284 TRANSIENT LOSS OF HLA B27
SR,—Because HLA antigens are genetically determined, an individual’s phenotype should not change. However, we have found some evidence that an HLA antigen may be lost transiently. The HLA phenotype of a 24-year-old female with ankylosing spondylitis with axial and peripheral involvement was Al, A2, -, B27 in 1974. A year later B27 was absent and in the following two years, three more tests in two different laboratories were twice negative and once positive for B27. This observation led us to repeat the test for HLA B27 antigen in some randomly selected patients. A similar result was obtained with eight patients (see table). TRANSIENT LOSS OF HLA
Fig. 1—Ptasma-chotesterol and
mean
B27
triglyceride levels.
* A.s.=Ankylosing spondylitis; R.A.=rheumatoid arthritis; R.s.=Reiter’s syndrome.
A.I.D.=anti-inflammatory drugs
other than steroids;
G.s.=gold salts;
s=steroids.
A standard microlymphocytotoxicity test was used and the antisera were checked by simultaneous testing of HLA B27 positive and HLA B27 negative patients. These results are thus unlikely to be due to laboratory error. Hormones, drugs, or antibodies formed during the disease may bind to lymphocytes, preventing the interaction of antibodies with HLA antigens. Svejgaard and Ryder’ suggested that HLA antigens interact with ligands such as hormones and Majsky and Jakoubkova2 described the transient loss of HLA antigens in a healthy woman during menstruation or supposed ovulation. HLA B27 is found in a high proportion of patients with ankylosing spondylitis or Reiter’s syndrome.3 Its absence in some cases may thus be only a transient loss.
Fig. 2-Results of H.M.G. treatment. Tubero-eruptive xanthomas on the right elbow before (above left) and after (above right) 56 weeks H.M.G. treatment; tendinous and tuberous xanthomas on right hand before (below left) and after (below right) 84 weeks H.M.G. treatment.
discontinued because of repeated episodes of arthritic xanthomatosis and during pregnancy. During pregnancy, plasmatriglycerides, which were unaffected by the drug treatment, also increased. After delivery H.M.G. was again given (3000 mg per day) and the plasma-cholesterol again decreased. During 84 weeks of treatment with H.M.G., the plasma-cholesterol level decreased on average by 24% with a maximum decrease of 38%. The tubero-eruptive xanthomas at the right elbow disappeared completely after 14 months of treatment and both the tendinous xanthomas on the dorsum of both hands and the tuberous xanthomas at the interphalangeal joints of all fingers regressed significantly after 84 weeks of treatment (fig. 2). Our results indicate that when combined with diet therapy, H.M.G. may be a promising non-toxic hypocholesterolasmic agent in the long-term treatment Of H.F.H. was
We thank the staff of the Lipid Research Center and especially Marielle Toussaint and Suzanne Parent for their collaboration.
Lipid Research Center, Department of Biochemistry, Laval University Hospital, Quebec, Canada G1V 4G2
P.-J. LUPIEN D. BRUN S. MOORJANI
Institut de
Rhumatologie,
Hôpital Cochin, 75014 Paris, France
B. AMOR A. KAHAN A. E. GEORGIADIS
HAZARDS WITH MONOAMINE-OXIDASE INHIBITORS: A PERSISTENT PROBLEM
SIR,—As a psychobiologist and director of a counselling service which sees many people with drug problems I have become concerned about an apparent increase in the prescribing of monoamine-oxidase inhibitors (M.A.O.I.S). These drugs have had a variable history of popularity with general practitioners, because of problems with overdosage and interaction with other drugs and certain foods. These risks should, by now, be well known, but in the year ended Sept. 30, 1977, we saw 35 clients who contacted us with crises arising out of the use of M.A.0. i.s; at least 4 of these crises were fatal During the year the total number of people seen with drug problems of all sorts was 119. In many cases the client claimed not to have been warned of the dangers of M.A.o.I.s in relation to other drugs or foods. Patients eating incompatible foods presented with hypertensive 1. Svejgaard, A., Ryder, L. D. Lancet, 1976, ii, 547. 2. Majsky, A., Jakoubkova, J. ibid. p. 859. 3. Amor, B., Feldmann, J. L., Delbarre, F., Hors, J.,
J. New Eng. J. Med. 1974, 290, 554.
Beaujan,
M.
M., Dausset,
SR,—Because HLA antigens are genetically determined, an individual’s phenotype should not change. However, we have found some evidence that an HLA antigen may be lost transiently. The HLA phenotype of a 24-year-old female with ankylosing spondylitis with axial and peripheral involvement was Al, A2, -, B27 in 1974. A year later B27 was absent and in the following two years, three more tests in two different laboratories were twice negative and once positive for B27. This observation led us to repeat the test for HLA B27 antigen in some randomly selected patients. A similar result was obtained with eight patients (see table). TRANSIENT LOSS OF HLA
Fig. 1—Ptasma-chotesterol and
mean
B27
triglyceride levels.
* A.s.=Ankylosing spondylitis; R.A.=rheumatoid arthritis; R.s.=Reiter’s syndrome.
A.I.D.=anti-inflammatory drugs
other than steroids;
G.s.=gold salts;
s=steroids.
A standard microlymphocytotoxicity test was used and the antisera were checked by simultaneous testing of HLA B27 positive and HLA B27 negative patients. These results are thus unlikely to be due to laboratory error. Hormones, drugs, or antibodies formed during the disease may bind to lymphocytes, preventing the interaction of antibodies with HLA antigens. Svejgaard and Ryder’ suggested that HLA antigens interact with ligands such as hormones and Majsky and Jakoubkova2 described the transient loss of HLA antigens in a healthy woman during menstruation or supposed ovulation. HLA B27 is found in a high proportion of patients with ankylosing spondylitis or Reiter’s syndrome.3 Its absence in some cases may thus be only a transient loss.
Fig. 2-Results of H.M.G. treatment. Tubero-eruptive xanthomas on the right elbow before (above left) and after (above right) 56 weeks H.M.G. treatment; tendinous and tuberous xanthomas on right hand before (below left) and after (below right) 84 weeks H.M.G. treatment.
discontinued because of repeated episodes of arthritic xanthomatosis and during pregnancy. During pregnancy, plasmatriglycerides, which were unaffected by the drug treatment, also increased. After delivery H.M.G. was again given (3000 mg per day) and the plasma-cholesterol again decreased. During 84 weeks of treatment with H.M.G., the plasma-cholesterol level decreased on average by 24% with a maximum decrease of 38%. The tubero-eruptive xanthomas at the right elbow disappeared completely after 14 months of treatment and both the tendinous xanthomas on the dorsum of both hands and the tuberous xanthomas at the interphalangeal joints of all fingers regressed significantly after 84 weeks of treatment (fig. 2). Our results indicate that when combined with diet therapy, H.M.G. may be a promising non-toxic hypocholesterolasmic agent in the long-term treatment Of H.F.H. was
We thank the staff of the Lipid Research Center and especially Marielle Toussaint and Suzanne Parent for their collaboration.
Lipid Research Center, Department of Biochemistry, Laval University Hospital, Quebec, Canada G1V 4G2
P.-J. LUPIEN D. BRUN S. MOORJANI
Institut de
Rhumatologie,
Hôpital Cochin, 75014 Paris, France
B. AMOR A. KAHAN A. E. GEORGIADIS
HAZARDS WITH MONOAMINE-OXIDASE INHIBITORS: A PERSISTENT PROBLEM
SIR,—As a psychobiologist and director of a counselling service which sees many people with drug problems I have become concerned about an apparent increase in the prescribing of monoamine-oxidase inhibitors (M.A.O.I.S). These drugs have had a variable history of popularity with general practitioners, because of problems with overdosage and interaction with other drugs and certain foods. These risks should, by now, be well known, but in the year ended Sept. 30, 1977, we saw 35 clients who contacted us with crises arising out of the use of M.A.0. i.s; at least 4 of these crises were fatal During the year the total number of people seen with drug problems of all sorts was 119. In many cases the client claimed not to have been warned of the dangers of M.A.o.I.s in relation to other drugs or foods. Patients eating incompatible foods presented with hypertensive 1. Svejgaard, A., Ryder, L. D. Lancet, 1976, ii, 547. 2. Majsky, A., Jakoubkova, J. ibid. p. 859. 3. Amor, B., Feldmann, J. L., Delbarre, F., Hors, J.,
J. New Eng. J. Med. 1974, 290, 554.
Beaujan,
M.
M., Dausset,
