834
J. D. Pickard, J. Stanley (Southampton General Hospital); J. Lagarrigue, V. Larrue (CHR Rangueil, Toulouse, France); 0. P. Dahl, R. Juul (Regionsykehuset I Trondheim, Norway).
gene-related peptide on postoperative neurological deficits following subarachnoid haemorrhage. Lancet 1990; 335: 869-72. 12. Jennett B, Bond A. Assessment of outcome after severe brain damage: a practical scale. Lancet 1975; i: 480-84. 13. Hanko
REFERENCES 1. Wilkins RH. Attempts at prevention or treatment of intracranial arterial spasm: an update. Neurosurgery 1986; 18: 808-25. 2. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. Br Med J 1989; 298: 636-42. 3. Amara SG, Jonas V, Rosenfeld MG, Ong ES, Evans RM. Alternative RNA processing in calcitonin gene expression generates mRNAs encoding different polypeptide products. Nature 1982; 298: 240-44. 4. Rosenfeld MG, Mermod J-J, Amara SG, et al. Production of a novel neuropeptide encoded by the calcitonin gene by tissue-specific RNA processing. Nature 1983; 304: 129-35. 5. Steenbergh PH, Hoppener JWM, Zandberg J, Van de Ven WJM, Jansz HS, Lips LJM. Calcitonin gene-related peptide coding sequence is conserved in the human genome and is expressed in medullary thyroid carcinoma. J Clin Endocrinol Metab 1984; 59: 358-60. 6. Steenbergh PH, Hoppener JWN, Zandberg J, Lips CJM, Jansz HS. A second human calcitonin/CGRP gene. FEBS Lett 1985; 183:
403-07. 7. Amara
SG, Arriza JL, Leff SE, Swanson LW, Evans RM, Rosenfeld
MG.
Expression in brain of a messenger RNA encoding a novel neuropeptide homologous to calcitonin gene-related peptide. Science 1985; 229: 1094-97. 8. Wimalawansa SJ, Emson
PC, MacIntyre I. Regional distribution of calcitonin gene-related peptide and its specific binding sites in rats with particular reference to the nervous system. Neuroendocrinology 1987;
46: 131-36. 9. Salmon P, Fitzgerald D, Lambe R, et al. A single rising intravenous dose tolerance and pharmacodynamic study of human calcitonin gene related peptide (CGRP) in healthy male volunteers. Clin Pharmacol Ther 1989; 45: 170. 10. Stanley JC, Martin JL, Barron ME, et al. A study of the cardiovascular and cerebrovascular effects of calcitonin gene-related peptide in human volunteers. J Physiol 1990; 427: 33P. 11. Johnston FG, Bell BA, Robertson IJA, et al. The effect of calcitonin
J, Hardebo J, Kahrstrom J, Owman C, Sundler F. Calcitonin
gene-related peptide is present in mammalian cerebrovascular nerve fibres and dilates pial and peripheral arteries. Neurosci Lett 1985; 57: 91-95.
R, Edvinsson L, Ekman R, Kingman T, McCulloch J. Innvervation of the feline cerebral vasculature by nerve fibres containing calcitonin gene-related peptide: trigeminal origin and co-existence with substance P. Neurosci Lett 1985; 62: 131-36. 15. Edvinsson L, Delgado-Zygmunt T, Ekman R, Jansen I, Svendgaard N-Aa, Uddman R. Involvement of perivascular sensory fibers in the pathophysiology of cerebral vasospasm following subarachnoid haemorrhage. J Cerebral Blood Flow Metab 1990; 10: 602-07. 16. Edvinsson L, Ekman R, Jansen I, Kingman TA, McCulloch J, Uddman R. Reduced levels of calcitonin gene-related peptide-like immunoreactivity in human brain vessels after subarachnoid haemorrhage. Neurosci Lett 1991; 121: 151-54. 17. Juul R, Edvinsson L, Gisvold SE, Ekman R, Brubakk AO, Fredriksen TA. Calcitonin gene-related peptide-LI in subarachnoid haemorrhage in man: signs of activation of the trigemino-cerebrovascular system. Br J Neurosurg 1990; 4: 171-80. 18. Hongo K, Tsukahara T, Kassell NF, Ogawa H. Effect of subarachnoid haemorrhage on calcitonin gene-related peptide-induced relaxation in rabbit basilar artery. Stroke 1989; 20: 100-04. 19. Edvinsson L, Ekman R, Jansen I, Ottosson A, Uddman R. Distribution, concentration and effects of neuropeptide Y, vasoactive intestinal polypeptide, calcitonin gene-related peptide, and substance P in human cerebral blood vessels. J Cerebral Blood Flow Metab 1985; 5: S545-46. 20. Naylor AR, Robertson IJA, Edwards CRW, et al. Cerebral vasospasm following subarachnoid haemorrhage: effect of calcitonin gene-related peptide on middle cerebral artery velocities using transcranial doppler. Surg Neurol 1991; 36: 278-80. 21. Kim P, Lorenz RR, Sundt TM, Vanhoutte PM. Release of endotheliumderived relaxing factor after subarachnoid haemorrhage. J Neurosurg 1989; 70: 108-14. 22. Byrne JV, Edwards DH, Griffiths TM, Bell BA. Delayed vasospasm after SAH is associated with inhibition of EDRF activity. J Neurol Neurosurg Psychiatry 1991; 54: 661. 14. Uddman
SHORT REPORTS High incidence of primary gastric lymphoma in northeastern Italy
We previously noted an extraordinarily high number of cases of primary gastric lymphoma (PG L) in northeastern Italy. We have now formally compared the incidence in Feltre, Italy, with that in three similar communities in the UK. Each community has a stable population served by a single endoscopy unit and histopathology laboratory. There were 13 times more cases of PGL in Feltre in 1986-91 than in the UK communities (66 vs 5 per 100 000 per 5 years). The incidence of gastric adenocarcinoma was also substantially higher in Feltre than in the UK (270 vs an average of 82 per 100 000 per 5 years), as was the prevalence of gastritis associated with Helicobacter pylori infection (87% of 1343 gastric biopsy samples in 1991).
Primary gastric lymphoma (PGL) is a rare tumour in countries, where it accounts for between 1% and 5 % of all malignant disorders of the stomach.1 Evidence that the incidence of PGL may be increasing2 and better understanding of its histopathology3 have led to greater interest in this type of lymphoma. Our study of the histopathology of PGLrevealed an extraordinarily high number of cases in northeastern Italy. We have formally compared the incidence of PGL in a small well-defined community in northeastern Italy with that in three western
communities in the UK. The study area is the local health service unit N4 (ULSN4) of the Veneto Region of Italy, centred around the city of Feltre. It has a stable population of 56 000 and is served by the Feltre City Hospital, which has a gastroenterology unit with excellent facilities for endoscopy. Biopsy samples taken at endoscopy are interpreted by one histopathologist (C. D.). Three British communities were chosen for comparison because of the stability of the local populations and the presence in each of a single local endoscopy unit. They are the Llanelli district in Wales (Prince Philip General Hospital), the Salisbury district in Wiltshire (Salisbury General Infirmary), and the Gloucester district in Gloucestershire (Gloucestershire Royal Hospital). All the histopathologists are aware of advances in knowledge about PGL, but have no special interest in the disorder. For each community studied, the number of gastroscopic examinations done in each of the years 1986-90 was noted, together
835
with the numbers of new cases of PGL, gastric adenocarcinoma, nodal Hodgkin’s disease, and non-Hodgkin lymphoma. All results
expressed as the number of cases per 100 000 individuals per 5 years. A detailed histopathological analysis was done for all gastric biopsy samples taken from 1355 patients in Feltre during 1991. The frequency of gastric biopsy samples showing PGL was 11-16 (average 13) times higher in Feltre than in the were
three UK communities (table). The age distributions of the Italian and British cohorts were similar (mean 62 [range 38-83] vs 62 [31-90] years) and the male/female ratio was 1 ’5/1 ’0 in both cohorts. Our findings also confirm the higher incidence of gastric carcinoma and of nodal non-Hodgkin lymphoma in northeastern Italy. Analysis of 1343 gastric biopsy samples taken in Feltre during 1991 showed 11 cases of PGL (98 per 100 000 per 5 years) and 25 of adenocarcinoma (223 per 100 000 per 5 years). Helicobacter pylori was detected in 87% of the samples, 584 (46%) of which showed severe gastritis with formation of lymphoid follicles.
We thank Dr Lesley Murray, Llanelli, Dr Bruce Addis, Salisbury, and Dr Neil Shepherd, Gloucester, for their help, and Prof Michael Marmot for advice.
REFERENCES
JJ, Enterline HT. Primary gastric lymphoma. A clinicopathologic study of 58 cases with long-term follow-up and literature
1. Brooks
review. Cancer 1983; 51: 701-11.
Hayes J, Dunn E. Has the incidence of primary gastric lymphoma increased? Cancer 1989; 63: 2073-76. 3. Isaacson PG, Spencer J. Malignant lymphoma of mucosa-associated lymphoma tissue. Histopathology 1987; 11: 445-62. 4. Buiatti E, Palli D, Decarli A, et al. A case-control study of gastric cancer and diet in Italy. Int J Cancer 1989; 44: 611-16. 5. Wotherspoon AC, Ortiz-Hidalgo C, Falzon MR, Isaacson PG. Helicobacter pylori associated gastritis and primary B-cell gastric lymphoma. Lancet 1991; 338: 1175-76. 6. Parsunnet J, Friedman GD, Vandersteen DP, et al. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med 1991; 325: 2.
1127-31. 7. Shallcross TM, Rathbone BJ, Heatley RG. Campylobacter pylori and non-ulcer dyspepsia. In: Rathbone BJ, Heatley RV, eds. Campylobacter pylori and gastroduodenal disease. Oxford: Blackwell Scientific, 1989: 155-56.
ABSOLUTE AND RELATIVE NUMBERS OF CASES OF PGL,
GASTRIC CARCINOMA, AND NODAL LYMPHOMA, 1986-90
ADDRESSES: Ospedale Civile, Feltre, Italy (C. Doglioni, MD, A. Moschini, MD, M de Boni, MD), and Department of Histopathology, University College and Middlesex School of Medicine, University Street, London WC1E6JJ, UK (A. C. Wotherspoon, MB, Prof P. G Isaacson, FRCPath). Correspondence to Prof Peter G. Isaacson
Urinary excretion of platelet-activating factor in haemolytic uraemic syndrome
That these findings reflect a truly high incidence of PGL in Feltre is supported by the similarity of the centres studied. None is a referral centre with a special interest in PGL or any other disorder that requires gastroscopy; thus, the endoscopy facilities are used only by the local population. Each centre is served by general histopathologists who are familiar with the latest ideas on the diagnosis of PGL but do not have a narrow special interest in the disease. The rate of gastroscopic examinations (per 100 000 per 5 years) is four times higher in Feltre than in the UK centres; this factor may account for the higher incidence of PGL. However, the ratio of PGL to gastric carcinoma is very high in Feltre (1 /4), despite the high incidence of gastric carcinoma; the ratio is between 1/13 and 1/18 in the UK centres. Furthermore, 4 cases of PGL are diagnosed for every 1000 gastroscopic examinations in Feltre compared with 1 per 1000 in the UK centres.
The previously reported high incidence of gastric carcinoma in areas of northern Italy4 is confirmed by this study, which suggests that predisposing factors may be shared by PGL and gastric carcinoma. H pylori infection may predispose to both disorders; 5,6 the rate of infection with this organism was much higher in Feltre patients undergoing gastroscopy (87%) than in patients undergoing routine gastroscopy in the UK (50-60%).7 Other environmental or dietary factors may also play a part, and the higher incidence of nodal non-Hodgkin lymphoma in Feltre may provide clues to these.
of the features of haemolytic uraemic syndrome (HUS), such as platelet activation and glomerular injury, could be brought about by platelet-activating factor (PAF), we have studied the urinary excretion of PAF in 10 children with HUS and in 10 healthy age-matched controls. Urinary PAF measured concentrations, by radioimmunoassay, were significantly higher in acutephase H US patients than in controls (mean 2·04 [SD 1·66] vs 0·72 [0·43] ng/mg creatinine, p < 0·05) but were similar to those in controls in samples taken after recovery. High PAF concentrations during the acute phase of HUS may reflect platelet activation and glomerular injury; the lower values after recovery suggest that urinary PAF may be a marker of disease
Since
some
activity.
Platelet-activating factor (PAF), a phospholipid produced by platelets and endothelial, mesangial, and other cells, promotes platelet aggregation and impairs renal function. Since the haemolytic uraemic syndrome (HUS) is characterised by platelet activation and injury to glomerular endothelial cells, we have investigated urinary excretion of PAF, which reflects renal synthesis,l during the acute phase of HUS and after recovery.
J. D. Pickard, J. Stanley (Southampton General Hospital); J. Lagarrigue, V. Larrue (CHR Rangueil, Toulouse, France); 0. P. Dahl, R. Juul (Regionsykehuset I Trondheim, Norway).
gene-related peptide on postoperative neurological deficits following subarachnoid haemorrhage. Lancet 1990; 335: 869-72. 12. Jennett B, Bond A. Assessment of outcome after severe brain damage: a practical scale. Lancet 1975; i: 480-84. 13. Hanko
REFERENCES 1. Wilkins RH. Attempts at prevention or treatment of intracranial arterial spasm: an update. Neurosurgery 1986; 18: 808-25. 2. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. Br Med J 1989; 298: 636-42. 3. Amara SG, Jonas V, Rosenfeld MG, Ong ES, Evans RM. Alternative RNA processing in calcitonin gene expression generates mRNAs encoding different polypeptide products. Nature 1982; 298: 240-44. 4. Rosenfeld MG, Mermod J-J, Amara SG, et al. Production of a novel neuropeptide encoded by the calcitonin gene by tissue-specific RNA processing. Nature 1983; 304: 129-35. 5. Steenbergh PH, Hoppener JWM, Zandberg J, Van de Ven WJM, Jansz HS, Lips LJM. Calcitonin gene-related peptide coding sequence is conserved in the human genome and is expressed in medullary thyroid carcinoma. J Clin Endocrinol Metab 1984; 59: 358-60. 6. Steenbergh PH, Hoppener JWN, Zandberg J, Lips CJM, Jansz HS. A second human calcitonin/CGRP gene. FEBS Lett 1985; 183:
403-07. 7. Amara
SG, Arriza JL, Leff SE, Swanson LW, Evans RM, Rosenfeld
MG.
Expression in brain of a messenger RNA encoding a novel neuropeptide homologous to calcitonin gene-related peptide. Science 1985; 229: 1094-97. 8. Wimalawansa SJ, Emson
PC, MacIntyre I. Regional distribution of calcitonin gene-related peptide and its specific binding sites in rats with particular reference to the nervous system. Neuroendocrinology 1987;
46: 131-36. 9. Salmon P, Fitzgerald D, Lambe R, et al. A single rising intravenous dose tolerance and pharmacodynamic study of human calcitonin gene related peptide (CGRP) in healthy male volunteers. Clin Pharmacol Ther 1989; 45: 170. 10. Stanley JC, Martin JL, Barron ME, et al. A study of the cardiovascular and cerebrovascular effects of calcitonin gene-related peptide in human volunteers. J Physiol 1990; 427: 33P. 11. Johnston FG, Bell BA, Robertson IJA, et al. The effect of calcitonin
J, Hardebo J, Kahrstrom J, Owman C, Sundler F. Calcitonin
gene-related peptide is present in mammalian cerebrovascular nerve fibres and dilates pial and peripheral arteries. Neurosci Lett 1985; 57: 91-95.
R, Edvinsson L, Ekman R, Kingman T, McCulloch J. Innvervation of the feline cerebral vasculature by nerve fibres containing calcitonin gene-related peptide: trigeminal origin and co-existence with substance P. Neurosci Lett 1985; 62: 131-36. 15. Edvinsson L, Delgado-Zygmunt T, Ekman R, Jansen I, Svendgaard N-Aa, Uddman R. Involvement of perivascular sensory fibers in the pathophysiology of cerebral vasospasm following subarachnoid haemorrhage. J Cerebral Blood Flow Metab 1990; 10: 602-07. 16. Edvinsson L, Ekman R, Jansen I, Kingman TA, McCulloch J, Uddman R. Reduced levels of calcitonin gene-related peptide-like immunoreactivity in human brain vessels after subarachnoid haemorrhage. Neurosci Lett 1991; 121: 151-54. 17. Juul R, Edvinsson L, Gisvold SE, Ekman R, Brubakk AO, Fredriksen TA. Calcitonin gene-related peptide-LI in subarachnoid haemorrhage in man: signs of activation of the trigemino-cerebrovascular system. Br J Neurosurg 1990; 4: 171-80. 18. Hongo K, Tsukahara T, Kassell NF, Ogawa H. Effect of subarachnoid haemorrhage on calcitonin gene-related peptide-induced relaxation in rabbit basilar artery. Stroke 1989; 20: 100-04. 19. Edvinsson L, Ekman R, Jansen I, Ottosson A, Uddman R. Distribution, concentration and effects of neuropeptide Y, vasoactive intestinal polypeptide, calcitonin gene-related peptide, and substance P in human cerebral blood vessels. J Cerebral Blood Flow Metab 1985; 5: S545-46. 20. Naylor AR, Robertson IJA, Edwards CRW, et al. Cerebral vasospasm following subarachnoid haemorrhage: effect of calcitonin gene-related peptide on middle cerebral artery velocities using transcranial doppler. Surg Neurol 1991; 36: 278-80. 21. Kim P, Lorenz RR, Sundt TM, Vanhoutte PM. Release of endotheliumderived relaxing factor after subarachnoid haemorrhage. J Neurosurg 1989; 70: 108-14. 22. Byrne JV, Edwards DH, Griffiths TM, Bell BA. Delayed vasospasm after SAH is associated with inhibition of EDRF activity. J Neurol Neurosurg Psychiatry 1991; 54: 661. 14. Uddman
SHORT REPORTS High incidence of primary gastric lymphoma in northeastern Italy
We previously noted an extraordinarily high number of cases of primary gastric lymphoma (PG L) in northeastern Italy. We have now formally compared the incidence in Feltre, Italy, with that in three similar communities in the UK. Each community has a stable population served by a single endoscopy unit and histopathology laboratory. There were 13 times more cases of PGL in Feltre in 1986-91 than in the UK communities (66 vs 5 per 100 000 per 5 years). The incidence of gastric adenocarcinoma was also substantially higher in Feltre than in the UK (270 vs an average of 82 per 100 000 per 5 years), as was the prevalence of gastritis associated with Helicobacter pylori infection (87% of 1343 gastric biopsy samples in 1991).
Primary gastric lymphoma (PGL) is a rare tumour in countries, where it accounts for between 1% and 5 % of all malignant disorders of the stomach.1 Evidence that the incidence of PGL may be increasing2 and better understanding of its histopathology3 have led to greater interest in this type of lymphoma. Our study of the histopathology of PGLrevealed an extraordinarily high number of cases in northeastern Italy. We have formally compared the incidence of PGL in a small well-defined community in northeastern Italy with that in three western
communities in the UK. The study area is the local health service unit N4 (ULSN4) of the Veneto Region of Italy, centred around the city of Feltre. It has a stable population of 56 000 and is served by the Feltre City Hospital, which has a gastroenterology unit with excellent facilities for endoscopy. Biopsy samples taken at endoscopy are interpreted by one histopathologist (C. D.). Three British communities were chosen for comparison because of the stability of the local populations and the presence in each of a single local endoscopy unit. They are the Llanelli district in Wales (Prince Philip General Hospital), the Salisbury district in Wiltshire (Salisbury General Infirmary), and the Gloucester district in Gloucestershire (Gloucestershire Royal Hospital). All the histopathologists are aware of advances in knowledge about PGL, but have no special interest in the disorder. For each community studied, the number of gastroscopic examinations done in each of the years 1986-90 was noted, together
835
with the numbers of new cases of PGL, gastric adenocarcinoma, nodal Hodgkin’s disease, and non-Hodgkin lymphoma. All results
expressed as the number of cases per 100 000 individuals per 5 years. A detailed histopathological analysis was done for all gastric biopsy samples taken from 1355 patients in Feltre during 1991. The frequency of gastric biopsy samples showing PGL was 11-16 (average 13) times higher in Feltre than in the were
three UK communities (table). The age distributions of the Italian and British cohorts were similar (mean 62 [range 38-83] vs 62 [31-90] years) and the male/female ratio was 1 ’5/1 ’0 in both cohorts. Our findings also confirm the higher incidence of gastric carcinoma and of nodal non-Hodgkin lymphoma in northeastern Italy. Analysis of 1343 gastric biopsy samples taken in Feltre during 1991 showed 11 cases of PGL (98 per 100 000 per 5 years) and 25 of adenocarcinoma (223 per 100 000 per 5 years). Helicobacter pylori was detected in 87% of the samples, 584 (46%) of which showed severe gastritis with formation of lymphoid follicles.
We thank Dr Lesley Murray, Llanelli, Dr Bruce Addis, Salisbury, and Dr Neil Shepherd, Gloucester, for their help, and Prof Michael Marmot for advice.
REFERENCES
JJ, Enterline HT. Primary gastric lymphoma. A clinicopathologic study of 58 cases with long-term follow-up and literature
1. Brooks
review. Cancer 1983; 51: 701-11.
Hayes J, Dunn E. Has the incidence of primary gastric lymphoma increased? Cancer 1989; 63: 2073-76. 3. Isaacson PG, Spencer J. Malignant lymphoma of mucosa-associated lymphoma tissue. Histopathology 1987; 11: 445-62. 4. Buiatti E, Palli D, Decarli A, et al. A case-control study of gastric cancer and diet in Italy. Int J Cancer 1989; 44: 611-16. 5. Wotherspoon AC, Ortiz-Hidalgo C, Falzon MR, Isaacson PG. Helicobacter pylori associated gastritis and primary B-cell gastric lymphoma. Lancet 1991; 338: 1175-76. 6. Parsunnet J, Friedman GD, Vandersteen DP, et al. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med 1991; 325: 2.
1127-31. 7. Shallcross TM, Rathbone BJ, Heatley RG. Campylobacter pylori and non-ulcer dyspepsia. In: Rathbone BJ, Heatley RV, eds. Campylobacter pylori and gastroduodenal disease. Oxford: Blackwell Scientific, 1989: 155-56.
ABSOLUTE AND RELATIVE NUMBERS OF CASES OF PGL,
GASTRIC CARCINOMA, AND NODAL LYMPHOMA, 1986-90
ADDRESSES: Ospedale Civile, Feltre, Italy (C. Doglioni, MD, A. Moschini, MD, M de Boni, MD), and Department of Histopathology, University College and Middlesex School of Medicine, University Street, London WC1E6JJ, UK (A. C. Wotherspoon, MB, Prof P. G Isaacson, FRCPath). Correspondence to Prof Peter G. Isaacson
Urinary excretion of platelet-activating factor in haemolytic uraemic syndrome
That these findings reflect a truly high incidence of PGL in Feltre is supported by the similarity of the centres studied. None is a referral centre with a special interest in PGL or any other disorder that requires gastroscopy; thus, the endoscopy facilities are used only by the local population. Each centre is served by general histopathologists who are familiar with the latest ideas on the diagnosis of PGL but do not have a narrow special interest in the disease. The rate of gastroscopic examinations (per 100 000 per 5 years) is four times higher in Feltre than in the UK centres; this factor may account for the higher incidence of PGL. However, the ratio of PGL to gastric carcinoma is very high in Feltre (1 /4), despite the high incidence of gastric carcinoma; the ratio is between 1/13 and 1/18 in the UK centres. Furthermore, 4 cases of PGL are diagnosed for every 1000 gastroscopic examinations in Feltre compared with 1 per 1000 in the UK centres.
The previously reported high incidence of gastric carcinoma in areas of northern Italy4 is confirmed by this study, which suggests that predisposing factors may be shared by PGL and gastric carcinoma. H pylori infection may predispose to both disorders; 5,6 the rate of infection with this organism was much higher in Feltre patients undergoing gastroscopy (87%) than in patients undergoing routine gastroscopy in the UK (50-60%).7 Other environmental or dietary factors may also play a part, and the higher incidence of nodal non-Hodgkin lymphoma in Feltre may provide clues to these.
of the features of haemolytic uraemic syndrome (HUS), such as platelet activation and glomerular injury, could be brought about by platelet-activating factor (PAF), we have studied the urinary excretion of PAF in 10 children with HUS and in 10 healthy age-matched controls. Urinary PAF measured concentrations, by radioimmunoassay, were significantly higher in acutephase H US patients than in controls (mean 2·04 [SD 1·66] vs 0·72 [0·43] ng/mg creatinine, p < 0·05) but were similar to those in controls in samples taken after recovery. High PAF concentrations during the acute phase of HUS may reflect platelet activation and glomerular injury; the lower values after recovery suggest that urinary PAF may be a marker of disease
Since
some
activity.
Platelet-activating factor (PAF), a phospholipid produced by platelets and endothelial, mesangial, and other cells, promotes platelet aggregation and impairs renal function. Since the haemolytic uraemic syndrome (HUS) is characterised by platelet activation and injury to glomerular endothelial cells, we have investigated urinary excretion of PAF, which reflects renal synthesis,l during the acute phase of HUS and after recovery.
