831 I suggest that caution be advised in the use of peritoneal lavage, for it is not some magical talisman but simply another variably valuable investigative tool. Like most other investigations its value is directly related to sound clinical indications for its use. Department of Surgery, University of British Columbia, Vancouver General Hospital,
JULIUS L. STOLLER
Vancouver, British Columbia, Canada
FATAL MULTISYSTEM TOXICITY AFTER CO-TRIMOXAZOLE
SiR,—Co-trimoxazole has been associated with severe damage to internal organsl-5 and neurological symptoms and signs.l,6 Of 655 adverse reactions to co-trimoxazole reported by Danish doctors from May 1, 1968, to March 31, 1977, 16 related to the central and peripheral nervous system and 5 to the special senses.7 We report here a case of cerebromedullospinal disconnection associated with lesions of the kidney, lung, and pancreas and cardiac arrhythmia after treatment with co-trimoxazole. The patient, a 62-year old man with no tendency to allergic reactions and in good health after an uncomplicated prostatectomy had bacteriuria diagnosed 3 weeks after the operation. Co-trimoxazole treatment was started (160 mg trimethoprim and 800 mg sulphamethoxazole twice daily) but after 8 days the patient had arthralgia and back pain. 2 days later he was admitted with a widespread pustulous eruption a temperature of 40-3° C cyanosis, tachycardia, and 90/60 mm Hg bloodpressure. X-rays showed diffuse lung infiltrations, and he was anuric within 24 h. On admission he
was treated with digoxin, frusemide and methylprednisolone intravenously, plasma, blood, dopamine and noradrenaline, artificial respiration, and peritoneal dialysis. Cultures from pustules, blood cerebrospinal fluid, urine, peritoneum, and the trachea were negative and he was treated with gentamicin, methicillin, and cephalothin sodium. After 3 days he had cardiac arrhythmia, and 2 days later he had a cardiac arrest, successfully treated by external cardiac massage and intravenous atropine. There was increasing evidence of damage to pancreas and liver (blood-sugar up to 750 mg/dl; lactic dehydrogenase 2200 units/I normal 150—450; bilirubin increasing to 4-7 mg/dl, normal 0.3-1.0) and at laparotomy 7 days after admission a severe hxmorrhagic pancreatitis was diagnosed. From the first day of admission he was thought unconscious, only reacting to pain. After a week he could open his eyes on
request and follow the examiner with theeyes, but he was otherwise global apractic, with rigid, reflexless extremities. After 2 months he had spontaneous respiration and, lateral gaze and would make small movements of tongue and lips. Except for these movements, he was mute, akinetic, and paralytic ; light and corneal reflexes, doll’s head reflex, and dilatation of the pupils when pinched in the face were normal, but he was without peripheral reactivity. This locked-in state ended by cardiac arrest after ten weeks. The necropsy showed acute tubulointerstitial nephropathy, acute pancreatitis, hepatic steatosis, and pulmonary fibrosis, several petechial hsemorrhages in the white substance of the hemispheres, and a 5 mm large haemorrhage caudally in the 1. Frisch, J. M. J. infect. Dis. 1973, 128, 607. 2. Kalowski, S., Mathew, T. H., Naura, R. S.,
Kincaid-Smith, P. Lancet, 1973,
i, 394. 3. Tamtamy, S. E. ibid. 1974, i, 929. 4. Knudsen, L., Weismann, K. Ugeskr. Lœg. 1977, 139, 1007. 5. Ramaiah, R. S., Gallagher, M. A., Biagi, R. W. Lancet, 1977, i, 604. 6 Grossman, A. B., Braimbridge, M. V., Ross Russell, R. W., Smith, S. E. ibid.
ii, 616. 7. Sundhedsstyrelsens
Bivirkningsnævn (Danish
Reactions). Unpublished.
State
Register for Adverse
corpus callosum. There were no macroscopic abnormalities in the brainstem. Our case was more severe than those reported by Kalowski et al .2 (acute tubular necrosis), Ramaiah et al.5 (anuria), and Knudsen and Weismann(liver and kidney damage). Our patient had toxic and/or allergic reactions affecting skin, lungs, kidneys, liver, pancreas, and central nervous system with probable loss of central neural control of the heart.8 Cerebromedullospinal disconnection may have been established before the first cardiac arrest but neurological examination and E.E.G. were not done until after the cardiac arrest, so the disconnection may have followed the cardiac arrest.9 There can be little doubt, however, that this case illustrates a fatal reaction to co-trimoxazole, since the patient was in fine health except for dysuria before treatment and from the eighth day of treatment he showed most of the reactions hitherto as-
sociated with co-trimoxazole. Department of Neurology and Intensive Care, Copenhagen Municipal Hospital, Copenhagen, Denmark
JØRGEN BRØCKNER ERIK BOISEN
PERHEXILENE MIMICKING BRONCHIAL CARCINOMA
SIR,-Perhexilene maleate is a useful anti-anginal drug, and side-effects, though common, are usually minor and reversible. We describe here a patient assumed to have carcinoma of the bronchus, but whose symptoms were subsequently attributed to perhexilene. A 63-year-old labourer was transferred to this hospital for He had been well until 3 months before admission when he began to have difficulty with balance, and he was said by his wife to be "walking like a drunk". He also complained of dizziness with no rotational element. Progressive dysaesthesiae in the feet started 2 months later. He had also lost 10 kg in weight over a 3 month period. Direct questioning revealed longstanding effort dyspnoea, mild orthopncea, and cough with mucopurulent sputum. 9 years earlier he had had a myocardial infarction after which hypertension was diagnosed. He was put on oxprenolol 80 mg and perhexilene 100 mg, both three times a day, 12 months before admission. He drank modest amounts of alcohol and he had stopped smoking 20 years previously. On examination he was emaciated and
investigation.
pyrexial (38 °C), blood-pressure 110/60 mm Hg, pulse 68/min, sinus rhythm. His chest was hyperinflated and he had consolidation in the right upper lobe. His voice was slightly hoarse and he was dysarthric. He had generalised wasting and the lower limbs were hypotonic. There was symmetrical loss of power and moderate ataxia in all four limbs, most severe in the legs. He was areflexic and the plantars were flexor. A rest tremor of the arms and titubation of the head were noted. On sensory examination he was found to have a panmodal loss in a
glove-and-stocking distribution. Hb was 13.5g/dl, white cells 13 500/1 (neutrophilia), erythrocyte-sedimentation-rate 90 mm/h, s.G.o.T. 739 iu/1, creatine phosphokinase 141 iu/1. Remainder of blood tests normal. A chest X-ray showed bilateral apical pleural thickening, calcification in both apices, and upper-lobe fibrosis. He also had consolidation of the right upper lobe and slight widening of the superior mediastinum. Bronchoscopy revealed no neoplasm. Nerve-conduction studies were compatible with a sensorimotor neuropathy affecting all four limbs. 3 days after admission he died of an overwhelming chest infection. Necropsy revealed no evidence of a bronchial carcinoma. The presumptive diagnosis had been bronchial carcinoma with non-metastatic neurological complications. However, investigations and necropsy findings failed to reveal a neoplasm. Perhexilene has been associated with proximal myopathy,l per8. 9. 1.
Korner, P. I. Physiol. Rev. 1971, 51, 312. Boisen, E., Siemkowicz, E. Lancet, 1976, i, 1381. Tomlinson, I. W., Rosenthal, F. D. Br. med. J. 1977, i, 1319.
832 muscle wasting and ataxia,3 and abnormalities of liver function.4 It has been the subject of an adverse-reactions warning.s We feel it likely that perhexilene was responsible for the symptom complex in this patient. This case emphasises the importance of first excluding an iatrogenic basis for a particular condition. K. D. DAWKINS National Hospitals for Nervous Diseases, London WC1N 3BG E. O’CONNOR
ipheral neuropathy,2
test results became negative after of the sera with heat-aggregated IgG. In contrast, IgM-I.F.A. test titres in cases of acute congenital or acquired toxoplasmosis were unaffected by this treatment. Thus treatment with heat-aggregated IgG can be used to differentiate false-positive IgM-i.F.A. test titres due to R.F. from those due
False-positive IgM-I.F,A.
treatment
to
specific IgM toxoplasma antibody.
A valuable contribution to this area is the report from the Wellcome Research Laboratories (Immun. Methods, 1976,13,
367). KOEBNER PHENOMENON, MORPHŒA, AND VIRAL EXANTHEMS
SjR,—The report by Dr Fenyk and colleagues (March 3,
p.
of sclerodermatous graft-versus-host disease limited to an area of measles exanthem prompts me to record a similar case. An 8-year-old girl had several large white macules with violaceous halos. These were localised to the trunk and were clinically and histologically compatible with morphoea. 3 months later she had severe varicella which healed with hypopigmentation leaving guttate macules (2-3 mm in diameter) on the trunk and extremities. Many of the post-varicella macules showed slightly depressed centres which histologically revealed focal homogenisation of the collagen, compatible with mor-
472)
phrea.
Fenyk et al. described the localised sclerodermatous changes in their patient as probable viral induction of the graft-versushost disease (G.V.H.D.). The reaction, however, strongly resembles a Koebner phenomenon in which the latent G.v.H.D. localises to areas of virally altered skin. In my patient, the viral lesions apparently caused Koebner phenomenon in latent mor-
Stanford University Medical Center, Stanford, California 94305, U.S.A. and Palo Alto Medical Research Foundation, Palo Alto, California
J. S. REMINGTON
FAMILY STUDY OF FARMER’S LUNG
SIR,-To evaluate factors that
may lead to farmer’s lung in individual while the other antigen-exposed members of the family remained symptom-free we have investigated the family of a patient known to have farmer’s lung. The clinical diagnosis of chronic farmer’s lung rested on the history, radiological changes, and a combined restrictive and obstructive ventilatory defect. Laboratory diagnosis was done by examining serum for precipitins against extracts of mouldy hay’ and Micropolyspora fceni culture filtrate antigens one
FAMILY CHARACTERISTICS
phoea (sclerodermatous change). Department of Dermatology, Oklahoma City Clinic, and University of Oklahoma Health Science Center, Oklahoma City, Oklahoma, U.S.A.
W.
J. SAHL
FALSE-POSITIVE IgM ANTI-TOXOPLASMA FLUORESCENT TEST DUE TO RHEUMATOID FACTOR
SIR,-The communication by Dr Yeni and colleagues (Jan. 28, p. 219) is interesting, but they do not refer to other work that has been done in this area. Our study (reported in Proc. Soc. exp. Biol. Med. 1975, 148, 1184) was prompted by the important observations of M. E. Camargo and colleagues, who described a high prevalence of Toxoplasma IgM-fluorescent antibody (I.F.A.) test titres in sera positive in the latex agglutination test for rheumatoid factor (R.F.) (Rev. Inst. Med. trop. Sdo Paulo, 1972, 14, 310). We looked for false-positive Toxoplasma IgM-I.F.A. test results in sera containing R.F. 8 (20%) of 41 sera which were positive for R.F. were positive in the Toxoplasma dye test and conventional Toxoplasma I.F.A. test. 3 of these 8 were also positive in the Toxoplasma IgM-I.F.A. test, and in 2 the results were considered to be false positives. Of the 33 R.F.-positive sera which were negative in both the dye test and conventional I.F.A. test, 3 were positive in the IgM-I.F.A. test. Of 51 sera from patients with suspected rheumatoid arthritis or other collagen vascular disorders, all of which were negative for R.F., none was positive for Toxoplasma antibodies in the IgM-I.F.A. test.
Sera from 15 adults with acute lymphadenopathic toxoplasmosis and 13 infants with proved congenital toxoplasmosis were also tested for the presence of R.F. Whereas none of the sera from the acquired cases had demonstrable R.F., 2 of the congenital cases had R.F. (1/320 in both). Abaza, A., and others. Nouv. Presse méd. 1973, 2, 2820. 3. Epstein, H. S. Afr. med. J. 1977, 51, 189. 4. Howard, D. J., Russell Rees, J. Br. med. J. 1976, i, 133. 5. Committee on Safety of Medicines. Adverse Reactions Series no. 15.
tomatic disease. The table shows the
degree of exposure to mouldy hay, precipitins against mouldy hay and M.F.C.F., and the percentage autologous complement consumption by M.F.C.F. (0.25 fLg M.F.C.F. in 0-ml 1/20 diluted serum). Serum precipitins against M.F.C.F. antigens were found not only in the affected farmer but also in his healthy son and symptom-free brother. This result is not surprising, because serum precipitins merely indicate exposure.3 M.F.C.F. antigens consumed complement not only in the serum of the patient but also in the serum of two other healthy relatives. However, only the serum of the patient with farmer’s lung had both precipitating and complement-consuming antibodies, whereas his relatives with either precipitating or complement-consuming antibodies were symptom-free. Perhaps both precipitating and complement-consuming antibodies to M. ftni antigens are necessary for farmer’s lung disease to develop. Our experience with farmer’s lung2 and pigeon-breeder’s disease4 supports this hypothesis. serum
1.
2.
1977.
(M.F.C.F.) and for autologous serum complement consumption by M.F.C.F.2 The sera of the family members were screened for precipitins and complement-consuming antibodies. HLA-typing of the family members was done to see if HLA type was related to serological reactivity to M. fani antigens or to symp-
July,
2. 3. 4.
Pepys, J. Hypersensitivity Diseases of the Lungs due to Fungi and Organic Dusts. Basle, 1969. Berrens, L., De Ridder, G., De Boer, F. Scand. J. resp. Dis., 1977, 58, 205. Salvaggio, J. Chest, 1972, 62, 242. Berrens, L., Guikers, C. L. H. Int. Archs Allergy, 1972, 43, 347.
JULIUS L. STOLLER
Vancouver, British Columbia, Canada
FATAL MULTISYSTEM TOXICITY AFTER CO-TRIMOXAZOLE
SiR,—Co-trimoxazole has been associated with severe damage to internal organsl-5 and neurological symptoms and signs.l,6 Of 655 adverse reactions to co-trimoxazole reported by Danish doctors from May 1, 1968, to March 31, 1977, 16 related to the central and peripheral nervous system and 5 to the special senses.7 We report here a case of cerebromedullospinal disconnection associated with lesions of the kidney, lung, and pancreas and cardiac arrhythmia after treatment with co-trimoxazole. The patient, a 62-year old man with no tendency to allergic reactions and in good health after an uncomplicated prostatectomy had bacteriuria diagnosed 3 weeks after the operation. Co-trimoxazole treatment was started (160 mg trimethoprim and 800 mg sulphamethoxazole twice daily) but after 8 days the patient had arthralgia and back pain. 2 days later he was admitted with a widespread pustulous eruption a temperature of 40-3° C cyanosis, tachycardia, and 90/60 mm Hg bloodpressure. X-rays showed diffuse lung infiltrations, and he was anuric within 24 h. On admission he
was treated with digoxin, frusemide and methylprednisolone intravenously, plasma, blood, dopamine and noradrenaline, artificial respiration, and peritoneal dialysis. Cultures from pustules, blood cerebrospinal fluid, urine, peritoneum, and the trachea were negative and he was treated with gentamicin, methicillin, and cephalothin sodium. After 3 days he had cardiac arrhythmia, and 2 days later he had a cardiac arrest, successfully treated by external cardiac massage and intravenous atropine. There was increasing evidence of damage to pancreas and liver (blood-sugar up to 750 mg/dl; lactic dehydrogenase 2200 units/I normal 150—450; bilirubin increasing to 4-7 mg/dl, normal 0.3-1.0) and at laparotomy 7 days after admission a severe hxmorrhagic pancreatitis was diagnosed. From the first day of admission he was thought unconscious, only reacting to pain. After a week he could open his eyes on
request and follow the examiner with theeyes, but he was otherwise global apractic, with rigid, reflexless extremities. After 2 months he had spontaneous respiration and, lateral gaze and would make small movements of tongue and lips. Except for these movements, he was mute, akinetic, and paralytic ; light and corneal reflexes, doll’s head reflex, and dilatation of the pupils when pinched in the face were normal, but he was without peripheral reactivity. This locked-in state ended by cardiac arrest after ten weeks. The necropsy showed acute tubulointerstitial nephropathy, acute pancreatitis, hepatic steatosis, and pulmonary fibrosis, several petechial hsemorrhages in the white substance of the hemispheres, and a 5 mm large haemorrhage caudally in the 1. Frisch, J. M. J. infect. Dis. 1973, 128, 607. 2. Kalowski, S., Mathew, T. H., Naura, R. S.,
Kincaid-Smith, P. Lancet, 1973,
i, 394. 3. Tamtamy, S. E. ibid. 1974, i, 929. 4. Knudsen, L., Weismann, K. Ugeskr. Lœg. 1977, 139, 1007. 5. Ramaiah, R. S., Gallagher, M. A., Biagi, R. W. Lancet, 1977, i, 604. 6 Grossman, A. B., Braimbridge, M. V., Ross Russell, R. W., Smith, S. E. ibid.
ii, 616. 7. Sundhedsstyrelsens
Bivirkningsnævn (Danish
Reactions). Unpublished.
State
Register for Adverse
corpus callosum. There were no macroscopic abnormalities in the brainstem. Our case was more severe than those reported by Kalowski et al .2 (acute tubular necrosis), Ramaiah et al.5 (anuria), and Knudsen and Weismann(liver and kidney damage). Our patient had toxic and/or allergic reactions affecting skin, lungs, kidneys, liver, pancreas, and central nervous system with probable loss of central neural control of the heart.8 Cerebromedullospinal disconnection may have been established before the first cardiac arrest but neurological examination and E.E.G. were not done until after the cardiac arrest, so the disconnection may have followed the cardiac arrest.9 There can be little doubt, however, that this case illustrates a fatal reaction to co-trimoxazole, since the patient was in fine health except for dysuria before treatment and from the eighth day of treatment he showed most of the reactions hitherto as-
sociated with co-trimoxazole. Department of Neurology and Intensive Care, Copenhagen Municipal Hospital, Copenhagen, Denmark
JØRGEN BRØCKNER ERIK BOISEN
PERHEXILENE MIMICKING BRONCHIAL CARCINOMA
SIR,-Perhexilene maleate is a useful anti-anginal drug, and side-effects, though common, are usually minor and reversible. We describe here a patient assumed to have carcinoma of the bronchus, but whose symptoms were subsequently attributed to perhexilene. A 63-year-old labourer was transferred to this hospital for He had been well until 3 months before admission when he began to have difficulty with balance, and he was said by his wife to be "walking like a drunk". He also complained of dizziness with no rotational element. Progressive dysaesthesiae in the feet started 2 months later. He had also lost 10 kg in weight over a 3 month period. Direct questioning revealed longstanding effort dyspnoea, mild orthopncea, and cough with mucopurulent sputum. 9 years earlier he had had a myocardial infarction after which hypertension was diagnosed. He was put on oxprenolol 80 mg and perhexilene 100 mg, both three times a day, 12 months before admission. He drank modest amounts of alcohol and he had stopped smoking 20 years previously. On examination he was emaciated and
investigation.
pyrexial (38 °C), blood-pressure 110/60 mm Hg, pulse 68/min, sinus rhythm. His chest was hyperinflated and he had consolidation in the right upper lobe. His voice was slightly hoarse and he was dysarthric. He had generalised wasting and the lower limbs were hypotonic. There was symmetrical loss of power and moderate ataxia in all four limbs, most severe in the legs. He was areflexic and the plantars were flexor. A rest tremor of the arms and titubation of the head were noted. On sensory examination he was found to have a panmodal loss in a
glove-and-stocking distribution. Hb was 13.5g/dl, white cells 13 500/1 (neutrophilia), erythrocyte-sedimentation-rate 90 mm/h, s.G.o.T. 739 iu/1, creatine phosphokinase 141 iu/1. Remainder of blood tests normal. A chest X-ray showed bilateral apical pleural thickening, calcification in both apices, and upper-lobe fibrosis. He also had consolidation of the right upper lobe and slight widening of the superior mediastinum. Bronchoscopy revealed no neoplasm. Nerve-conduction studies were compatible with a sensorimotor neuropathy affecting all four limbs. 3 days after admission he died of an overwhelming chest infection. Necropsy revealed no evidence of a bronchial carcinoma. The presumptive diagnosis had been bronchial carcinoma with non-metastatic neurological complications. However, investigations and necropsy findings failed to reveal a neoplasm. Perhexilene has been associated with proximal myopathy,l per8. 9. 1.
Korner, P. I. Physiol. Rev. 1971, 51, 312. Boisen, E., Siemkowicz, E. Lancet, 1976, i, 1381. Tomlinson, I. W., Rosenthal, F. D. Br. med. J. 1977, i, 1319.
832 muscle wasting and ataxia,3 and abnormalities of liver function.4 It has been the subject of an adverse-reactions warning.s We feel it likely that perhexilene was responsible for the symptom complex in this patient. This case emphasises the importance of first excluding an iatrogenic basis for a particular condition. K. D. DAWKINS National Hospitals for Nervous Diseases, London WC1N 3BG E. O’CONNOR
ipheral neuropathy,2
test results became negative after of the sera with heat-aggregated IgG. In contrast, IgM-I.F.A. test titres in cases of acute congenital or acquired toxoplasmosis were unaffected by this treatment. Thus treatment with heat-aggregated IgG can be used to differentiate false-positive IgM-i.F.A. test titres due to R.F. from those due
False-positive IgM-I.F,A.
treatment
to
specific IgM toxoplasma antibody.
A valuable contribution to this area is the report from the Wellcome Research Laboratories (Immun. Methods, 1976,13,
367). KOEBNER PHENOMENON, MORPHŒA, AND VIRAL EXANTHEMS
SjR,—The report by Dr Fenyk and colleagues (March 3,
p.
of sclerodermatous graft-versus-host disease limited to an area of measles exanthem prompts me to record a similar case. An 8-year-old girl had several large white macules with violaceous halos. These were localised to the trunk and were clinically and histologically compatible with morphoea. 3 months later she had severe varicella which healed with hypopigmentation leaving guttate macules (2-3 mm in diameter) on the trunk and extremities. Many of the post-varicella macules showed slightly depressed centres which histologically revealed focal homogenisation of the collagen, compatible with mor-
472)
phrea.
Fenyk et al. described the localised sclerodermatous changes in their patient as probable viral induction of the graft-versushost disease (G.V.H.D.). The reaction, however, strongly resembles a Koebner phenomenon in which the latent G.v.H.D. localises to areas of virally altered skin. In my patient, the viral lesions apparently caused Koebner phenomenon in latent mor-
Stanford University Medical Center, Stanford, California 94305, U.S.A. and Palo Alto Medical Research Foundation, Palo Alto, California
J. S. REMINGTON
FAMILY STUDY OF FARMER’S LUNG
SIR,-To evaluate factors that
may lead to farmer’s lung in individual while the other antigen-exposed members of the family remained symptom-free we have investigated the family of a patient known to have farmer’s lung. The clinical diagnosis of chronic farmer’s lung rested on the history, radiological changes, and a combined restrictive and obstructive ventilatory defect. Laboratory diagnosis was done by examining serum for precipitins against extracts of mouldy hay’ and Micropolyspora fceni culture filtrate antigens one
FAMILY CHARACTERISTICS
phoea (sclerodermatous change). Department of Dermatology, Oklahoma City Clinic, and University of Oklahoma Health Science Center, Oklahoma City, Oklahoma, U.S.A.
W.
J. SAHL
FALSE-POSITIVE IgM ANTI-TOXOPLASMA FLUORESCENT TEST DUE TO RHEUMATOID FACTOR
SIR,-The communication by Dr Yeni and colleagues (Jan. 28, p. 219) is interesting, but they do not refer to other work that has been done in this area. Our study (reported in Proc. Soc. exp. Biol. Med. 1975, 148, 1184) was prompted by the important observations of M. E. Camargo and colleagues, who described a high prevalence of Toxoplasma IgM-fluorescent antibody (I.F.A.) test titres in sera positive in the latex agglutination test for rheumatoid factor (R.F.) (Rev. Inst. Med. trop. Sdo Paulo, 1972, 14, 310). We looked for false-positive Toxoplasma IgM-I.F.A. test results in sera containing R.F. 8 (20%) of 41 sera which were positive for R.F. were positive in the Toxoplasma dye test and conventional Toxoplasma I.F.A. test. 3 of these 8 were also positive in the Toxoplasma IgM-I.F.A. test, and in 2 the results were considered to be false positives. Of the 33 R.F.-positive sera which were negative in both the dye test and conventional I.F.A. test, 3 were positive in the IgM-I.F.A. test. Of 51 sera from patients with suspected rheumatoid arthritis or other collagen vascular disorders, all of which were negative for R.F., none was positive for Toxoplasma antibodies in the IgM-I.F.A. test.
Sera from 15 adults with acute lymphadenopathic toxoplasmosis and 13 infants with proved congenital toxoplasmosis were also tested for the presence of R.F. Whereas none of the sera from the acquired cases had demonstrable R.F., 2 of the congenital cases had R.F. (1/320 in both). Abaza, A., and others. Nouv. Presse méd. 1973, 2, 2820. 3. Epstein, H. S. Afr. med. J. 1977, 51, 189. 4. Howard, D. J., Russell Rees, J. Br. med. J. 1976, i, 133. 5. Committee on Safety of Medicines. Adverse Reactions Series no. 15.
tomatic disease. The table shows the
degree of exposure to mouldy hay, precipitins against mouldy hay and M.F.C.F., and the percentage autologous complement consumption by M.F.C.F. (0.25 fLg M.F.C.F. in 0-ml 1/20 diluted serum). Serum precipitins against M.F.C.F. antigens were found not only in the affected farmer but also in his healthy son and symptom-free brother. This result is not surprising, because serum precipitins merely indicate exposure.3 M.F.C.F. antigens consumed complement not only in the serum of the patient but also in the serum of two other healthy relatives. However, only the serum of the patient with farmer’s lung had both precipitating and complement-consuming antibodies, whereas his relatives with either precipitating or complement-consuming antibodies were symptom-free. Perhaps both precipitating and complement-consuming antibodies to M. ftni antigens are necessary for farmer’s lung disease to develop. Our experience with farmer’s lung2 and pigeon-breeder’s disease4 supports this hypothesis. serum
1.
2.
1977.
(M.F.C.F.) and for autologous serum complement consumption by M.F.C.F.2 The sera of the family members were screened for precipitins and complement-consuming antibodies. HLA-typing of the family members was done to see if HLA type was related to serological reactivity to M. fani antigens or to symp-
July,
2. 3. 4.
Pepys, J. Hypersensitivity Diseases of the Lungs due to Fungi and Organic Dusts. Basle, 1969. Berrens, L., De Ridder, G., De Boer, F. Scand. J. resp. Dis., 1977, 58, 205. Salvaggio, J. Chest, 1972, 62, 242. Berrens, L., Guikers, C. L. H. Int. Archs Allergy, 1972, 43, 347.
