329 after transfer-factor treatment could be the result of interferon induction. Interferon has been shown to improve patients with cytomegalovirus’ and may have done so in the cases by Thomas et al. The interferon induced by transfer factor is active for 2-3 days so that in chronic diseases, long-term transfer-factor therapy may be necessary to eliminate persistent vinesses
This has been my experience with chronic active hepatitis (to be reported elsewhere). I suggested therefore that transfer factor be given twice a week for prolonged periods when treating viral diseases. ruses.
I thank Sallie Graham for technical assistance.
Department of Immunotherapy, Wadley Institutes of Molecular Medicine, Dallas, Texas 75235, U.S.A.
AMANULLAH KHAN
RESPIRATORY DISEASE ASSOCIATED WITH PRACTOLOL
SiR,-Marshall
et
al.l suggest that corticosteroids
or
im-
munosuppressive agents might be beneficial for the respiratory disease associated with practolol therapy. This might be true if the untoward effects of practolol were immunologically produced but in my experience steroids do not benefit the lung condition once it has become chronic. Unlike the sclerosing peritonitis, lung lesions do not appear after stopping practolol. The other lesions disappear within a month or two of the end of therapy. The patients who have developed pleural and lung lesions have become respiratory cripples, but the incidence of sideeffects in patients treated with practolol seems very variable. Zacharias2 reported that 38 of 170 treated patients developed oculomucocutaneous lesions and in Finland,2 110 of 80 000 treated patients had the oculomucocutaneous syndrome and 11 had sclerosing peritonitis, but in these studies no mention was made of the incapacitating dyspnreic syndrome. Guy’s Hospital St Thomas Street, London SE1 9RT
A. W. FRANKLAND
PERIPHERAL NEUROPATHY WITH DISOPYRAMIDE
SIR,-We have seen treatment with
a case
of sensorimotor
neuropathy after
disopyramide.
A 72-year-old woman presented with a 4-year history of intermittent attacks of fast atrial fibrillation’during which she had dyspnoea, angina at rest, and occasional syncope. These attacks were not controlled by digoxin, and she complained of dry eyes with practolol. Other beta blockers had not averted the attacks and she became nauseated with quinidine. 6 months before admission disopyramide phosphate (’Norpace’) 150 mg four times a day had been prescribed with complete relief of the tachycardia. 18 days later burning in both feet developed. 3 weeks later disopyramide base (’Rythmodan’) 100 mg three times a day was substituted for the norpace, and 8 days later the burning became intolerable, despite vitamin supplements. The rythmodan was withdrawn and she was started on sustained-release quinidine (’Kinidin Durules’) with good effect. She was admitted to this hospital 4 months after the initial treatment with disopyramide. She drank no alcohol and did not smoke. She complained of severe dysaesthesiae in her feet sufficient to prevent her walking. There were no other neuro5. O’Reilly, R. J. and others. Clin. Immun. Immunopath. 1976, 6, 51. 1. Marshall, A. J., and others. Lancet, 1977, ii, 1254. 2. Zacharias, F. J. Proc. R. Soc. Med. 1977, 70, suppl. 5, 24. 3. Idanpaan-Heikkila, J. E., Hastbacka, J., Jarvinen, H. J. J. Lancet, 1977, ii, 1354.
logical symptoms. Her blood-pressure was 135/85 mm Hg, pulse 60/min regular; she was well perfused and all peripheral pulses were present. Slight weakness of hip and knee flexion and extension, and dorsiflexion of the feet was elicited, more marked on the left. Vibration sense was absent to the iliac spines and joint position was absent in the feet, but normal at the ankle. Testing for touch, pain, temperature, and two-point discrimination was normal, and no hyperalgesia could be demonstrated. Motor and sensory examination of the upper limbs was normal. Laboratory tests on blood and cerebrospinal fluid were normal. Nerve-conduction studies were compatible with a mixed sensorimotor neuropathy of large-fibre type affecting mainly the lower limbs. The patient was given physiotherapy, and carbamazepine provided some symptomatic relief of the dysaesthesix. At the time of discharge her symptoms had improved considerably and she was able to walk unaided. 4 months later she was symptom-free. Most side-effects encountered with disopyramide are related to its anticholinergic properties. It may also lower cardiac output and peripheral perfusion.! Peripheral neuropathy has not previously been reported, although paraesthesiae2.3 and/or numbness4 have been seen. Nerve-conduction studies in patients with symptoms of dysaesthesiae might reveal more cases of disopyramide neuropathy. K. D. DAWKINS National Hospitals for Nervous Diseases, London WC1 J. GIBSON
CLOSED-ANGLE GLAUCOMA IN PATIENT ON DISOPYRAMIDE woman receiving oral disopyramide the ophthalmology ward with acute closedangle glaucoma with symptoms localised to the right eye. The pressures were 40 mm Hg in the right eye and 35 mm Hg in the left eye on applanation tonometry. Gonioscopy revealed bilateral narrow angles closed through 360°. The patient was treated with 2% pilocarpine and 0.25% eserine eye-drops until the pressures were controlled, and 3 days later bilateral peripheral iridectomy was done. Postoperatively her pressures remained controlled, and the patient was discharged on disopyramide tablets 100 mg four times daily. She had recently been treated in the medical wards for supraventricular paroxysmal tachycardia, and, because this had not been controlled by propranolol, she was given oral disopyramide 100 mg three times a day for 6 days and then 200 mg three times a day for a further 6 days. Her symptoms of glaucoma had started on the 7th day of this regime. We have found no previous report of closed-angle glaucoma precipitated by disopyramide, but the anticholinergic activity of this drug has been demonstrated in vitroand in vivo.1i A drug history should be taken from all patients with closedangle glaucoma, and clinicians should remember that the anticholinergic activity of disopyramide may produce glaucoma in a susceptible patient. This drug is being widely used for the prevention and treatment of arrhythmias. All patients who are to be treated in this way should be asked if they have a family history of glaucoma, and if there is any doubt, they should be assessed gonioscopically.
SIR,-A 66-year-old
was
admitted
to
Department of Ophthalmology, Stobhill General Hospital, Glasgow G21 3UW
G. E. TROPE V. M. D. HIND
1. Befeler, B., and others. Angiology, 1975, 26, suppl. 1, p. 99. 2. Jennings, G., and others. Lancet, 1976, i, 51. 3. Zainal, N., and others. J. int. med. Res. 1976, 4, suppl. 1, p. 71. 4. Hopkins, A. M. Personal communication. 5. Mokler, C. M., Hillman, R. A. Pharmac. Res. Commun. 1972, 4, 6. McHaffie, D. J., Guz, A., Johnston, A. Lancet, 1977, i, 859.
171.
This has been my experience with chronic active hepatitis (to be reported elsewhere). I suggested therefore that transfer factor be given twice a week for prolonged periods when treating viral diseases. ruses.
I thank Sallie Graham for technical assistance.
Department of Immunotherapy, Wadley Institutes of Molecular Medicine, Dallas, Texas 75235, U.S.A.
AMANULLAH KHAN
RESPIRATORY DISEASE ASSOCIATED WITH PRACTOLOL
SiR,-Marshall
et
al.l suggest that corticosteroids
or
im-
munosuppressive agents might be beneficial for the respiratory disease associated with practolol therapy. This might be true if the untoward effects of practolol were immunologically produced but in my experience steroids do not benefit the lung condition once it has become chronic. Unlike the sclerosing peritonitis, lung lesions do not appear after stopping practolol. The other lesions disappear within a month or two of the end of therapy. The patients who have developed pleural and lung lesions have become respiratory cripples, but the incidence of sideeffects in patients treated with practolol seems very variable. Zacharias2 reported that 38 of 170 treated patients developed oculomucocutaneous lesions and in Finland,2 110 of 80 000 treated patients had the oculomucocutaneous syndrome and 11 had sclerosing peritonitis, but in these studies no mention was made of the incapacitating dyspnreic syndrome. Guy’s Hospital St Thomas Street, London SE1 9RT
A. W. FRANKLAND
PERIPHERAL NEUROPATHY WITH DISOPYRAMIDE
SIR,-We have seen treatment with
a case
of sensorimotor
neuropathy after
disopyramide.
A 72-year-old woman presented with a 4-year history of intermittent attacks of fast atrial fibrillation’during which she had dyspnoea, angina at rest, and occasional syncope. These attacks were not controlled by digoxin, and she complained of dry eyes with practolol. Other beta blockers had not averted the attacks and she became nauseated with quinidine. 6 months before admission disopyramide phosphate (’Norpace’) 150 mg four times a day had been prescribed with complete relief of the tachycardia. 18 days later burning in both feet developed. 3 weeks later disopyramide base (’Rythmodan’) 100 mg three times a day was substituted for the norpace, and 8 days later the burning became intolerable, despite vitamin supplements. The rythmodan was withdrawn and she was started on sustained-release quinidine (’Kinidin Durules’) with good effect. She was admitted to this hospital 4 months after the initial treatment with disopyramide. She drank no alcohol and did not smoke. She complained of severe dysaesthesiae in her feet sufficient to prevent her walking. There were no other neuro5. O’Reilly, R. J. and others. Clin. Immun. Immunopath. 1976, 6, 51. 1. Marshall, A. J., and others. Lancet, 1977, ii, 1254. 2. Zacharias, F. J. Proc. R. Soc. Med. 1977, 70, suppl. 5, 24. 3. Idanpaan-Heikkila, J. E., Hastbacka, J., Jarvinen, H. J. J. Lancet, 1977, ii, 1354.
logical symptoms. Her blood-pressure was 135/85 mm Hg, pulse 60/min regular; she was well perfused and all peripheral pulses were present. Slight weakness of hip and knee flexion and extension, and dorsiflexion of the feet was elicited, more marked on the left. Vibration sense was absent to the iliac spines and joint position was absent in the feet, but normal at the ankle. Testing for touch, pain, temperature, and two-point discrimination was normal, and no hyperalgesia could be demonstrated. Motor and sensory examination of the upper limbs was normal. Laboratory tests on blood and cerebrospinal fluid were normal. Nerve-conduction studies were compatible with a mixed sensorimotor neuropathy of large-fibre type affecting mainly the lower limbs. The patient was given physiotherapy, and carbamazepine provided some symptomatic relief of the dysaesthesix. At the time of discharge her symptoms had improved considerably and she was able to walk unaided. 4 months later she was symptom-free. Most side-effects encountered with disopyramide are related to its anticholinergic properties. It may also lower cardiac output and peripheral perfusion.! Peripheral neuropathy has not previously been reported, although paraesthesiae2.3 and/or numbness4 have been seen. Nerve-conduction studies in patients with symptoms of dysaesthesiae might reveal more cases of disopyramide neuropathy. K. D. DAWKINS National Hospitals for Nervous Diseases, London WC1 J. GIBSON
CLOSED-ANGLE GLAUCOMA IN PATIENT ON DISOPYRAMIDE woman receiving oral disopyramide the ophthalmology ward with acute closedangle glaucoma with symptoms localised to the right eye. The pressures were 40 mm Hg in the right eye and 35 mm Hg in the left eye on applanation tonometry. Gonioscopy revealed bilateral narrow angles closed through 360°. The patient was treated with 2% pilocarpine and 0.25% eserine eye-drops until the pressures were controlled, and 3 days later bilateral peripheral iridectomy was done. Postoperatively her pressures remained controlled, and the patient was discharged on disopyramide tablets 100 mg four times daily. She had recently been treated in the medical wards for supraventricular paroxysmal tachycardia, and, because this had not been controlled by propranolol, she was given oral disopyramide 100 mg three times a day for 6 days and then 200 mg three times a day for a further 6 days. Her symptoms of glaucoma had started on the 7th day of this regime. We have found no previous report of closed-angle glaucoma precipitated by disopyramide, but the anticholinergic activity of this drug has been demonstrated in vitroand in vivo.1i A drug history should be taken from all patients with closedangle glaucoma, and clinicians should remember that the anticholinergic activity of disopyramide may produce glaucoma in a susceptible patient. This drug is being widely used for the prevention and treatment of arrhythmias. All patients who are to be treated in this way should be asked if they have a family history of glaucoma, and if there is any doubt, they should be assessed gonioscopically.
SIR,-A 66-year-old
was
admitted
to
Department of Ophthalmology, Stobhill General Hospital, Glasgow G21 3UW
G. E. TROPE V. M. D. HIND
1. Befeler, B., and others. Angiology, 1975, 26, suppl. 1, p. 99. 2. Jennings, G., and others. Lancet, 1976, i, 51. 3. Zainal, N., and others. J. int. med. Res. 1976, 4, suppl. 1, p. 71. 4. Hopkins, A. M. Personal communication. 5. Mokler, C. M., Hillman, R. A. Pharmac. Res. Commun. 1972, 4, 6. McHaffie, D. J., Guz, A., Johnston, A. Lancet, 1977, i, 859.
171.
