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Acute Polyradiculoneuropathy Complicating Systemic Lupus Erythematosus

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Acute Polyradiculoneuropathy Complicating Systemic Lupus Erythematosus Postgraduate Medical Journal (1986) 62, 291-294 Postgrad Med J: first published as 10.1136/pgmj.62.726.291 on 1 April 1986. Downloaded from Acute polyradiculoneuropathy complicating systemic lupus erythematosus Stephen H. Morgan, Robin P. Kennett, Christopher Dudley, Charles Mackworth- Young, Richard Hull and Graham R.V. Hughes* The Rheumatology andNeurology Units, The Royal Postgraduate Medical School, Hammersmith Hospital, London W12, UK. Summary: Two elderly patients with systemic lupus erythematosus (SLE) are presented. Both developed an acute polyradiculoneuropathy which is an unusual complication of this disease. Features of their presentation are discussed. Introduction The neurological manifestations of systemic lupus tremities. Over the next week similar symptoms de- erythematosus (SLE) may be protean (Johnson & veloped in the arms. Past history included chorea in Richardson, 1968). Cerebral involvement was a childhood and more recently, grittiness ofthe eyes and feature of one of the earliest patients described by pleuritic chest pains. Kaposi (1872), but peripheral nerve disorders are seen When examined in 1984 he looked ill. There was a much less frequently. In a recent prospective study of synovitis of the small joints of both hands and feet. copyright. patients presenting with SLE to the Hammersmith There was marked facial diplegia but no other bulbar Hospital (Grigor et al., 1978), 3 patients (6%) had a signs. There was a flaccid and global weakness of all peripheral neuropathy but only 1 was an ascending limbs, in the MRC grading range 2-3. The truncal polyradiculoneuropathy of the Guillain-Barre type. muscles were too weak to flex the body against gravity. We now document 2 patients who have presented with There was hypaesthesia and hypalgesia of the fingers this complication of SLE in the last year. and below the knees bilaterally. Position sense was impaired in the fingers and toes, and vibration sense was lost below the anterior superior iliac spines. There http://pmj.bmj.com/ Case reports was no evidence of sphincter or autonomic disfunc- tion. Case I Investigations showed a hypochromic normocytic anaemia (haemoglobin 8.6 g/dl) and throm- A 58 year old male psychotherapist first developed an bocytopenia (114 x 106/1). The biochemical renal fun- acute symmetrical polyarthropathy in 1982. This was ction was impaired (creatinine 160 jLmol/l, urea in a rheumatoid distribution, and improved on treat- 15.8 mmol/l, creatinine clearance 27 ml/minute). on September 25, 2021 by guest. Protected ment with indomethacin. There was 3.2 g ofproteinuria/24 hours. The ESR was In 1984 there was a recurrence ofarthritis with fever 108 mm/hour and C-reactive protein (CRP) 2.0 tLmol/ and night sweats. He was again treated with indometh- 1. The antinuclear antibody (ANA) titre was 1:6400 acin, but a few weeks later developed visual hallucina- with a homogenous pattern on immunofluorescence, tions, poor concentration, anorexia and weight loss. A but the DNA binding was normal and antibodies to month later progressive weakness ofboth legs became ENAs were not detected. A minor salivary gland apparent, with numbness and tingling of the ex- biopsy was consistent with Sj6gren's syndrome. The serum levels of IgG and IgM were elevated (21.4 and *Present address: Rheumatology Department, St Thomas' 7.4 g/l respectively), and tests for immune complexes Hospital, Lambeth Palace Rd, London S.E.1, UK. (Clq binding and mRFBA) were strongly positive Correspondence: S.H. Morgan, M.B., M.R.C.P., Division of along with moderate cryoglobulinaemia. Serological Inherited Metabolic Diseases, Clinical Research Centre, tests for syphilis, hepatitis surface antigen and lupus Northwick Park Hospital, Harrow, Middlesex, UK. anti-coagulant were all negative. Renal biopsy demon- Accepted: 24 September 1985 strated a mesangio-proliferative glomerulonephritis © The Fellowship of Postgraduate Medicine, 1986 292 CLINICAL REPORTS Postgrad Med J: first published as 10.1136/pgmj.62.726.291 on 1 April 1986. Downloaded from with deposits of IgA, IgG, IgM and C3. The cerebros- rays showed bilateral osteonecrosis of the femoral pinal fluid (CSF) was acellular with an elevated heads. She underwent total hip replacement on the left protein content (1.09 g/l), but without oligoclonal IgG in 1981 and on the right in 1983. bands. She was admitted in late 1983 with right upper The motor nerve conduction velocities were quadrant abdominal pain and vomiting. Acute moderately reduced at 43, 46 and 31 m/s on recording cholecystitis was diagnosed. The following week she from the median, ulnar and peroneal nerves respec- developed progressive weakness in her arms and legs. tively. The median, ulnar and tibial nerve distal motor Simultaneously, she noticed continuous tingling in the latencies were prolonged at 6.1, 4.2 and 8.5 ms respec- fingers and toes which spread proximally to the wrists tively. The ulnar F-wave response was delayed (38 ms) and ankles over 5 days. There was no sphincter and median and peroneal F-waves were absent. The disturbance. On examination, she had global weak- sensory nerve action potentials were small at 5, 8 and ness ofboth arms (MRC grade 4 range), most marked 7 pV on recording from the median, ulnar and sural in the extensor muscles, she could just flex her body nerves respectively. These findings were consistent against gravity with the truncal muscles, and she had with the diagnosis of acute inflammatory global weakness of the legs (MRC grade 4) most polyradiculoneuropathy (Eisen & Humphreys, 1974). marked in the flexors. Only the biceps tendon reflexes The abductor pollicis brevis muscle action potential were retained and the plantar responses were flexor. was small (0.5 fV) but there was no evidence of There was hypaesthesia and hypalgesia of all fingers conduction block in motor fibres of the median nerve. and both legs below the knees. Vibration sense was lost Reduction of the muscle action potential amplitude is below the sternum, joint position sense was impaired considered to indicate poor prognosis in the Guillain- in the fingers and toes and 2-point discrimination was Barre syndrome (Brown & Feasby, 1984). of abnormally high threshold in the peripheries. Prednisolone, 1 mg/kg/day, was started, but his There was a mild normochromic normocytic condition deteriorated with increased sensory distur- anaemia (Hb 12.8 g/dl), and thrombocytopenia bance. He was given four, 5 litre plasma exchanges, (80 x 106/1). The ESR was 54 mm/hour and the DNA followed by a single intravenous pulse of 500mg binding was normal with a positive ANA at 1: 160. The cyclophosphamide, and maintenance azathioprine CSF protein was raised (l.1 g/l) with no cells or was started. There was clinical improvement and by organisms present. The distal motor latencies oncopyright. the time ofdischarge, power was in the MRC grade 4- recording from the median, ulnar and peroneal nerves 4+ range. There was also a fall in the ESR and were delayed at 7.8, 5.6 and 9.9 ms respectively. The immunoglobulin levels, and renal function returned to median F-wave response was delayed at 42ms. The normal. Nerve conduction studies 2 months after the motor nerve conduction velocities were only slightly onset of the illness showed improvement with motor reduced (median nerve 46.5 m/s, ulnar nerve 48 m/s). nerve conduction velocities of 48 and 49 m/s on The sensory nerve action potentials were absent. These recording from the median and ulnar nerves. The findings were consistent with a diagnosis of acute http://pmj.bmj.com/ median nerve distal motor latency was 5 ms and the inflammatory polyneuropathy (Eisen & Humphreys, ulnar 4.3 ms, and the F-wave latencies were less 1974). delayed (median 36 ms, ulnar 35 ms). The sensory The weakness gradually improved, and she was able nerve action potentials remained small (median 7 jiV, to walk 8 weeks following the start of her illness ulnar 5 ILV). despite no change in the maintenance dose of pred- nisolone. Case 2 on September 25, 2021 by guest. Protected In 1977 a 50 year old woman was admitted with Discussion epistaxes, and a profound thrombocytopenia (15 x 106/1) with a mild normochromic normocytic The Guillain-Barre syndrome (GBS), consisting of anaemia. She gave a history ofmyalgia, arthralgia and acute, usually predominantly motor neuropathy with fatigue over the 6 years prior to this. A diagnosis of areflexia and raised CSF protein, was first described in SLE was made when she subsequently developed a 1916 (Guillain et al.). Since then there has been florid polyarthritis with a raised ESR of 120 mm/hour, controversy over diagnostic criteria, although guide- a positive ANA (1:640) and LE cell phenomenon. lines have recently been proposed (Editorial, 1978). It Treatment was initially prednisolone alone, but azath- is generally agreed that the eponym 'Guillain-Barre ioprine was added later. On this combination she syndrome' should be reserved for those cases where an developed further purpura and, after bone marrow underlying aetiology is not found (Marshall, 1963; examination, azathioprine was implicated as the cause Asbury, 1981), the remainder being called 'acute of thrombocytopenia and was discontinued. inflammatory polyradiculoneuropathy'. In a large In 1980 she complained of pain in both hips and X- literature review of 1,100 cases of 'Guillain-Barre CLINICAL REPORTS 293 Postgrad Med J: first published as 10.1136/pgmj.62.726.291 on 1 April 1986. Downloaded from syndrome' (Leneman, 1966), 66% had an established (Rodriquez-Iturbe et al., 1973). associated illness. Ofthese, only 14 (less than 2%) were Both patients satisfy the revised ARA criteria for related to a connective tissue disease; SLE having the diagnosis of SLE (Tan et al., 1982), although been diagnosed in 7 cases. This emphasizes that neither had antibodies against double stranded DNA polyradiculoneuropathy rarely complicates SLE, and (dsDNA), or ENAs, despite the high titre of antinu- may appear by chance alone.
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