81
stop an episode. We therefore continued pyridoxine and began maintenance treatment with phenobarbitone, which reduced the frequency and severity of the attacks but did not relieve the touch-induced myoclonus. All episodes could be stopped by forcibly flexing the infant. These findings led to a diagnosis of startle disease. Although no defmite family history could be obtained because the father and his family do not live in the UK, two first cousins (paternal) had had neonatal convulsions but are now healthy
REFERENCES 1. Kirstein L, Silfverskiold B. A family with emotionally precipitated drop seizures. Acta Psychiatr Scand 1958; 33: 471-76. 2. Suhren O, Bruyn GW, Tuynman JA. Hyperekplexia: a hereditary startle syndrome. J Neurol Sci 1966; 3: 577-605. 3. Andermann F, Andermann E. Startle disorders of man: hyperekplexia,
jumping and startle epilepsy. Brain Dev 1988; 10: 213-22. C, Roze JC, David A, Veccierini MF, Renaud P, Mouzard A. Hyperekplexia or stiff baby syndrome. Arch Dis Child 1991; 66:
4. Tohier
on no treatment.
We speculated that the abnormalities might be due to low GABA concentrations. A CSF sample was taken on day 14. Free GABA, measured by ion-exchange chromatography with fluorescence detection, was abnormally low (11nmol/1 compared with normal range for newborn infants of 20-100 mnolfl).8 Clonazepam was introduced on day 28 and phenobarbitone was gradually withdrawn. The infant showed great improvement; a normal tone pattern developed and she now has only a few nocturnal myoclonic episodes, though nose tappingb can still elicit a startle response. At 9 weeks, the CSF free GABA concentration was 35 nmol/1, in the low normal range for this age. The infant is now 3 months old and is at home with an apnoea alarm in use. She has mild general hypotonia with greater tone in the upper limbs, but no fisting.
Hyperactivity of the brainstem centres, especially of the rhomboencephalic reticular formation, has been suggested as the cause of startle disease.2,3,7 Several nuclei in the medullary and pontine reticular formation are primary sources of serotoninergic innervation in the brain; thus it is possible that serotoninergic hyperexcitability is a primary cause of the disorder, especially since it has been successfully treated with the serotonin antagonist clonazepam.2 Some of the symptoms of startle disease are similar to those of opioid-induced hypertonicity, so it could be a defect of the endogenous opiate pathway.9 A genetic defect resulting in low brain and CSF GABA is another possibility. GABA is an important inhibitory neurotransmitter, and low concentrations could produce hyperexcitability in the nervous system. A low threshold to epileptic stimulil3 and high amplitude of somatosensory responses5 have also been described in this disorder. The improvement with clonazepam could be explained by potentiation of GABA transmission, brought about by increasing the sensitivity of the GABA receptor, which in turn could lead to an increase in free CSF GABA. If startle disease is primarily due to low GABA concentrations, the best treatment should be vigabatrin. However, this drug can produce microvacuolation in myelinated tracts in animals, so it could interfere with myelination in very immature infants. The mechanism by which acute flexion of the trunk10 abolishes the signs of this disorder remains a mystery. Our case also illustrates the difficulties of clinical diagnosis of startle disease. Although the infant had all the classic signs, we were initially cautious. The myoclonic movements produced a lot of artifacts on the EEG so it was difficult to rule out electrical seizures. The apnoea and abnormal eye movements also hinted at an epileptiform basis. However, the production of myoclonic jerks in response to touch and their inhibition by swaddling and flexing, together with the persistent startle response to nose tapping,6 helped to clinch the diagnosis. We suggest that measurement of CSF GABA concentration is helpful in the diagnosis of this disorder and that the GABA neurotransmitter system is implicated in its pathogenesis. L. M. S. D. is supported by the Medical Research Council. We thank Dr D. Wertheim and Miss M. Hayden for electrophysiological investigation, the Magnetic Resonance Imaging Unit for MRI and MRS studies, and our colleagues for helpful discussions.
460-61. 5. Markand ON,
Garg BP, Weaver (hyperekplexia): electrophysiological
DD. Familial startle disease studies. Arch Neurol 1984; 41:
71-74. 6. Shahar E, Brand
N, Uziel Y, Barak Y. Nose tapping test inducing a generalized flexor spasm: a hallmark of hyperekplexia. Acta Paediatr Scand 1991; 80: 1073-77.
7.
Morley DJ, Weaver DD, Garg BP, Markand O. Hyperekplexia:
an
inherited disorder of the startle response. Clin Genet 1982; 21: 388-96. 8. Carchon HA, Jaeken J, Jansen E, Eggermont E. Reference values for free gamma-aminobutyric acid determined by ion-exchange chromatography and fluorescence detection in the cerebrospinal fluid of children. Clin Chim Acta 1991; 201: 83-88. 9. Weinger MB. "Stiff baby" syndrome: an expression of the same neural circuitry responsible for opiate-induced muscle rigidity? Anesthesiology
1987; 66: 580-81. 10.
Dalla Bernardina B. Startle disease: avoidable cause of sudden infant death. Lancet 1989; i: 216.
Vigevano F, Di Capua M,
an
ADDRESSES: Department of Paediatrics and Neonatal Medicine, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK (L. M. S. Dubowitz, MD, H. Bouza, MD, M. F. Hird, MRCP), and Department of Paediatrics, Universitair Ziekenhuis Gasthuisberg, Leuven, Belgium (J. Jaeken, PhD). Correspondence to Dr L. M. S. Dubowitz.
Detection of Chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction
In 1986, Chlamydia trachomatis elementary bodies were found by direct immunofluorescence (DIF) in synovial-fluid cell deposits and synovialmembrane biopsy samples from five of eight patients with sexually acquired reactive arthritis (SARA) but in none of eight controls with other types of arthritis. Cells from the original slides (stored at 4°C) have now been examined by a polymerase chain reaction (PCR) that amplifies DNA for the major outer membrane protein of C trachomatis. Chlamydial DNA was found in samples from four DIF-positive patients, one DIF-negative patient, and one DIFnegative control. Overall, there was 80% concordance for DIF and PCR results. This study supports our previous finding of chlamydiae in joints in reactive arthritis.
in about 1 % of men with and disease definitely associated non-gonococcal urethritis, with sexually transmitted infection has been called sexually acquired reactive arthritis (SARA).1 Serovars of Chlamydia trachomatis account for up to 50% of cases of nongonococcal urethritis and for other genital-tract diseases
Reactive arthritis
develops
82
COMPARISON OF PCR AND DIF RESULTS
NA= not available.
*Reclprocal titre 64.
including cervicitis and salpingitis. The association between C trachomatis infection and SARA was strengthened when, by means of a direct immunofluorescence (DIF) method, we detected C trachomatis in the joints of patients with SARA2 and seronegative arthritis.3 A polymerase chain reaction (PCR) designed to amplify a conserved region of the major outer membrane protein (MOMP) gene of C trachomatis is at least as sensitive as DIF for detection of chlamydiae in genital-tract specimens. We have shown that the PCR can detect chlamydiae on slides prepared for examination by D IF. We have examined by PCR smears of synovial-fluid cell deposits and synovial-membrane biopsy sections prepared for our original study.2 The synovial-fluid cell deposits and synovial-membrane biopsy sections had been fixed on MicroTrak (Syva, UK) slides, stained with the MicroTrak reagent (fluorescein-conjugated C trachomatis monoclonal antibody), covered with a cover-slip, and stored at 4°C for about 6 years. The samples came from eight patients with SARA and eight controls; they were originally examined by DIF for fluroescent C trachomatis elementary bodies. The cells were scraped from the slidess for examination by PCR. The presence or absence of elementary bodies in each sample was not disclosed until the results of the PCR assay were available.
PCR results are compared with our previous DIF and serological findings in the table. Fluorescent elementary bodies were detected originally in synovial-fluid cell deposits, synovial-membrane specimens, or both, from five SARA patients. In the other three patients, evidence of current or recent C trachomatis infection was provided by positive genital-tract DIF (not shown) with or without serum or synovial-fluid IgG antibody reciprocal titres of 64 or above. Four of five DIF-positive samples and one DIF-negative sample were positive by PCR. All the controls had been negative by DIF, but one was positive by PCR; no material for PCR was available for one control. Thus, of fifteen pairs of samples with complete data, the results were concordant for twelve (80%). Our finding of C trachoma tis elementary bodies in joints of patients with SARA2 was not confirmed by others using DIF,6although there was some support from electron microscopy and immunochemistry7 and from the use of probes to detect chlamydial rRNA. 8,9 However, the development of a highly sensitive PCR that could be used on samples fixed on slides enabled us to re-examine our original slides and so directly support our original observations.
There was 80% concordance between the DIF and PCR results. The discordant results could be due to loss of chlamydial elementary bodies during storage or in the process of transfer from slide to PCR reaction mixture. The detection of chlamydiae by the PCR in one of the DIF-negative control specimens did cause some concern. However, that patient, a young woman, was initially thought to have had early rheumatoid arthritis, but she had had an acute episode of polyarthritis in both knees associated with a rash; both features resolved over 5 months without further evidence of rheumatoid disease. We are aware and have had experience of the DNA contamination that can arise with PCR methods. Because spurious results may be generated, it is most important to ensure the validity of the PCR result before questioning any clinical diagnosis. Nevertheless, provided that adequate precautions are taken to prevent contamination, we believe that this technique will be applicable for samples from other patients and will be valuable to those workers who are not confident about use of the DIF technique owing to its subjectivity. Use of PCR based on a chlamydial plasmid failed to detect chlamydial DNA in the joints of other patients with SARA.1O It is possible that intra-articular chlamydiae can lose plasmids, but the reason for the failure of one PCR and the success of ours, based on DNA associated with the MOMP of C trachomatis, is not known. It is clear, however, that the PCR we used is more sensitive than any other chlamydial detection procedure apart from DIF. REFERENCES 1. Keat AC, Maini RN, Nkwazi GC, Pegrum GD, Ridgway GL, Scott JT. Role of Chlamydia trachomatis and HLA-B27 in sexually acquired reactive arthritis. Br Med J 1978; i: 605-07. 2. Keat A, Thomas B, Dixey J, Osborn M, Sonnex C, Taylor-Robinson D. Chlamydia trachomatis and reactive arthritis: the missing link. Lancet 1987; i: 72-74. 3. Taylor-Robinson D, Thomas BJ, Dixey J, Osborn MF, Furr PM, Keat AC. Evidence that Chlamydia trachomatis causes seronegative arthritis in women. Ann Rheum Dis 1988; 47: 295-99. 4. Palmer HM, Gilroy CB, Thomas BJ, Hay PE, Gilchrist C, TaylorRobinson D. Detection of Chlamydia trachomatis by the polymerase chain reaction in swabs and urine from men with non-gonococcal urethritis. J Clin Pathol 1991; 44: 321-25. 5. Gilroy CB, Thomas BJ, Taylor-Robinson D. Small numbers of Chlamydia trachomatis elementary bodies on slides detected by the polymerase chain reaction. J Clin Pathol 1992; 45: 531-32. 6. Wong ML, Poole ES, Williams G, Highton J. A prospective and retrospective study of Chlamydia trachomatis in affected tissues of patients with reactive arthritis using a specific monoclonal antibody. Proc Univ Otago Med School 1986; 64: 77-78. 7. Schumacher HR, Magge S, Cherian PV, et al. Light and electron microscopic studies on the synovial membrane in Reiter’s syndrome. Arthritis Rheum 1988; 31: 937-46. 8. Rahman MU, Cheema MA, Schumacher HR, Hudson AP. Detection of chlamydial RNA in the synovium of Reiter’s syndrome patients by molecular hybridization. Arthritis Rheum 1990; 33 (suppl): S25. 9. Hammer M, Nettelnbreker E, Hope S, Schmitz E, Pörschke K, Zeidler H. Chlamydial rRNA in the joints of patients with Chlamydia-induced arthritis and undifferentiated arthritis. Clin Exp Rheum 1992; 10: 63-66. 10. Wordsworth BP, Hughes RA, Allan I, Keat AC, Bell JI. Chlamydial DNA is absent from the joints of patients with sexually acquired reactive arthritis. Br J Rheumatol 1990; 29: 208-10.
ADDRESSES Division of Sexually Transmitted Diseases, Clinical Research Centre, Harrow, Middlesex, and Jefferiss Wing, St Mary’s Hospital, London (Prof D. Taylor-Robinson, FRCPath, C. B. Gilroy, BSc, B. J. Thomas, PhD.), and Department of Rheumatology, Westminster Hospital, London, UK (A. C. S. Keat, FRCP). Correspondence to Prof D. Taylor-Robinson, Division of Sexually Transmitted Diseases, Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ, UK.
stop an episode. We therefore continued pyridoxine and began maintenance treatment with phenobarbitone, which reduced the frequency and severity of the attacks but did not relieve the touch-induced myoclonus. All episodes could be stopped by forcibly flexing the infant. These findings led to a diagnosis of startle disease. Although no defmite family history could be obtained because the father and his family do not live in the UK, two first cousins (paternal) had had neonatal convulsions but are now healthy
REFERENCES 1. Kirstein L, Silfverskiold B. A family with emotionally precipitated drop seizures. Acta Psychiatr Scand 1958; 33: 471-76. 2. Suhren O, Bruyn GW, Tuynman JA. Hyperekplexia: a hereditary startle syndrome. J Neurol Sci 1966; 3: 577-605. 3. Andermann F, Andermann E. Startle disorders of man: hyperekplexia,
jumping and startle epilepsy. Brain Dev 1988; 10: 213-22. C, Roze JC, David A, Veccierini MF, Renaud P, Mouzard A. Hyperekplexia or stiff baby syndrome. Arch Dis Child 1991; 66:
4. Tohier
on no treatment.
We speculated that the abnormalities might be due to low GABA concentrations. A CSF sample was taken on day 14. Free GABA, measured by ion-exchange chromatography with fluorescence detection, was abnormally low (11nmol/1 compared with normal range for newborn infants of 20-100 mnolfl).8 Clonazepam was introduced on day 28 and phenobarbitone was gradually withdrawn. The infant showed great improvement; a normal tone pattern developed and she now has only a few nocturnal myoclonic episodes, though nose tappingb can still elicit a startle response. At 9 weeks, the CSF free GABA concentration was 35 nmol/1, in the low normal range for this age. The infant is now 3 months old and is at home with an apnoea alarm in use. She has mild general hypotonia with greater tone in the upper limbs, but no fisting.
Hyperactivity of the brainstem centres, especially of the rhomboencephalic reticular formation, has been suggested as the cause of startle disease.2,3,7 Several nuclei in the medullary and pontine reticular formation are primary sources of serotoninergic innervation in the brain; thus it is possible that serotoninergic hyperexcitability is a primary cause of the disorder, especially since it has been successfully treated with the serotonin antagonist clonazepam.2 Some of the symptoms of startle disease are similar to those of opioid-induced hypertonicity, so it could be a defect of the endogenous opiate pathway.9 A genetic defect resulting in low brain and CSF GABA is another possibility. GABA is an important inhibitory neurotransmitter, and low concentrations could produce hyperexcitability in the nervous system. A low threshold to epileptic stimulil3 and high amplitude of somatosensory responses5 have also been described in this disorder. The improvement with clonazepam could be explained by potentiation of GABA transmission, brought about by increasing the sensitivity of the GABA receptor, which in turn could lead to an increase in free CSF GABA. If startle disease is primarily due to low GABA concentrations, the best treatment should be vigabatrin. However, this drug can produce microvacuolation in myelinated tracts in animals, so it could interfere with myelination in very immature infants. The mechanism by which acute flexion of the trunk10 abolishes the signs of this disorder remains a mystery. Our case also illustrates the difficulties of clinical diagnosis of startle disease. Although the infant had all the classic signs, we were initially cautious. The myoclonic movements produced a lot of artifacts on the EEG so it was difficult to rule out electrical seizures. The apnoea and abnormal eye movements also hinted at an epileptiform basis. However, the production of myoclonic jerks in response to touch and their inhibition by swaddling and flexing, together with the persistent startle response to nose tapping,6 helped to clinch the diagnosis. We suggest that measurement of CSF GABA concentration is helpful in the diagnosis of this disorder and that the GABA neurotransmitter system is implicated in its pathogenesis. L. M. S. D. is supported by the Medical Research Council. We thank Dr D. Wertheim and Miss M. Hayden for electrophysiological investigation, the Magnetic Resonance Imaging Unit for MRI and MRS studies, and our colleagues for helpful discussions.
460-61. 5. Markand ON,
Garg BP, Weaver (hyperekplexia): electrophysiological
DD. Familial startle disease studies. Arch Neurol 1984; 41:
71-74. 6. Shahar E, Brand
N, Uziel Y, Barak Y. Nose tapping test inducing a generalized flexor spasm: a hallmark of hyperekplexia. Acta Paediatr Scand 1991; 80: 1073-77.
7.
Morley DJ, Weaver DD, Garg BP, Markand O. Hyperekplexia:
an
inherited disorder of the startle response. Clin Genet 1982; 21: 388-96. 8. Carchon HA, Jaeken J, Jansen E, Eggermont E. Reference values for free gamma-aminobutyric acid determined by ion-exchange chromatography and fluorescence detection in the cerebrospinal fluid of children. Clin Chim Acta 1991; 201: 83-88. 9. Weinger MB. "Stiff baby" syndrome: an expression of the same neural circuitry responsible for opiate-induced muscle rigidity? Anesthesiology
1987; 66: 580-81. 10.
Dalla Bernardina B. Startle disease: avoidable cause of sudden infant death. Lancet 1989; i: 216.
Vigevano F, Di Capua M,
an
ADDRESSES: Department of Paediatrics and Neonatal Medicine, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK (L. M. S. Dubowitz, MD, H. Bouza, MD, M. F. Hird, MRCP), and Department of Paediatrics, Universitair Ziekenhuis Gasthuisberg, Leuven, Belgium (J. Jaeken, PhD). Correspondence to Dr L. M. S. Dubowitz.
Detection of Chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction
In 1986, Chlamydia trachomatis elementary bodies were found by direct immunofluorescence (DIF) in synovial-fluid cell deposits and synovialmembrane biopsy samples from five of eight patients with sexually acquired reactive arthritis (SARA) but in none of eight controls with other types of arthritis. Cells from the original slides (stored at 4°C) have now been examined by a polymerase chain reaction (PCR) that amplifies DNA for the major outer membrane protein of C trachomatis. Chlamydial DNA was found in samples from four DIF-positive patients, one DIF-negative patient, and one DIFnegative control. Overall, there was 80% concordance for DIF and PCR results. This study supports our previous finding of chlamydiae in joints in reactive arthritis.
in about 1 % of men with and disease definitely associated non-gonococcal urethritis, with sexually transmitted infection has been called sexually acquired reactive arthritis (SARA).1 Serovars of Chlamydia trachomatis account for up to 50% of cases of nongonococcal urethritis and for other genital-tract diseases
Reactive arthritis
develops
82
COMPARISON OF PCR AND DIF RESULTS
NA= not available.
*Reclprocal titre 64.
including cervicitis and salpingitis. The association between C trachomatis infection and SARA was strengthened when, by means of a direct immunofluorescence (DIF) method, we detected C trachomatis in the joints of patients with SARA2 and seronegative arthritis.3 A polymerase chain reaction (PCR) designed to amplify a conserved region of the major outer membrane protein (MOMP) gene of C trachomatis is at least as sensitive as DIF for detection of chlamydiae in genital-tract specimens. We have shown that the PCR can detect chlamydiae on slides prepared for examination by D IF. We have examined by PCR smears of synovial-fluid cell deposits and synovial-membrane biopsy sections prepared for our original study.2 The synovial-fluid cell deposits and synovial-membrane biopsy sections had been fixed on MicroTrak (Syva, UK) slides, stained with the MicroTrak reagent (fluorescein-conjugated C trachomatis monoclonal antibody), covered with a cover-slip, and stored at 4°C for about 6 years. The samples came from eight patients with SARA and eight controls; they were originally examined by DIF for fluroescent C trachomatis elementary bodies. The cells were scraped from the slidess for examination by PCR. The presence or absence of elementary bodies in each sample was not disclosed until the results of the PCR assay were available.
PCR results are compared with our previous DIF and serological findings in the table. Fluorescent elementary bodies were detected originally in synovial-fluid cell deposits, synovial-membrane specimens, or both, from five SARA patients. In the other three patients, evidence of current or recent C trachomatis infection was provided by positive genital-tract DIF (not shown) with or without serum or synovial-fluid IgG antibody reciprocal titres of 64 or above. Four of five DIF-positive samples and one DIF-negative sample were positive by PCR. All the controls had been negative by DIF, but one was positive by PCR; no material for PCR was available for one control. Thus, of fifteen pairs of samples with complete data, the results were concordant for twelve (80%). Our finding of C trachoma tis elementary bodies in joints of patients with SARA2 was not confirmed by others using DIF,6although there was some support from electron microscopy and immunochemistry7 and from the use of probes to detect chlamydial rRNA. 8,9 However, the development of a highly sensitive PCR that could be used on samples fixed on slides enabled us to re-examine our original slides and so directly support our original observations.
There was 80% concordance between the DIF and PCR results. The discordant results could be due to loss of chlamydial elementary bodies during storage or in the process of transfer from slide to PCR reaction mixture. The detection of chlamydiae by the PCR in one of the DIF-negative control specimens did cause some concern. However, that patient, a young woman, was initially thought to have had early rheumatoid arthritis, but she had had an acute episode of polyarthritis in both knees associated with a rash; both features resolved over 5 months without further evidence of rheumatoid disease. We are aware and have had experience of the DNA contamination that can arise with PCR methods. Because spurious results may be generated, it is most important to ensure the validity of the PCR result before questioning any clinical diagnosis. Nevertheless, provided that adequate precautions are taken to prevent contamination, we believe that this technique will be applicable for samples from other patients and will be valuable to those workers who are not confident about use of the DIF technique owing to its subjectivity. Use of PCR based on a chlamydial plasmid failed to detect chlamydial DNA in the joints of other patients with SARA.1O It is possible that intra-articular chlamydiae can lose plasmids, but the reason for the failure of one PCR and the success of ours, based on DNA associated with the MOMP of C trachomatis, is not known. It is clear, however, that the PCR we used is more sensitive than any other chlamydial detection procedure apart from DIF. REFERENCES 1. Keat AC, Maini RN, Nkwazi GC, Pegrum GD, Ridgway GL, Scott JT. Role of Chlamydia trachomatis and HLA-B27 in sexually acquired reactive arthritis. Br Med J 1978; i: 605-07. 2. Keat A, Thomas B, Dixey J, Osborn M, Sonnex C, Taylor-Robinson D. Chlamydia trachomatis and reactive arthritis: the missing link. Lancet 1987; i: 72-74. 3. Taylor-Robinson D, Thomas BJ, Dixey J, Osborn MF, Furr PM, Keat AC. Evidence that Chlamydia trachomatis causes seronegative arthritis in women. Ann Rheum Dis 1988; 47: 295-99. 4. Palmer HM, Gilroy CB, Thomas BJ, Hay PE, Gilchrist C, TaylorRobinson D. Detection of Chlamydia trachomatis by the polymerase chain reaction in swabs and urine from men with non-gonococcal urethritis. J Clin Pathol 1991; 44: 321-25. 5. Gilroy CB, Thomas BJ, Taylor-Robinson D. Small numbers of Chlamydia trachomatis elementary bodies on slides detected by the polymerase chain reaction. J Clin Pathol 1992; 45: 531-32. 6. Wong ML, Poole ES, Williams G, Highton J. A prospective and retrospective study of Chlamydia trachomatis in affected tissues of patients with reactive arthritis using a specific monoclonal antibody. Proc Univ Otago Med School 1986; 64: 77-78. 7. Schumacher HR, Magge S, Cherian PV, et al. Light and electron microscopic studies on the synovial membrane in Reiter’s syndrome. Arthritis Rheum 1988; 31: 937-46. 8. Rahman MU, Cheema MA, Schumacher HR, Hudson AP. Detection of chlamydial RNA in the synovium of Reiter’s syndrome patients by molecular hybridization. Arthritis Rheum 1990; 33 (suppl): S25. 9. Hammer M, Nettelnbreker E, Hope S, Schmitz E, Pörschke K, Zeidler H. Chlamydial rRNA in the joints of patients with Chlamydia-induced arthritis and undifferentiated arthritis. Clin Exp Rheum 1992; 10: 63-66. 10. Wordsworth BP, Hughes RA, Allan I, Keat AC, Bell JI. Chlamydial DNA is absent from the joints of patients with sexually acquired reactive arthritis. Br J Rheumatol 1990; 29: 208-10.
ADDRESSES Division of Sexually Transmitted Diseases, Clinical Research Centre, Harrow, Middlesex, and Jefferiss Wing, St Mary’s Hospital, London (Prof D. Taylor-Robinson, FRCPath, C. B. Gilroy, BSc, B. J. Thomas, PhD.), and Department of Rheumatology, Westminster Hospital, London, UK (A. C. S. Keat, FRCP). Correspondence to Prof D. Taylor-Robinson, Division of Sexually Transmitted Diseases, Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ, UK.
