longer deserves (although it certainly did from 1988 to 1990) for indiscriminately encouraging markets, and also opprobrium it certainly does deserve (currently) for interfering obsessively in increasing central control of a supposedly newly devolved NHS. In the end we are left with the contracting process and the purchaser's ability to identify need-yet the rhetoric of consumerism. This may produce two forces for higher spending. Firstly, rationing based on purchasers' priorities translated into contracts with providers may still be politically unacceptable (hence the recent problems over interleukin at the Christie Hospital, Manchester). Yet, secondly, consumers will demand "production line" medicine and "trendy" procedures, whether they meet need, defined by experts, or not. In aggregate these forces will push for higher NHS spending. This may be fine. After all, Britain is a very low spender on health. And public spending is the most effective and efficient way to increase expenditure on health. The problem hitherto has been the conventional wisdom, on the right and the left, that only moving to an insurance based or partly private financing system could boost aggregate spending. It would be an ironv to be savoured if the long term fallout of the review was higher public spending and little or no reliance on competitive markets. CALUM R PATON

Cenitre tor Hcalth Planning and Management, Keele University, Keele, Staftfordshire SF5 5SP

11am C. Revisiting the initcrnial ntarket. BAI7 1991;302:250-1. (2 Februarv.) 2 Brindle D. I'atients facc February 12 1991:6.

httrdlc to joinl NHS quietues. (Guardiant

Drug Points Digoxin toxicity presenting as dysphagia and dysphonia Drs M F CORDEIRO and K G ARNOLD (Geriatric Department, University College Hospital, London NW1 OPE) write: A 93 year old woman was referred by her general practitioner with a two month history of worsening dysphagia (initially solids but progressing to liquids), dysphonia, nausea, anorexia, and weight loss (13 kg in four months). Six months previously her general practitioner had started treatment with digoxin for rapid atrial fibrillation. On admission to hospital she was taking 0 125 mg digoxin a day. On examination she was found to be cachectic, but no other abnormal clinical signs were present. Her plasma urea and electrolyte concentrations were normal, as was her chest x ray film, and an electrocardiogram confirmed her to be in atrial fibrillation. A barium swallow examination two days later showed no abnormality apart from evidence of oesophageal muscle incoordination. She was referred to the ear, nose, and throat department for investigation of her dvsphonia. Indirect laryngopharyngoscopy showed no abnormalities, as did oesphagopharyngoscopy. Serum digoxin concentration on the day of admission was extremely high at 6 1 nmol/l (normal range 0-9-2 6 nmolll nine hours after dose). Digoxin was therefore stopped and electrocardiography was performed daily to monitor her cardiac state. Four days after digoxin was stopped her serum digoxin concentration was 1 3 nmol/l. Over the next few days her dysphagia and dvsphonia progressively improved and she was discharged three weeks later without any medication but with a normal electrocardiogram and complete resolution of her presenting symptoms.

BMJ VOLUME 302

27 APRIL 1991

The cause of this patient's dysphagia and dysphonia could, after investigation, be attributed only to her toxic serum concentration of digoxin.' Once the digoxin had been discontinued her symptoms resolved. There has been one previous report of digoxin toxicity manifested by dysphagia,2 but no mechanism of oesophageal dysfunction has been elucidated. Perhaps, in the light of the above, further investigations into the effects of digoxin on smooth muscle (other than cardiac or intestinal sphincteric muscle') should be undertaken. Dysphagia and dysphonia may be occasional symptoms of digoxin toxicity. I Park (iD, Spector R, (iold erg MJ, Feldman RD. Digoxin toxicity in patients with high serum digoxin concentrations.

Am 71ed Sci 1987;294:423-8.

hemiparesis (Committee on Safety of Medicines, personal communication, 1990). Slow acetylator state has been implicated as a predisposing factor in the development of some toxic reactions induced by sulphasalazine,' but the acetylator status was not determined in our patient. Several drugs have been incriminated as causing chorea.4 We have been unable to find any reports of chorea produced by sulphasalazine. Digoxin is unlikely to have been responsible in our patient as she had been taking the same dose for some time before the onset of the chorea. We cannot, however, exclude a synergistic effect. If a person taking sulphasalazine develops fidgetiness or frank chorea for which no other cause can be found, we would suggest that this drug should also be considered as a possible cause.

2 Kelton JG, Sctullin DC. Digitalis toxicity manifested by dvs-

phagia. JIMA 1978;239:613-4. 3 Gazes PC, Holmes CR, Moseley \V, Pratt-Thomas HR. Acute haemorrhage and necrosis of the intestines associated with digitalization. Circulatton 1961;24:358-64.

Chorea precipitated by sulphasalazine Drs A G QUINN and W R ELLIS (Department of Medicine, Dryburn Hospital, Durham) and Drs D BURN and N CARTLIDGE (Department of Neurology, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP) write: A 70 year old woman was admitted to hospital for investigation of a five month history of diarrhoea. Involuntary movements of her right arm had been present for four weeks. Six weeks before admission she had started taking sulphasalazine 1 g four times daily. There was no history of movement disorder, rheumatic fever, or psychiatric illness, and no family history of chorea. She had undergone partial thyroidectomy five years before. She was also taking digoxin and a frusemide and potassium combination diuretic (Lasikal). Her general practitioner confirmed that no other drugs had been prescribed in the past two years and that she had never received neuroleptics. On examination she appeared well and was alert and fully orientated. Her pulse was 76 beats/min and blood pressure 140/80 mm Hg, and she had a soft pansvstolic murmur. She had mild choreiform movements of her right upper arm but no other focal neurological signs. Results of a full blood count, erythrocyte sedimentation rate, and biochemical profile including thyroid function tests were all normal. Results of an autoantibody screen were negative and serum magnesium concentration was within normal limits. No pathogens were found on stool culture or microscopy. She was discharged, taking the same drugs, and readmitted four weeks later for flexible sigmoidoscopy. Repeat neurological examination at that time showed a generalised choreiform movement disorder. No other neurological signs were detected. The reflexes were symmetrical and not depressed, and there were no other focal signs. Flexible sigmoidoscopy and mucosal biopsy showed no evidence of inflammatory bowel disease. The possibility of a drug induced chorea was considered in view of the temporal relation between the onset of the symptoms and starting sulphasalazine. Sulphasalazine was withdrawn; other drugs, including digoxin, were continued. Over the next eight weeks the chorea slowly improved. Repeat neurological examination four months later had entirely normal results. Our patient developed a progressive movement disorder two weeks after starting sulphasalazine, which resolved when this drug was discontinued. We believe that the time course and response to withdrawal incriminates sulphasalazine as the cause of the movement disorder. A number of adverse neurological reactions associated with sulphasalazine use have been described. These include sensorimotor neuropathy, ataxia, tremor, encephalopathy, and

1 Price TR. Sensorimotor neuropathy with sulphasalazine. Postgrad.Medj 1985;61:147-8. 2 Hermann GG. Sulphasalazine: adverse effects. Dig Dis Sci 1984;29:781-2. 3 Skeith KJ, Russell AS. Adverse reactions to sulphasalazine. J Rheumatol 1988;15:529-30. 4 Padberg GW, Bruyn GW. Chorea: differential diagnosis. In: Handbook of clinical neurology. Vol 5. 1986:549-64.

Influence of oral contraceptives on body temperature Dr R H B MEYBOOM (Netherlands Pharmacovigilance Centre, PO Box 5406, 2280 HK Rijswijk, The Netherlands) writes: One of the physiological effects of progesterone is a slight rise in body temperature, up to 0 5°C. " Mid-cycle temperature rise may be used as evidence of ovulation and the formation of a corpus luteum. Although progestagens are a basic constituent of oral contraceptives, the possibility of an influence on temperature is not mentioned in the usual sources of information on side effects. 3 6 A recent case report to The Netherlands Pharmacovigilance Centre described a 35 year old woman with longstanding rise in body temperature of about 0 5°C, which in the evening reached subfebrile values up to 38°C, in suspected association with Microgynon 30 (levonorgestrel 150 itg, ethinyloestradiol 30 [tg). No medical cause was found and the course of the temperature after stopping and during rechallenge, as established by daily rectal assessment of morning temperature, was consistent with an effect of the contraceptive agent. Although the influence of progesterone on temperature is well known, there is a remarkable paucity of data in current physiology textbooks concerning this effect.2 With regard to oral contraceptives, only one reference was found in the medical literature, but without quantification and comment.9 A body temperature raised by 0 5&C may be mistaken for a subfebrile temperature and may be a cause of unnecessary concern and medical investigations. More information on the influence of progestagens on temperature is needed. The product information of all oral contraceptives containing a progestagen should mention the possibility of a slight rise in body temperature. I De Mouzon J, Iestart J, lcfe reB Pouly Jl., Frsdman B. Iitllne relationships between basal body temperature and ovulation or plasma progestins. Fertil Steril 1984;41:254-9. 2 Keele CA, Neil E, Joels N. Samson W'right's applied phs'siologv. Oxford: Oxford University Press, 1983. 3 Association of the British Pharmaccutical Industry. ABPI data sheet compendium. London: Datapharm, 1990. 4 Wade A. Martindale: the extra pharmacopoeia. 29th ed. Lotsdon: Pharmaceutical Plress, 1989. 5 Dukes MN, ed. Mevler's side effects of drugs. 11th cd. Amstcrdam: Elsevier, 1988. 6 Dasies D)M. Texthook of adverse drug reactions. 3rd ed. Oxtord: Oxford University P'ress, 1985. 7 Meyboom RHB, M\artin DJ. 136ienvltedittg van de lichaatnstemperatuur door orale anticotcceptisa. Huisarts Wet 199(0;33:

488-90. 8

GUtvton AC. Iexibook of' medical physiologv. I'hiladelpilia:

Saunders, 1986. 9 Spona J, Schneider WHF. Central and peripheral parametcrs of the menstrual cy,cle under the influence of a new combined oral

cotttraceptive. A-cta Obstet (vnecol Scand 1976;suppl 54:45-5(0.

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Influence of oral contraceptives on body temperature.

longer deserves (although it certainly did from 1988 to 1990) for indiscriminately encouraging markets, and also opprobrium it certainly does deserve...
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