1539
and diphtheria fall below 0-1
IU/ml, and our data will be available
shortly. Cutts and Begg object to implications for developing countries being drawn from our study and they cite a report of lower efficiency of transfer of transplacental antibodies to tetanus toxoid antibodies in African than in French infants.2 However, that study clearly showed that higher levels of tetanus toxoid antibody were
transferred to African infants if their mothers had been immunised
during pregnancy. The critical point is that protection against neonatal tetanus results from passively acquired antibodies and, as shown by studies in Thailand,3these can suppress the response to active immunisation of 2-month-old infants with tetanus toxoid. Our investigations in Oxford (Feb 29, p 507) also indicate that in infants with high maternal antibody concentrations, lower titres of serum antibodies to tetanus and pertussis are evident at 5 months of age after completion of the primary course of three immunisations at 2, 3, and 4 months of age. Thus, despite the clear overall benefits of both the accelerated programme of immunisation and immunisation of pregnant mothers against tetanus, there is a need to recognise the potential difficulties that may arise from the reduction in immune responses resulting from (i) suppression by passively acquired maternal antibodies and (ii) possible immune immaturity. If protection decreases over time, further natural exposure to diphtheria or pertussis may result in disease. ROBERT BOOY E. RICHARD MOXON RICHARD T. MAYON-WHITE STUART J. AITKEN HELEN GRIFFITHS HELEN M. CHAPEL
Department of Paediatrics, John Radcliffe Hospital,
Headington, Oxford OX3 9DU, UK
1. Melville-Smith ME, Seagroatt VA, Watkins JT. A comparison of enzyme-linked immunosorbent assay (ELISA) with the toxin neutralization test m mice as a method for the estimation of tetanus anti-toxin in human sera. J Biol Stand 1983; 11: 137-44. 2. Gendrel D, Richard-Lenobele D, Picaud C, Francoual C, Blot P. Placental transfer of tetanus antibodies and protection of the newborn. J Trop Paediatr 1990; 36: 279-82. 3. Sangpetchsong V, Impat A, Dhiensiri K, Podhipala A. Effect of passive immunity to tetanus in DTP vaccinated infants. SE Asian J Trop Med Pub Health 1985; 16: 117-23.
Cystic fibrosis carrier screening at first diagnosis of pregnancy in general practice SiR,—Several pilot programmes for cystic fibrosis (CF) carrier screening in the general British population are now being evaluated (see, for example, Watson et all). Strategies investigated involve pre-pregnancy screening, when patient motivation and later recall may be low; or hospital antenatal clinic screening, when there is little time for counselling and reflection and where positive tests lead to undesirably late termination of pregnancy. We report here a successful pilot study of an alternative approach-namely, testing offered at first diagnosis of pregnancy, allowing carrier testing to be completed within the first trimester and allowing discussion of reproductive options and antenatal diagnosis without undue pressure.
The study is based in a south Manchester two-partner training general practice (population 4400) in which there are 50-60 births per year. A preliminary feasibility survey in 1990, the year before the pilot study, showed that 96% of pregnancies were diagnosed at 6-14 weeks (average 8 weeks). However, this early opportunity for screening was generally lost because the average delay between first GP
booking and first hospital antenatal
clinic
appointment was 4
weeks, taking many patients into the second trimester. From Sept 1, 1991, CF carrier screening has been offered to all patients at the time of the antenatal booking consultation at the practice. This consultation includes routine general medical history, obstetric history, and choice of place of delivery. An explanatory leaflet is given, after discussion of CF carrier screening within the context of other antenatal tests offered during pregnancy. After permission has been obtained, patients are randomised to maternal or to couple testing. A saliva sample is obtained from the woman at
that time and
women
in the
couple-testing
group
are
asked to obtain a saliva sample from the father. They take home the leaflet with a sample kit for their partner to be returned the following morning. The results of the test, with a risk estimation for the pregnancy, are sent to the patients by post within 10 days with a copy to the GP. Laboratory tests involve four gene probes (AF508, G551D, G542X, 621 + 1G > T), detecting 83.5% of CF carriers in our
population.
So far 44 pregnancies have been screened. 1 carrier has been detected in the maternal-testing group; her partner tested negative. 2 carriers were detected in the couple-testing group, and both partners tested negative. 1 partner in the couple-testing group declined the test and the maternal sample tested negative. 14 pregnancies were not included in the pilot study, for the following reasons: 1 patient aged 17 years declined the test, then requested termination, changed her mind, and delivered prematurely; 4 booked after 14 weeks for antenatal care; 7 requested termination for reasons unrelated to CF; and 2 patients miscarried before antenatal booking. Preliminary results from questionnaires and interview indicate that women have a positive attitude to CF carrier screening and to general practice as the preferred place for counselling and testing. There is no evidence at this stage that the procedure has caused excessive anxiety (Spielberger scale). Our study will be extended to other local general practices because we believe that general practice provides the ideal setting for very early pregnancy screening and general genetic counselling. Here it becomes an integral part of primary health care and permits assessment of the psychological impact of screening on patients, partners, and families. This is a valuable model for the closer integration of primary and secondary health-care services. This work is supported by the Wolfson Foundation and the North Western Regional Health Authority. Brooklands Medical Practice,
H.
J. HARRIS
Manchester
D. SCOTCHER
Department of Medical Genetics, St Mary’s Hospital, Manchester M13 OJH, UK
D. CRAUFURD A. WALLACE R. HARRIS
Mayall E, Chapple J, et al. Screening for carriers of cystic fibrosis through primary health care services. Br Med J 1991; 303: 504-07.
1. Watson EK,
Population screening for cystic fibrosis SIR,-We are involved in a pilot project of population screening for cystic fibrosis (CF) carriers, using mouthwash samples to screen for four mutations (AF508, G551D, G542X, 621 + 1G>T). We offered all members of staff in our division of molecular and medical genetics confidential screening for carrier status and report here the uptake of testing in this genetically interested and informed group of adults, predominantly of reproductive age. In December, 1991, three posters advertising the availability of confidential screening were displayed prominently, giving two contact names (a clinical geneticist and a nurse genetics counsellor). Those requesting screening were given an information leaflet (devised for our population screening programme) and then interviewed privately to establish whether there was a family history of CF, to check that they understood the inheritance of CF, and to confirm that neither they, their partner, nor anyone else in their family were pregnant. We also reminded them that a negative test result would reduce their carrier risk (to 1 in 130 for caucasians), but not eliminate it. Each mouthwash sample was given a coded reference number, the identity being known only to the clinicians offering the service. The results were handed to staff members personally one week later, together with a copy for them to pass on to their general practitioner. There are 110 members of staff in the division, of whom 80 are female (73%). 18 requested screening during the first three days, and 5 more presented a month later, while being screened for hepatitis B immunity status, when a personal verbal offer of CF screening was made. Of the 23 staff requesting screening, 20 were female (87%). 1 female had her test postponed because a relative was in late pregnancy at that time. The uptake rate for CF carrier screening was therefore about 20%. No carriers were detected.
1540
ten Kate et al2 found that more than half of respondents to a survey thought they would make use of CF carrier screening if it were offered. Watson et al,3 recruiting patients by speaking directly to them, achieved an uptake of 66% in general practice and 87% in family-planning clinics. It is sometimes postulated that low uptake of health screening is partly based on lack of knowledge but an uptake rate of only 20% in a medical genetics department suggests that factors other than ignorance are responsible for a lack of much spontaneous enthusiasm for screening. Our fmding, if confirmed, may be relevant to the design and cost assessments of population screening programmes.
Division of Medical and Molecular Genetics,
UMDS, Guy’s Hospital, London SE1 9RT, UK
FRANCES A. FLINTER ANNE SILVER CHRISTOPHER G. MATHEW MARTIN BOBROW
RM, Robertson NH, Vaudin SA, Sthwantz M, Little S. Development of multiplex ARMS test for the simultaneous detection of four common CF mutations. Am J Hum Genet 1991; 49 (supply: 195. 2. ten Kate LF, Tjimstra TJ. Carrier screening for CF. Lancet 1989; ii: 973-74. 3. Watson EK, Mayall E, Chapple J, et al. Screening for carriers of CF through primary health care services. Br Med J 1991; 303: 504-07. 1. Ferrie
Severe dyserythropoiesis and autoimmune thrombocytopenia associated with ingestion of kelp supplements SIR,-As availability and consumption of dietary health supplements increases, concern has been expressed about the safety of some preparations. Preparations containing kelp are now widely available. Kelp can concentrate various heavy metals, and kelp preparations can contain substantial concentrations of arsenic.1
Urinary arsenic excretion in patients with peripheral neuropathy who have been taking kelp tablets may be increased2 and seaweed ingestion has seen linked with chronic thyroiditis.3 Arsenic intoxication can cause bone marrow depression and megaloblastic changes.4,5 There have been no reports, however, of arsenic-related autoimmune thrombocytopenia or dyserythropoiesis and thrombocytopenia due to arsenic in kelp preparations. We report a patient who had been taking a preparation of kelp found to contain substantial quantities of arsenic. A 54-year-old woman presented with a one week history of abnormal bleeding and petechiae. She was otherwise well and had no relevant medical history. She had been taking a proprietary vitamin tablet and kelp tablets for the previous six weeks (three 550 mg kelp tablets daily with extra calcium.) The only abnormal findings were widespread bruises and petechiae. Haemoglobin (Hb) was 12-2 g/dl, white cells 4-7 x 109/1, and platelets 16 x 109/1. The red cell indices were normal with occasional macrocytes. Antiplatelet antibodies were raised (IgG 28 and IgM 26 ng per 106 platelets; normal, 0-11.0 and 0-1-42, respectively). Serum vitamin B12 and red cell folate, and direct antiglobulin test were normal. Bone marrow aspiration and trephine biopsy showed an increase in megakaryocytes consistent with autoimmune thrombocytopenic purpura. In addition, erythropoiesis was grossly abnormal with increased megaloblasts, large binucleate and trinucleate forms, delayed nuclear maturation with pyknosis, vacuolation, and cytoplasmic bridging. Myeloid and lymphoid lines were normal. Sucrose lysis and Ham’s tests with the patient’s serum and serum from a pool of seven donors were negative. Monocyte CD 14 and neutrophil CD 16 expression were normal. HbF was less than 1%. Electron microscopy of bone marrow was normal with no evidence of double endoplasmic reticulum in the erythroid precursors. Analysis of the kelp tablets showed that they contained 1-3 ug/g arsenic; the patient had therefore been ingesting 2-2 ug arsenic daily. Autoimmune thrombocytopenic purpura with dyserythropoiesis of unknown aetiology was diagnosed. Kelp was withdrawn and the autoimmune thrombocytopenia was treated with intravenous immunoglobulin and prednisolone, with good response. The patient was subsequently treated with azathioprine and her platelet count stabilised around 60 x 109/1. Bone marrow aspiration and trephine biopsy were repeated after three months and showed
virtual complete reversal of the dyserythropoietic features and normal megakaryocyte morphology. Severe dyserythropoiesis is a rare, usually congenital, and generally irreversible condition. Congenital dyserythropoietic anaemia, paroxysmal nocturnal haemoglobinuria, and myelodysplastic syndrome, which are the commonest causes, were excluded by our investigations. We postulate that kelp was responsible for the severe dyserythropoiesis in this patient and it may also have been implicated in either the pathogenesis of the autoimmune thrombocytopenia or the exacerbation of a preexisting condition. Physicians need to be aware of the potentially dangerous contaminants in some kelp preparations. Department of Haematology, Royal London Hospital,
KATHRYN G. PYE STEPHEN M. KELSEY
London E1 1 BB, UK
National Poisons Unit,
Guy’s Hospital, London
IVAN M. HOUSE
Department of Haematology, Royal London Hospital
ADRIAN C. NEWLAND
1. Norman JA, Pickford CJ, Sanders TW, Waller M. Human intake of arsenic and iodine from seaweed-based food supplements and health foods available in the UK. Food
Addit Contam 1987; 5: 103-09. 2. Walkiw O, Douglas DE. Health food supplements prepared from kelp-a source of elevated urinary arsenic. Clin Toxicol 1975; 8: 325-31. 3. Okamura K, Inoue K, Omae T. A case of Hashimoto’s thyroiditis with thyroid immunological abnormality manifested after habitual ingestion of seaweed. Acta Endocrinol 1978; 88: 703-12. 4. Kyle RA, Pease GL. Hematologic aspects of arsenic intoxication. N Engl J Med 1965; 273: 18-23. 5. Westhoff DD, Samaha RJ, Barnes A. Arsenic intoxication as a cause of megaloblastic anaemia. Blood 1975; 45: 241-46.
Practicability of early treatment of acute stroke SIR,-As Dr Sandercock and Mr Willems point out in their contribution to the Stroke Octet (Feb 29, p 537), hardly any of the potential treatments for acute stroke has yet been adequately evaluated in controlled trials and none has been shown to be effective. This view has encouraged a nihilistic attitude, so that in parts of Britain only about half of patients with acute stroke are admittedl and the need for urgent medical treatment is infrequently given by general practitioners as a reason for requesting admission.2 If hospital care is thought necessary for other reasons, this perceived lack of urgency could delay admission beyond the stage when salvage of ischaemic brain is feasible, and many clinicians doubt that adequate acute stroke trials can be conducted in Britain. As a group of general physicians and geriatricians with an interest in stroke, we set out to test this conjecture by surveying all acute stroke admissions to hospitals in seven health districts over 3 months. We included all patients with a new stroke (according to World Health Organisation clinical criteria) in which limb weakness was evident, admitted at any time because of neurological deficit rather than another complication. We excluded patients who were not admitted, with stroke that took place in hospital, with transient ischaemic attacks whose deficits had resolved before they were seen, ADMISSION DELAY AND PREVIOUS DISABILITIES IN PATIENTS ADMITTED TO GENERAL AND GERIATRIC MEDICAL WARDS
*6
more
patemts admitted directly to stroke
units.
and diphtheria fall below 0-1
IU/ml, and our data will be available
shortly. Cutts and Begg object to implications for developing countries being drawn from our study and they cite a report of lower efficiency of transfer of transplacental antibodies to tetanus toxoid antibodies in African than in French infants.2 However, that study clearly showed that higher levels of tetanus toxoid antibody were
transferred to African infants if their mothers had been immunised
during pregnancy. The critical point is that protection against neonatal tetanus results from passively acquired antibodies and, as shown by studies in Thailand,3these can suppress the response to active immunisation of 2-month-old infants with tetanus toxoid. Our investigations in Oxford (Feb 29, p 507) also indicate that in infants with high maternal antibody concentrations, lower titres of serum antibodies to tetanus and pertussis are evident at 5 months of age after completion of the primary course of three immunisations at 2, 3, and 4 months of age. Thus, despite the clear overall benefits of both the accelerated programme of immunisation and immunisation of pregnant mothers against tetanus, there is a need to recognise the potential difficulties that may arise from the reduction in immune responses resulting from (i) suppression by passively acquired maternal antibodies and (ii) possible immune immaturity. If protection decreases over time, further natural exposure to diphtheria or pertussis may result in disease. ROBERT BOOY E. RICHARD MOXON RICHARD T. MAYON-WHITE STUART J. AITKEN HELEN GRIFFITHS HELEN M. CHAPEL
Department of Paediatrics, John Radcliffe Hospital,
Headington, Oxford OX3 9DU, UK
1. Melville-Smith ME, Seagroatt VA, Watkins JT. A comparison of enzyme-linked immunosorbent assay (ELISA) with the toxin neutralization test m mice as a method for the estimation of tetanus anti-toxin in human sera. J Biol Stand 1983; 11: 137-44. 2. Gendrel D, Richard-Lenobele D, Picaud C, Francoual C, Blot P. Placental transfer of tetanus antibodies and protection of the newborn. J Trop Paediatr 1990; 36: 279-82. 3. Sangpetchsong V, Impat A, Dhiensiri K, Podhipala A. Effect of passive immunity to tetanus in DTP vaccinated infants. SE Asian J Trop Med Pub Health 1985; 16: 117-23.
Cystic fibrosis carrier screening at first diagnosis of pregnancy in general practice SiR,—Several pilot programmes for cystic fibrosis (CF) carrier screening in the general British population are now being evaluated (see, for example, Watson et all). Strategies investigated involve pre-pregnancy screening, when patient motivation and later recall may be low; or hospital antenatal clinic screening, when there is little time for counselling and reflection and where positive tests lead to undesirably late termination of pregnancy. We report here a successful pilot study of an alternative approach-namely, testing offered at first diagnosis of pregnancy, allowing carrier testing to be completed within the first trimester and allowing discussion of reproductive options and antenatal diagnosis without undue pressure.
The study is based in a south Manchester two-partner training general practice (population 4400) in which there are 50-60 births per year. A preliminary feasibility survey in 1990, the year before the pilot study, showed that 96% of pregnancies were diagnosed at 6-14 weeks (average 8 weeks). However, this early opportunity for screening was generally lost because the average delay between first GP
booking and first hospital antenatal
clinic
appointment was 4
weeks, taking many patients into the second trimester. From Sept 1, 1991, CF carrier screening has been offered to all patients at the time of the antenatal booking consultation at the practice. This consultation includes routine general medical history, obstetric history, and choice of place of delivery. An explanatory leaflet is given, after discussion of CF carrier screening within the context of other antenatal tests offered during pregnancy. After permission has been obtained, patients are randomised to maternal or to couple testing. A saliva sample is obtained from the woman at
that time and
women
in the
couple-testing
group
are
asked to obtain a saliva sample from the father. They take home the leaflet with a sample kit for their partner to be returned the following morning. The results of the test, with a risk estimation for the pregnancy, are sent to the patients by post within 10 days with a copy to the GP. Laboratory tests involve four gene probes (AF508, G551D, G542X, 621 + 1G > T), detecting 83.5% of CF carriers in our
population.
So far 44 pregnancies have been screened. 1 carrier has been detected in the maternal-testing group; her partner tested negative. 2 carriers were detected in the couple-testing group, and both partners tested negative. 1 partner in the couple-testing group declined the test and the maternal sample tested negative. 14 pregnancies were not included in the pilot study, for the following reasons: 1 patient aged 17 years declined the test, then requested termination, changed her mind, and delivered prematurely; 4 booked after 14 weeks for antenatal care; 7 requested termination for reasons unrelated to CF; and 2 patients miscarried before antenatal booking. Preliminary results from questionnaires and interview indicate that women have a positive attitude to CF carrier screening and to general practice as the preferred place for counselling and testing. There is no evidence at this stage that the procedure has caused excessive anxiety (Spielberger scale). Our study will be extended to other local general practices because we believe that general practice provides the ideal setting for very early pregnancy screening and general genetic counselling. Here it becomes an integral part of primary health care and permits assessment of the psychological impact of screening on patients, partners, and families. This is a valuable model for the closer integration of primary and secondary health-care services. This work is supported by the Wolfson Foundation and the North Western Regional Health Authority. Brooklands Medical Practice,
H.
J. HARRIS
Manchester
D. SCOTCHER
Department of Medical Genetics, St Mary’s Hospital, Manchester M13 OJH, UK
D. CRAUFURD A. WALLACE R. HARRIS
Mayall E, Chapple J, et al. Screening for carriers of cystic fibrosis through primary health care services. Br Med J 1991; 303: 504-07.
1. Watson EK,
Population screening for cystic fibrosis SIR,-We are involved in a pilot project of population screening for cystic fibrosis (CF) carriers, using mouthwash samples to screen for four mutations (AF508, G551D, G542X, 621 + 1G>T). We offered all members of staff in our division of molecular and medical genetics confidential screening for carrier status and report here the uptake of testing in this genetically interested and informed group of adults, predominantly of reproductive age. In December, 1991, three posters advertising the availability of confidential screening were displayed prominently, giving two contact names (a clinical geneticist and a nurse genetics counsellor). Those requesting screening were given an information leaflet (devised for our population screening programme) and then interviewed privately to establish whether there was a family history of CF, to check that they understood the inheritance of CF, and to confirm that neither they, their partner, nor anyone else in their family were pregnant. We also reminded them that a negative test result would reduce their carrier risk (to 1 in 130 for caucasians), but not eliminate it. Each mouthwash sample was given a coded reference number, the identity being known only to the clinicians offering the service. The results were handed to staff members personally one week later, together with a copy for them to pass on to their general practitioner. There are 110 members of staff in the division, of whom 80 are female (73%). 18 requested screening during the first three days, and 5 more presented a month later, while being screened for hepatitis B immunity status, when a personal verbal offer of CF screening was made. Of the 23 staff requesting screening, 20 were female (87%). 1 female had her test postponed because a relative was in late pregnancy at that time. The uptake rate for CF carrier screening was therefore about 20%. No carriers were detected.
1540
ten Kate et al2 found that more than half of respondents to a survey thought they would make use of CF carrier screening if it were offered. Watson et al,3 recruiting patients by speaking directly to them, achieved an uptake of 66% in general practice and 87% in family-planning clinics. It is sometimes postulated that low uptake of health screening is partly based on lack of knowledge but an uptake rate of only 20% in a medical genetics department suggests that factors other than ignorance are responsible for a lack of much spontaneous enthusiasm for screening. Our fmding, if confirmed, may be relevant to the design and cost assessments of population screening programmes.
Division of Medical and Molecular Genetics,
UMDS, Guy’s Hospital, London SE1 9RT, UK
FRANCES A. FLINTER ANNE SILVER CHRISTOPHER G. MATHEW MARTIN BOBROW
RM, Robertson NH, Vaudin SA, Sthwantz M, Little S. Development of multiplex ARMS test for the simultaneous detection of four common CF mutations. Am J Hum Genet 1991; 49 (supply: 195. 2. ten Kate LF, Tjimstra TJ. Carrier screening for CF. Lancet 1989; ii: 973-74. 3. Watson EK, Mayall E, Chapple J, et al. Screening for carriers of CF through primary health care services. Br Med J 1991; 303: 504-07. 1. Ferrie
Severe dyserythropoiesis and autoimmune thrombocytopenia associated with ingestion of kelp supplements SIR,-As availability and consumption of dietary health supplements increases, concern has been expressed about the safety of some preparations. Preparations containing kelp are now widely available. Kelp can concentrate various heavy metals, and kelp preparations can contain substantial concentrations of arsenic.1
Urinary arsenic excretion in patients with peripheral neuropathy who have been taking kelp tablets may be increased2 and seaweed ingestion has seen linked with chronic thyroiditis.3 Arsenic intoxication can cause bone marrow depression and megaloblastic changes.4,5 There have been no reports, however, of arsenic-related autoimmune thrombocytopenia or dyserythropoiesis and thrombocytopenia due to arsenic in kelp preparations. We report a patient who had been taking a preparation of kelp found to contain substantial quantities of arsenic. A 54-year-old woman presented with a one week history of abnormal bleeding and petechiae. She was otherwise well and had no relevant medical history. She had been taking a proprietary vitamin tablet and kelp tablets for the previous six weeks (three 550 mg kelp tablets daily with extra calcium.) The only abnormal findings were widespread bruises and petechiae. Haemoglobin (Hb) was 12-2 g/dl, white cells 4-7 x 109/1, and platelets 16 x 109/1. The red cell indices were normal with occasional macrocytes. Antiplatelet antibodies were raised (IgG 28 and IgM 26 ng per 106 platelets; normal, 0-11.0 and 0-1-42, respectively). Serum vitamin B12 and red cell folate, and direct antiglobulin test were normal. Bone marrow aspiration and trephine biopsy showed an increase in megakaryocytes consistent with autoimmune thrombocytopenic purpura. In addition, erythropoiesis was grossly abnormal with increased megaloblasts, large binucleate and trinucleate forms, delayed nuclear maturation with pyknosis, vacuolation, and cytoplasmic bridging. Myeloid and lymphoid lines were normal. Sucrose lysis and Ham’s tests with the patient’s serum and serum from a pool of seven donors were negative. Monocyte CD 14 and neutrophil CD 16 expression were normal. HbF was less than 1%. Electron microscopy of bone marrow was normal with no evidence of double endoplasmic reticulum in the erythroid precursors. Analysis of the kelp tablets showed that they contained 1-3 ug/g arsenic; the patient had therefore been ingesting 2-2 ug arsenic daily. Autoimmune thrombocytopenic purpura with dyserythropoiesis of unknown aetiology was diagnosed. Kelp was withdrawn and the autoimmune thrombocytopenia was treated with intravenous immunoglobulin and prednisolone, with good response. The patient was subsequently treated with azathioprine and her platelet count stabilised around 60 x 109/1. Bone marrow aspiration and trephine biopsy were repeated after three months and showed
virtual complete reversal of the dyserythropoietic features and normal megakaryocyte morphology. Severe dyserythropoiesis is a rare, usually congenital, and generally irreversible condition. Congenital dyserythropoietic anaemia, paroxysmal nocturnal haemoglobinuria, and myelodysplastic syndrome, which are the commonest causes, were excluded by our investigations. We postulate that kelp was responsible for the severe dyserythropoiesis in this patient and it may also have been implicated in either the pathogenesis of the autoimmune thrombocytopenia or the exacerbation of a preexisting condition. Physicians need to be aware of the potentially dangerous contaminants in some kelp preparations. Department of Haematology, Royal London Hospital,
KATHRYN G. PYE STEPHEN M. KELSEY
London E1 1 BB, UK
National Poisons Unit,
Guy’s Hospital, London
IVAN M. HOUSE
Department of Haematology, Royal London Hospital
ADRIAN C. NEWLAND
1. Norman JA, Pickford CJ, Sanders TW, Waller M. Human intake of arsenic and iodine from seaweed-based food supplements and health foods available in the UK. Food
Addit Contam 1987; 5: 103-09. 2. Walkiw O, Douglas DE. Health food supplements prepared from kelp-a source of elevated urinary arsenic. Clin Toxicol 1975; 8: 325-31. 3. Okamura K, Inoue K, Omae T. A case of Hashimoto’s thyroiditis with thyroid immunological abnormality manifested after habitual ingestion of seaweed. Acta Endocrinol 1978; 88: 703-12. 4. Kyle RA, Pease GL. Hematologic aspects of arsenic intoxication. N Engl J Med 1965; 273: 18-23. 5. Westhoff DD, Samaha RJ, Barnes A. Arsenic intoxication as a cause of megaloblastic anaemia. Blood 1975; 45: 241-46.
Practicability of early treatment of acute stroke SIR,-As Dr Sandercock and Mr Willems point out in their contribution to the Stroke Octet (Feb 29, p 537), hardly any of the potential treatments for acute stroke has yet been adequately evaluated in controlled trials and none has been shown to be effective. This view has encouraged a nihilistic attitude, so that in parts of Britain only about half of patients with acute stroke are admittedl and the need for urgent medical treatment is infrequently given by general practitioners as a reason for requesting admission.2 If hospital care is thought necessary for other reasons, this perceived lack of urgency could delay admission beyond the stage when salvage of ischaemic brain is feasible, and many clinicians doubt that adequate acute stroke trials can be conducted in Britain. As a group of general physicians and geriatricians with an interest in stroke, we set out to test this conjecture by surveying all acute stroke admissions to hospitals in seven health districts over 3 months. We included all patients with a new stroke (according to World Health Organisation clinical criteria) in which limb weakness was evident, admitted at any time because of neurological deficit rather than another complication. We excluded patients who were not admitted, with stroke that took place in hospital, with transient ischaemic attacks whose deficits had resolved before they were seen, ADMISSION DELAY AND PREVIOUS DISABILITIES IN PATIENTS ADMITTED TO GENERAL AND GERIATRIC MEDICAL WARDS
*6
more
patemts admitted directly to stroke
units.
