more than coincidental. This is the first report of such a side-effect in association with chloroquine. The vitiligo could have been secondary to the underlying autoimmune disease but, to the best of our knowledge, an association between vitiligo and RA has not been previously described. Similarly we can only postulate that the improvement in the vitiligo was a result of the chloroquine withdrawal and not due to the natural history of the skin disease or due to the treatment with the placebo.
Downloaded from http://rheumatology.oxfordjournals.org/ at University of Otago on July 27, 2015
C. J. MENKES,* G. ANDREU,! F. HESHMATI,!
20 50
Patient 4
LETTERS TO THE EDITOR L. A. GONGGRYP, A. A. KALLA
Department of Medicine, Rheumatic Diseases Unit, University of Cape Town, South Africa Accepted 17 July 1992
Juvenile Arthritis and Coeliac Disease SIR—We read with interest the case report: Oligoarthritis—a Presenting Feature of Occult Coeliac Disease [9]. We now report a case of arthritis and coeliac disease affecting a child. Our patient a 21-year-old Caucasian woman, first presented at 2.5 years of age with symmetrical polyarthritis affecting elbows, wrists, fingers and knees. There was fever but not the characteristic pattern of Still's disease, there was no rash. She had had diarrhoea from the age of 8 months, this was attributed to gluten intolerance and treated by dietary restriction; it subsided progressively and disappeared by 3 years of age. Four months before the onset of arthritis, she had had 'enteritis' treated by antibiotics. Her grandfather had iritis and lumbar pain. On physical examination, apart from the prominent arthritis, there was a polylymphoadenopathy and a moderate enlargement of the spleen. Laboratory tests revealed an increased erythrocyte sedimentation rate; rheumatoid factors were negative, as were anti-nuclear antibodies. A diagnosis of chronic juvenile arthritis was made, and she was treated with aspirin and gold salts. This, treatment had only moderate success in controlling arthritis. Seven years later, she was referred to our Rheumatology Department for local treatment with osmic acid for chronic bilateral synovitis of the knee. X-rays showed small erosions of both carpal and metacarpophalangeal joints. Her height was 117 cm (2 SD below normal) and she weighed 16.5 kg (3 SD below normal). Apart from a moderate increase of lipid content in the faeces (4.5 g compared to a norm of 2 g) with the presence of soaps, no other malabsorption feature (anaemia, hypoproteinemia, hypocalcaemia, hypokaliemia, evidence of osteomalacia) was detectable, HLA B27 was positive. Between 1980 and 1987, she had some painful crises, and remained on anti-inflammatory symptomatic treatment. In 1987, when she was 16 years of age, the statoponderal delay was still present and the possibility of occult coeliac disease was raised, a jejunal biopsy was performed which demonstrated villous atrophy. A glutenfree diet was then commenced.
There was a spectacular recovery in height and weight (respectively, 14 cm and 10 kg) within 2 years; a complete disappearance of the arthritis and an improvement in enteric histology was confirmed after 1 year of treatment. The patient has carried on with the diet and has no articular complaint apart from minimal painless hydarthrosis of the left knee. A few years ago, osteo-articular manifestations of this intestinal disorder were thought to be extremely rare [7, 8], and mainly due to the depletion of calcium, potassium and magnesium [6-9] or to metabolic bone disease (osteomalacia and/or osteoporosis) [5, 7-9]. It now seems obvious that a diagnosis of malabsorption syndrome should have been suspected earlier. In chronic juvenile arthritis, there can be a growth disturbance but weight is infrequently impaired. The age of onset is unusual, since the early 1980s after Prier et al. [1] and Addelizi et al. [10], some cases [ 2 , 4 , 5 , 9 ] concerning adults, have been published, the youngest patient was 15 years of age [6]. Our patient did not have either of the two major features of malabsorption present in occult coeliac disease of the adult, osteomalacia and anaemia [6-8]. The intestinal manifestations largely preceded the articular ones, and were considered as cured in the absence of diarrhoea. The presence of H L A B27, although not usual, was present in two of the six patients studied by Bourne [5]; one of them had radiological sacro-iliitis, which until now has not presented in our patient. Even though the etiology of the disease may be questionable, the therapeutic proof of gluten withdrawal, is reliable evidence. M. SIMOES, B. AMOR
Rheumatology Department, Hdpital Cochin, 27, ruedu Fg Saint Jacques, 75674 Paris Cedex 14, France Accepted 15 July 1992 1. Prier A, Le Quintrec Y, Camus JP, Gendre JP, Bradel P. Polyarthrites inflammatoires associees a une atrophie villositaire du grele. Rev Rhum 1980;47:661-5. 2. Gendre JP, Luboinski J, Prier A, Camus JP, Le Quintrec Y. Anomalies de la muqueuse jejunale et polyarthrite rhumatoide: 30 cas. Gastroenterol Clin Biol 1982;6:772-5. 3. Alcalay M. Les manifestations articulaires des maladies inflammatoires chroniques de 1'intestin. Gastroenterol Clin Biol 1982;6:755-8. 4. Parke AL, Fagan DA, Chadwick VS, Hughes GR. Coeliac disease and rheumatoid arthritis. Ann Rheum Dis 1984; 43:378-80. 5. Bourne JT, Kumar P, Huskisson EC, Mageed R, Unsworth DJ, Wojtulewski JA. Arthritis and coeliac disease. Ann Rheum Db 1985;44:592-8. 6. Pinals RS. Arthritis associated with gluten sensitive enteropathy. / Rheumatol 1986;13:201-3. 7. Bouhnik Y, Rambaud JC. Manifestations systfmiques associees a la maladie coeliaque de l'adulte. Gastroenterol Clin Biol 1991;15:28-33. 8. Bouhnik Y, Prost A, Rambaud JC. Les manifestations syst£miques des ente'rocolopathies chroniques. In: Kahn MF, Ed. Les maladies systtmiques. 3 ed. Paris: Flammarion/Me'decine-sciences, 1991. 9. Chakravarty K, Scott DGI. Oligoarthritis. A presenting feature of occult coeliac disease. Br J Rheumatol 1992; 31:348-50. 10. Addelizzi RA, Pecora AA, Chiesa JC. Coeliac disease: case report with an associated arthropathy. Am J Gastroenterol 1983;I2:475-93.
Gouty Arthropathy and Synovial Uric Acid SIR—In western societies acute gout is most common in the first metatarsophalangeal (MTP), the ankle and the knee joint [1,2]. There are no inherent physiological or
Downloaded from http://rheumatology.oxfordjournals.org/ at University of Otago on July 27, 2015
1. Nordlund JJ, Lerner AB. Vitiligo. Arch Dermatol 1982; 118:5-8. 2. Dawber RPR. Clinical associations of vitiligo. Postgrad Med J 1970;46:276-7. 3. Burns-Cox CJ, Pearson JEG. Addison's disease, vitiligo and multiple autoantibodies. Postgrad Med J 1972;48:115-17. 4. Wade A (ed). Martindale. The extra pharmacopoeia, 27th edn London: Pharmaceutical Press, 1977;343-8. 5. Dukes MNG (ed). Meyler's side effects of drugs, 11th edn, Amsterdam: Elsevier, 1988;584. 6. Robins AH (ed). Biological perspectives on human pigmentation. Cambridge: Cambridge University Press, 1991 ;136-7. 7. Levontine A, Almeyda J. Drug induced changes in pigmentation. Br J Rheumatol 1973;89:105-12. 8. Levy H. Chloroquine induced pigmentation. S Afr Med J 1982;62:735-7. 9. Alarcon-Segovia D. Repigmentation of vitiligo under penicillamine treatment for rheumatoid arthritis. Arch Dermatol 1982;118:962. 10. Collen RJ, et al. Primary ovarian failure, juvenile rheumatoid arthritis and vitiligo. Am J Dis Child 1979;133:548-600.
791
