472
experience and of reports of inefficacy in larger numbers of patients with ITJ>8 and HIV-related thrombocytopenia,9 we do not share the view that alpha-interferon is a safe and possibly better alternative to intravenous immunoglobulin1 and would urge considerable caution in the
of this
use
treatment
in ITP. F. MATTHEY S. ARDEMAN
Department of Haematology. Edgware General Hospital Department of Haematology, London Hospital,
L. JONES A. C. NEWLAND
London E1 1BB, UK
1. Proctor
SJ, Jackson G, Carey P, Stark A. Short-course alpha-interferon therapy in unresponsive immune thrombocytopenic purpura. Lancet 1988; i: 947. 2. Ellis ME, Neal KR, Leen CLS, Newland AC. Alpha 2a recombinant interferon in HIV associated thrombocytopema. Br Med J 1987; 295: 1519. 3. Burman P, Karlsson FA, Öberg K, Alm G. Autoimmune thyroid disease in interferon-treated patients. Lancet 1985; ii: 100-01. 4. Costanzi JJ, Cooper MR, Scarffe JH, et al. Phase II study of recombinant alpha-2 interferon in resistant multiple myeloma. J Clin Oncol 1985; 3: 654-59. 5. Talpaz M, Kantarjian HM, Mc Credie KB, et al. Clinical investigation of human alpha interferon in chronic myelogenous leukaemia. Blood 1987; 69: 1280-88. 6. Hunt BJ, Roter B, Davies SC, Hedge U. Raised levels of platelet associated immunoproteins in the initial thrombocytopenia seen with alpha interferon. Br J Haematol 1988; 69: 143 (abstract). 7. Giles FJ, Singer CRJ, Gray AG, et al. Alpha-interferon therapy for essential thrombocythaemia. Lancet 1988; ii. 70-72. 8. Bellucci S, Bordessoule D, Coiffier B, Tabah I. Interferon alpha 2b therapy m adult chronic thrombocytopenic purpura. Br J Haematol 1989; 73: 578-79. 9. Taillan B, Fuzibet JG, Pesce A, et al. Alpha-interferon in thrombocytopenic purpura. severe
Lancet
1988; ii: 170.
Diagnosis of malaria SIR,-Dr Hengy and Dr Gozal (Jan 13, p 121) remark on the difficulty of routine detection of Plasmodium falciparum in blood films from patients on chloroquine/proguanil prophylaxis. I have also observed that scanty trophozoites in a thick film from such a patient were practically unrecognisable, and were missed by the worker who first examined them. They were detected in this instance by long careful examination of a thin film, where their abnormal character did not prevent recognition. A thin film is often regarded as being useful for more accurate species diagnosis, following a positive thick film. However, in the face of a negative thick film, examination of the thin film can still be valuable. In theory, thick fihns should be thirty times more efficient than thin in the detection of infection,1 but the loss of parasites that occurs during thick-film staining reduces this advantage to about ten times. A 30 min thin-film examination is reported as being marginally more sensitive than a 3 min thick-film examination.2 The effectiveness of a thin-film is more pronounced with respect to P vivax and P ovale since erythrocytes infected with these species tend to accumulate along the edges and in the tail of the thin blood film. Finally, Hengy and Gozal’s report shows the value of an independent check on negative blood film results in any laboratory where malaria diagnosis is done.3 PHLS Malaria Reference Laboratory, London School of Hygiene and Tropical Medicine, London WC1 E 7HT, UK
D. C. WARHURST
Use and limitations of light microscopy for diagnosing malaria at the primary care level. Bull WHO 1988, 66: 621-26. 2. Dowling MAC, Shute GT. A comparative study of thick and thin blood films in the diagnosis of scanty malaria parasitaemia. Bull WHO 1966; 34: 249-67. 3. Raghavan K. Statistical considerations in the microscopical diagnosis of malaria, with special reference to the role of cross checking. Bull WHO 1966; 34: 788-91. 1.
Payne D
health
Cerebral malaria: what is unarousable coma? SIR,-Dr Leaver and his colleagues (Jan 6,
p 44) suggest that alterations in consciousness less severe than unarousable coma should be included in studies of severe malaria. In our experience with African children such patients may deteriorate rapidly. If malaria is clinically suspected, any
patients
with
impairment of consciousness warrants immediate and appropriate treatment for this life-threatening condition.1 For research purposes, however, we do not agree with the use of a summation of the Glasgow coma score (GCS) in the definition of cerebral malaria. The GCS was designed to monitor coma2 and does not provide a complete neurological description of the patient. The summation of the responses is unfounded since their values are determined by their rank order and therefore do not represent discrete quantities,3and in summation of these values, information is lost.’ These criticisms are especially pertinent to the Adelaide modification of the GCS for childrens (who bear the brunt of cerebral malaria in Africa) since the responses vary with age. However, the scoring system devised by Molyneux et al6 is useful because of its simplicity and independence of age. The World Health Organisation’s definitionidentifies patients in whom the impairment of consciousness cannot be attributed to fever alone, while the score suggested by Leaver et al does not. Unlike Leaver and colleagues, we have found the motor response of the GCS to be the easiest to interpret and have used this in the initial assessment of consciousness in our young patients with malaria. This was also the experience with Thai adults.8 Thereafter it is reasonable to use coma scores to monitor progress. We agree that reports of neurological involvement in malaria should include a stratification of severity, but this should consist of a clinical description of each category and should not be reduced to a single score. Proposals for new defmitions and classifications should include full details of the patients on whom these are based, including the parasitological diagnosis and exclusion of other diseases.
Kilifi, Kenya
C. R. J. C. NEWTON G. PASVOL P. A. WINSTANLEY
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, UK
D. A. WARRELL
Kilifi Research Unit, PO Box 428,
1 Warrell DA. Cerebral malaria. Q J Med 1989, 265: 369-71. 2. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical side. Lancet 1974; ii 81-84. 3. Teasdale G, Jennert B, Murray L, Murray G. Glasgow coma scale. to sum or not to sum? Lancet 1983, ii 678. 4. Teasdale G, Murray G, Parker L, Jennett B. Adding up the Glasgow coma scale. Acta Neurochir 1979; 28 (suppl). 13-16. 5. Reilly PL, Simpson DA, Sprod R, Thomas L. Assessing the conscious level in infants and young children: a paediatric version of the Glasgow coma scale. Child Nerv Syst 1988; 4: 30-33. 6. Molyneux ME, Taylor TE, Wirima JJ, Borgstein A. Clinical features and prognostic indictors in paediatnc cerebral malana: a study of 131 comatose Malawian children Q J Med 1989; 71: 441-59. 7. World Health Organisation. Malaria action programme: severe and complicated malaria Trans R Soc Trop Med Hyg 1986; 80: 1-50. 8. Warrell DA, Looareesuwan S, Warrell MJ, et al. Dexamethasone proves deleterious in cerebral malaria: a double-blind trial in 100 comatose patients. N Engl J Med 1982; 306: 313-19.
Runway malaria SIR,-Dr Phillips-Howard and colleagues (Jan 13, p 119) highlight the increase in malaria imported to Britain from West Africa, and Dr Signorelli and Dr Messineo (Jan 20, p 164) remind us of the risk of airport malaria when people in non-endemic areas near international airports acquire the disease from "commuter" mosquitoes arriving in aeroplanes from Africa. We report a patient with imported as well as airport malaria and have termed this "runway malaria". A 63-year-old British woman who had lived in Johannesburg, South Africa, for thirteen years returned to the UK in July, 1989. Nine days after arrival she was treated at home for gastroenteritis. Five days later, following three rigors, she became jaundiced and was referred to hospital with suspected viral hepatitis. On admission she was unwell, hypotensive, and oliguric, and proved to have 5% parasitaemia with Plasmodium falciparum. She was treated with intravenous quinine and eventually made a good recovery, though she had several common complications of severe malaria and its treatment-hypotension, renal failure, pulmonary oedema, thrombocytopenia, and hypoglycaemia.
experience and of reports of inefficacy in larger numbers of patients with ITJ>8 and HIV-related thrombocytopenia,9 we do not share the view that alpha-interferon is a safe and possibly better alternative to intravenous immunoglobulin1 and would urge considerable caution in the
of this
use
treatment
in ITP. F. MATTHEY S. ARDEMAN
Department of Haematology. Edgware General Hospital Department of Haematology, London Hospital,
L. JONES A. C. NEWLAND
London E1 1BB, UK
1. Proctor
SJ, Jackson G, Carey P, Stark A. Short-course alpha-interferon therapy in unresponsive immune thrombocytopenic purpura. Lancet 1988; i: 947. 2. Ellis ME, Neal KR, Leen CLS, Newland AC. Alpha 2a recombinant interferon in HIV associated thrombocytopema. Br Med J 1987; 295: 1519. 3. Burman P, Karlsson FA, Öberg K, Alm G. Autoimmune thyroid disease in interferon-treated patients. Lancet 1985; ii: 100-01. 4. Costanzi JJ, Cooper MR, Scarffe JH, et al. Phase II study of recombinant alpha-2 interferon in resistant multiple myeloma. J Clin Oncol 1985; 3: 654-59. 5. Talpaz M, Kantarjian HM, Mc Credie KB, et al. Clinical investigation of human alpha interferon in chronic myelogenous leukaemia. Blood 1987; 69: 1280-88. 6. Hunt BJ, Roter B, Davies SC, Hedge U. Raised levels of platelet associated immunoproteins in the initial thrombocytopenia seen with alpha interferon. Br J Haematol 1988; 69: 143 (abstract). 7. Giles FJ, Singer CRJ, Gray AG, et al. Alpha-interferon therapy for essential thrombocythaemia. Lancet 1988; ii. 70-72. 8. Bellucci S, Bordessoule D, Coiffier B, Tabah I. Interferon alpha 2b therapy m adult chronic thrombocytopenic purpura. Br J Haematol 1989; 73: 578-79. 9. Taillan B, Fuzibet JG, Pesce A, et al. Alpha-interferon in thrombocytopenic purpura. severe
Lancet
1988; ii: 170.
Diagnosis of malaria SIR,-Dr Hengy and Dr Gozal (Jan 13, p 121) remark on the difficulty of routine detection of Plasmodium falciparum in blood films from patients on chloroquine/proguanil prophylaxis. I have also observed that scanty trophozoites in a thick film from such a patient were practically unrecognisable, and were missed by the worker who first examined them. They were detected in this instance by long careful examination of a thin film, where their abnormal character did not prevent recognition. A thin film is often regarded as being useful for more accurate species diagnosis, following a positive thick film. However, in the face of a negative thick film, examination of the thin film can still be valuable. In theory, thick fihns should be thirty times more efficient than thin in the detection of infection,1 but the loss of parasites that occurs during thick-film staining reduces this advantage to about ten times. A 30 min thin-film examination is reported as being marginally more sensitive than a 3 min thick-film examination.2 The effectiveness of a thin-film is more pronounced with respect to P vivax and P ovale since erythrocytes infected with these species tend to accumulate along the edges and in the tail of the thin blood film. Finally, Hengy and Gozal’s report shows the value of an independent check on negative blood film results in any laboratory where malaria diagnosis is done.3 PHLS Malaria Reference Laboratory, London School of Hygiene and Tropical Medicine, London WC1 E 7HT, UK
D. C. WARHURST
Use and limitations of light microscopy for diagnosing malaria at the primary care level. Bull WHO 1988, 66: 621-26. 2. Dowling MAC, Shute GT. A comparative study of thick and thin blood films in the diagnosis of scanty malaria parasitaemia. Bull WHO 1966; 34: 249-67. 3. Raghavan K. Statistical considerations in the microscopical diagnosis of malaria, with special reference to the role of cross checking. Bull WHO 1966; 34: 788-91. 1.
Payne D
health
Cerebral malaria: what is unarousable coma? SIR,-Dr Leaver and his colleagues (Jan 6,
p 44) suggest that alterations in consciousness less severe than unarousable coma should be included in studies of severe malaria. In our experience with African children such patients may deteriorate rapidly. If malaria is clinically suspected, any
patients
with
impairment of consciousness warrants immediate and appropriate treatment for this life-threatening condition.1 For research purposes, however, we do not agree with the use of a summation of the Glasgow coma score (GCS) in the definition of cerebral malaria. The GCS was designed to monitor coma2 and does not provide a complete neurological description of the patient. The summation of the responses is unfounded since their values are determined by their rank order and therefore do not represent discrete quantities,3and in summation of these values, information is lost.’ These criticisms are especially pertinent to the Adelaide modification of the GCS for childrens (who bear the brunt of cerebral malaria in Africa) since the responses vary with age. However, the scoring system devised by Molyneux et al6 is useful because of its simplicity and independence of age. The World Health Organisation’s definitionidentifies patients in whom the impairment of consciousness cannot be attributed to fever alone, while the score suggested by Leaver et al does not. Unlike Leaver and colleagues, we have found the motor response of the GCS to be the easiest to interpret and have used this in the initial assessment of consciousness in our young patients with malaria. This was also the experience with Thai adults.8 Thereafter it is reasonable to use coma scores to monitor progress. We agree that reports of neurological involvement in malaria should include a stratification of severity, but this should consist of a clinical description of each category and should not be reduced to a single score. Proposals for new defmitions and classifications should include full details of the patients on whom these are based, including the parasitological diagnosis and exclusion of other diseases.
Kilifi, Kenya
C. R. J. C. NEWTON G. PASVOL P. A. WINSTANLEY
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, UK
D. A. WARRELL
Kilifi Research Unit, PO Box 428,
1 Warrell DA. Cerebral malaria. Q J Med 1989, 265: 369-71. 2. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical side. Lancet 1974; ii 81-84. 3. Teasdale G, Jennert B, Murray L, Murray G. Glasgow coma scale. to sum or not to sum? Lancet 1983, ii 678. 4. Teasdale G, Murray G, Parker L, Jennett B. Adding up the Glasgow coma scale. Acta Neurochir 1979; 28 (suppl). 13-16. 5. Reilly PL, Simpson DA, Sprod R, Thomas L. Assessing the conscious level in infants and young children: a paediatric version of the Glasgow coma scale. Child Nerv Syst 1988; 4: 30-33. 6. Molyneux ME, Taylor TE, Wirima JJ, Borgstein A. Clinical features and prognostic indictors in paediatnc cerebral malana: a study of 131 comatose Malawian children Q J Med 1989; 71: 441-59. 7. World Health Organisation. Malaria action programme: severe and complicated malaria Trans R Soc Trop Med Hyg 1986; 80: 1-50. 8. Warrell DA, Looareesuwan S, Warrell MJ, et al. Dexamethasone proves deleterious in cerebral malaria: a double-blind trial in 100 comatose patients. N Engl J Med 1982; 306: 313-19.
Runway malaria SIR,-Dr Phillips-Howard and colleagues (Jan 13, p 119) highlight the increase in malaria imported to Britain from West Africa, and Dr Signorelli and Dr Messineo (Jan 20, p 164) remind us of the risk of airport malaria when people in non-endemic areas near international airports acquire the disease from "commuter" mosquitoes arriving in aeroplanes from Africa. We report a patient with imported as well as airport malaria and have termed this "runway malaria". A 63-year-old British woman who had lived in Johannesburg, South Africa, for thirteen years returned to the UK in July, 1989. Nine days after arrival she was treated at home for gastroenteritis. Five days later, following three rigors, she became jaundiced and was referred to hospital with suspected viral hepatitis. On admission she was unwell, hypotensive, and oliguric, and proved to have 5% parasitaemia with Plasmodium falciparum. She was treated with intravenous quinine and eventually made a good recovery, though she had several common complications of severe malaria and its treatment-hypotension, renal failure, pulmonary oedema, thrombocytopenia, and hypoglycaemia.
