238 Journal of the Royal Society of Medicine Volume 84 April 1991 to an agent like clozapine might be prophylactic. The latter agent has been shown to have minimal central antidopaminergic effects4 and would therefore be expected to produce much fewer extrapyramidal side-effects. Acknowledgnent: We gratefully acknowledge support from the South African Medical Research Council. References 1 Levinson DF, Simpson GM. Serious nonextrapyramidal adverse effects of neuroleptics: sudden death, agranulocytosis, and hepatotoxicity. In: Meltzer HY, ed. Psychopharmacology, the third generation of progress. New York: Raven, 1987:1431-36 -2 Flaherty JA, Lahmeyer HW. Laryngeal-pharyngeal dystonia as a possible-cause of asphyxia with haloperidol treatment. Am J Psychiatry 1978;135:1414-15 3 Leestma JE, Koenig KL. Sudden death and phenothiazines. Arch Gen Psychiatry 1968;18:137-48 4 Baldessarini RJ. Drugs and the treatment of psychiatric disorders. In: Gilman A, Goodman LS, Rall TW, Murad F, eds. Goodman and Gilman's the pharmacological basis oftherapeutics, 7th edn, New York: MacMillan, 1985:387-445 (Accepted 23 March 1990) Guillain-Barre syndrome in a patient with hairy cell leukaemia S C Tayal MD MRCPI D S Rowbotham MBBS S K Bansal FRCP Department of Medicine for the Elderly, Ryhope General Hospital, Sunderland SR2 OLY Keywords: Guillain-Barr6 syndrome; hairy cell leukaemia; autoimmunity; lymphocyte subpopulations Hairy cell leukaemia (HCL) is a chronic form of leukaemia that predominantly affects middle aged men. Neurological complications have been reported in only 5% of patients, mainly due to infections' or leukaemic infiltration2 of the central nervous system. We describe a patient with Guillain-Barre syndrome (GBS) associated with HCL which, to our knowledge, has not been described in the literature. Case report A 78-year-old retired miner was admitted with a 2-week history of progressive weakness of limbs, constipation and retention of urine. There was no preceding history of viral illness. He was on captopril 25 mg twice daily and hydrochlorothiazide 5 mg daily for hypertension. On examination he was heavily built, apxial and had a blood pressure of 170/85 mmHg. Cardiovascular, respiratory and abdominal examination were all normal. Neurological examination revealed higher functions and cranial nerves to be unaffected. Muscular fasciculations were pret in all limbs, with power grade 3/5 proximally and 4/5 distally. There was generalized areflexia and both plantars were equivocal. Sensation was intact. Laboratory data: haemoglobin 14.1 g/dl, whole blood count 10.2x 19/L with lymphocytes 4.78x 1(AL, platelets 216x109/L, erythrocyte sedimentation rate 10mm/h-and peripheral blood smear showed abnormal moonuclear cells. Biochemical results showed plasma sodium 121 mmol/l, potassium 3.05 mmol/l, urea, creatinine and glucose were normal. The CSF was clear, sterile with normal-cell conts8 and a protein level of 1.1 g/l and JgG of 0.1 gll. Monospot test was negative, viral titres were insignificant and blood culture sterile. Bone marrow emnation showed malignant lymphoproliferative morphology suggestive of hairy cell leukaemia. Whole blood count cell markers in theperipheral blood confirmed B cell monoclonal proliferation (CD22- activated B cells 96%, CD19-pre B cells 71% and lambda 80%) and a reactive T cell subpopulation (CD4-OKT4 24% and CD8-OKT8 4%). Electromyography and nerve conduction studies were reported as showing severe motor and sensory peripheral neuropathy with predominant demyelination and a degree of secondary axonal degeneration. Treaitment was commenced with subcutaneous interferon 3 million IU three times a week for 2 weeks and intravenous methylprednisolone 500 mg daily for 3 days. The illness was complicated by deep vein thrombosis, multiple pulmonary emboli and supraventricular -tachycardia. The patient died of progressive respiratory failure 4 weeks after admission. Postmortem examination cofirmed the diagnosis of GBS. The infla tory infiltrate was predominantly perivascular in an epineural and extrafascicular distribution and showed a heterogeneous mixture of mononuclear inflammatory cells. mmimunoperoxidase studies for immunoglobulin light chains showed a polyclonal staining pattern. There was no evidence of direct leukaemia/lymphomatous infiltration on the nerves. Discussion Both GBS and HCL are very uncommon diseases making a chance association unlikely. Cases of GBS may have an underlying cause other than previous viral infection; for example Hodgkin's disease, neoplasms, metabolic disease and a variety of endocrine conditions3. However, GBS has not been reported previously either as the presenting feature or as a complication of HCL. GBS is8an immunologically-mediated disease caused by a delayed hypersensitivity reaction provoked, in a manner not yet understood, by antecedent viral infection or other conditions. Under certain circumstan, partial and perhaps transient immunosuppression could serve as one con- tributing factor in triggering GBS4. In a proportion of patients with GBS alterations in peripheral blood lymphocyte subpopulations have been described'. These include an increased helper/suppressor T-cell ratio due to a reduction in'the OK0P (suppressor cells) subpopulation. B cell and OKT4 (helper cells) populations remained normal. In our patient there was a predominant neoplastic B cell population. The reactive T cell population showed a helper/suppressr ratio of 6: 1 (normal 2: 1) due to loss of OKT8 cells. Thus depreaion of these'OK8 cells in GBS'might permit the development of autoimmunity to myelin igens and so play an important role in pathogenesis. The m anismn whereby HCL was associated with this abnormal T-helper and s r cells ratio is not clear.- However it is likely that the development:of GBS in this patient reflects an effect of tICL upon the immune status of the patient. Acknowledgment Our thanks to Dr P Ince, Consultant Neuro- pathologist, General Hospital, Newcastle-Upon-Tyne,for reviewing the hitology and advice. References 1 Kimmel DW, Hermann HC, ONeill BP. Neurolgical comlicati of hairy cell leukaemia. Arch Neurol 1984;41:202-3 0141-07468/91/ -: 040238*240.00/0 o 1991 The Royal Society of Medicine