- Email: [email protected]
MANAGING LASSA FEVER
926 MANAGING LASSA FEVER
SIR,-Earlier this year we admitted a patient to the high security at Coppetts Wood Hospital, who was subsequently confirmed to have Lassa fever. His illness had started 6 days after a small furry animal, presumably a multimammate rat, had run across his face while he was camping in Sierra Leone, and the illness followed the
unit
teichopsia, though no headache. The picture is non-specific and in my view not adequate evidence of migraine. (3) Food exclusions lasted for 5 days with each challenge; this period is insufficient to permit assessment of the much longer term pattern of attacks, and indeed of any response to dietetic treatment. Without a prolonged period of assessment it is impossible to guess whether these exclusions are of therapeutic use, and a formal trial is necessary both of the effects of continued dietary provocation and of the efficacy (or otherwise) of dietary exclusion. This applies equally to the putative role of sodium cromoglycate. (4) The table reporting the positive responses to wheat, milk, and eggs shows only the responses to intradermal tests. Thus this interesting work does not give adequate evidence that the symptoms produced were migrainous, and the protective effect clamied for sodium cromoglycate is not well supported by the emergence of only "partial protection" in three patients and a placebo response in one in a series of nine patients. Since no therapeutic role can yet be assigned to cromoglycate on this evidence, and since exclusion diets are notoriously impracticable, especially if needed in a disorder affecting 10 to 20% of the population, we need a great deal more evidence before accepting the contention of the title of this paper and its implications.
customary course for a moderate attack of Lassa fever. Lassa virus was isolated from blood but not urine during the acute phase of the illness, which lasted 10 days. 6 days after the end of the febrile stage, his blood still contained virus though urine remained free. Subsequent blood cultures were negative. However, virus was detected in a single sample or urine obtained 16 days after the acute phase had ended. The persistence of virus in urine after an attack of Lassa fever is well recognised but it is perhaps less widely appreciated that virus may persist in blood. In our experience with Lassa fever in the UK viraemia has ceased when the fever has settled though viruria may persist for several weeks. Your editorial (Sept 29, p 728) has emphasised the delayed appearance of neutralising antibody in both Lassa fever and the closely related Argentine haemorrhagic fever, which may explain the persistence of virus in the blood of some patients during convalescence. Persistent viraemia as well as viruria present a hazard to clinical and laboratory staff looking after the
Department of Neurology, Hull Royal Infirmary, Hull HU3 2JZ
patient. Infectious Disease Department, Royal Free Hospital, Coppetts Wood Hospital,
London N10 1JN Reference
Special Pathogens CAMR Porton Down, Salisbury, Wilts
Laboratory,
BLOOD R. T. D. EMOND W. R. C. WEIR E. T. W. BOWEN G. LLOYD T. SOUTHEE
SIR,-Since the determinants of the ABO and Lewis blood-group
antigens and of carcinoembryonic antigens (CEA) share the same glycoprotein carrier molecules,l does maternofetal ABO incompatibility enable the mother to recognise CEA? If so, a group 0 woman sensitised against a group A fetus may have a lower than usual risk of certain cancers. Indeed Bagshawe and Beer and Billingham have shown that maternofetal ABO incompatibility confers on the mother a protective effect against cancer of the trophoblast.’3’ A study of 924 patients from the general surgery department serologically grouped by the blood transfusion centre showed the male/female ratio among patients with digestive-tract cancers to be
RTD, Bannister B, Lloyd G, Southee TJ, Bowen ETW. A case ofLassa fever: Clinical and virological findings. Br Med 1982; J 285: 1001-02.
FOOD ALLERGY AND MIGRAINE
SIR,-The paper by Dr Monro and her colleagues (Sept 29, p 719) interesting but seems to me to draw unwarranted conclusions:
(1) A study of nine highly selected patients does not permit generalisation to migraine as a whole. (2) The patients were challenged with foods on three occasions. Only one response was reported. People rarely react in the same way on three consecutive occasions, particularly with migraine. (3) Many migraine precipitants have nothing to do with allergy: delaying meals, sleep disturbances, hormonal changes in women, exposure to light or cold, travelling, stress, for example. (4) Triggering mechanisms cannot be equated with cause. It would have been more accurate-particularly since papers in The Lancet are sometimes covered in the national press, as this one have said that allergy as a triggering mechanism of migraine is still a hypothesis. This paper does not provide proof: for that, patients would have to have had the appropriate dietary restriction, and if necessary sodium cromoglycate, for several months during which all of them would have had to be free from migraine. Dr Seymour Diamond and I have recently analysed 327
was-to
questionnaires
on
diet-precipitated migraine completed by
members of the American Association for the Study of Headache and by British physicians interested in migraine: not one mentioned a single pip and I have never heard a patient mention such a precipitant during my 20 years of special interest in migraine. City of London Migraine Clinic, London ÈC1M 6DX
GROUPS, SEX, AND FREQUENCY OF COLORECTAL CARCINOMA
1. Emond
is
J. M. S. PEARCE
about 1-4. The distribution of the various ABO blood groups in the patients was the same as in the normal population. In the normal population the ratio of males/females for all the ABO blood groups was 1, but among group 0 patients it was 1 - 7, and among group A patients it was 1-3. Our study of 501 subjects with colorectal . adenocarcinoma from the same department gave very similar results ,
(see table). More
recent
studies
describe
DISTRIBUTION OF ABO BLOOD GROUPS AMONG COLORECTAL CARCINOMA
J. N. BLAU
SIR,-The claim by Dr Monro and her colleagues that migraine is food-allergic disease is a dramatic declaration. But is it true? The production of IgE immune complexes by food triggers and their suppression by sodium cromoglycate in three patients is of interest,
a
but insufficient support for their assertion in the absence of clear clinical evidence. I would make the following comments: (1) Nine patients are too few for the study of a common disorder. (2) The symptoms allegedly provoked by dietary challenge are headaches, flatulence, nausea, and diarrhoea. Only one patient had
novel
fucolipids type
2
accumulating in human adenocarcinoma.The chemical structures which determine Le blood groups are of type 1. A "sugarcarbohydrate antigen" 19tumour marker, made up of a Lewislike determinant in which fucose 1-2 is replaced by sialic acid, has been identified with the aid of monoclonal antibodies.Number 19 chromosome is thought to encode for Lewis enzyme, and number 9 chromosome is thought to encode for ABO enzymes. Koprowski et al suggested that if Le(a- b-) subjects were unable to synthesise the 5 sugar antigen they would constitute a protected population.5
"-1 = male.
F=female.
*p<0-012.
tp<0’019.
501
PATIENTS WITH
SIR,-Earlier this year we admitted a patient to the high security at Coppetts Wood Hospital, who was subsequently confirmed to have Lassa fever. His illness had started 6 days after a small furry animal, presumably a multimammate rat, had run across his face while he was camping in Sierra Leone, and the illness followed the
unit
teichopsia, though no headache. The picture is non-specific and in my view not adequate evidence of migraine. (3) Food exclusions lasted for 5 days with each challenge; this period is insufficient to permit assessment of the much longer term pattern of attacks, and indeed of any response to dietetic treatment. Without a prolonged period of assessment it is impossible to guess whether these exclusions are of therapeutic use, and a formal trial is necessary both of the effects of continued dietary provocation and of the efficacy (or otherwise) of dietary exclusion. This applies equally to the putative role of sodium cromoglycate. (4) The table reporting the positive responses to wheat, milk, and eggs shows only the responses to intradermal tests. Thus this interesting work does not give adequate evidence that the symptoms produced were migrainous, and the protective effect clamied for sodium cromoglycate is not well supported by the emergence of only "partial protection" in three patients and a placebo response in one in a series of nine patients. Since no therapeutic role can yet be assigned to cromoglycate on this evidence, and since exclusion diets are notoriously impracticable, especially if needed in a disorder affecting 10 to 20% of the population, we need a great deal more evidence before accepting the contention of the title of this paper and its implications.
customary course for a moderate attack of Lassa fever. Lassa virus was isolated from blood but not urine during the acute phase of the illness, which lasted 10 days. 6 days after the end of the febrile stage, his blood still contained virus though urine remained free. Subsequent blood cultures were negative. However, virus was detected in a single sample or urine obtained 16 days after the acute phase had ended. The persistence of virus in urine after an attack of Lassa fever is well recognised but it is perhaps less widely appreciated that virus may persist in blood. In our experience with Lassa fever in the UK viraemia has ceased when the fever has settled though viruria may persist for several weeks. Your editorial (Sept 29, p 728) has emphasised the delayed appearance of neutralising antibody in both Lassa fever and the closely related Argentine haemorrhagic fever, which may explain the persistence of virus in the blood of some patients during convalescence. Persistent viraemia as well as viruria present a hazard to clinical and laboratory staff looking after the
Department of Neurology, Hull Royal Infirmary, Hull HU3 2JZ
patient. Infectious Disease Department, Royal Free Hospital, Coppetts Wood Hospital,
London N10 1JN Reference
Special Pathogens CAMR Porton Down, Salisbury, Wilts
Laboratory,
BLOOD R. T. D. EMOND W. R. C. WEIR E. T. W. BOWEN G. LLOYD T. SOUTHEE
SIR,-Since the determinants of the ABO and Lewis blood-group
antigens and of carcinoembryonic antigens (CEA) share the same glycoprotein carrier molecules,l does maternofetal ABO incompatibility enable the mother to recognise CEA? If so, a group 0 woman sensitised against a group A fetus may have a lower than usual risk of certain cancers. Indeed Bagshawe and Beer and Billingham have shown that maternofetal ABO incompatibility confers on the mother a protective effect against cancer of the trophoblast.’3’ A study of 924 patients from the general surgery department serologically grouped by the blood transfusion centre showed the male/female ratio among patients with digestive-tract cancers to be
RTD, Bannister B, Lloyd G, Southee TJ, Bowen ETW. A case ofLassa fever: Clinical and virological findings. Br Med 1982; J 285: 1001-02.
FOOD ALLERGY AND MIGRAINE
SIR,-The paper by Dr Monro and her colleagues (Sept 29, p 719) interesting but seems to me to draw unwarranted conclusions:
(1) A study of nine highly selected patients does not permit generalisation to migraine as a whole. (2) The patients were challenged with foods on three occasions. Only one response was reported. People rarely react in the same way on three consecutive occasions, particularly with migraine. (3) Many migraine precipitants have nothing to do with allergy: delaying meals, sleep disturbances, hormonal changes in women, exposure to light or cold, travelling, stress, for example. (4) Triggering mechanisms cannot be equated with cause. It would have been more accurate-particularly since papers in The Lancet are sometimes covered in the national press, as this one have said that allergy as a triggering mechanism of migraine is still a hypothesis. This paper does not provide proof: for that, patients would have to have had the appropriate dietary restriction, and if necessary sodium cromoglycate, for several months during which all of them would have had to be free from migraine. Dr Seymour Diamond and I have recently analysed 327
was-to
questionnaires
on
diet-precipitated migraine completed by
members of the American Association for the Study of Headache and by British physicians interested in migraine: not one mentioned a single pip and I have never heard a patient mention such a precipitant during my 20 years of special interest in migraine. City of London Migraine Clinic, London ÈC1M 6DX
GROUPS, SEX, AND FREQUENCY OF COLORECTAL CARCINOMA
1. Emond
is
J. M. S. PEARCE
about 1-4. The distribution of the various ABO blood groups in the patients was the same as in the normal population. In the normal population the ratio of males/females for all the ABO blood groups was 1, but among group 0 patients it was 1 - 7, and among group A patients it was 1-3. Our study of 501 subjects with colorectal . adenocarcinoma from the same department gave very similar results ,
(see table). More
recent
studies
describe
DISTRIBUTION OF ABO BLOOD GROUPS AMONG COLORECTAL CARCINOMA
J. N. BLAU
SIR,-The claim by Dr Monro and her colleagues that migraine is food-allergic disease is a dramatic declaration. But is it true? The production of IgE immune complexes by food triggers and their suppression by sodium cromoglycate in three patients is of interest,
a
but insufficient support for their assertion in the absence of clear clinical evidence. I would make the following comments: (1) Nine patients are too few for the study of a common disorder. (2) The symptoms allegedly provoked by dietary challenge are headaches, flatulence, nausea, and diarrhoea. Only one patient had
novel
fucolipids type
2
accumulating in human adenocarcinoma.The chemical structures which determine Le blood groups are of type 1. A "sugarcarbohydrate antigen" 19tumour marker, made up of a Lewislike determinant in which fucose 1-2 is replaced by sialic acid, has been identified with the aid of monoclonal antibodies.Number 19 chromosome is thought to encode for Lewis enzyme, and number 9 chromosome is thought to encode for ABO enzymes. Koprowski et al suggested that if Le(a- b-) subjects were unable to synthesise the 5 sugar antigen they would constitute a protected population.5
"-1 = male.
F=female.
*p<0-012.
tp<0’019.
501
PATIENTS WITH