- Email: [email protected]
Imatinib for chronic myeloid leukaemia: a NICE mess
CORRESPONDENCE
strategy is developed, but some fresh thinking is required. Stephen G O’Brien Department of Haematology, University of Newcastle, Royal Victoria Infirmary, Newcastle NE1 4LP, UK 1
Barbour V. Imatinib for chronic myeloid leukaemia: a NICE mess. Lancet 2001; 358: 1478.
Sir—Allan van Oosterom and colleagues (Oct 27, p 1421)1 report on the efficacy of imatinib in the treatment of gastrointestinal stromal tumours. This finding could extend the use of imatinib to tyrosine kinase dependent tumours other than those limited to chronic myeloid leukaemia and Philadelphia positive acute myeloid leukaemia.2 Mild cutaneous rashes to imatinib were noted in 22 (55%) of 40 patients in van Oosterom and colleagues’ study, but two patients had a severe reaction requiring dose modification. Brouard and colleagues3 reported a patient who developed an acute generalised exanthematous pustulosis while taking imatinib. However, to date no rashes other than non-specific maculopapular eruptions have been reported. We noted an erosive oral lichenoid reaction (figure), which promptly cleared after imatinib was stopped. The ulcerations started on the buccal mucosa as radiating lattice-like striae, which eventually eroded, and progressed to involve the dorsum of the tongue. Symptoms arose 12 weeks after imatinib was started. Histopathology revealed a lichenoid infiltrate concentrated perivascularly, and a negative direct immunoflurosence excluded immunobullous disease. Clinical responses to chronic myeloid leukaemia and gastrointestinal stromal tumours have been promising, and we can expect to see more patients on imatinib in the near future. In this subset of patients in whom the use of imatinib is indicated, this potential
Erosive lichenoid reaction to imatinib confined to oral mucosa in a patient with chronic myeloid leukaemia
THE LANCET • Vol 358 • December 1, 2001
side-effect of the drug must be borne in mind, and, most importantly, must be differentiated from idiopathic lichen planus, immunobullous eruptions, and oral graft versus host disease. *Davin Lim, Jim Muir Department of Dermatology, Mater Hospital, Southbank, Brisbane, Australia (e-mail: [email protected]) 1
2
3
van Oosterom A, Judson I, Verweij J, et al. Safety and efficacy of imatinib (STI 571) in metastatic gastrointestinal stromal tumours: a phase I study. Lancet 2001; 358: 1421–23. Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001; 344: 1031–37. Brouard M, Saurat JH. Cutaneous reactions to STI 571. N Engl J Med 2001; 345: 618–19.
heparin are used than in Europe, with different intervals between the siting of epidurals and administration of thromboprophylaxsis.4 We believe that enough clinical information is available to facilitate a proper discussion of the risks and benefits associated with this procedure with the concerned patients. This process will further refine the technique of selective deafferentation to speed and improve physiological recovery from major surgery. *Jones Kurian, Venkat Raghavan, Pushparaj Shetty Department of Anaesthetics, St George’s Hospital, London SW17 0QT, UK (e-mail: [email protected]) 1 2
Use of epidurals during and after surgery 3
Sir—We wish to resolve the dilemma highlighted by A Williams (Aug 25, p 673)1 facing anaesthetists about the use of intraoperative and postoperative epidural analgesia in the presence of prophylactic anticoagulation. Williams has no reservations about the efficacy and usefulness of epidural analgesia during the postoperative period but is not sure whether epidural anaesthesia alone confers substantial protection against venous thrombosis, and whether we should continue following the conventional guidelines, which do allow concomitant use of epidurals and prophylactic anticoagulation. We do not think the first question will ever be resolved with 100% certainty, as for any question or controversy in clinical medicine. In a comprehensive systematic review looking at the effects of neuraxial blockade on postoperative morbidity and mortality, Rodgers and colleagues2 reported a significant overall reduction of mortality by about one-third in patients assigned neuraxial blockade. Neuraxial blockade reduced the odds of deep-vein thrombosis by 44% and pulmonary embolism by 55%, along with significant reduction in transfusion requirements, pneumonia, and respiratory depression. Rodgers and colleagues are supporting more widespread use of neuraxial blockade. The incidence of neurological dysfunction resulting from haemorrhagic complications associated with central neural blockade is estimated to be less than one in 150 000 epidurals.3 Most of the reported cases are from North America, where much larger doses of low-molecular-weight
4
Williams AE. Expectations placed on anaesthetists. Lancet 2001; 358: 673–74. Rodgers A, Walker N, Schug S, et al. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. BMJ 2000; 321: 1493. Horlocker TT. Low molecular weight heparin and neuraxial anesthesia. Thromb Res 2001; 101: V141–54. Breivik H. Neurological complications in association with spinal and epidural analgesia—again. Acta Anaesthesiol Scan 1998; 42: 609–13.
Cholesterol and all-cause mortality in Honolulu Sir—Irwin Schatz and colleagues (Aug 4, p 351)1 report that low plasma cholesterol concentrations are associated with all-cause mortality in elderly men and that long-term persistence of low cholesterol increases the risk of death. It is unfortunate that they do not report data on the association between cholesterol and cause-specific mortality. The well-known U-shaped curve that describes the relation between cholesterol and mortality results from different associations that cholesterol concentrations have with different causes of death.2 Iribarren and colleagues3 reported, in the same cohort studied by Schatz and colleagues, that the higher mortality seen in individuals who had low cholesterol concentrations was due mainly to the presence of cancer, liver disease, and haemorrhagic stroke. At the other end of the curve, the association between cholesterol and mortality for cardiovascular disease in the elderly is similar to that seen in younger people when signs of disease and frailty are taken in account.4 Schatz and colleagues do not think that frailty measures can explain the increased mortality in individuals with persistent low cholesterol concentrations. However, their data
1903
For personal use. Only reproduce with permission from The Lancet Publishing Group.
strategy is developed, but some fresh thinking is required. Stephen G O’Brien Department of Haematology, University of Newcastle, Royal Victoria Infirmary, Newcastle NE1 4LP, UK 1
Barbour V. Imatinib for chronic myeloid leukaemia: a NICE mess. Lancet 2001; 358: 1478.
Sir—Allan van Oosterom and colleagues (Oct 27, p 1421)1 report on the efficacy of imatinib in the treatment of gastrointestinal stromal tumours. This finding could extend the use of imatinib to tyrosine kinase dependent tumours other than those limited to chronic myeloid leukaemia and Philadelphia positive acute myeloid leukaemia.2 Mild cutaneous rashes to imatinib were noted in 22 (55%) of 40 patients in van Oosterom and colleagues’ study, but two patients had a severe reaction requiring dose modification. Brouard and colleagues3 reported a patient who developed an acute generalised exanthematous pustulosis while taking imatinib. However, to date no rashes other than non-specific maculopapular eruptions have been reported. We noted an erosive oral lichenoid reaction (figure), which promptly cleared after imatinib was stopped. The ulcerations started on the buccal mucosa as radiating lattice-like striae, which eventually eroded, and progressed to involve the dorsum of the tongue. Symptoms arose 12 weeks after imatinib was started. Histopathology revealed a lichenoid infiltrate concentrated perivascularly, and a negative direct immunoflurosence excluded immunobullous disease. Clinical responses to chronic myeloid leukaemia and gastrointestinal stromal tumours have been promising, and we can expect to see more patients on imatinib in the near future. In this subset of patients in whom the use of imatinib is indicated, this potential
Erosive lichenoid reaction to imatinib confined to oral mucosa in a patient with chronic myeloid leukaemia
THE LANCET • Vol 358 • December 1, 2001
side-effect of the drug must be borne in mind, and, most importantly, must be differentiated from idiopathic lichen planus, immunobullous eruptions, and oral graft versus host disease. *Davin Lim, Jim Muir Department of Dermatology, Mater Hospital, Southbank, Brisbane, Australia (e-mail: [email protected]) 1
2
3
van Oosterom A, Judson I, Verweij J, et al. Safety and efficacy of imatinib (STI 571) in metastatic gastrointestinal stromal tumours: a phase I study. Lancet 2001; 358: 1421–23. Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001; 344: 1031–37. Brouard M, Saurat JH. Cutaneous reactions to STI 571. N Engl J Med 2001; 345: 618–19.
heparin are used than in Europe, with different intervals between the siting of epidurals and administration of thromboprophylaxsis.4 We believe that enough clinical information is available to facilitate a proper discussion of the risks and benefits associated with this procedure with the concerned patients. This process will further refine the technique of selective deafferentation to speed and improve physiological recovery from major surgery. *Jones Kurian, Venkat Raghavan, Pushparaj Shetty Department of Anaesthetics, St George’s Hospital, London SW17 0QT, UK (e-mail: [email protected]) 1 2
Use of epidurals during and after surgery 3
Sir—We wish to resolve the dilemma highlighted by A Williams (Aug 25, p 673)1 facing anaesthetists about the use of intraoperative and postoperative epidural analgesia in the presence of prophylactic anticoagulation. Williams has no reservations about the efficacy and usefulness of epidural analgesia during the postoperative period but is not sure whether epidural anaesthesia alone confers substantial protection against venous thrombosis, and whether we should continue following the conventional guidelines, which do allow concomitant use of epidurals and prophylactic anticoagulation. We do not think the first question will ever be resolved with 100% certainty, as for any question or controversy in clinical medicine. In a comprehensive systematic review looking at the effects of neuraxial blockade on postoperative morbidity and mortality, Rodgers and colleagues2 reported a significant overall reduction of mortality by about one-third in patients assigned neuraxial blockade. Neuraxial blockade reduced the odds of deep-vein thrombosis by 44% and pulmonary embolism by 55%, along with significant reduction in transfusion requirements, pneumonia, and respiratory depression. Rodgers and colleagues are supporting more widespread use of neuraxial blockade. The incidence of neurological dysfunction resulting from haemorrhagic complications associated with central neural blockade is estimated to be less than one in 150 000 epidurals.3 Most of the reported cases are from North America, where much larger doses of low-molecular-weight
4
Williams AE. Expectations placed on anaesthetists. Lancet 2001; 358: 673–74. Rodgers A, Walker N, Schug S, et al. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. BMJ 2000; 321: 1493. Horlocker TT. Low molecular weight heparin and neuraxial anesthesia. Thromb Res 2001; 101: V141–54. Breivik H. Neurological complications in association with spinal and epidural analgesia—again. Acta Anaesthesiol Scan 1998; 42: 609–13.
Cholesterol and all-cause mortality in Honolulu Sir—Irwin Schatz and colleagues (Aug 4, p 351)1 report that low plasma cholesterol concentrations are associated with all-cause mortality in elderly men and that long-term persistence of low cholesterol increases the risk of death. It is unfortunate that they do not report data on the association between cholesterol and cause-specific mortality. The well-known U-shaped curve that describes the relation between cholesterol and mortality results from different associations that cholesterol concentrations have with different causes of death.2 Iribarren and colleagues3 reported, in the same cohort studied by Schatz and colleagues, that the higher mortality seen in individuals who had low cholesterol concentrations was due mainly to the presence of cancer, liver disease, and haemorrhagic stroke. At the other end of the curve, the association between cholesterol and mortality for cardiovascular disease in the elderly is similar to that seen in younger people when signs of disease and frailty are taken in account.4 Schatz and colleagues do not think that frailty measures can explain the increased mortality in individuals with persistent low cholesterol concentrations. However, their data
1903
For personal use. Only reproduce with permission from The Lancet Publishing Group.