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.
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.
