- Email: [email protected]
SCREENING FOR CYSTIC FIBROSIS
1238 POSSIBLE ASSOCIATION OF ALZHEIMER’S DISEASE WITH HLA-BW15 AND CYTOMEGALOVIRUS INFECTION
brain damage, and there is evidence9 that slow infections such as subacute sclerosing panencephalitis may be caused by conventional viruses acting in an unusual way. Murine c.M.v. suppresses humoral,lO cellmediated," and interferon" responses of the host to other antigens, and its possible involvement in disease need not be related to its direct cytopathogenic effect but could result from the initiation of an abnormal immune response, or by acting synergistically with other viruses. The possible association of HLA-BW15 with Alzheimer’s disease, and an immune response trait to c.M.v. is interesting, but it is much too early to conclude that virus is implicated in Alzheimer’s disease. Further studies are needed.
can cause severe some
SIR,-We have HLA-typed 86 inpatients with Alzheimer’s senile dementia and 38 inpatients with Alzheimer’s presenile dementia, for seven A locus and thirteen B locus antigens by a standard microlymphocytoxicity method. Alzheimer’s disease was diagnosed clinically (insidious onset, memory loss, intellectual and personality deterioration, with typical progression, in the absence of hypertension, strokes, or other secondary causes of dementia) with the onset before and after the age of 65 in the presenile and senile groups, respectively. HLA frequencies were compared (chi-squared test) with those in 458 controls who were not age matched (there is no evidence of postnatal selection at the HLA loci’). Table I shows the results of typing for BW 15. The frequency of BW 15in the presenile group was 32% (r<001), in the senile group 27% (r<001), and in both groups combined 28.2% (p
I-FREQUENCY
OF
We thank the consultant
psychiatrists who allowed us to study their
patients. Department of Psychiatry, University of Leeds,
E. B. RENVOIZE
Leeds LS2 9LT Public Health Leeds
HLA-BW15
Regional
Laboratory,
M. H. HAMBLING M.D. PEPPER
Blood Transfusion Centre,
S. M. RAJAH
Leeds
SCREENING FOR CYSTIC FIBROSIS
SIR,-Dr Crossley and her colleagues (March 3, p. 472) have measured serum-immunoreactive-trypsin (I.R.T.) in children with cystic fibrosis and in controls. They found abnormally high levels of serum-i.R.T. in infants with cystic fibrosis and in older patients with residual pancreatic function. They suggest the use of dried blood-spot screening for cystic fibrosis in the newborn and felt that their findings supported the hypothesis of "back-leakage" of pancreatic acrinar contents into the
A study2 of 34 patients with Alzheimer’s senile and presenile dementia revealed no significant association with the HLA system except with CW3 (P<0.05, before correction for the number of antigens tested). BW15 is in strong linkage disequilibrium with CW3.3 There is evidence4 for an association between cytomegalovirus (c.M.v.) susceptibility and the murine major histocompatibility complex, and there may be a similar association in healthy adults with BW15.5 We therefore measured complement-fixation antibody titres to c.M.v. in the sera of 33 of the patients with BW15, and 81 with other tissue-types (table II). 86% had antibodies at a titre of 1/16, and significantly more patients with BW15 had titres 1/64 (p=0.0013, chi-squared
serum.
test). TABLE II-COMPLEMENT-FIXING ANTIBODIES TO C.M.V.
*Mean age
of BW15-positives 73.1
years,
BW15-negatives
73-2 years.
et al.6 found a significantly increased incidence of antibodies in demented patients than in schizophrenics or a mixed group of patients with other psychiatric disorders. They postulated that age difference and the problem of maintaining hygienic conditions among demented patients could be
Lycke
c.M.v.
partly responsible. Could c.M.v. play a tion in the
role in Alzheimer’s disease? c.mt.v. infecin immunosuppressed adults8
fetus,7 neonateand
_
1. 2. 3.
Bender, K., and others Tissue Antigens, 1976, 7, 118. Henschke, P. J., Bell, D. A., Cape, R. D. T. ibid. 1978,12,132. Mayr, W. R. in Histocompatibility Testing 1975 (edited by F. Kissmeyer-
Nielsen); p. 330. Copenhagen, 1975. 4. Chalmer, J. E., Mackenzie, J. S., Stanley, N. F. J. gen. Virol. 1977, 5. Pereira, R. S., James, D. C. O., Stern, H. Br. med J. 1978. ii, 126. 6. Lycke, E., Norrby, R., Roos, B. Br. J. Psychiat. 1974, 124, 273 7. Stern, H., and others, Lancet, 1969, ii, 443. 8. Dorfman, L. J. Neurology, 1973, 23, 136.
Our cystic-fibrosis children usually either have severe lung disease with mild steatorrhcea or severe maldigestion with lesser pulmonary problems. We therefore measured serum-proteases in cystic-fibrosis patients and controls to see if there was any support for the following hypothesis: since lack of antitrypsin is associated with lung damage, plasma-trypsin in excess of antitrypsin might be responsible for the lung damage in cystic fibrosis. Early, severe pancreatic damage causes pronounced maldigestion but little rise in serum-protease levels, and therefore less lung damage; on the other hand, subtotal pancreatic damage allows some digestion but also maintains high serum-protease levels which cause more striking lung damage. General protease and trypsin levels were measured spectrophotometrically using a modification of the method of Erlanger, Kojowsky and Cohen. Trypsin-inhibitor capacity levels were measured by a modification of the method of Eriksson. There were 10 cystic-fibrosis patients and 54 controls all of whom were hospital inpatients or outpatients. Only 2 cysticfibrosis patients were less than one year old and samples were taken before and after food from these children. Our results showed no significant difference between protease and trypsin levels in cystic-fibrosis patients and controls. The protease levels were from 0 to 10.4 mg/ml and the trypsin levels from 0 to 2 mg/ml. In 5 control children, chosen because they were undergoing cardiac catheterisation, levels of protease and trypsin in the pulmonary arteries and veins were similar. Trvpsininhibiting capacities of sera from cystic-fibrosis children were however, smce higher than those of controls (r<0001); trypsin-inhibiting capacity is related to infection, the variation may be due to this. The difference between our results and those of Crossley et al. may be explained by the differing measuring techniques
37, 107. 9.
Agnarsdóttir,
G. in Recent Advances
in
Clinical
Virology
edited by A P
Waterson), p. 21. 1977, Edinburgh, 1977. 10. Osborn, J. E., Medearis, D. N. Proc. Soc. exp. Biol Med. 1967. 124, 347 11. Howard, R J., Miller, J., Najarian, J. S. Clin. exp. Immuno. 1974. 18, 119
1239 used. Our trypsin levels were measured spectrophotometrically and theirs by radioimmunoassay, and it would appear that their immunoassay measures trypsin bound to inhibitor as well as free trypsin. In addition, the number of our young cysticfibrosis patients was small. These positive results from New Zealand encourage us to continue our investigations. B. PHILLIPS Medical Department, Booth Hall Children’s Manchester M9 2AA
J. A. DAVIS
Hospital,
M. GOODE
creased risk of endometrial cancer. Therefore we strongly urge the addition of 7-13 days of a progestagen each month so that the benefits of oestrogen may be achieved with no increased risk of endometrial lesions. Department of Obstetrics and Gynxcology, King’s College Hospital,
MARGARET THOM
Department of Obstetrics and Gynaecology, Birmingham and Midland Hospital for Women, Birmingham 11
MICHAEL PATTERSON
ŒSTROGEN THERAPY AND ENDOMETRIAL CARCINOMA
SIR,-Your editorial of May 26 makes
many controversial the that side-effects of points. oestrogen therapy are still under scrutiny but one would have thought that the benefits of oestrogen over placebo are now well accepted by all but the occasional provocative leader writer, having been clarified by the double-blind trial of Campbell and Whitehead’1 and interminable correspondence in the columns of The Lancet over the past year. Hammond2 and his team from Duke have shown the longterm metabolic benefit of oestrogen by significantly lower rates of strokes, heart-attacks, hypertension, osteoporosis, and fractures. They also confirmed an increased incidence of carcinoma of the endometrium with a risk ratio of9.3.3 The great value of this and the Antunes paper cited by you is that details of therapy are given.’ Only 1 of Hammond’s 11 oestrogen-taking patients with cancer was receiving progestagen ("rarely") during her twenty-four years of high-dose cyclical therapy for gonadal dysgenesis. In the Antunes paper none of the 64 patients with cancer of the uterus had taken progestagen: half were on continuous therapy and 9 were receiving stilboestrol (your conclusion was that continuous therapy was as safe as cyclical oestrogen therapy). 7 of Jick’s5 patients had received "progesterone" but no details of type, duration or frequency are given: you conclude that we should refrain from including progestagens in the regimen. We have probably the largest menopause clinic in Europe and have not been able to reproduce these findings and do not support the prediction of Jick et al. that the annual rate of cancer of the uterus in oestrogen users is 20/1000. During the past six years we have had no cases of carcinoma in endometrial biopsies of 1000 non-hysterectomised patients whose treatment we have initiated and supervised. Of the 4 patients who had been referred from elsewhere, 3 had had unopposed continuous oestrogen for in excess of twelve years and the other showed no evidence of carcinoma after four weeks of modifying
It is
true
’
progestagen. Few would doubt that many years of unopposed cestrogens may, in susceptible patients, produce endometrial cancer, but there is good evidence that the addition of progestagen prevents this increased rate of cancer6 and also hyperplasia.7 Our current data strongly support this in that the incidence of cystic hyperplasia with thirteen days of progestagen is 0% whether the oestrogen is given orally or by subcutaneous implant. It is 3% with 7-10 days of progestagen, 7% if low dose cyclical oestrogen is used, and 15% with high-dose cyclical oestrogen. Furthermore, all of 60 patients with cystic hyperplasia had the lesion reversed to normal by two twenty-one-day courses of norethisterone. There is no published evidence that low-dose cyclical oestrogen with progestagen is in any way associated with an in1. Campbell, S., Whitehead, M. Clins Obstet. Gynœc. 1977, 4, 31. 2 Hammond, C. B., and others Am. J. Obstet. Gynec. 1979, 133, 525. 3 Hammond, C. B., and others ibid. p. 537. 4. Antunes, C. M. F., and others New Engl. J. Med. 300, 9. 5 Jick, H., and others ibid. p. 218. 6. Gambrell, R. D. Maturitas, 1978, 1, 107. 7. Sturdee, D., Wade-Evans, T., Paterson, M. E. L., Thom, M., Studd, Br. med. J. 1978, i, 1575.
J. W. W.
J W OHM . S TURD
London SE5
SIR,-When you cite work which questions the effect of on menopausal flushes, it only serves to show that if
cestrogens
searches the literature hard enough one can find papers which prove almost anything. Unfortunately, while maximising the risks and minimising the benefits of oestrogen therapy, you have quoted us as stating that cestrogens only prevent bone loss when administered immediately after the menopause. In fact, we stated clearly in the paper to which you refer’ that, although this effect of oestrogen was most obvious immediately after the menopause, this did not mean that oestrogen therapy at a later stage was ineffective. You also cite the early paper by Aitken et al.,2 in which they made this claim, but failed to quote their subsequent paper which appeared in your own columns,3 in which they withdrew it. Bone resorption can be suppressed and bone loss reduced or prevented by oestrogen therapy at any time after the menopause but the effect is most apparent in the early years because that is the time when loss of bone proceeds most rapidly in untreated subjects.4 one
M.R.C. Mineral Metabolism Leeds General Infirmary, Leeds LS1 3EX
Unit,
B. E. C. NORDIN
PELVIC ACTINOMYCOSIS AND INTRAUTERINE CONTRACEPTIVE DEVICES
SIR,-Five women with severe genital-tract actinomycosis have been detected in two hospitals in the North East Thames region in two years. This is the largest published series of patients in the U.K. with clinical pelvic actinomycosis. Four patients had an intrauterine contraceptive device (LU.D.) at the time of diagnosis, confirming the association between i.u.D. usage and pelvic actinomycosis reported from Europe and North America. 1-12 The clinical features of the patients are summarised in the table. The diagnoses were established only after microscopic examination of surgical specimens. Bacteriological examination of blood, vaginal specimens, and pus in abscesses and peritoneal cavity failed to reveal any evidence of actinomyces. Major surgery was required in all cases, and the immediate
postoperative
recovery
was
complicated by
a
presumed
sep-
ticaemia in one patient and by problems with wound healing in two others. Loss of fertility and ovarian function were usual
sequelx. Actinomycosis 1.
is often very difficult
to
diagnose,
and it may
Horsman, A., Gallagher, J. C., Simpson, M., Mordin, B. E. C. Br. med. J. 1977, ii, 789. 2. Aitken, J. M., Holt, D. M., Lindsay, R. ibid. 1973, iii, 515. 3. Lindsay, R., Holt, D. M., Aitken, J. M., Macdonald, E. B., Anderson, J. B., Clarke, A. C. Lancet, 1976, i, 1038. 4. Horsman, A., Simpson, M., Kirby, P. A., Nordin, B. E. C. Br. J. Radiol. 1977, 50, 504. 5. Henderson, S. R. Obstet. Gynec. 1973, 41, 726. 6. Schiffer, M A , Elguezabal, A., Sultana, M., Allen, A. ibid. 1975, 45, 67. 7. Lomax, C W, Harbert, G. M., Jr., Thornton, W. N. ibid. 1976, 48, 431. 8. Dische, F E, Hurt, J M., Davidson, N J. H., Puntambeker, S. J. Obstet. Gvnœc Br. Commonw 1974, 81, 724. 9. Barnham, M., Burton, A C, Copland, O. Br med. J. 1978, i, 719 10. O’Brien, P. K., Roth-Mayo, L. Can. med. Ass. J. 1975, 112, 596. 11. van Jauer, P-C., Busch, B. Zbl. Gynœk. 197, 97, 228 12. Purdie. P. W., Carty, M. J., McLeod, T. I. F Br. med. J. 1977, ii, 1392.
brain damage, and there is evidence9 that slow infections such as subacute sclerosing panencephalitis may be caused by conventional viruses acting in an unusual way. Murine c.M.v. suppresses humoral,lO cellmediated," and interferon" responses of the host to other antigens, and its possible involvement in disease need not be related to its direct cytopathogenic effect but could result from the initiation of an abnormal immune response, or by acting synergistically with other viruses. The possible association of HLA-BW15 with Alzheimer’s disease, and an immune response trait to c.M.v. is interesting, but it is much too early to conclude that virus is implicated in Alzheimer’s disease. Further studies are needed.
can cause severe some
SIR,-We have HLA-typed 86 inpatients with Alzheimer’s senile dementia and 38 inpatients with Alzheimer’s presenile dementia, for seven A locus and thirteen B locus antigens by a standard microlymphocytoxicity method. Alzheimer’s disease was diagnosed clinically (insidious onset, memory loss, intellectual and personality deterioration, with typical progression, in the absence of hypertension, strokes, or other secondary causes of dementia) with the onset before and after the age of 65 in the presenile and senile groups, respectively. HLA frequencies were compared (chi-squared test) with those in 458 controls who were not age matched (there is no evidence of postnatal selection at the HLA loci’). Table I shows the results of typing for BW 15. The frequency of BW 15in the presenile group was 32% (r<001), in the senile group 27% (r<001), and in both groups combined 28.2% (p
I-FREQUENCY
OF
We thank the consultant
psychiatrists who allowed us to study their
patients. Department of Psychiatry, University of Leeds,
E. B. RENVOIZE
Leeds LS2 9LT Public Health Leeds
HLA-BW15
Regional
Laboratory,
M. H. HAMBLING M.D. PEPPER
Blood Transfusion Centre,
S. M. RAJAH
Leeds
SCREENING FOR CYSTIC FIBROSIS
SIR,-Dr Crossley and her colleagues (March 3, p. 472) have measured serum-immunoreactive-trypsin (I.R.T.) in children with cystic fibrosis and in controls. They found abnormally high levels of serum-i.R.T. in infants with cystic fibrosis and in older patients with residual pancreatic function. They suggest the use of dried blood-spot screening for cystic fibrosis in the newborn and felt that their findings supported the hypothesis of "back-leakage" of pancreatic acrinar contents into the
A study2 of 34 patients with Alzheimer’s senile and presenile dementia revealed no significant association with the HLA system except with CW3 (P<0.05, before correction for the number of antigens tested). BW15 is in strong linkage disequilibrium with CW3.3 There is evidence4 for an association between cytomegalovirus (c.M.v.) susceptibility and the murine major histocompatibility complex, and there may be a similar association in healthy adults with BW15.5 We therefore measured complement-fixation antibody titres to c.M.v. in the sera of 33 of the patients with BW15, and 81 with other tissue-types (table II). 86% had antibodies at a titre of 1/16, and significantly more patients with BW15 had titres 1/64 (p=0.0013, chi-squared
serum.
test). TABLE II-COMPLEMENT-FIXING ANTIBODIES TO C.M.V.
*Mean age
of BW15-positives 73.1
years,
BW15-negatives
73-2 years.
et al.6 found a significantly increased incidence of antibodies in demented patients than in schizophrenics or a mixed group of patients with other psychiatric disorders. They postulated that age difference and the problem of maintaining hygienic conditions among demented patients could be
Lycke
c.M.v.
partly responsible. Could c.M.v. play a tion in the
role in Alzheimer’s disease? c.mt.v. infecin immunosuppressed adults8
fetus,7 neonateand
_
1. 2. 3.
Bender, K., and others Tissue Antigens, 1976, 7, 118. Henschke, P. J., Bell, D. A., Cape, R. D. T. ibid. 1978,12,132. Mayr, W. R. in Histocompatibility Testing 1975 (edited by F. Kissmeyer-
Nielsen); p. 330. Copenhagen, 1975. 4. Chalmer, J. E., Mackenzie, J. S., Stanley, N. F. J. gen. Virol. 1977, 5. Pereira, R. S., James, D. C. O., Stern, H. Br. med J. 1978. ii, 126. 6. Lycke, E., Norrby, R., Roos, B. Br. J. Psychiat. 1974, 124, 273 7. Stern, H., and others, Lancet, 1969, ii, 443. 8. Dorfman, L. J. Neurology, 1973, 23, 136.
Our cystic-fibrosis children usually either have severe lung disease with mild steatorrhcea or severe maldigestion with lesser pulmonary problems. We therefore measured serum-proteases in cystic-fibrosis patients and controls to see if there was any support for the following hypothesis: since lack of antitrypsin is associated with lung damage, plasma-trypsin in excess of antitrypsin might be responsible for the lung damage in cystic fibrosis. Early, severe pancreatic damage causes pronounced maldigestion but little rise in serum-protease levels, and therefore less lung damage; on the other hand, subtotal pancreatic damage allows some digestion but also maintains high serum-protease levels which cause more striking lung damage. General protease and trypsin levels were measured spectrophotometrically using a modification of the method of Erlanger, Kojowsky and Cohen. Trypsin-inhibitor capacity levels were measured by a modification of the method of Eriksson. There were 10 cystic-fibrosis patients and 54 controls all of whom were hospital inpatients or outpatients. Only 2 cysticfibrosis patients were less than one year old and samples were taken before and after food from these children. Our results showed no significant difference between protease and trypsin levels in cystic-fibrosis patients and controls. The protease levels were from 0 to 10.4 mg/ml and the trypsin levels from 0 to 2 mg/ml. In 5 control children, chosen because they were undergoing cardiac catheterisation, levels of protease and trypsin in the pulmonary arteries and veins were similar. Trvpsininhibiting capacities of sera from cystic-fibrosis children were however, smce higher than those of controls (r<0001); trypsin-inhibiting capacity is related to infection, the variation may be due to this. The difference between our results and those of Crossley et al. may be explained by the differing measuring techniques
37, 107. 9.
Agnarsdóttir,
G. in Recent Advances
in
Clinical
Virology
edited by A P
Waterson), p. 21. 1977, Edinburgh, 1977. 10. Osborn, J. E., Medearis, D. N. Proc. Soc. exp. Biol Med. 1967. 124, 347 11. Howard, R J., Miller, J., Najarian, J. S. Clin. exp. Immuno. 1974. 18, 119
1239 used. Our trypsin levels were measured spectrophotometrically and theirs by radioimmunoassay, and it would appear that their immunoassay measures trypsin bound to inhibitor as well as free trypsin. In addition, the number of our young cysticfibrosis patients was small. These positive results from New Zealand encourage us to continue our investigations. B. PHILLIPS Medical Department, Booth Hall Children’s Manchester M9 2AA
J. A. DAVIS
Hospital,
M. GOODE
creased risk of endometrial cancer. Therefore we strongly urge the addition of 7-13 days of a progestagen each month so that the benefits of oestrogen may be achieved with no increased risk of endometrial lesions. Department of Obstetrics and Gynxcology, King’s College Hospital,
MARGARET THOM
Department of Obstetrics and Gynaecology, Birmingham and Midland Hospital for Women, Birmingham 11
MICHAEL PATTERSON
ŒSTROGEN THERAPY AND ENDOMETRIAL CARCINOMA
SIR,-Your editorial of May 26 makes
many controversial the that side-effects of points. oestrogen therapy are still under scrutiny but one would have thought that the benefits of oestrogen over placebo are now well accepted by all but the occasional provocative leader writer, having been clarified by the double-blind trial of Campbell and Whitehead’1 and interminable correspondence in the columns of The Lancet over the past year. Hammond2 and his team from Duke have shown the longterm metabolic benefit of oestrogen by significantly lower rates of strokes, heart-attacks, hypertension, osteoporosis, and fractures. They also confirmed an increased incidence of carcinoma of the endometrium with a risk ratio of9.3.3 The great value of this and the Antunes paper cited by you is that details of therapy are given.’ Only 1 of Hammond’s 11 oestrogen-taking patients with cancer was receiving progestagen ("rarely") during her twenty-four years of high-dose cyclical therapy for gonadal dysgenesis. In the Antunes paper none of the 64 patients with cancer of the uterus had taken progestagen: half were on continuous therapy and 9 were receiving stilboestrol (your conclusion was that continuous therapy was as safe as cyclical oestrogen therapy). 7 of Jick’s5 patients had received "progesterone" but no details of type, duration or frequency are given: you conclude that we should refrain from including progestagens in the regimen. We have probably the largest menopause clinic in Europe and have not been able to reproduce these findings and do not support the prediction of Jick et al. that the annual rate of cancer of the uterus in oestrogen users is 20/1000. During the past six years we have had no cases of carcinoma in endometrial biopsies of 1000 non-hysterectomised patients whose treatment we have initiated and supervised. Of the 4 patients who had been referred from elsewhere, 3 had had unopposed continuous oestrogen for in excess of twelve years and the other showed no evidence of carcinoma after four weeks of modifying
It is
true
’
progestagen. Few would doubt that many years of unopposed cestrogens may, in susceptible patients, produce endometrial cancer, but there is good evidence that the addition of progestagen prevents this increased rate of cancer6 and also hyperplasia.7 Our current data strongly support this in that the incidence of cystic hyperplasia with thirteen days of progestagen is 0% whether the oestrogen is given orally or by subcutaneous implant. It is 3% with 7-10 days of progestagen, 7% if low dose cyclical oestrogen is used, and 15% with high-dose cyclical oestrogen. Furthermore, all of 60 patients with cystic hyperplasia had the lesion reversed to normal by two twenty-one-day courses of norethisterone. There is no published evidence that low-dose cyclical oestrogen with progestagen is in any way associated with an in1. Campbell, S., Whitehead, M. Clins Obstet. Gynœc. 1977, 4, 31. 2 Hammond, C. B., and others Am. J. Obstet. Gynec. 1979, 133, 525. 3 Hammond, C. B., and others ibid. p. 537. 4. Antunes, C. M. F., and others New Engl. J. Med. 300, 9. 5 Jick, H., and others ibid. p. 218. 6. Gambrell, R. D. Maturitas, 1978, 1, 107. 7. Sturdee, D., Wade-Evans, T., Paterson, M. E. L., Thom, M., Studd, Br. med. J. 1978, i, 1575.
J. W. W.
J W OHM . S TURD
London SE5
SIR,-When you cite work which questions the effect of on menopausal flushes, it only serves to show that if
cestrogens
searches the literature hard enough one can find papers which prove almost anything. Unfortunately, while maximising the risks and minimising the benefits of oestrogen therapy, you have quoted us as stating that cestrogens only prevent bone loss when administered immediately after the menopause. In fact, we stated clearly in the paper to which you refer’ that, although this effect of oestrogen was most obvious immediately after the menopause, this did not mean that oestrogen therapy at a later stage was ineffective. You also cite the early paper by Aitken et al.,2 in which they made this claim, but failed to quote their subsequent paper which appeared in your own columns,3 in which they withdrew it. Bone resorption can be suppressed and bone loss reduced or prevented by oestrogen therapy at any time after the menopause but the effect is most apparent in the early years because that is the time when loss of bone proceeds most rapidly in untreated subjects.4 one
M.R.C. Mineral Metabolism Leeds General Infirmary, Leeds LS1 3EX
Unit,
B. E. C. NORDIN
PELVIC ACTINOMYCOSIS AND INTRAUTERINE CONTRACEPTIVE DEVICES
SIR,-Five women with severe genital-tract actinomycosis have been detected in two hospitals in the North East Thames region in two years. This is the largest published series of patients in the U.K. with clinical pelvic actinomycosis. Four patients had an intrauterine contraceptive device (LU.D.) at the time of diagnosis, confirming the association between i.u.D. usage and pelvic actinomycosis reported from Europe and North America. 1-12 The clinical features of the patients are summarised in the table. The diagnoses were established only after microscopic examination of surgical specimens. Bacteriological examination of blood, vaginal specimens, and pus in abscesses and peritoneal cavity failed to reveal any evidence of actinomyces. Major surgery was required in all cases, and the immediate
postoperative
recovery
was
complicated by
a
presumed
sep-
ticaemia in one patient and by problems with wound healing in two others. Loss of fertility and ovarian function were usual
sequelx. Actinomycosis 1.
is often very difficult
to
diagnose,
and it may
Horsman, A., Gallagher, J. C., Simpson, M., Mordin, B. E. C. Br. med. J. 1977, ii, 789. 2. Aitken, J. M., Holt, D. M., Lindsay, R. ibid. 1973, iii, 515. 3. Lindsay, R., Holt, D. M., Aitken, J. M., Macdonald, E. B., Anderson, J. B., Clarke, A. C. Lancet, 1976, i, 1038. 4. Horsman, A., Simpson, M., Kirby, P. A., Nordin, B. E. C. Br. J. Radiol. 1977, 50, 504. 5. Henderson, S. R. Obstet. Gynec. 1973, 41, 726. 6. Schiffer, M A , Elguezabal, A., Sultana, M., Allen, A. ibid. 1975, 45, 67. 7. Lomax, C W, Harbert, G. M., Jr., Thornton, W. N. ibid. 1976, 48, 431. 8. Dische, F E, Hurt, J M., Davidson, N J. H., Puntambeker, S. J. Obstet. Gvnœc Br. Commonw 1974, 81, 724. 9. Barnham, M., Burton, A C, Copland, O. Br med. J. 1978, i, 719 10. O’Brien, P. K., Roth-Mayo, L. Can. med. Ass. J. 1975, 112, 596. 11. van Jauer, P-C., Busch, B. Zbl. Gynœk. 197, 97, 228 12. Purdie. P. W., Carty, M. J., McLeod, T. I. F Br. med. J. 1977, ii, 1392.