- Email: [email protected]
IS COELIAC DISEASE A PREMALIGNANT STATE?
903
using the MRC method first followed by the GP method for the next 30 patients. Though the differences were smaller (5-5 and 4-8 mm Hg for systolic and diastolic, respectively) the GP continued to record significantly higher pressures (p < 0-01). To ensure that the results were not accounted for by differences in end points the nurse and GP measured BP in 20 patients using a dual stethoscope. The mean was 1-3 mm Hg higher for the GP on systolic pressures and 0-5 mm Hg lower on diastolic pressures. When we substituted
far had no specific complication from this during endoprosthesis insertion; the length of incision is considerably smaller than that
so
used for the extraction of duct stones. Sphincterotomy has been greatly facilitated by the introduction of a sphincterotome which can be used over a guidewire. Gastrointestinal Unit, Leicester Royal Infirmary, Leicester LEI 5WW
DAVID L. CARR-LOCKE
another male GP on 8 patients the pressor effect remained a mean of 13 3 mm Hg higher on diastolic pressures (p < 0-001) though it was less on systolic pressures (mean 3-75 mm Hg, not significant). The same was true when a female GP was substituted on 15 patients. Diastolic BP was 9-7 mm Hg higher than the nurse-recorded The systolic pressure was only 3-2 mm Hg pressure (p<0-001). higher (not significant). Thus the pressor effect of doctors in hospital demonstrated in Milan2 is also present in a GP’s surgery in Lancashire. The implication is that doctors may be identifying a population differing from the mild hypertensives defined by the MRC trial and may be treating people for whom there is no evidence that treatment is advantageous to outcome. It may be that home monitoring more closely reflects the MRC trial pressures, but this remains speculative. The situation is analogous to that of random blood glucose estimations being used to manage diabetes mellitus. Until the glycosylated haemaglobin equivalent in hypertension is identified we are left with a snapshot of a moving picture. The MRC trial demonstrates that despite the effort to obtain scientific accuracy a clinical trial must remain clinically relevant. General Practice, Kildonan House,
Horwich, Bolton, Lancashire
P. J. ELLIS E. MARSHALL
Mount Sinai Medical Center, New York, NY, USA
S. J. ELLIS
1. Wilcox
RG, Mitchell JRA, Hampton JR. Treatment of high blood pressure: should clinical practice be based on results of clinical trials? Br Med J 1986, 293: 433-37. 2. Mancia G, Bertinieri G, Grassi G, et al Effects of blood-pressure measurement by the doctor on patient’s blood pressure and heart rate. Lancet 1983; ii: 695-98. 3 Medical Research Council Working Party, MRC trial of treatment of mild hypertension: principal results. Br Med J 1985; 291: 97-104.
ENDOSCOPE EXCHANGE IN BILIARY PROSTHESIS PROCEDURES
SiR,—Iwould like to support the technique of catheter and wire-guided endoscope exchange for the insertion of biliary endoprostheses described by Dr Martin (Sept 3, p 542). We, too, have used this technique where necessary. To clarify certain details for endoscopists embarking on such procedures for the first time I would make the following comments. I would recommend a 0-9 mm (0-035 in) ’Teflon’ coated 400 cm guidewire passed through a standard diagnostic ERCP catheter whenever the ERCP catheter has been passed across a malignant bileduct stricture since this facilitates any later therapeutic procedure. Not all makes and types of diagnostic catheter will permit the passage of such a guidewire since the proximal and distal end of the catheter itself vary in design. This point should be checked on before the catheter is used. A 37 mm duodenoscope, such as the Fujinon ‘DUOXT’ can be used for diagnostic and therapeutic purposes and does not require the exchange technique described by Martin et al, which is more appropriate to duodenoscopes with a 42mm channel. The 6F pigtail catheter described by Martin et al, although normally used as a nasobiliary drainage catheter, is described in their technique as pernasal but it is, presumably, used via the oral route in this situation since the catheter is subsequently used as a guide for the second duodenoscope. In common with the technique of a combined transhepatic and endoscopic approach to the insertion of a biliary endoprosthesis I would commend the use of a Dormia basket to grasp the guidewire during passage of the second duodenoscope; we find this more secure than biopsy forceps and less damaging to the wire, if reuse is
intended. It is not my experience that never
an
required for the passage of a 1
endoscopic sphincterotomy is OF endoprosthesis, and we have
IS COELIAC DISEASE A PREMALIGNANT STATE?
SiR,-Since the original report from Bristol in 1962 that small-intestinal lymphoma might complicate coeliac disease, it has become clear that patients with coeliac disease have a 50-100 fold greater risk of malignant lymphoma than the general population,z,3 Hodgkin’s lymphoma2 and non-Hodgkin’s lymphoma, especially of T cell origin’4may develop in coeliac patients. The symptoms of coeliac disease and of the complicating lymphoma are initially similar, so the diagnosis of the lymphoma is often made late, with a correspondingly poor prognosis.2 We have found a tumourassociated antigen in the serum of patients with active Hodgkin’s and non-Hodgkin’s lymphomas and a decrease in the antigen during remission.’ This antigen was identified by a monoclonal antibody, CM-H-9, which binds specifically to placental isoferritin (PLF). Because of the strong association between coeliac disease and lymphoma, we screened a population of children with active and non-active coeliac disease for serum PLF. A group of age-matched children with other gastrointestinal disorders were the controls. 16 children with active and 16 with non-active coeliac disease were studied. The diagnosis of coeliac disease was made according to ESPGAN criteria.6 32 children with diarrhoea, constipation, and abdominal pain served as controls. The mean age of the children was 8 (SD 11) years. Serum PLF and normal ferritin were measured in two different ELISAs.5 The figure shows that most of the patients with active coeliac disease had high serum levels of PLF. These values (mean 124-7 [SE26] U/ml) were significantly higher than those in the control group (mean 14 [2-8] U/ml) or in patients with coeliac disease in remission (mean 38 [14] U/ml) (p = 0-0004 and p = 002, respectively; Wilcoxon test). The values in the control and remission groups were similar. 3 patients were studied during active and non-active disease stages: the level of PLF decreased during remission (table). Unlike PLF, the serum level of normal ferrtin was similar in the three groups and was normal (mean 27-7 [8’5] ng/ml). Our results indicate that in the absence of lymphoma, patients with active coeliac disease have high levels of PLF-an antigen associated with lymphoma. PLF is normally found in the serum of pregnant women.7 In addition to lymphomas, PLF has been found in premalignant and early stage breast cancer,8 and in patients with AIDS-related complex.9
PLF levels in
serum of patients with coeliac disease and other gastrointestinal (GI) disorders.
Bars represent
mean
and SE.
904 LEVELS OF PLF IN
3 COELIAC PATIENTS
STUDIED DURING ACTIVE
AND NON-ACTIVE DISEASE
PLF suppresses T cell function in vitro.’° Its presence in the above conditions, which are associated with immunosuppression, may indicate an immunosuppressive role in vivo. Suppressor cell activity induced by x-gliadin has been demonstrated in coeliac disease." The high levels of PLF in active coeliac disease and its decrease during remission in the absence of x-gliadin suggest that PLF has a role in the induction of immunosuppression during active disease. It is often asked whether a gluten-free diet protects against lymphoma in coeliac disease. We assume that the appearance of PLF may be one of the steps required for the development of malignancy. A gluten-free diet, by reversing this state, might prevent lymphoma. Patients on a gluten-free diet in whom PLF does not decrease may prove to be in a higher risk group for the development of malignancy when other factors are controlled. Monitoring PLF values in coeliac patients may help to identify high-risk patients and thereby enable early diagnosis. We thank Mrs B.
Zingerman for technical assistance.
Rogoff Medical Research Institute and Pediatnc Gastroenterology and Nutrition Unit, Beilmson Hospital and the Sackler School of Medicine, Tel-Aviv University, 49100 Tel-Aviv, Israel 1. 2
3 4 5.
C. MOROZ H. MARCUS I. ZAHAVI G. DINARI
Gough KR, Read AE, Naish JM.
Intestinal reticulosis as a complication of idiopathic steatorrhoea Gut 1962; 3: 232-39. Swinson CM, Slavin G, Coles EC, Booth CC Coeliac disease and malignancy. Lancet 1983, i: 111-15 Cooper BT, Read AE Coeliac disease and lymphoma Q J Med 1987; 240: 269-74. Isaacson PG, O’Connor NTJ, Spencer J, et al Malignant histiocytosis of the intestine: a T-cell lymphoma Lancet 1985; ii 688-91. Moroz C, Bessler H, Lurie Y, Shaklai M New monoclonal antibody enzymoassay for specific measurement of placental ferritin isotype in hematologic malignancies.
Exp Hematol 1987, 15: 258-63. Diagnostic criteria m coeliac disease. Acta Paediatr Scand 1970; 59:
6. Meeuwisse GW
461-63 7. Moroz C, Bessler H, Sirota L,
et al. Difference in placental ferritin levels measured by a specific monoclonal antibody enzymoassay in preterm and term delivery. Clin Exp
Immunol 1987; 69: 702-06. 8. Moroz C, Kan M, Chaimof Ch, et al. Ferritin bearing lymphocytes in the diagnosis of breast cancer Cancer 1984; 54: 84-89.
9. Moroz C, Mirsrock SL, Siegal FP Isoferritin in HIV infection Relation to clinical stage, CD8 lymphocyte binding and the pathogenesis of AIDS. AIDS (in press). 10. Matzner Y, Konijn AM, Shlomai Z Ben-Basat H Differential effect of isolated placental isoferritin on in-vitro T lymphocyte function. Br J Haematol 1985; 59: 443-48 11 O’Farrelly C, Whelan CA, Feighery CF, Weir DG Suppressor-cell activity in coeliac disease induced by alpha-gliadin, a dietary antigen. Lancet 1984; ii. 1305-07.
HAS THE INCIDENCE OF PNEUMOCYSTIS CARINII PNEUMONIA IN CANCER PATIENTS INCREASED WITH THE AIDS EPIDEMIC?
SiR,—The mode of transmission of Pneumocystis carinii has not fully established In man P carinii pneumonia (PCP) is believed to develop when an earlier infection is reactivated, especially in patients immunosuppressed after chemotherapy.3,4 However, PCP may be acquired as a de-novo airborne infectionS or by person-to-person transmission in hospita1.1,3,6 The incidence of been
PCP at M. D. Anderson Cancer Center had been low and stable for the past two decades.’ But between 1981 and 1986 the number of patients with AIDs and PCP at our institution rose dramatically, an increase that may have influenced the transmission of this pathogen inside the hospital to our cancer patients. Thus we retrospectively analysed all cases of PCP in our cancer population during 1980-87. The medical and necropsy records of all patients who acquired PCP during 1980-87 were reviewed. Patients who were HIVpositive or had AIDS (Centers for Disease Control criteria) were
yt:.AH
patients and number of AIDS registrations. Observed significantly greater8 than expected (O’73/IOOOO in 1980-82): p=001, 1982-84 and 1983-85; p <0’001,1984-86; and p=0002, 1 985-E7.
Incidence of PCP in
cancer
calculated as the number of PCP hospital registrations, because the number of admissions does not reflect outpatient care, which is common among cancer patients. Average incidences were calculated as three-year moving averages to decrease variability in rare events. Between January, 1980, and December, 1987, PCP was identified in 21 patients (13 female) being treated for cancer (aged 10-83 years, median 34). In 15 patients a haematological malignancy and in 6 a solid tumour were the underlying disease. 5 of the 21 patients had undergone allogeneic bone marrow transplantation (BMT) and PCP developed 2-8 months later; this was not related to the annual number of allogeneic BMTs (table). Except for 1 patient with breast cancer, all patients had received immunosuppressive treatment during the month before pneumonia developed, and 17 had also received corticosteroids. The table also shows the yearly distribution of PCP cases and the number of AIDS registrations during 1980-87. Most cases (19 of 21) occurred during or after 1984 when the number of AIDS patients increased significantly. The correlation between the number of AIDS registrations and the average rate of PCP in cancer patients is shown in the figure. The peak incidence of PCP occurred in 1984-86, with a corresponding increase in the number of AIDS registrations. The decrease in AIDS registrations in 1985-87 was followed by a lower rate of PCP in cancer patients. The number of observed cases was significantly higher than expected for most
excluded. Incidence cases
rates were
per 10 000
periods. No epidemiological relation could
be established between staff Since medical staff caring for cancer patients were mostly not involved with AIDS patients, transmission of PCP by doctors and nurses was unlikely. No room or section of the hospital was associated with an increased number of PCP cases. However, the AIDS clinic adjoined the leukaemia outpatient clinic and AIDS and cancer patients mingled freely. Our study suggests a relation between the incidence of PCP in immunocompromised cancer patients and the number of AIDS patients cared for at this institution over the past eight years. We believe this represents a true increase in PCP rather than reflecting improved methods of diagnosis and increased awareness of
members and PCP
NUMBER OF PCP
cases.
CASES, AIDS REGISTRATIONS, AND PATIENTS WHO UNDERWENT BMT
using the MRC method first followed by the GP method for the next 30 patients. Though the differences were smaller (5-5 and 4-8 mm Hg for systolic and diastolic, respectively) the GP continued to record significantly higher pressures (p < 0-01). To ensure that the results were not accounted for by differences in end points the nurse and GP measured BP in 20 patients using a dual stethoscope. The mean was 1-3 mm Hg higher for the GP on systolic pressures and 0-5 mm Hg lower on diastolic pressures. When we substituted
far had no specific complication from this during endoprosthesis insertion; the length of incision is considerably smaller than that
so
used for the extraction of duct stones. Sphincterotomy has been greatly facilitated by the introduction of a sphincterotome which can be used over a guidewire. Gastrointestinal Unit, Leicester Royal Infirmary, Leicester LEI 5WW
DAVID L. CARR-LOCKE
another male GP on 8 patients the pressor effect remained a mean of 13 3 mm Hg higher on diastolic pressures (p < 0-001) though it was less on systolic pressures (mean 3-75 mm Hg, not significant). The same was true when a female GP was substituted on 15 patients. Diastolic BP was 9-7 mm Hg higher than the nurse-recorded The systolic pressure was only 3-2 mm Hg pressure (p<0-001). higher (not significant). Thus the pressor effect of doctors in hospital demonstrated in Milan2 is also present in a GP’s surgery in Lancashire. The implication is that doctors may be identifying a population differing from the mild hypertensives defined by the MRC trial and may be treating people for whom there is no evidence that treatment is advantageous to outcome. It may be that home monitoring more closely reflects the MRC trial pressures, but this remains speculative. The situation is analogous to that of random blood glucose estimations being used to manage diabetes mellitus. Until the glycosylated haemaglobin equivalent in hypertension is identified we are left with a snapshot of a moving picture. The MRC trial demonstrates that despite the effort to obtain scientific accuracy a clinical trial must remain clinically relevant. General Practice, Kildonan House,
Horwich, Bolton, Lancashire
P. J. ELLIS E. MARSHALL
Mount Sinai Medical Center, New York, NY, USA
S. J. ELLIS
1. Wilcox
RG, Mitchell JRA, Hampton JR. Treatment of high blood pressure: should clinical practice be based on results of clinical trials? Br Med J 1986, 293: 433-37. 2. Mancia G, Bertinieri G, Grassi G, et al Effects of blood-pressure measurement by the doctor on patient’s blood pressure and heart rate. Lancet 1983; ii: 695-98. 3 Medical Research Council Working Party, MRC trial of treatment of mild hypertension: principal results. Br Med J 1985; 291: 97-104.
ENDOSCOPE EXCHANGE IN BILIARY PROSTHESIS PROCEDURES
SiR,—Iwould like to support the technique of catheter and wire-guided endoscope exchange for the insertion of biliary endoprostheses described by Dr Martin (Sept 3, p 542). We, too, have used this technique where necessary. To clarify certain details for endoscopists embarking on such procedures for the first time I would make the following comments. I would recommend a 0-9 mm (0-035 in) ’Teflon’ coated 400 cm guidewire passed through a standard diagnostic ERCP catheter whenever the ERCP catheter has been passed across a malignant bileduct stricture since this facilitates any later therapeutic procedure. Not all makes and types of diagnostic catheter will permit the passage of such a guidewire since the proximal and distal end of the catheter itself vary in design. This point should be checked on before the catheter is used. A 37 mm duodenoscope, such as the Fujinon ‘DUOXT’ can be used for diagnostic and therapeutic purposes and does not require the exchange technique described by Martin et al, which is more appropriate to duodenoscopes with a 42mm channel. The 6F pigtail catheter described by Martin et al, although normally used as a nasobiliary drainage catheter, is described in their technique as pernasal but it is, presumably, used via the oral route in this situation since the catheter is subsequently used as a guide for the second duodenoscope. In common with the technique of a combined transhepatic and endoscopic approach to the insertion of a biliary endoprosthesis I would commend the use of a Dormia basket to grasp the guidewire during passage of the second duodenoscope; we find this more secure than biopsy forceps and less damaging to the wire, if reuse is
intended. It is not my experience that never
an
required for the passage of a 1
endoscopic sphincterotomy is OF endoprosthesis, and we have
IS COELIAC DISEASE A PREMALIGNANT STATE?
SiR,-Since the original report from Bristol in 1962 that small-intestinal lymphoma might complicate coeliac disease, it has become clear that patients with coeliac disease have a 50-100 fold greater risk of malignant lymphoma than the general population,z,3 Hodgkin’s lymphoma2 and non-Hodgkin’s lymphoma, especially of T cell origin’4may develop in coeliac patients. The symptoms of coeliac disease and of the complicating lymphoma are initially similar, so the diagnosis of the lymphoma is often made late, with a correspondingly poor prognosis.2 We have found a tumourassociated antigen in the serum of patients with active Hodgkin’s and non-Hodgkin’s lymphomas and a decrease in the antigen during remission.’ This antigen was identified by a monoclonal antibody, CM-H-9, which binds specifically to placental isoferritin (PLF). Because of the strong association between coeliac disease and lymphoma, we screened a population of children with active and non-active coeliac disease for serum PLF. A group of age-matched children with other gastrointestinal disorders were the controls. 16 children with active and 16 with non-active coeliac disease were studied. The diagnosis of coeliac disease was made according to ESPGAN criteria.6 32 children with diarrhoea, constipation, and abdominal pain served as controls. The mean age of the children was 8 (SD 11) years. Serum PLF and normal ferritin were measured in two different ELISAs.5 The figure shows that most of the patients with active coeliac disease had high serum levels of PLF. These values (mean 124-7 [SE26] U/ml) were significantly higher than those in the control group (mean 14 [2-8] U/ml) or in patients with coeliac disease in remission (mean 38 [14] U/ml) (p = 0-0004 and p = 002, respectively; Wilcoxon test). The values in the control and remission groups were similar. 3 patients were studied during active and non-active disease stages: the level of PLF decreased during remission (table). Unlike PLF, the serum level of normal ferrtin was similar in the three groups and was normal (mean 27-7 [8’5] ng/ml). Our results indicate that in the absence of lymphoma, patients with active coeliac disease have high levels of PLF-an antigen associated with lymphoma. PLF is normally found in the serum of pregnant women.7 In addition to lymphomas, PLF has been found in premalignant and early stage breast cancer,8 and in patients with AIDS-related complex.9
PLF levels in
serum of patients with coeliac disease and other gastrointestinal (GI) disorders.
Bars represent
mean
and SE.
904 LEVELS OF PLF IN
3 COELIAC PATIENTS
STUDIED DURING ACTIVE
AND NON-ACTIVE DISEASE
PLF suppresses T cell function in vitro.’° Its presence in the above conditions, which are associated with immunosuppression, may indicate an immunosuppressive role in vivo. Suppressor cell activity induced by x-gliadin has been demonstrated in coeliac disease." The high levels of PLF in active coeliac disease and its decrease during remission in the absence of x-gliadin suggest that PLF has a role in the induction of immunosuppression during active disease. It is often asked whether a gluten-free diet protects against lymphoma in coeliac disease. We assume that the appearance of PLF may be one of the steps required for the development of malignancy. A gluten-free diet, by reversing this state, might prevent lymphoma. Patients on a gluten-free diet in whom PLF does not decrease may prove to be in a higher risk group for the development of malignancy when other factors are controlled. Monitoring PLF values in coeliac patients may help to identify high-risk patients and thereby enable early diagnosis. We thank Mrs B.
Zingerman for technical assistance.
Rogoff Medical Research Institute and Pediatnc Gastroenterology and Nutrition Unit, Beilmson Hospital and the Sackler School of Medicine, Tel-Aviv University, 49100 Tel-Aviv, Israel 1. 2
3 4 5.
C. MOROZ H. MARCUS I. ZAHAVI G. DINARI
Gough KR, Read AE, Naish JM.
Intestinal reticulosis as a complication of idiopathic steatorrhoea Gut 1962; 3: 232-39. Swinson CM, Slavin G, Coles EC, Booth CC Coeliac disease and malignancy. Lancet 1983, i: 111-15 Cooper BT, Read AE Coeliac disease and lymphoma Q J Med 1987; 240: 269-74. Isaacson PG, O’Connor NTJ, Spencer J, et al Malignant histiocytosis of the intestine: a T-cell lymphoma Lancet 1985; ii 688-91. Moroz C, Bessler H, Lurie Y, Shaklai M New monoclonal antibody enzymoassay for specific measurement of placental ferritin isotype in hematologic malignancies.
Exp Hematol 1987, 15: 258-63. Diagnostic criteria m coeliac disease. Acta Paediatr Scand 1970; 59:
6. Meeuwisse GW
461-63 7. Moroz C, Bessler H, Sirota L,
et al. Difference in placental ferritin levels measured by a specific monoclonal antibody enzymoassay in preterm and term delivery. Clin Exp
Immunol 1987; 69: 702-06. 8. Moroz C, Kan M, Chaimof Ch, et al. Ferritin bearing lymphocytes in the diagnosis of breast cancer Cancer 1984; 54: 84-89.
9. Moroz C, Mirsrock SL, Siegal FP Isoferritin in HIV infection Relation to clinical stage, CD8 lymphocyte binding and the pathogenesis of AIDS. AIDS (in press). 10. Matzner Y, Konijn AM, Shlomai Z Ben-Basat H Differential effect of isolated placental isoferritin on in-vitro T lymphocyte function. Br J Haematol 1985; 59: 443-48 11 O’Farrelly C, Whelan CA, Feighery CF, Weir DG Suppressor-cell activity in coeliac disease induced by alpha-gliadin, a dietary antigen. Lancet 1984; ii. 1305-07.
HAS THE INCIDENCE OF PNEUMOCYSTIS CARINII PNEUMONIA IN CANCER PATIENTS INCREASED WITH THE AIDS EPIDEMIC?
SiR,—The mode of transmission of Pneumocystis carinii has not fully established In man P carinii pneumonia (PCP) is believed to develop when an earlier infection is reactivated, especially in patients immunosuppressed after chemotherapy.3,4 However, PCP may be acquired as a de-novo airborne infectionS or by person-to-person transmission in hospita1.1,3,6 The incidence of been
PCP at M. D. Anderson Cancer Center had been low and stable for the past two decades.’ But between 1981 and 1986 the number of patients with AIDs and PCP at our institution rose dramatically, an increase that may have influenced the transmission of this pathogen inside the hospital to our cancer patients. Thus we retrospectively analysed all cases of PCP in our cancer population during 1980-87. The medical and necropsy records of all patients who acquired PCP during 1980-87 were reviewed. Patients who were HIVpositive or had AIDS (Centers for Disease Control criteria) were
yt:.AH
patients and number of AIDS registrations. Observed significantly greater8 than expected (O’73/IOOOO in 1980-82): p=001, 1982-84 and 1983-85; p <0’001,1984-86; and p=0002, 1 985-E7.
Incidence of PCP in
cancer
calculated as the number of PCP hospital registrations, because the number of admissions does not reflect outpatient care, which is common among cancer patients. Average incidences were calculated as three-year moving averages to decrease variability in rare events. Between January, 1980, and December, 1987, PCP was identified in 21 patients (13 female) being treated for cancer (aged 10-83 years, median 34). In 15 patients a haematological malignancy and in 6 a solid tumour were the underlying disease. 5 of the 21 patients had undergone allogeneic bone marrow transplantation (BMT) and PCP developed 2-8 months later; this was not related to the annual number of allogeneic BMTs (table). Except for 1 patient with breast cancer, all patients had received immunosuppressive treatment during the month before pneumonia developed, and 17 had also received corticosteroids. The table also shows the yearly distribution of PCP cases and the number of AIDS registrations during 1980-87. Most cases (19 of 21) occurred during or after 1984 when the number of AIDS patients increased significantly. The correlation between the number of AIDS registrations and the average rate of PCP in cancer patients is shown in the figure. The peak incidence of PCP occurred in 1984-86, with a corresponding increase in the number of AIDS registrations. The decrease in AIDS registrations in 1985-87 was followed by a lower rate of PCP in cancer patients. The number of observed cases was significantly higher than expected for most
excluded. Incidence cases
rates were
per 10 000
periods. No epidemiological relation could
be established between staff Since medical staff caring for cancer patients were mostly not involved with AIDS patients, transmission of PCP by doctors and nurses was unlikely. No room or section of the hospital was associated with an increased number of PCP cases. However, the AIDS clinic adjoined the leukaemia outpatient clinic and AIDS and cancer patients mingled freely. Our study suggests a relation between the incidence of PCP in immunocompromised cancer patients and the number of AIDS patients cared for at this institution over the past eight years. We believe this represents a true increase in PCP rather than reflecting improved methods of diagnosis and increased awareness of
members and PCP
NUMBER OF PCP
cases.
CASES, AIDS REGISTRATIONS, AND PATIENTS WHO UNDERWENT BMT