Hence, alfuzosin can be considered effective in the decreased ... in his usual state of good health. ..... S A 97-yr-old Chinese lady has had bindings of her.
British Journal of Rheumatology 1998;37:1135–1141
LETTERS TO THE EDITOR anti-Jo-1 and anticardiolipin antibodies were negative. C3, C4 and thyroid hormones were within normal limits. Serological tests for HIV, Toxoplasma, cytomegalovirus, herpes virus and Epstein–Barr virus were negative. The evolution of analytical values is shown in Table I. An electromyogram performed on the left side of the body showed an increase in the insertional activity of the muscle with numerous fibrillation potentials and positive sharp waves at rest. The motor units showed decreased amplitude and duration, and increased polyphasic potentials. A magnetic resonance imaging (MRI ) exploration showed findings consistent with inflammation of muscles, and a right deltoid muscle biopsy revealed an infiltrate of lymphocytes and plasma cells in the muscle and perimysial tissues with an occasional polymorphonuclear leucocyte. There was necrosis of muscle fibres with phagocytosis and regeneration. An occult neoplasm was eliminated by performing X-ray films of the chest, urinalysis, ultrasonographic study of the abdomen, barium enema and gastroscopy. The patient has been receiving treatment with alfuzosin during the last year due to BPH. This drug was interrupted at admission; nonetheless, 3 days after there was no clinical or analytical improvement, so prednisone treatment was started at a dose of 1 mg/kg/day. On the following days, improvement in clinical and blood chemistry was found. Several drugs have been described as causing agentinduced dermatomyositis (phenylbutazone [7], statins [8, 9], hydroxyurea [10], -penicillamine [11, 12]). In this case, we have reported a new drug (alfuzosin) as a possible inducer of dermatomyositis. Alfuzosin is a quinazoline, a -adrenoceptor antagonist, which has 1 been associated with an increase in ANA, e.g. with prazosin [13], although this report has been discussed [14]. Relevant information was found on Medline. The literature found was published between 1966 and 1997 on autoimmune syndrome ( lupus erythematosus, dermatomyositis) induced by quinazoline. Only one report was found: a lupus erythematosus induced by doxazosin [15]. Nevertheless, an increase in ANA has been found in several cases [13, 16 ]. In our case, the quick response to corticosteroids
Alfuzosin-associated Dermatomyositis SAlfuzosin, a quinazoline derivative, is a selective antagonist of a -adrenoceptors. It causes a contraction 1 of prostatic, prostatic capsule, proximal urethral and bladder base smooth muscle, thereby reducing the tone of these genitourinary structures. Consequently, elevated urethral tone, resistance and pressure, bladder outlet resistance and bladder instability, associated with benign prostatic hyperplasia (BPH ), are reduced. Hence, alfuzosin can be considered effective in the symptomatic treatment of BHP. Adverse effects of alfuzosin have been evaluated in short- and long-term clinical trials. The most common side-effects seen in treated patients (usual daily dose 7.5–10 mg) were dizziness, headache, somnolence, diarrhoea, nausea, skin rash, asthenia and dry mouth These side-effects were generally reported as mild and improved after cessation of therapy. No unexpected or serious adverse effects and discontinuations are significant in clinical trials [1–6 ]. Alfuzosin is available in most European and Asian countries, and registration applications have been submitted to other countries. We recorded a probable alfuzosin-induced dermatomyositis in a man. This finding has not been previously reported for patients who have received alfuzosin for the treatment of BPH. A 75-yr-old man was admitted to the hospital. His symptoms included a gradually increasing proximal upper and lower limb muscle pain and weakness during a 4 day duration, accompanied by facial rash and periungual lesions. Prior to his admission, he had been in his usual state of good health. He denied fever or weight loss, but he had noticed fatigue. On admission, the patient appeared well. Muscle examination showed marked weakness involving the proximal limbs, with tenderness and swelling in deltoid, biceps and triceps areas. There was an erythematous rash with prominent oedema affecting malar areas and the bridge of the nose, periungual purpuric spots and erythematous plaques over the finger joints. The rest of the physical examination was normal. Laboratory examination revealed a normal, complete blood count. The erythrocyte sedimentation rate ( ESR) was 28 mm/h, creatine kinase (CK ) was 2109 U/l (normal values 25–190 U/l ), of which 100% was MM, lactate dehydrogenase (LDH ) was 856 U/l (normal values 230–460 U/l ), aldolase 24.5 U/l (normal values 0–7.5), serum aspartate aminotransferase (AST ) 250 U/l (normal values 10–35 U/l ) and alanine aminotransferase (ALT ) 113 U/l (normal values 9–43 U/l ). The rest of the biochemical tests, including gammaglutamyl transpeptidase (GGT ) and alkaline phosphatase, were normal. The ANA was positive, with a titre of 1/80 with a speckled pattern. Anti-dsDNA, anti-Ro, anti-La, anti-Sm, anti-RNP,
TABLE I Analytical evolution (all values are in U/I )
Normal value 1st day 3rd day 9th day 19th day 25th day
AST
ALT
Aldolase
CK
LDH
10–35 250 216 96 70 61
9–43 103 77 55 37 34
0–7.5 19.8 24.5 12.6 10.5 4.7
25–190 2109 2579 1046 762 665
230–460 856 1941 615 546 495
© 1998 British Society for Rheumatology 1135
1136
BRITISH JOURNAL OF RHEUMATOLOGY VOL. 37 NO. 10
could be consistent with a drug-induced phenomenon. On the other hand, the normality of immunological values (ANA, C3, C4, ENA and anti-Jo), and the negative search for the neoplasic syndrome, mitigate the diagnosis of causes other than pharmacological ones. Therefore, we recommend that clinical signs of patients who have been treated long term with quinazolines be monitored for possible autoimmune syndrome induced by quinazoline. P. V-C, J. B-B,* A. N-R*
Rheumatology Service and *Pharmacy Service, Hospital General University of Elche, 03202 Elche, Spain Accepted 12 May 1998 Correspondence to: P. Vela-Casasempere, Reumatologı´a, Servicio de Medicina Interna, C/Huertos y Molinos s/n, Hospital General Universitario de Elche, 03202 Elche, Spain. 1. Jardin A, Bensadoun H, Delauche-Cavallier MC, Attali P. Alfuzosin for treatment of benign prostatic hypertrophy. The BPH-ALF Group. Lancet 1991;337:1457–61. 2. Buzelin JM, Hebert M, Blondin P. Alpha-blocking treatment with alfuzosin in symptomatic benign prostatic hyperplasia: comparative study with prazosin. The PRAZALF Group. Br J Urol 1993;72:922–7. 3. Jardin A, Bensadoun H, Delauche-Cavallier MC, StallaBourdillon A, Attali P. Long-term treatment of benign prostatic hyperplasia with alfuzosin: a 24–30 month survey. BPHALF Group. Br J Urol 1994;74:579–84. 4. Multicenter observational trial on symptomatic treatment of benign prostatic hyperplasia with alfuzosin: clinical evaluation of impact on patient’s quality of life. The Italian Alfuzosin Cooperative Group. Eur Urol 1995;27:128–34. 5. Lukacs B, Blondin P, MacCarthy C, Du Boys B, Grippon P, Lassale C. Safety profile of 3 months’ therapy with alfuzosin in 13,389 patients suffering from benign prostatic hypertrophy. Eur Urol 1996;29:29–35. 6. Buzelin JM, Roth S, Geffriaud-Ricouard C, Delauche-Cavallier MC. Efficacy and safety of sustained-release alfuzosin 5 mg in patients with benign prostatic hyperplasia. ALGEBI Study Group. Eur Urol 1997,31:190–8. 7. Curran JJ, Jamieson TW. Dermatomyositis-like syndrome associated with phenylbutazone therapy. J Rheumatol 1987;14: 397–8. 8. Hill C, Zeitz C, Kirkham B. Dermatomyositis with lung involvement in a patient treated with simvastatin. Aust NZ J Med 1995;25:745–6. 9. Rodriguez-Garcia JL, Serrano Commino M. Lovastatinassociated dermatomyositis. Postgrad Med J 1996;72:694. 10. Senet P, Aractingi S, Porneuf M, Perrin P, Duterque M. Hydroxyurea-induced dermatomyositis-like eruption. Br J Dermatol 1995;133:455–9. 11. Takahashi K, Ogita T, Okudaira H, Yoshinoya S, Yoshizawa H, Miyamoto T. D-penicillamine-induced polymyositis in patients with rheumatoid arthritis. Arthritis Rheum 1986;29: 560–4. 12. Bahadoran P, Castanet J, Lacour JP, Perrin C, Del Giudice P, Mannocci N et al. Pseudo-dermatomyositis induced by longterm hydroxyurea therapy: report of two cases. Br J Dermatol 1996;134:1161–3. 13. Marshall AJ, McGraw ME, Barritt DW. Positive antinuclear factor tests with prazosin. Br Med J 1979;1:165–6. 14. Wilson JD, Bullock JY, Booth RJ. Influence of prazosin on the development of antinuclear antibodies in hypertensive patients. Clin Pharmacol Ther 1979;26:209–12. 15. Feurle GE. Doxazosin-induced lupus erythematodes. Dtsch Med Wochenschr 1992;117:157. 16. Bainbridge CV. Prazosin and ANA. Am Fam Physician 1981;24:41–2.
Cavitary Lung Tuberculosis in a Rheumatoid Arthritis Patient Treated with Low-dose Methotrexate and Steroid Pulse Therapy SRheumatoid arthritis (RA) patients are frequently treated by immunosuppressive agents and steroids, which may increase the risk of opportunistic infections. Corticosteroid pulse therapy (CPT ) produces relatively mild side-effects [1, 2] and the infection rate during lowdose methotrexate (MTX ) ranges from 0 to 27%, with an increased risk soon after the onset of therapy [3]. Several pathogens have previously been reported in RA patients treated by CPT and low-dose MTX. We report a case of upper lobe cavitary tuberculosis ( TB) in a patient with RA under this treatment. In 1991, M.M., a white female aged 40 yr who had been suffering from RA since 1988, first came to our clinic. She had previously undergone treatment with NSAIDs, low-dose steroids (LDS) (prednisone 5 mg daily), hydroxychloroquine and oral gold salts, but with poor response. Diagnosis of RA was confirmed, according to the 1987 ACR criteria; she had acute arthritic symptoms, rheumatoid nodules, serum IgM factor and decreased levels of complement fractions and glucose in synovial fluid. She was a non-smoker, and no clinical, functional and/or radiographic chest abnormality was found. She started salazosulphapyridine and methylprednisolone 4 mg daily, and continued hydroxychloroquine; clinical remission was reached in ~6 weeks. Over the next 3 yr, only one short clinical relapse occurred, continuing drug administration. In January 1994, arthritis flared up again with early radiographic changes of the joints. Total oral prednisone equivalent administered since initial presentation was 4.47 g. Previously administered drugs were suspended and oral MTX (7.5 mg weekly) was started, together with NSAIDs and Deflazacort 6 and 12 mg on alternate days. After 2 months, steroids were gradually tapered. Chest X-ray did not reveal any abnormality. In September 1994, active arthritis reappeared; methylprednisolone 8 mg daily was administered, without clinical improvement. To obtain a prompt resolution of symptoms and to avoid high-dose oral steroids, a 3 day course of CPT (1 g methylprednisolone i.v. daily) was followed by a clinical remission; 10 days later, 4 mg methylprednisolone daily were administered. In December 1994, the patient complained of a persistent cough, with little sputum and no fever; increased sedimentation rate and normal white cell count were found. Chest X-ray and tomography revealed right upper lobe cavitation and contralateral nodules ( Fig. 1), without evident clinical signs on physical chest examination. Any past history of TB was excluded. Direct microscopic examination of the sputum revealed the presence of Mycobacterium tuberculosis (MT ) and sputum cultured for acid/alcoholfast bacilli grew MT. This confirmed the diagnosis of TB and definitively excluded other forms of nodular lung lesions such as malignancy and rheumatoid pulmonary involvement.
LETTERS TO THE EDITOR
MTX was stopped and steroids were tapered off, while rifampicin 600 mg, ethambutol 1.5 g and isoniazid 300 mg daily were started immediately. Determination of drug susceptibility revealed the efficacy of all three. After 6 months, rifampicin was suspended, while ethambutol and isoniazid were continued for a further 3 months. X-ray control after 5 months showed complete resolution of the cavitation with residual contralateral calcified nodules, confirmed later by radiographic controls. In the following years, M.M. started parenteral gold salts, but suffered from severe articular damage and leucocytoclastic vasculitis together with mixed cryoglobulinaemia, and underwent three surgical prostheses. Class II HLA determination revealed the presence of DR4 antigen. This is a case of RA in a middle-aged woman who developed a cavitary TB after low-dose MTX and CPT. We chose this therapy to obtain prompt control of the flare-up of arthritis, sparing high-dose oral steroids, and to achieve clinical remission by MTX alone. Irrespective of treatment, the susceptibility to common infections of patients with RA does not seem to have increased [4]. Nevertheless, these patients are frequently treated with immunosuppressive agents and, among these, CPT and low-dose MTX have been associated with an increased risk of opportunistic infections [1–4]. No case of TB was reported before 1995 during low-dose MTX [3] and CPT; only three other cases of cytomegalovirus infections, one of Pneumocystis carinii pneumonia and one of herpes zoster have been reported since then [5–9]. TB infection has been reported in three rheumatic patients who underwent low-dose MTX and were affected by diseases different from RA [3, 10]. In our patient, the onset of lung infection appears to be closely related to MTX and CPT, because of the interval between drug administration and the onset of TB, and the lack of other risk factors for opportunistic infection. The role of low-dose oral steroids administered to our patient after CPT remains doubtful; in
F. 1.—Chest X-ray revealing right upper lobe cavitation and contralateral nodules.
1137
fact, although a cumulative dose of >700 mg of prednisone seems to be related to enhanced risk of infection [11], no increased rate or inhibited host defence mechanism has been reported at doses below 10 mg of prednisone daily [3]. No conclusive statement about the prevailing role played by MTX or CPT can be advanced. On the other hand, corticosteroids seem to play an important role in TB infection by promoting reactivation of latent infection [12] rather than the onset of primary infection, and our patient had no past history of MT infection. Therefore, TB could be mainly dependent on MTX treatment, but a predisposing role played by the combination of the two drugs cannot be excluded. In conclusion, this case underlines the necessity of close monitoring for severe opportunistic infections in rheumatoid patients during treatment with CPT and MTX, particularly those with an aggressive disease or with its markers. C. G, N. P, E. M, C. R, F. G, G. M
‘Salvatore Maugeri’ Foundation, Medical Center of Rehabilitation, IRCCS, Localita` S.Stefano in Lanteria, 82037 Telese Terme (BN), Italy Accepted 28 May 1998 Correspondence to: C. di Girolamo. 1. Weusten BLAM, Jacobs JWG, Bijlsma JWJ. Corticosteroid pulse therapy in active rheumatoid arthritis. Semin Arthritis 1993;23:183–92. 2. Van der Veen MJ, Bijlsma JWJ. The effect of methylprednisolone pulse therapy on methotrexate treatment of rheumatoid arthritis. Clin Rheumatol 1993;12:500–5. 3. Boerbooms AMT, Kerstens PJSM, van Loenhout JWA, Mulder J, van de Putte LBA. Infections during low-dose methotrexate treatment in rheumatoid arthritis. Semin Arthritis Rheum 1995;24:411–21. 4. van der Veen MJ, van der Heide A, Kruize AA, Bijlsma JWJ. Infection rate and use of antibiotics in patients with rheumatoid arthritis treated with methotrexate. Ann Rheum Dis 1994;53:224–8. 5. Aglas F, Rainer F, Herman J, Gretler J, Huttl E, Domej W et al. Interstitial pneumonia due to cytomegalovirus following low-dose methotrexate treatment for rheumatoid arthritis. Arthritis Rheum 1995;38:291–6. 6. Bowman S, Mowat A. Cytomegalovirus in methotrexate-treated rheumatoid arthritis patients: comment on the concise communication by Aglas et al. Arthritis Rheum 1995;38:1861–6. 7. Okuda Y, Oyama T, Oyama H, Miyamoto T, Takasugi K. Pneumocystis carinii pneumonia associated with low-dose methotrexate treatment for malignant rheumatoid arthritis. Ryumachi 1995;35:699–704 (in Japanese). 8. Thomas E, Olive P, Mazyad H, Blotman F. Cytomegalovirusinduced pneumonia in a rheumatoid arthritis patient treated with low dose methotrexate. Clin Exp Rheumatol 1997;15:583–4. 9. Lyon CC, Thompson D. Herpes zoster encephalomyelitis associated with low-dose methotrexate for rheumatoid arthritis. J Rheumatol 1997;24:589–91. 10. Belzunegui J, Plazaola I, Uriarte E, Pego JM. Primary tuberculosis muscle abscess in a patient with systemic lupus erythematosus. Br J Rheumatol 1995;34:1177–8. 11. Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in patients taking glucocorticosteroids. Rev Infect Dis 1989; 11:954–63. 12. Cisneros JR, Murray KM. Corticosteroids in tuberculosis. Ann Pharmacother 1996;30:1298–303.
1138
BRITISH JOURNAL OF RHEUMATOLOGY VOL. 37 NO. 10
Similar Response of Adrenocorticotrophic Hormone, Cortisol and Prolactin to Surgery in Rheumatoid Arthritis and Osteoarthritis SStudies by Chikanza et al. [1] showed a diurnal cortisol rhythm which was at the lower limit of normal in patients with rheumatoid arthritis (RA) and a failure to increase cortisol levels following surgery. They also found increased levels of prolactin in patients with RA and an abnormal increase in prolactin levels after surgery [2]. They conclude that in RA a defective hypothalamic-pituitary-adrenal axis response and excessive prolactin reaction lead to a pro-inflammatory hormonal status which might play a role in the pathogenesis of RA [3]. The aim of this study was to confirm these findings. Nine patients with rheumatoid factor-positive RA and 10 patients with osteoarthritis (OA) who needed total knee or hip replacement were studied. Seven RA patients were using disease-modifying anti-rheumatic drugs (DMARDs). All OA patients, and all but one RA patients, were treated with NSAIDs. At 7:30 a.m. before surgery, and on the following 4 days, blood was collected for the determination of plasma adrenocorticotrophic hormone (ACTH ), plasma cortisol and serum prolactin levels. There was no significant difference in age (RA: mean [...] 63.3 [3.5] yr, OA: 66.4 [2.1 yr]). Mean ESR in RA patients was 25.6 [3.4] mm/h. Before surgery, plasma cortisol levels in patients with RA and in patients with OA were 0.48 [0.04] mmol/l and 0.58 [0.04] mmol/l, respectively (Fig. 1A). Following surgery, no significant changes were found either within or between groups. Before surgery, ACTH levels were in the normal range, both in the RA patients (6.7 [1.3] pmol/l ) and the OA patients (5.32 [1.2] pmol/l ) ( Fig. 1B). The first day after surgery, a comparable decrease was seen in both groups with a return to pre-
operative levels in the following days. There were no significant differences in prolactin levels before surgery between both groups nor were there any significant changes after surgery (not shown). These observations are in disagreement with the study of Chikanza et al. [1, 2]. Firstly, we found higher levels of cortisol in both RA and OA patients. This might be related to the fact that in our study patients’ blood was drawn at 7:30 a.m. and in Chikanza’s study at 9:00 a.m. Before surgery, in our patients cortisol levels were in the upper range of normal and we attributed this to stress in anticipation of the operation; perhaps the patients in the study of Chikanza had received more sedative drugs as pre-medication than the patients in our study. Another explanation could be the influence of anti-rheumatic therapy on the HPA axis. In the study by Chikanza et al., the diurnal rhythm of cortisol was studied in 10 patients with active RA, 10 patients with non-inflammatory arthritis (NIA) and in 10 patients with osteomyelitis (OM ); whereas all patients with RA were treated with NSAIDs, only five of the NIA and none of the OM patients were. Nine RA patients were also treated with a DMARD. The RA patients showed the lowest cortisol values, the NIA patients higher values and the OM patients the highest values. The high cortisol values of the OM patients are to be expected because of their active inflammation, but one would expect the same values in the RA patients with a comparable degree of inflammation. The fact that this was not found might suggest a hypothalamic defect, but might also be the result of the use of NSAIDs and/or DMARDs. One of the possible mechanisms by which cytokines may activate the HPA axis is through the synthesis of prostaglandins, which stimulate the secretion of corticotrophin releasing hormone (CRH ) [4–6 ]. Studies in animals have shown that the effect of cytokines on
F. 1.—Cortisol (A) and adrenocorticotrophic hormone (ACTH ) (B) levels in patients with RA (—) and OA (– – –). Values were taken at 7:30 a.m. on day 0 (day of surgery) and on days 1–4 after surgery. Values are the mean ± S.E.M.
LETTERS TO THE EDITOR
CRH release could be antagonized by blocking the cyclooxygenase pathway and thereby prostaglandin synthesis by NSAIDs [7, 8]. Through this mechanism, NSAIDs might cause a decreased cortisol response. In the study of Chikanza et al. [1, 2], the reactions to surgery were studied in 10 patients with RA, nine with OA and 10 with OM. Before surgery, cortisol levels were similar in RA and OA, but higher in OM patients (not using NSAIDs). After operation, RA patients showed no increased cortisol levels, whereas OM and OA patients did. This difference after surgery cannot be explained by the use of NSAIDs as this was comparable in RA and OA. A possible influence of DMARDs on the HPA axis cannot be excluded. Secondly, we did not observe higher levels of prolactin before the operation in patients with RA nor an excessive secretion after surgery. This might be explained by a difference in disease activity, as illustrated by the ESR: mean [..] 25.6 [10.3] vs 56.9 [18] mm/h in the study by Chikanza et al. However, our findings of normal prolactin levels in RA are in agreement with recent studies in which no significant difference was found in prolactin levels between patients with RA and controls [9, 10]. In conclusion, we found neither a defective response of the pituitary–adrenal axis nor an excessive prolactin secretion in patients with RA. We therefore question the existence of a defective hypothalamic response in patients with RA and suggest that a possible influence of NSAIDs on the HPA axis should be considered. This study was supported by a grant from ‘Het Nationaal Reumafonds’ of The Netherlands. A. E, F. H, R. L, M. W M,* A. H,† C. S,‡ D.-J. R, L. P
Departments of Rheumatology, *Orthopedics, †Endocrinology and ‡Chemical Endocrinology, University Hospital Nijmegen and St Maartenskliniek, Nijmegen, The Netherlands Accepted 1 June 1998 Correspondence to: Agnes Eijsbouts, Department of Rheumatology, University Hospital Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands. 1. Chikanza IC, Petrou P, Kingsley G, Chrousos G, Panayi GS. Defective hypothalamic response to immune and inflammatory stimuli in patients with rheumatoid arthritis. Arthritis Rheum 1992;35:1281–8. 2. Chikanza IC, Petrou P, Chrousos G, Kingsley G, Panayi GS. Excessive and dysregulated secretion of prolactin in rheumatoid arthritis: immunopathogenetic and therapeutic implications. Br J Rheumatol 1993;32:445–8. 3. Chikanza IC, Chrousos G, Panayi GS. Abnormal neuroendocrine immune communications in patients with rheumatoid arthritis. Eur J Clin Invest 1992;22:635–7. 4. Katsuura G, Gottschall PE, Dahl RR, Arimura A. Adrenocorticotrophin release induced by intracerebroventricular injection of recombinant human interleukin-1 in rats: possible involvement of prostaglandin. Endocrinology 1988;122:1773–9. 5. Watanabe T, Morimoto A, Sakata Y, Murakami N. ACTH response induced by interleukin-1 is mediated by CRF secretion stimulated by hypothalamic PGE. Experientia 1990;46:481–4. 6. Navarra P, Tsagarakis S, Faria MS, Rees LH, Besser GM, Grossman AB. Interleukins-1 and -6 stimulate the release of
7.
8.
9. 10.
1139
corticotropin-releasing hormone-41 from rat hypothalamus in vitro via the eicosanoid cyclooxygenase pathway. Endocrinology 1991;128:37–44. Rivier C, Vale W. Stimulatory effect of interleukin-1 on adrenocorticotropin secretion in the rat: Is it modulated by prostaglandins? Endocrinology 1991;129:384–8. Morimoto A, Murakami N, Nakamori T, Sakata Y, Watanabe T. Possible involvement of prostaglandin E in development of ACTH response in rats induced by human recombinant interleukin-1. J Physiol 1989;411:245–56. Templ E, Koeller M, Riedl M, Wagner O, Graninger W, Luger A. Anterior pituitary function in patients with newly diagnosed rheumatoid arthritis. Br J Rheumatol 1996;35:350–6. Kassimos D, Choy E, Grossman A, Chikanza I, Panayi G. Endogenous opioid tone in patients with rheumatoid arthritis. Br J Rheumatol 1996;35:436–40.
Re: Management of Idiopathic Carpal Tunnel Syndrome SThe survey by Pal et al. [1] revealed an interesting variation in the management of idiopathic carpal tunnel syndrome (ICTS ) by British rheumatologists, but the guidelines proposed by the authors are untenable. ICTS is one of the commonest and simplest conditions that we are asked to treat. It is primarily a clinical diagnosis based principally on a suggestive history, and perhaps reinforced by one or more physical signs. Neurophysiological assessment is superfluous in most cases and is potentially misleading. Steroid injection of the carpal tunnel is easy to perform, usually rapidly effective and has a low complication rate. It can also serve as a specific and sensitive diagnostic test for the condition. Failure of response indicates either an incorrect diagnosis or median nerve compression of a degree which is unamenable to local steroid therapy. In the latter situation, the physical signs should be unequivocal and the diagnosis readily confirmable by electromyography ( EMG) and nerve conduction studies (NCS ) prior to surgery. The false-negative rate for EMG and NCS in the diagnosis of ICTS is unknown, but milder or intermittent cases of median nerve compression may not be associated with a measurable slowing of sensory nerve conduction velocity, the minimum diagnostic criterion for CTS [2]. Apart from further increasing the demand on an already overburdened service, insisting on neurophysiological verification of the diagnosis of ICTS prior to treatment may deny patients a very simple, safe and effective treatment, or at least delay it for weeks or months. Phalen [3] considered that ‘electrodiagnostic studies surely are not necessary in every patient with carpal tunnel syndrome’ and that a good response to a local steroid injection ‘provides excellent confirmation of the diagnosis’. A pragmatic policy is to reserve EMG and NCS for cases in which there is reasonable doubt about the diagnosis, or where conservative treatment has proved ineffective [4]. N. J. S
Department of Rheumatology, Edith Cavell Hospital, Bretton Gate, Peterborough PE3 9GZ Accepted 5 June 1998
1140
BRITISH JOURNAL OF RHEUMATOLOGY VOL. 37 NO. 10
1. Pal B, Morris J, Keenan J, Mangion P. Management of idiopathic carpal tunnel syndrome (ICTS ): a survey of rheumatologists’ practice and proposed guidelines. Br J Rheumatol 1997;36: 1328–30. 2. Boniface SJ, Morris I, Macleod A. How does neurophysiological assessment influence the management and outcome of patients with carpal tunnel syndrome? Br J Rheumatol 1994;33:1169–70. 3. Phalen GS. Reflections on 21 years’ experience with the carpaltunnel syndrome. J Am Med Assoc 1970;212:1365–7. 4. Richards AJ. How does neurophysiological assessment influence the management and outcome of patients with carpal tunnel syndrome? [Letter] Br J Rheumatol 1995;34:581.
purposedly fused in extreme flexion. Other deformities include dystrophic toe nails, loss of medial arch support, ankle valgus and displaced heel pad. In motion, she practically walks on her buried small toes, although she still retains remarkably good ankle flexion and extension. Ironically, the practice of bindings was the privilege and class symbol of the ladies of wealthy and aristocratic families of the Ching Dynasty (1644–1912), China. The gait, which is small-stepped and shifting, is intended to be graceful and genteel. Such small feet, known as the ‘the three inches of the golden lily’, are rarities and seldom seen nowadays. S. K. M
Binding Feet, the Living Legacy of the Ching Dynasty (1644–1912), China
Department of Medicine, The Chinese University of Hong Kong, Room E, 17 Floor, CNT Tower, 338 Hennessy Road, Wanchai, Hong Kong Accepted 1 June 1998
SA 97-yr-old Chinese lady has had bindings of her forefeet since childhood ( Fig. 1). The small toes were
(a)
(b)
(c)
(d)
LETTERS TO THE EDITOR
1141
(e) F. 1.—(a) Standing view, both feet. (b) Dorsal surface, apparent missing small toes. (c) Volar surface of left foot, showing extreme flexion of small clawed toes. (d) Volar surface of left foot, close-up view, in plantar flexion. (e) Lateral view of left foot, displaced heel pad, apparent missing toes.
