Sara Freeman

LONDON – Patients with rheumatoid arthritis who have had a heart attack for the first time do not appear to be getting medications recommended to prevent a further cardiovascular event, according to the findings of a large Danish study.

Aspirin, statins, and beta-blockers – cardioprotective medications that are given as the standard of care to most patients immediately following a myocardial infarction – were all less frequently prescribed to patients with rheumatoid arthritis (RA) than to members of the general patient population.

Indeed, 1 month after an MI, the odds ratios for the prescription of these drugs were 0.75 (95% confidence interval, 0.63-0.90) for aspirin, 0.68 (95% CI, 0.57-0.82) for a statin, and 0.76 (95% CI, 0.63-0.91) for beta-blockers. These results did not change greatly at follow-ups of 3 months, 6 months, or 1 year.

The increased risk of cardiovascular disease in RA patients is well known and could result from a number of causes, including the presence of classical risk factors such as dyslipidemia and hypertension, possible adverse effects of RA treatment, and an accelerated atherosclerotic process driven by the high levels of inflammation characteristic of the rheumatic disease.

"What’s not been considered, [however,] and perhaps the simplest explanation, is whether or not there is undertreatment of [RA] patients," Dr. Jesper Lindhardsen, of the cardiology department at Gentofte University Hospital, Copenhagen, said at a press briefing during the annual European Congress of Rheumatology.

To determine whether patients with RA were being given standard cardioprotective medications after a first MI, he and his colleagues analyzed data from several Danish patient registries, including those giving prescription records, details of comorbidities, and income.

The study population consisted of 66,389 patients who had had a first heart attack between 2002 and 2009. Of these, 875 (1.3%) had RA. The median age was 72.6 years for RA patients and 69.4 years for patients without RA.

At baseline, the use of cardioprotective medications by patients with and without RA were relatively similar or the same, at 27% and 25.1%, respectively, for aspirin; 19.1% and 19.1% for a statin; 23.9% and 22.5% for a beta-blocker; and 3.3% and 2.2% for clopidogrel.

Although aspirin, statin, and beta-blocker use was later found to be lower in the RA patients than in the non-RA patients throughout the early post-MI period, there was no significant difference in the prescription of clopidogrel at 1, 3, or 6 months or at 1 year.

Commenting on the findings in an interview, Dr. Lindhardsen conceded that this data raises more questions than it answers. For one thing, it’s not known what medications patients were taking before they had their heart attack, which could influence the findings.

Dr. Georg Schett, who is chief of rheumatology at the University of Erlangen-Nuremberg, Germany, but was not involved in the study, said the findings illustrate that the high cardiovascular risk in patients with RA is still not being taken seriously enough.

Speaking at a press conference, Dr. Schett said that "the risk of cardiovascular disease in RA is similar to diabetes, but people sometimes forget this."

Indeed, Dr. Lindhardsen and his colleagues recently published data showing that RA is associated with the same risk of MI as diabetes (Ann. Rheum. Dis. 2011;70:929-34).

With regard to this post-MI data, Dr. Lindhardsen stressed the importance of communication between the cardiologist discharging a patient and the rheumatologist responsible for the patient’s long-term care to ensure that standard cardioprotective medications are being used.

"We have quantitative data. Now we need more qualitative data," Dr. Lindhardsen observed in an interview. The next steps are to try to determine the reasons RA patients get fewer prescriptions for these standard post-MI drugs, he said.

Dr. Lindhardsen and Dr. Schett had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis who have had a heart attack for the first time do not appear to be getting medications recommended to prevent a further cardiovascular event, according to the findings of a large Danish study.

Aspirin, statins, and beta-blockers – cardioprotective medications that are given as the standard of care to most patients immediately following a myocardial infarction – were all less frequently prescribed to patients with rheumatoid arthritis (RA) than to members of the general patient population.

Indeed, 1 month after an MI, the odds ratios for the prescription of these drugs were 0.75 (95% confidence interval, 0.63-0.90) for aspirin, 0.68 (95% CI, 0.57-0.82) for a statin, and 0.76 (95% CI, 0.63-0.91) for beta-blockers. These results did not change greatly at follow-ups of 3 months, 6 months, or 1 year.

The increased risk of cardiovascular disease in RA patients is well known and could result from a number of causes, including the presence of classical risk factors such as dyslipidemia and hypertension, possible adverse effects of RA treatment, and an accelerated atherosclerotic process driven by the high levels of inflammation characteristic of the rheumatic disease.

"What’s not been considered, [however,] and perhaps the simplest explanation, is whether or not there is undertreatment of [RA] patients," Dr. Jesper Lindhardsen, of the cardiology department at Gentofte University Hospital, Copenhagen, said at a press briefing during the annual European Congress of Rheumatology.

To determine whether patients with RA were being given standard cardioprotective medications after a first MI, he and his colleagues analyzed data from several Danish patient registries, including those giving prescription records, details of comorbidities, and income.

The study population consisted of 66,389 patients who had had a first heart attack between 2002 and 2009. Of these, 875 (1.3%) had RA. The median age was 72.6 years for RA patients and 69.4 years for patients without RA.

At baseline, the use of cardioprotective medications by patients with and without RA were relatively similar or the same, at 27% and 25.1%, respectively, for aspirin; 19.1% and 19.1% for a statin; 23.9% and 22.5% for a beta-blocker; and 3.3% and 2.2% for clopidogrel.

Although aspirin, statin, and beta-blocker use was later found to be lower in the RA patients than in the non-RA patients throughout the early post-MI period, there was no significant difference in the prescription of clopidogrel at 1, 3, or 6 months or at 1 year.

Commenting on the findings in an interview, Dr. Lindhardsen conceded that this data raises more questions than it answers. For one thing, it’s not known what medications patients were taking before they had their heart attack, which could influence the findings.

Dr. Georg Schett, who is chief of rheumatology at the University of Erlangen-Nuremberg, Germany, but was not involved in the study, said the findings illustrate that the high cardiovascular risk in patients with RA is still not being taken seriously enough.

Speaking at a press conference, Dr. Schett said that "the risk of cardiovascular disease in RA is similar to diabetes, but people sometimes forget this."

Indeed, Dr. Lindhardsen and his colleagues recently published data showing that RA is associated with the same risk of MI as diabetes (Ann. Rheum. Dis. 2011;70:929-34).

With regard to this post-MI data, Dr. Lindhardsen stressed the importance of communication between the cardiologist discharging a patient and the rheumatologist responsible for the patient’s long-term care to ensure that standard cardioprotective medications are being used.

"We have quantitative data. Now we need more qualitative data," Dr. Lindhardsen observed in an interview. The next steps are to try to determine the reasons RA patients get fewer prescriptions for these standard post-MI drugs, he said.

Dr. Lindhardsen and Dr. Schett had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis who have had a heart attack for the first time do not appear to be getting medications recommended to prevent a further cardiovascular event, according to the findings of a large Danish study.

Aspirin, statins, and beta-blockers – cardioprotective medications that are given as the standard of care to most patients immediately following a myocardial infarction – were all less frequently prescribed to patients with rheumatoid arthritis (RA) than to members of the general patient population.

Indeed, 1 month after an MI, the odds ratios for the prescription of these drugs were 0.75 (95% confidence interval, 0.63-0.90) for aspirin, 0.68 (95% CI, 0.57-0.82) for a statin, and 0.76 (95% CI, 0.63-0.91) for beta-blockers. These results did not change greatly at follow-ups of 3 months, 6 months, or 1 year.

The increased risk of cardiovascular disease in RA patients is well known and could result from a number of causes, including the presence of classical risk factors such as dyslipidemia and hypertension, possible adverse effects of RA treatment, and an accelerated atherosclerotic process driven by the high levels of inflammation characteristic of the rheumatic disease.

"What’s not been considered, [however,] and perhaps the simplest explanation, is whether or not there is undertreatment of [RA] patients," Dr. Jesper Lindhardsen, of the cardiology department at Gentofte University Hospital, Copenhagen, said at a press briefing during the annual European Congress of Rheumatology.

To determine whether patients with RA were being given standard cardioprotective medications after a first MI, he and his colleagues analyzed data from several Danish patient registries, including those giving prescription records, details of comorbidities, and income.

The study population consisted of 66,389 patients who had had a first heart attack between 2002 and 2009. Of these, 875 (1.3%) had RA. The median age was 72.6 years for RA patients and 69.4 years for patients without RA.

At baseline, the use of cardioprotective medications by patients with and without RA were relatively similar or the same, at 27% and 25.1%, respectively, for aspirin; 19.1% and 19.1% for a statin; 23.9% and 22.5% for a beta-blocker; and 3.3% and 2.2% for clopidogrel.

Although aspirin, statin, and beta-blocker use was later found to be lower in the RA patients than in the non-RA patients throughout the early post-MI period, there was no significant difference in the prescription of clopidogrel at 1, 3, or 6 months or at 1 year.

Commenting on the findings in an interview, Dr. Lindhardsen conceded that this data raises more questions than it answers. For one thing, it’s not known what medications patients were taking before they had their heart attack, which could influence the findings.

Dr. Georg Schett, who is chief of rheumatology at the University of Erlangen-Nuremberg, Germany, but was not involved in the study, said the findings illustrate that the high cardiovascular risk in patients with RA is still not being taken seriously enough.

Speaking at a press conference, Dr. Schett said that "the risk of cardiovascular disease in RA is similar to diabetes, but people sometimes forget this."

Indeed, Dr. Lindhardsen and his colleagues recently published data showing that RA is associated with the same risk of MI as diabetes (Ann. Rheum. Dis. 2011;70:929-34).

With regard to this post-MI data, Dr. Lindhardsen stressed the importance of communication between the cardiologist discharging a patient and the rheumatologist responsible for the patient’s long-term care to ensure that standard cardioprotective medications are being used.

"We have quantitative data. Now we need more qualitative data," Dr. Lindhardsen observed in an interview. The next steps are to try to determine the reasons RA patients get fewer prescriptions for these standard post-MI drugs, he said.

Dr. Lindhardsen and Dr. Schett had no conflicts of interest to declare.

LONDON – Close relatives of patients with acute myeloid leukemia and myelodysplastic syndromes can be reassured that they are not at increased risk of developing these diseases themselves, according to the findings of a large population-based registry trial.

"Among over 20,000 first-degree relatives of almost 7,000 AML [acute myeloid leukemia] patients, we found no excess risk of developing AML, MDS [myelodysplastic syndromes], or any myeloid neoplasms as a group," said Dr. Magnus Björkholm, a professor of medicine at Karolinska University Hospital, Solna and the Karolinska Institute, both in Stockholm.

Speaking at the annual congress of the European Hematology Association, Dr. Björkholm reported that there was also no strong genetic predisposition for first-degree relatives of patients with MDS to develop myeloid or other hematological neoplasms.

"If you read Wikipedia today, it says that the risk of developing AML is increased threefold in first-degree relatives of patients with AML," Dr. Björkholm observed. "But there is really limited data on the extent of familial aggregation of AML and MDS in the population.

Indeed, the Wikipedia entry cites a paper (J. Natl. Cancer Inst. 1969;42:517-24) from 1969 as the source of this claim, and results of early studies found an increased risk of leukemia among relatives of patients were actually accounted for by cases of chronic lymphocytic leukemia.

"We believe a better understanding on the role for genetic factors in the causation of AML/MDS is of major importance to patients, their families, and healthcare professionals," Dr. Björkholm said, explaining the rationale behind the research.

Using data from the Swedish Cancer Registry, the Swedish Population Registry, and the Swedish Multigenerational Registry, Dr. Björkholm and colleagues identified 6,962 patients diagnosed with AML from Jan. 1, 1958 until Dec. 31, 2004 and 1,388 MDS patients diagnosed from 1993 – the date when MDS was first included in the Swedish Cancer Registry – through Dec. 31, 2004. There were 20,579 first-degree relatives of the AML patients and 3,994 first-degree relatives of the MDS patients.

For each AML and MDS patient, four population-matched control subjects of a similar age, year of birth, and country of residence were randomly selected from the Swedish population, and their first-degree relatives were also identified. In all, there were 27,827 AML controls and 90,406 AML control relatives, and 5,312 MDS controls and 15,818 MDS control relatives.

No excess risk of AML (hazard ratio 0.94) or other myeloid or lymphoid malignancies was statistically significant in relatives of patients with AML with one exception – relatives of patients with AML did have an increased risk of polycythemia vera (HR 2.28, P less than .05). The risks for any hematopoietic or solid malignancies were significantly increased statistically, but only modestly, with risk ratios of 1.16 and 1.09, respectively.

First-degree relatives of AML patients who were diagnosed at a younger age (20 years or less) did, however, have a higher chance of developing AML, myeloid neoplasms, or multiple myeloma, based on small numbers in the sample. Dr. Björkholm suggested that genes predisposing to malignancy in general, environmental factors, or both, might be shared in these families.

No significant excess risks were seen among first-degree relatives of MDS patients.

"The lack of familial aggregation in AML and MDS is rather striking," Dr. Björkholm admitted. It is also "in stark contrast to findings in other myelo- and lymphoproliferative disorders."

In an interview, he emphasized, "The main message is that first-degree relatives of patients with acute myeloid leukemia do not have an increased risk of developing acute myeloid leukemia, which is in contrast to many other solid and hematological malignancies."

Dr. Björkholm also noted that patients are often told by their physicians that there is a two to three times increased risk of their siblings or children developing leukemia. The current findings suggest that this is unlikely, considering the large cohort of subjects that was studied.

"From a global point of view, this [study] is probably the best you can do."

Dr. Björkholm stated he had no conflicts of interest. The study received financial support from the Adolf H. Lundin Charitable Foundation, Karolinska Institute Foundations, Stockholm County Council, Swedish Cancer Society, and the Division of Intramural Research Programs at the National Cancer Institute of the National Institutes of Health.

LONDON – Close relatives of patients with acute myeloid leukemia and myelodysplastic syndromes can be reassured that they are not at increased risk of developing these diseases themselves, according to the findings of a large population-based registry trial.

"Among over 20,000 first-degree relatives of almost 7,000 AML [acute myeloid leukemia] patients, we found no excess risk of developing AML, MDS [myelodysplastic syndromes], or any myeloid neoplasms as a group," said Dr. Magnus Björkholm, a professor of medicine at Karolinska University Hospital, Solna and the Karolinska Institute, both in Stockholm.

Speaking at the annual congress of the European Hematology Association, Dr. Björkholm reported that there was also no strong genetic predisposition for first-degree relatives of patients with MDS to develop myeloid or other hematological neoplasms.

"If you read Wikipedia today, it says that the risk of developing AML is increased threefold in first-degree relatives of patients with AML," Dr. Björkholm observed. "But there is really limited data on the extent of familial aggregation of AML and MDS in the population.

Indeed, the Wikipedia entry cites a paper (J. Natl. Cancer Inst. 1969;42:517-24) from 1969 as the source of this claim, and results of early studies found an increased risk of leukemia among relatives of patients were actually accounted for by cases of chronic lymphocytic leukemia.

"We believe a better understanding on the role for genetic factors in the causation of AML/MDS is of major importance to patients, their families, and healthcare professionals," Dr. Björkholm said, explaining the rationale behind the research.

Using data from the Swedish Cancer Registry, the Swedish Population Registry, and the Swedish Multigenerational Registry, Dr. Björkholm and colleagues identified 6,962 patients diagnosed with AML from Jan. 1, 1958 until Dec. 31, 2004 and 1,388 MDS patients diagnosed from 1993 – the date when MDS was first included in the Swedish Cancer Registry – through Dec. 31, 2004. There were 20,579 first-degree relatives of the AML patients and 3,994 first-degree relatives of the MDS patients.

For each AML and MDS patient, four population-matched control subjects of a similar age, year of birth, and country of residence were randomly selected from the Swedish population, and their first-degree relatives were also identified. In all, there were 27,827 AML controls and 90,406 AML control relatives, and 5,312 MDS controls and 15,818 MDS control relatives.

No excess risk of AML (hazard ratio 0.94) or other myeloid or lymphoid malignancies was statistically significant in relatives of patients with AML with one exception – relatives of patients with AML did have an increased risk of polycythemia vera (HR 2.28, P less than .05). The risks for any hematopoietic or solid malignancies were significantly increased statistically, but only modestly, with risk ratios of 1.16 and 1.09, respectively.

First-degree relatives of AML patients who were diagnosed at a younger age (20 years or less) did, however, have a higher chance of developing AML, myeloid neoplasms, or multiple myeloma, based on small numbers in the sample. Dr. Björkholm suggested that genes predisposing to malignancy in general, environmental factors, or both, might be shared in these families.

No significant excess risks were seen among first-degree relatives of MDS patients.

"The lack of familial aggregation in AML and MDS is rather striking," Dr. Björkholm admitted. It is also "in stark contrast to findings in other myelo- and lymphoproliferative disorders."

In an interview, he emphasized, "The main message is that first-degree relatives of patients with acute myeloid leukemia do not have an increased risk of developing acute myeloid leukemia, which is in contrast to many other solid and hematological malignancies."

Dr. Björkholm also noted that patients are often told by their physicians that there is a two to three times increased risk of their siblings or children developing leukemia. The current findings suggest that this is unlikely, considering the large cohort of subjects that was studied.

"From a global point of view, this [study] is probably the best you can do."

Dr. Björkholm stated he had no conflicts of interest. The study received financial support from the Adolf H. Lundin Charitable Foundation, Karolinska Institute Foundations, Stockholm County Council, Swedish Cancer Society, and the Division of Intramural Research Programs at the National Cancer Institute of the National Institutes of Health.

LONDON – Close relatives of patients with acute myeloid leukemia and myelodysplastic syndromes can be reassured that they are not at increased risk of developing these diseases themselves, according to the findings of a large population-based registry trial.

"Among over 20,000 first-degree relatives of almost 7,000 AML [acute myeloid leukemia] patients, we found no excess risk of developing AML, MDS [myelodysplastic syndromes], or any myeloid neoplasms as a group," said Dr. Magnus Björkholm, a professor of medicine at Karolinska University Hospital, Solna and the Karolinska Institute, both in Stockholm.

Speaking at the annual congress of the European Hematology Association, Dr. Björkholm reported that there was also no strong genetic predisposition for first-degree relatives of patients with MDS to develop myeloid or other hematological neoplasms.

"If you read Wikipedia today, it says that the risk of developing AML is increased threefold in first-degree relatives of patients with AML," Dr. Björkholm observed. "But there is really limited data on the extent of familial aggregation of AML and MDS in the population.

Indeed, the Wikipedia entry cites a paper (J. Natl. Cancer Inst. 1969;42:517-24) from 1969 as the source of this claim, and results of early studies found an increased risk of leukemia among relatives of patients were actually accounted for by cases of chronic lymphocytic leukemia.

"We believe a better understanding on the role for genetic factors in the causation of AML/MDS is of major importance to patients, their families, and healthcare professionals," Dr. Björkholm said, explaining the rationale behind the research.

Using data from the Swedish Cancer Registry, the Swedish Population Registry, and the Swedish Multigenerational Registry, Dr. Björkholm and colleagues identified 6,962 patients diagnosed with AML from Jan. 1, 1958 until Dec. 31, 2004 and 1,388 MDS patients diagnosed from 1993 – the date when MDS was first included in the Swedish Cancer Registry – through Dec. 31, 2004. There were 20,579 first-degree relatives of the AML patients and 3,994 first-degree relatives of the MDS patients.

For each AML and MDS patient, four population-matched control subjects of a similar age, year of birth, and country of residence were randomly selected from the Swedish population, and their first-degree relatives were also identified. In all, there were 27,827 AML controls and 90,406 AML control relatives, and 5,312 MDS controls and 15,818 MDS control relatives.

No excess risk of AML (hazard ratio 0.94) or other myeloid or lymphoid malignancies was statistically significant in relatives of patients with AML with one exception – relatives of patients with AML did have an increased risk of polycythemia vera (HR 2.28, P less than .05). The risks for any hematopoietic or solid malignancies were significantly increased statistically, but only modestly, with risk ratios of 1.16 and 1.09, respectively.

First-degree relatives of AML patients who were diagnosed at a younger age (20 years or less) did, however, have a higher chance of developing AML, myeloid neoplasms, or multiple myeloma, based on small numbers in the sample. Dr. Björkholm suggested that genes predisposing to malignancy in general, environmental factors, or both, might be shared in these families.

No significant excess risks were seen among first-degree relatives of MDS patients.

"The lack of familial aggregation in AML and MDS is rather striking," Dr. Björkholm admitted. It is also "in stark contrast to findings in other myelo- and lymphoproliferative disorders."

In an interview, he emphasized, "The main message is that first-degree relatives of patients with acute myeloid leukemia do not have an increased risk of developing acute myeloid leukemia, which is in contrast to many other solid and hematological malignancies."

Dr. Björkholm also noted that patients are often told by their physicians that there is a two to three times increased risk of their siblings or children developing leukemia. The current findings suggest that this is unlikely, considering the large cohort of subjects that was studied.

"From a global point of view, this [study] is probably the best you can do."

Dr. Björkholm stated he had no conflicts of interest. The study received financial support from the Adolf H. Lundin Charitable Foundation, Karolinska Institute Foundations, Stockholm County Council, Swedish Cancer Society, and the Division of Intramural Research Programs at the National Cancer Institute of the National Institutes of Health.

LONDON – Close relatives of patients with acute myeloid leukemia and myelodysplastic syndromes can be reassured that they are not at increased risk of developing these diseases themselves, according to the findings of a large population-based registry trial.

"Among over 20,000 first-degree relatives of almost 7,000 AML [acute myeloid leukemia] patients, we found no excess risk of developing AML, MDS [myelodysplastic syndromes], or any myeloid neoplasms as a group," said Dr. Magnus Björkholm, a professor of medicine at Karolinska University Hospital, Solna and the Karolinska Institute, both in Stockholm.

Speaking at the annual congress of the European Hematology Association, Dr. Björkholm reported that there was also no strong genetic predisposition for first-degree relatives of patients with MDS to develop myeloid or other hematological neoplasms.

"If you read Wikipedia today, it says that the risk of developing AML is increased threefold in first-degree relatives of patients with AML," Dr. Björkholm observed. "But there is really limited data on the extent of familial aggregation of AML and MDS in the population.

Indeed, the Wikipedia entry cites a paper (J. Natl. Cancer Inst. 1969;42:517-24) from 1969 as the source of this claim, and results of early studies found an increased risk of leukemia among relatives of patients were actually accounted for by cases of chronic lymphocytic leukemia.

"We believe a better understanding on the role for genetic factors in the causation of AML/MDS is of major importance to patients, their families, and healthcare professionals," Dr. Björkholm said, explaining the rationale behind the research.

Using data from the Swedish Cancer Registry, the Swedish Population Registry, and the Swedish Multigenerational Registry, Dr. Björkholm and colleagues identified 6,962 patients diagnosed with AML from Jan. 1, 1958 until Dec. 31, 2004 and 1,388 MDS patients diagnosed from 1993 – the date when MDS was first included in the Swedish Cancer Registry – through Dec. 31, 2004. There were 20,579 first-degree relatives of the AML patients and 3,994 first-degree relatives of the MDS patients.

For each AML and MDS patient, four population-matched control subjects of a similar age, year of birth, and country of residence were randomly selected from the Swedish population, and their first-degree relatives were also identified. In all, there were 27,827 AML controls and 90,406 AML control relatives, and 5,312 MDS controls and 15,818 MDS control relatives.

No excess risk of AML (hazard ratio 0.94) or other myeloid or lymphoid malignancies was statistically significant in relatives of patients with AML with one exception – relatives of patients with AML did have an increased risk of polycythemia vera (HR 2.28, P less than .05). The risks for any hematopoietic or solid malignancies were significantly increased statistically, but only modestly, with risk ratios of 1.16 and 1.09, respectively.

First-degree relatives of AML patients who were diagnosed at a younger age (20 years or less) did, however, have a higher chance of developing AML, myeloid neoplasms, or multiple myeloma, based on small numbers in the sample. Dr. Björkholm suggested that genes predisposing to malignancy in general, environmental factors, or both, might be shared in these families.

No significant excess risks were seen among first-degree relatives of MDS patients.

"The lack of familial aggregation in AML and MDS is rather striking," Dr. Björkholm admitted. It is also "in stark contrast to findings in other myelo- and lymphoproliferative disorders."

In an interview, he emphasized, "The main message is that first-degree relatives of patients with acute myeloid leukemia do not have an increased risk of developing acute myeloid leukemia, which is in contrast to many other solid and hematological malignancies."

Dr. Björkholm also noted that patients are often told by their physicians that there is a two to three times increased risk of their siblings or children developing leukemia. The current findings suggest that this is unlikely, considering the large cohort of subjects that was studied.

"From a global point of view, this [study] is probably the best you can do."

Dr. Björkholm stated he had no conflicts of interest. The study received financial support from the Adolf H. Lundin Charitable Foundation, Karolinska Institute Foundations, Stockholm County Council, Swedish Cancer Society, and the Division of Intramural Research Programs at the National Cancer Institute of the National Institutes of Health.

LONDON – Close relatives of patients with acute myeloid leukemia and myelodysplastic syndromes can be reassured that they are not at increased risk of developing these diseases themselves, according to the findings of a large population-based registry trial.

"Among over 20,000 first-degree relatives of almost 7,000 AML [acute myeloid leukemia] patients, we found no excess risk of developing AML, MDS [myelodysplastic syndromes], or any myeloid neoplasms as a group," said Dr. Magnus Björkholm, a professor of medicine at Karolinska University Hospital, Solna and the Karolinska Institute, both in Stockholm.

Speaking at the annual congress of the European Hematology Association, Dr. Björkholm reported that there was also no strong genetic predisposition for first-degree relatives of patients with MDS to develop myeloid or other hematological neoplasms.

"If you read Wikipedia today, it says that the risk of developing AML is increased threefold in first-degree relatives of patients with AML," Dr. Björkholm observed. "But there is really limited data on the extent of familial aggregation of AML and MDS in the population.

Indeed, the Wikipedia entry cites a paper (J. Natl. Cancer Inst. 1969;42:517-24) from 1969 as the source of this claim, and results of early studies found an increased risk of leukemia among relatives of patients were actually accounted for by cases of chronic lymphocytic leukemia.

"We believe a better understanding on the role for genetic factors in the causation of AML/MDS is of major importance to patients, their families, and healthcare professionals," Dr. Björkholm said, explaining the rationale behind the research.

Using data from the Swedish Cancer Registry, the Swedish Population Registry, and the Swedish Multigenerational Registry, Dr. Björkholm and colleagues identified 6,962 patients diagnosed with AML from Jan. 1, 1958 until Dec. 31, 2004 and 1,388 MDS patients diagnosed from 1993 – the date when MDS was first included in the Swedish Cancer Registry – through Dec. 31, 2004. There were 20,579 first-degree relatives of the AML patients and 3,994 first-degree relatives of the MDS patients.

For each AML and MDS patient, four population-matched control subjects of a similar age, year of birth, and country of residence were randomly selected from the Swedish population, and their first-degree relatives were also identified. In all, there were 27,827 AML controls and 90,406 AML control relatives, and 5,312 MDS controls and 15,818 MDS control relatives.

No excess risk of AML (hazard ratio 0.94) or other myeloid or lymphoid malignancies was statistically significant in relatives of patients with AML with one exception – relatives of patients with AML did have an increased risk of polycythemia vera (HR 2.28, P less than .05). The risks for any hematopoietic or solid malignancies were significantly increased statistically, but only modestly, with risk ratios of 1.16 and 1.09, respectively.

First-degree relatives of AML patients who were diagnosed at a younger age (20 years or less) did, however, have a higher chance of developing AML, myeloid neoplasms, or multiple myeloma, based on small numbers in the sample. Dr. Björkholm suggested that genes predisposing to malignancy in general, environmental factors, or both, might be shared in these families.

No significant excess risks were seen among first-degree relatives of MDS patients.

"The lack of familial aggregation in AML and MDS is rather striking," Dr. Björkholm admitted. It is also "in stark contrast to findings in other myelo- and lymphoproliferative disorders."

In an interview, he emphasized, "The main message is that first-degree relatives of patients with acute myeloid leukemia do not have an increased risk of developing acute myeloid leukemia, which is in contrast to many other solid and hematological malignancies."

Dr. Björkholm also noted that patients are often told by their physicians that there is a two to three times increased risk of their siblings or children developing leukemia. The current findings suggest that this is unlikely, considering the large cohort of subjects that was studied.

"From a global point of view, this [study] is probably the best you can do."

Dr. Björkholm stated he had no conflicts of interest. The study received financial support from the Adolf H. Lundin Charitable Foundation, Karolinska Institute Foundations, Stockholm County Council, Swedish Cancer Society, and the Division of Intramural Research Programs at the National Cancer Institute of the National Institutes of Health.

LONDON – Close relatives of patients with acute myeloid leukemia and myelodysplastic syndromes can be reassured that they are not at increased risk of developing these diseases themselves, according to the findings of a large population-based registry trial.

"Among over 20,000 first-degree relatives of almost 7,000 AML [acute myeloid leukemia] patients, we found no excess risk of developing AML, MDS [myelodysplastic syndromes], or any myeloid neoplasms as a group," said Dr. Magnus Björkholm, a professor of medicine at Karolinska University Hospital, Solna and the Karolinska Institute, both in Stockholm.

Speaking at the annual congress of the European Hematology Association, Dr. Björkholm reported that there was also no strong genetic predisposition for first-degree relatives of patients with MDS to develop myeloid or other hematological neoplasms.

"If you read Wikipedia today, it says that the risk of developing AML is increased threefold in first-degree relatives of patients with AML," Dr. Björkholm observed. "But there is really limited data on the extent of familial aggregation of AML and MDS in the population.

Indeed, the Wikipedia entry cites a paper (J. Natl. Cancer Inst. 1969;42:517-24) from 1969 as the source of this claim, and results of early studies found an increased risk of leukemia among relatives of patients were actually accounted for by cases of chronic lymphocytic leukemia.

"We believe a better understanding on the role for genetic factors in the causation of AML/MDS is of major importance to patients, their families, and healthcare professionals," Dr. Björkholm said, explaining the rationale behind the research.

Using data from the Swedish Cancer Registry, the Swedish Population Registry, and the Swedish Multigenerational Registry, Dr. Björkholm and colleagues identified 6,962 patients diagnosed with AML from Jan. 1, 1958 until Dec. 31, 2004 and 1,388 MDS patients diagnosed from 1993 – the date when MDS was first included in the Swedish Cancer Registry – through Dec. 31, 2004. There were 20,579 first-degree relatives of the AML patients and 3,994 first-degree relatives of the MDS patients.

For each AML and MDS patient, four population-matched control subjects of a similar age, year of birth, and country of residence were randomly selected from the Swedish population, and their first-degree relatives were also identified. In all, there were 27,827 AML controls and 90,406 AML control relatives, and 5,312 MDS controls and 15,818 MDS control relatives.

No excess risk of AML (hazard ratio 0.94) or other myeloid or lymphoid malignancies was statistically significant in relatives of patients with AML with one exception – relatives of patients with AML did have an increased risk of polycythemia vera (HR 2.28, P less than .05). The risks for any hematopoietic or solid malignancies were significantly increased statistically, but only modestly, with risk ratios of 1.16 and 1.09, respectively.

First-degree relatives of AML patients who were diagnosed at a younger age (20 years or less) did, however, have a higher chance of developing AML, myeloid neoplasms, or multiple myeloma, based on small numbers in the sample. Dr. Björkholm suggested that genes predisposing to malignancy in general, environmental factors, or both, might be shared in these families.

No significant excess risks were seen among first-degree relatives of MDS patients.

"The lack of familial aggregation in AML and MDS is rather striking," Dr. Björkholm admitted. It is also "in stark contrast to findings in other myelo- and lymphoproliferative disorders."

In an interview, he emphasized, "The main message is that first-degree relatives of patients with acute myeloid leukemia do not have an increased risk of developing acute myeloid leukemia, which is in contrast to many other solid and hematological malignancies."

Dr. Björkholm also noted that patients are often told by their physicians that there is a two to three times increased risk of their siblings or children developing leukemia. The current findings suggest that this is unlikely, considering the large cohort of subjects that was studied.

"From a global point of view, this [study] is probably the best you can do."

Dr. Björkholm stated he had no conflicts of interest. The study received financial support from the Adolf H. Lundin Charitable Foundation, Karolinska Institute Foundations, Stockholm County Council, Swedish Cancer Society, and the Division of Intramural Research Programs at the National Cancer Institute of the National Institutes of Health.

LONDON – Women with both rheumatoid arthritis and systemic lupus erythematosus were more than twice as likely as women without these diseases to have pregnancy-related hypertension, and the risk has not lessened in recent years despite improved treatment, according to 10-years’ worth of admission and discharge data from several Canadian hospitals.

Such women were more likely to undergo a cesarean section, and their newborns were more likely to be born prematurely, be small for gestational age (SGA), and require intensive care, compared with children born to women without RA or SLE.

"We wanted to look at what obstetrical and neonatal outcomes have been like over the past 10 years in both RA and in lupus," study author and rheumatologist Dr. Cheryl Barnabe said in an interview during a poster session at the annual European Congress of Rheumatology.

To do so, Dr. Barnabe and colleagues used an administrative database maintained by the Canadian government to examine the outcomes of 38 women with RA and 95 with SLE who were admitted and discharged from hospitals in Calgary for obstetric reasons. Outcomes were compared with expectant women who did not have either condition, with four times as many controls as cases.

"We found that the RA and lupus patients stayed in hospital longer [after delivery], approximately double the percentage of patients [in both groups] had C-sections done, and there were more postpartum infections in the lupus patients compared to the lupus controls [6.3% vs. 1.3%, P less than .004]," observed Dr. Barnabe, a clinical scholar in the department of medicine at the University of Calgary in Alberta.

Adjusted odds ratios (ORs) for preeclampsia or eclampsia were 2.8 (95% confidence interval 1.0-7.8) for RA and 2.0 (95% CI 1.0-3.7) for SLE.

The mean length of hospital stay was 0.9 days longer for women with RA than for those without (P less than .003) and 1.8 days longer for those with SLE than for those without (P less than .001).

One-third (34.2%) of women with RA and 43.2% of women with SLE underwent cesarean section compared with 21.2% of RA controls and 23.7% of SLE controls. The adjusted ORs for cesarean section in RA and SLE were 2.3 (95% CI 0.9-4.7) and 2.8 (95% CI 1.5-4.0), respectively.

Babies were more frequently premature, with 2.6% vs. 0.7% born between 28 and 34 weeks’ gestation in women with and without RA, and 18.4% vs. 8% born at 34-37 weeks’ gestation. Corresponding values for the children of women with SLE were 8.4% vs. 1.9% at 28-34 weeks and 23.2% vs. 5.1% at 34-37 weeks. Three (3.2%) women with SLE but none without gave birth at less than 28 weeks’ gestation.

The adjusted ORs for premature delivery were 2.7 (95% CI 1.0-7.0) for RA and 6.6 (95% CI 3.5-12.3) for SLE.

Not surprisingly, the need for intensive care was higher among children born to women with RA or SLE than among the babies of women in the control groups. Adjusted ORs for SGA were 3.0 and 2.8 for RA and SLE, respectively.

These findings suggest the need for improved multidisciplinary management of women with arthritic conditions who are pregnant, Dr. Barnabe suggested.

"I think this shows that we can’t just assume that if we treat disease activity well enough we will affect obstetrical outcomes," she said.

"We should liaise with the obstetricians and the maternal-fetal medicine specialists and others to ensure that blood pressures are well controlled during pregnancy and make sure the disease activity is well controlled, and that will hopefully optimize these outcomes," Dr. Barnabe added. "I think a combined clinic is probably the best way to approach this."

Dr. Barnabe disclosed receiving a scholarship from the Arthritis Society, UCB, and the Canadian Rheumatologists Association for her master’s degree. A coauthor has received financial support from Alberta Innovative Health Solutions.

LONDON – Women with both rheumatoid arthritis and systemic lupus erythematosus were more than twice as likely as women without these diseases to have pregnancy-related hypertension, and the risk has not lessened in recent years despite improved treatment, according to 10-years’ worth of admission and discharge data from several Canadian hospitals.

Such women were more likely to undergo a cesarean section, and their newborns were more likely to be born prematurely, be small for gestational age (SGA), and require intensive care, compared with children born to women without RA or SLE.

"We wanted to look at what obstetrical and neonatal outcomes have been like over the past 10 years in both RA and in lupus," study author and rheumatologist Dr. Cheryl Barnabe said in an interview during a poster session at the annual European Congress of Rheumatology.

To do so, Dr. Barnabe and colleagues used an administrative database maintained by the Canadian government to examine the outcomes of 38 women with RA and 95 with SLE who were admitted and discharged from hospitals in Calgary for obstetric reasons. Outcomes were compared with expectant women who did not have either condition, with four times as many controls as cases.

"We found that the RA and lupus patients stayed in hospital longer [after delivery], approximately double the percentage of patients [in both groups] had C-sections done, and there were more postpartum infections in the lupus patients compared to the lupus controls [6.3% vs. 1.3%, P less than .004]," observed Dr. Barnabe, a clinical scholar in the department of medicine at the University of Calgary in Alberta.

Adjusted odds ratios (ORs) for preeclampsia or eclampsia were 2.8 (95% confidence interval 1.0-7.8) for RA and 2.0 (95% CI 1.0-3.7) for SLE.

The mean length of hospital stay was 0.9 days longer for women with RA than for those without (P less than .003) and 1.8 days longer for those with SLE than for those without (P less than .001).

One-third (34.2%) of women with RA and 43.2% of women with SLE underwent cesarean section compared with 21.2% of RA controls and 23.7% of SLE controls. The adjusted ORs for cesarean section in RA and SLE were 2.3 (95% CI 0.9-4.7) and 2.8 (95% CI 1.5-4.0), respectively.

Babies were more frequently premature, with 2.6% vs. 0.7% born between 28 and 34 weeks’ gestation in women with and without RA, and 18.4% vs. 8% born at 34-37 weeks’ gestation. Corresponding values for the children of women with SLE were 8.4% vs. 1.9% at 28-34 weeks and 23.2% vs. 5.1% at 34-37 weeks. Three (3.2%) women with SLE but none without gave birth at less than 28 weeks’ gestation.

The adjusted ORs for premature delivery were 2.7 (95% CI 1.0-7.0) for RA and 6.6 (95% CI 3.5-12.3) for SLE.

Not surprisingly, the need for intensive care was higher among children born to women with RA or SLE than among the babies of women in the control groups. Adjusted ORs for SGA were 3.0 and 2.8 for RA and SLE, respectively.

These findings suggest the need for improved multidisciplinary management of women with arthritic conditions who are pregnant, Dr. Barnabe suggested.

"I think this shows that we can’t just assume that if we treat disease activity well enough we will affect obstetrical outcomes," she said.

"We should liaise with the obstetricians and the maternal-fetal medicine specialists and others to ensure that blood pressures are well controlled during pregnancy and make sure the disease activity is well controlled, and that will hopefully optimize these outcomes," Dr. Barnabe added. "I think a combined clinic is probably the best way to approach this."

Dr. Barnabe disclosed receiving a scholarship from the Arthritis Society, UCB, and the Canadian Rheumatologists Association for her master’s degree. A coauthor has received financial support from Alberta Innovative Health Solutions.

LONDON – Women with both rheumatoid arthritis and systemic lupus erythematosus were more than twice as likely as women without these diseases to have pregnancy-related hypertension, and the risk has not lessened in recent years despite improved treatment, according to 10-years’ worth of admission and discharge data from several Canadian hospitals.

Such women were more likely to undergo a cesarean section, and their newborns were more likely to be born prematurely, be small for gestational age (SGA), and require intensive care, compared with children born to women without RA or SLE.

"We wanted to look at what obstetrical and neonatal outcomes have been like over the past 10 years in both RA and in lupus," study author and rheumatologist Dr. Cheryl Barnabe said in an interview during a poster session at the annual European Congress of Rheumatology.

To do so, Dr. Barnabe and colleagues used an administrative database maintained by the Canadian government to examine the outcomes of 38 women with RA and 95 with SLE who were admitted and discharged from hospitals in Calgary for obstetric reasons. Outcomes were compared with expectant women who did not have either condition, with four times as many controls as cases.

"We found that the RA and lupus patients stayed in hospital longer [after delivery], approximately double the percentage of patients [in both groups] had C-sections done, and there were more postpartum infections in the lupus patients compared to the lupus controls [6.3% vs. 1.3%, P less than .004]," observed Dr. Barnabe, a clinical scholar in the department of medicine at the University of Calgary in Alberta.

Adjusted odds ratios (ORs) for preeclampsia or eclampsia were 2.8 (95% confidence interval 1.0-7.8) for RA and 2.0 (95% CI 1.0-3.7) for SLE.

The mean length of hospital stay was 0.9 days longer for women with RA than for those without (P less than .003) and 1.8 days longer for those with SLE than for those without (P less than .001).

One-third (34.2%) of women with RA and 43.2% of women with SLE underwent cesarean section compared with 21.2% of RA controls and 23.7% of SLE controls. The adjusted ORs for cesarean section in RA and SLE were 2.3 (95% CI 0.9-4.7) and 2.8 (95% CI 1.5-4.0), respectively.

Babies were more frequently premature, with 2.6% vs. 0.7% born between 28 and 34 weeks’ gestation in women with and without RA, and 18.4% vs. 8% born at 34-37 weeks’ gestation. Corresponding values for the children of women with SLE were 8.4% vs. 1.9% at 28-34 weeks and 23.2% vs. 5.1% at 34-37 weeks. Three (3.2%) women with SLE but none without gave birth at less than 28 weeks’ gestation.

The adjusted ORs for premature delivery were 2.7 (95% CI 1.0-7.0) for RA and 6.6 (95% CI 3.5-12.3) for SLE.

Not surprisingly, the need for intensive care was higher among children born to women with RA or SLE than among the babies of women in the control groups. Adjusted ORs for SGA were 3.0 and 2.8 for RA and SLE, respectively.

These findings suggest the need for improved multidisciplinary management of women with arthritic conditions who are pregnant, Dr. Barnabe suggested.

"I think this shows that we can’t just assume that if we treat disease activity well enough we will affect obstetrical outcomes," she said.

"We should liaise with the obstetricians and the maternal-fetal medicine specialists and others to ensure that blood pressures are well controlled during pregnancy and make sure the disease activity is well controlled, and that will hopefully optimize these outcomes," Dr. Barnabe added. "I think a combined clinic is probably the best way to approach this."

Dr. Barnabe disclosed receiving a scholarship from the Arthritis Society, UCB, and the Canadian Rheumatologists Association for her master’s degree. A coauthor has received financial support from Alberta Innovative Health Solutions.

LONDON – Women with both rheumatoid arthritis and systemic lupus erythematosus were more than twice as likely as women without these diseases to have pregnancy-related hypertension, and the risk has not lessened in recent years despite improved treatment, according to 10-years’ worth of admission and discharge data from several Canadian hospitals.

Such women were more likely to undergo a cesarean section, and their newborns were more likely to be born prematurely, be small for gestational age (SGA), and require intensive care, compared with children born to women without RA or SLE.

"We wanted to look at what obstetrical and neonatal outcomes have been like over the past 10 years in both RA and in lupus," study author and rheumatologist Dr. Cheryl Barnabe said in an interview during a poster session at the annual European Congress of Rheumatology.

To do so, Dr. Barnabe and colleagues used an administrative database maintained by the Canadian government to examine the outcomes of 38 women with RA and 95 with SLE who were admitted and discharged from hospitals in Calgary for obstetric reasons. Outcomes were compared with expectant women who did not have either condition, with four times as many controls as cases.

"We found that the RA and lupus patients stayed in hospital longer [after delivery], approximately double the percentage of patients [in both groups] had C-sections done, and there were more postpartum infections in the lupus patients compared to the lupus controls [6.3% vs. 1.3%, P less than .004]," observed Dr. Barnabe, a clinical scholar in the department of medicine at the University of Calgary in Alberta.

Adjusted odds ratios (ORs) for preeclampsia or eclampsia were 2.8 (95% confidence interval 1.0-7.8) for RA and 2.0 (95% CI 1.0-3.7) for SLE.

The mean length of hospital stay was 0.9 days longer for women with RA than for those without (P less than .003) and 1.8 days longer for those with SLE than for those without (P less than .001).

One-third (34.2%) of women with RA and 43.2% of women with SLE underwent cesarean section compared with 21.2% of RA controls and 23.7% of SLE controls. The adjusted ORs for cesarean section in RA and SLE were 2.3 (95% CI 0.9-4.7) and 2.8 (95% CI 1.5-4.0), respectively.

Babies were more frequently premature, with 2.6% vs. 0.7% born between 28 and 34 weeks’ gestation in women with and without RA, and 18.4% vs. 8% born at 34-37 weeks’ gestation. Corresponding values for the children of women with SLE were 8.4% vs. 1.9% at 28-34 weeks and 23.2% vs. 5.1% at 34-37 weeks. Three (3.2%) women with SLE but none without gave birth at less than 28 weeks’ gestation.

The adjusted ORs for premature delivery were 2.7 (95% CI 1.0-7.0) for RA and 6.6 (95% CI 3.5-12.3) for SLE.

Not surprisingly, the need for intensive care was higher among children born to women with RA or SLE than among the babies of women in the control groups. Adjusted ORs for SGA were 3.0 and 2.8 for RA and SLE, respectively.

These findings suggest the need for improved multidisciplinary management of women with arthritic conditions who are pregnant, Dr. Barnabe suggested.

"I think this shows that we can’t just assume that if we treat disease activity well enough we will affect obstetrical outcomes," she said.

"We should liaise with the obstetricians and the maternal-fetal medicine specialists and others to ensure that blood pressures are well controlled during pregnancy and make sure the disease activity is well controlled, and that will hopefully optimize these outcomes," Dr. Barnabe added. "I think a combined clinic is probably the best way to approach this."

Dr. Barnabe disclosed receiving a scholarship from the Arthritis Society, UCB, and the Canadian Rheumatologists Association for her master’s degree. A coauthor has received financial support from Alberta Innovative Health Solutions.

LONDON – Women with both rheumatoid arthritis and systemic lupus erythematosus were more than twice as likely as women without these diseases to have pregnancy-related hypertension, and the risk has not lessened in recent years despite improved treatment, according to 10-years’ worth of admission and discharge data from several Canadian hospitals.

Such women were more likely to undergo a cesarean section, and their newborns were more likely to be born prematurely, be small for gestational age (SGA), and require intensive care, compared with children born to women without RA or SLE.

"We wanted to look at what obstetrical and neonatal outcomes have been like over the past 10 years in both RA and in lupus," study author and rheumatologist Dr. Cheryl Barnabe said in an interview during a poster session at the annual European Congress of Rheumatology.

To do so, Dr. Barnabe and colleagues used an administrative database maintained by the Canadian government to examine the outcomes of 38 women with RA and 95 with SLE who were admitted and discharged from hospitals in Calgary for obstetric reasons. Outcomes were compared with expectant women who did not have either condition, with four times as many controls as cases.

"We found that the RA and lupus patients stayed in hospital longer [after delivery], approximately double the percentage of patients [in both groups] had C-sections done, and there were more postpartum infections in the lupus patients compared to the lupus controls [6.3% vs. 1.3%, P less than .004]," observed Dr. Barnabe, a clinical scholar in the department of medicine at the University of Calgary in Alberta.

Adjusted odds ratios (ORs) for preeclampsia or eclampsia were 2.8 (95% confidence interval 1.0-7.8) for RA and 2.0 (95% CI 1.0-3.7) for SLE.

The mean length of hospital stay was 0.9 days longer for women with RA than for those without (P less than .003) and 1.8 days longer for those with SLE than for those without (P less than .001).

One-third (34.2%) of women with RA and 43.2% of women with SLE underwent cesarean section compared with 21.2% of RA controls and 23.7% of SLE controls. The adjusted ORs for cesarean section in RA and SLE were 2.3 (95% CI 0.9-4.7) and 2.8 (95% CI 1.5-4.0), respectively.

Babies were more frequently premature, with 2.6% vs. 0.7% born between 28 and 34 weeks’ gestation in women with and without RA, and 18.4% vs. 8% born at 34-37 weeks’ gestation. Corresponding values for the children of women with SLE were 8.4% vs. 1.9% at 28-34 weeks and 23.2% vs. 5.1% at 34-37 weeks. Three (3.2%) women with SLE but none without gave birth at less than 28 weeks’ gestation.

The adjusted ORs for premature delivery were 2.7 (95% CI 1.0-7.0) for RA and 6.6 (95% CI 3.5-12.3) for SLE.

Not surprisingly, the need for intensive care was higher among children born to women with RA or SLE than among the babies of women in the control groups. Adjusted ORs for SGA were 3.0 and 2.8 for RA and SLE, respectively.

These findings suggest the need for improved multidisciplinary management of women with arthritic conditions who are pregnant, Dr. Barnabe suggested.

"I think this shows that we can’t just assume that if we treat disease activity well enough we will affect obstetrical outcomes," she said.

"We should liaise with the obstetricians and the maternal-fetal medicine specialists and others to ensure that blood pressures are well controlled during pregnancy and make sure the disease activity is well controlled, and that will hopefully optimize these outcomes," Dr. Barnabe added. "I think a combined clinic is probably the best way to approach this."

Dr. Barnabe disclosed receiving a scholarship from the Arthritis Society, UCB, and the Canadian Rheumatologists Association for her master’s degree. A coauthor has received financial support from Alberta Innovative Health Solutions.

LONDON – Women with both rheumatoid arthritis and systemic lupus erythematosus were more than twice as likely as women without these diseases to have pregnancy-related hypertension, and the risk has not lessened in recent years despite improved treatment, according to 10-years’ worth of admission and discharge data from several Canadian hospitals.

Such women were more likely to undergo a cesarean section, and their newborns were more likely to be born prematurely, be small for gestational age (SGA), and require intensive care, compared with children born to women without RA or SLE.

"We wanted to look at what obstetrical and neonatal outcomes have been like over the past 10 years in both RA and in lupus," study author and rheumatologist Dr. Cheryl Barnabe said in an interview during a poster session at the annual European Congress of Rheumatology.

To do so, Dr. Barnabe and colleagues used an administrative database maintained by the Canadian government to examine the outcomes of 38 women with RA and 95 with SLE who were admitted and discharged from hospitals in Calgary for obstetric reasons. Outcomes were compared with expectant women who did not have either condition, with four times as many controls as cases.

"We found that the RA and lupus patients stayed in hospital longer [after delivery], approximately double the percentage of patients [in both groups] had C-sections done, and there were more postpartum infections in the lupus patients compared to the lupus controls [6.3% vs. 1.3%, P less than .004]," observed Dr. Barnabe, a clinical scholar in the department of medicine at the University of Calgary in Alberta.

Adjusted odds ratios (ORs) for preeclampsia or eclampsia were 2.8 (95% confidence interval 1.0-7.8) for RA and 2.0 (95% CI 1.0-3.7) for SLE.

The mean length of hospital stay was 0.9 days longer for women with RA than for those without (P less than .003) and 1.8 days longer for those with SLE than for those without (P less than .001).

One-third (34.2%) of women with RA and 43.2% of women with SLE underwent cesarean section compared with 21.2% of RA controls and 23.7% of SLE controls. The adjusted ORs for cesarean section in RA and SLE were 2.3 (95% CI 0.9-4.7) and 2.8 (95% CI 1.5-4.0), respectively.

Babies were more frequently premature, with 2.6% vs. 0.7% born between 28 and 34 weeks’ gestation in women with and without RA, and 18.4% vs. 8% born at 34-37 weeks’ gestation. Corresponding values for the children of women with SLE were 8.4% vs. 1.9% at 28-34 weeks and 23.2% vs. 5.1% at 34-37 weeks. Three (3.2%) women with SLE but none without gave birth at less than 28 weeks’ gestation.

The adjusted ORs for premature delivery were 2.7 (95% CI 1.0-7.0) for RA and 6.6 (95% CI 3.5-12.3) for SLE.

Not surprisingly, the need for intensive care was higher among children born to women with RA or SLE than among the babies of women in the control groups. Adjusted ORs for SGA were 3.0 and 2.8 for RA and SLE, respectively.

These findings suggest the need for improved multidisciplinary management of women with arthritic conditions who are pregnant, Dr. Barnabe suggested.

"I think this shows that we can’t just assume that if we treat disease activity well enough we will affect obstetrical outcomes," she said.

"We should liaise with the obstetricians and the maternal-fetal medicine specialists and others to ensure that blood pressures are well controlled during pregnancy and make sure the disease activity is well controlled, and that will hopefully optimize these outcomes," Dr. Barnabe added. "I think a combined clinic is probably the best way to approach this."

Dr. Barnabe disclosed receiving a scholarship from the Arthritis Society, UCB, and the Canadian Rheumatologists Association for her master’s degree. A coauthor has received financial support from Alberta Innovative Health Solutions.

LONDON – Although a potentially serious complication, perforation of the gastrointestinal tract is rare, judging from the findings of an analysis of more than 140,000 patients with rheumatoid arthritis.

Upper or lower GI tract perforation occurred in 696 (0.5%) of patients, with an overall, unadjusted incidence rate of 1.7 cases per 1,000 person-years, according to a report by Dr. Jeffrey Curtis.

"For [most of] the rheumatoid arthritis patients someone has in their practice, [GI perforation] is going to be very uncommon; I think that should be reassuring," Dr. Curtis said during an interview at the annual European Congress of Rheumatology.

"We also observed that there were cases [of GI perforation] for every biologic group," added Dr. Curtis, a rheumatologist, epidemiologist, and associate professor of medicine at the University of Alabama at Birmingham. This should help dispel any concerns that the adverse event might occur with certain biologic agents used to treat RA, he suggested.

In a retrospective study, Dr. Curtis and his associates analyzed records of 143,433 RA patients from a large U.S.-based administrative claims database for the years 2001-2009. The investigators used a validated algorithm to identify cases of upper and lower GI perforation and to determine predictive factors. The median follow-up was 2.5 years.

Older age was found to be a predictor of GI perforation, with adjusted relative risks of 1.6 and 2.1 for people aged 40-64 years and 65 years, respectively, compared with RA patients younger than 40 years. The mean age of the 142,737 patients who did not have a GI perforation was 57.6 years, and the mean age of the 696 patients who did was 62 years (P less than .01).

Diverticulitis and diverticulosis without diverticulitis were also significantly more common in patients who experienced a GI perforation than in those who did not, although the incidence was still low, with rates of 2.9% vs. 0.3% and 1.4% vs. 0.4%, respectively (both P less than .01). Diverticulitis but not diverticulosis was a significant risk factor for perforation.

The main risk factors among the RA medication groups of most relevance were the use of oral glucocorticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), not biologics and not really the disease-modifying antirheumatic drugs (DMARDs), Dr. Curtis said in the interview. Indeed, the incidence of GI perforation was highest in patients who used glucocorticoids in combination with DMARDs other than methotrexate (3.03 per 1,000 patient years).

Steroid monotherapy carried an incidence of 2.86 per 1,000 patient-years. Steroids used in combination with methotrexate and biologics also increased the risk of the GI complications (2.24 and 1.87 per 1,000 patient-years, respectively).

The rates of GI perforations in patients treated with biologics, methotrexate, or other DMARDs without steroids were 1.02, 1.08, and 1.71 per 1,000 patient-years, respectively. NSAID use was associated with an incidence rate of 1.68 per 1,000 patient-years.

"In contrast to about 10 years ago, when there was a lot more GI bleeding with perforation in the upper GI tract, there are population studies now suggesting that we need to be more worried about perforations of the lower GI tract," Dr. Curtis said.

In the study, 80% of the perforations seen were in the lower GI tract, so the use of gastroprotective medications may not be that useful.

"I think that the relative contribution of NSAIDs [to GI perforation] is probably diminished, just because we are seeing more lower now than upper."

Although still important, upper GI bleeding and peptic ulcer disease are perhaps less critical than antecedent diverticulitis and its associated complications.

Minimization of NSAID and steroid use is probably warranted in higher-risk patients, Dr. Curtis advised. "In somebody with a history of diverticulitis, I would be very cautious," he noted.

Dr. Curtis disclosed research and consulting relationships with Abbot, Amgen, BMS, Centocor, CORRONA, Crescendo, Pfizer, Roche, and UCB.

LONDON – Although a potentially serious complication, perforation of the gastrointestinal tract is rare, judging from the findings of an analysis of more than 140,000 patients with rheumatoid arthritis.

Upper or lower GI tract perforation occurred in 696 (0.5%) of patients, with an overall, unadjusted incidence rate of 1.7 cases per 1,000 person-years, according to a report by Dr. Jeffrey Curtis.

"For [most of] the rheumatoid arthritis patients someone has in their practice, [GI perforation] is going to be very uncommon; I think that should be reassuring," Dr. Curtis said during an interview at the annual European Congress of Rheumatology.

"We also observed that there were cases [of GI perforation] for every biologic group," added Dr. Curtis, a rheumatologist, epidemiologist, and associate professor of medicine at the University of Alabama at Birmingham. This should help dispel any concerns that the adverse event might occur with certain biologic agents used to treat RA, he suggested.

In a retrospective study, Dr. Curtis and his associates analyzed records of 143,433 RA patients from a large U.S.-based administrative claims database for the years 2001-2009. The investigators used a validated algorithm to identify cases of upper and lower GI perforation and to determine predictive factors. The median follow-up was 2.5 years.

Older age was found to be a predictor of GI perforation, with adjusted relative risks of 1.6 and 2.1 for people aged 40-64 years and 65 years, respectively, compared with RA patients younger than 40 years. The mean age of the 142,737 patients who did not have a GI perforation was 57.6 years, and the mean age of the 696 patients who did was 62 years (P less than .01).

Diverticulitis and diverticulosis without diverticulitis were also significantly more common in patients who experienced a GI perforation than in those who did not, although the incidence was still low, with rates of 2.9% vs. 0.3% and 1.4% vs. 0.4%, respectively (both P less than .01). Diverticulitis but not diverticulosis was a significant risk factor for perforation.

The main risk factors among the RA medication groups of most relevance were the use of oral glucocorticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), not biologics and not really the disease-modifying antirheumatic drugs (DMARDs), Dr. Curtis said in the interview. Indeed, the incidence of GI perforation was highest in patients who used glucocorticoids in combination with DMARDs other than methotrexate (3.03 per 1,000 patient years).

Steroid monotherapy carried an incidence of 2.86 per 1,000 patient-years. Steroids used in combination with methotrexate and biologics also increased the risk of the GI complications (2.24 and 1.87 per 1,000 patient-years, respectively).

The rates of GI perforations in patients treated with biologics, methotrexate, or other DMARDs without steroids were 1.02, 1.08, and 1.71 per 1,000 patient-years, respectively. NSAID use was associated with an incidence rate of 1.68 per 1,000 patient-years.

"In contrast to about 10 years ago, when there was a lot more GI bleeding with perforation in the upper GI tract, there are population studies now suggesting that we need to be more worried about perforations of the lower GI tract," Dr. Curtis said.

In the study, 80% of the perforations seen were in the lower GI tract, so the use of gastroprotective medications may not be that useful.

"I think that the relative contribution of NSAIDs [to GI perforation] is probably diminished, just because we are seeing more lower now than upper."

Although still important, upper GI bleeding and peptic ulcer disease are perhaps less critical than antecedent diverticulitis and its associated complications.

Minimization of NSAID and steroid use is probably warranted in higher-risk patients, Dr. Curtis advised. "In somebody with a history of diverticulitis, I would be very cautious," he noted.

Dr. Curtis disclosed research and consulting relationships with Abbot, Amgen, BMS, Centocor, CORRONA, Crescendo, Pfizer, Roche, and UCB.

LONDON – Although a potentially serious complication, perforation of the gastrointestinal tract is rare, judging from the findings of an analysis of more than 140,000 patients with rheumatoid arthritis.

Upper or lower GI tract perforation occurred in 696 (0.5%) of patients, with an overall, unadjusted incidence rate of 1.7 cases per 1,000 person-years, according to a report by Dr. Jeffrey Curtis.

"For [most of] the rheumatoid arthritis patients someone has in their practice, [GI perforation] is going to be very uncommon; I think that should be reassuring," Dr. Curtis said during an interview at the annual European Congress of Rheumatology.

"We also observed that there were cases [of GI perforation] for every biologic group," added Dr. Curtis, a rheumatologist, epidemiologist, and associate professor of medicine at the University of Alabama at Birmingham. This should help dispel any concerns that the adverse event might occur with certain biologic agents used to treat RA, he suggested.

In a retrospective study, Dr. Curtis and his associates analyzed records of 143,433 RA patients from a large U.S.-based administrative claims database for the years 2001-2009. The investigators used a validated algorithm to identify cases of upper and lower GI perforation and to determine predictive factors. The median follow-up was 2.5 years.

Older age was found to be a predictor of GI perforation, with adjusted relative risks of 1.6 and 2.1 for people aged 40-64 years and 65 years, respectively, compared with RA patients younger than 40 years. The mean age of the 142,737 patients who did not have a GI perforation was 57.6 years, and the mean age of the 696 patients who did was 62 years (P less than .01).

Diverticulitis and diverticulosis without diverticulitis were also significantly more common in patients who experienced a GI perforation than in those who did not, although the incidence was still low, with rates of 2.9% vs. 0.3% and 1.4% vs. 0.4%, respectively (both P less than .01). Diverticulitis but not diverticulosis was a significant risk factor for perforation.

The main risk factors among the RA medication groups of most relevance were the use of oral glucocorticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), not biologics and not really the disease-modifying antirheumatic drugs (DMARDs), Dr. Curtis said in the interview. Indeed, the incidence of GI perforation was highest in patients who used glucocorticoids in combination with DMARDs other than methotrexate (3.03 per 1,000 patient years).

Steroid monotherapy carried an incidence of 2.86 per 1,000 patient-years. Steroids used in combination with methotrexate and biologics also increased the risk of the GI complications (2.24 and 1.87 per 1,000 patient-years, respectively).

The rates of GI perforations in patients treated with biologics, methotrexate, or other DMARDs without steroids were 1.02, 1.08, and 1.71 per 1,000 patient-years, respectively. NSAID use was associated with an incidence rate of 1.68 per 1,000 patient-years.

"In contrast to about 10 years ago, when there was a lot more GI bleeding with perforation in the upper GI tract, there are population studies now suggesting that we need to be more worried about perforations of the lower GI tract," Dr. Curtis said.

In the study, 80% of the perforations seen were in the lower GI tract, so the use of gastroprotective medications may not be that useful.

"I think that the relative contribution of NSAIDs [to GI perforation] is probably diminished, just because we are seeing more lower now than upper."

Although still important, upper GI bleeding and peptic ulcer disease are perhaps less critical than antecedent diverticulitis and its associated complications.

Minimization of NSAID and steroid use is probably warranted in higher-risk patients, Dr. Curtis advised. "In somebody with a history of diverticulitis, I would be very cautious," he noted.

Dr. Curtis disclosed research and consulting relationships with Abbot, Amgen, BMS, Centocor, CORRONA, Crescendo, Pfizer, Roche, and UCB.

LONDON – Although a potentially serious complication, perforation of the gastrointestinal tract is rare, judging from the findings of an analysis of more than 140,000 patients with rheumatoid arthritis.

Upper or lower GI tract perforation occurred in 696 (0.5%) of patients, with an overall, unadjusted incidence rate of 1.7 cases per 1,000 person-years, according to a report by Dr. Jeffrey Curtis.

"For [most of] the rheumatoid arthritis patients someone has in their practice, [GI perforation] is going to be very uncommon; I think that should be reassuring," Dr. Curtis said during an interview at the annual European Congress of Rheumatology.

"We also observed that there were cases [of GI perforation] for every biologic group," added Dr. Curtis, a rheumatologist, epidemiologist, and associate professor of medicine at the University of Alabama at Birmingham. This should help dispel any concerns that the adverse event might occur with certain biologic agents used to treat RA, he suggested.

In a retrospective study, Dr. Curtis and his associates analyzed records of 143,433 RA patients from a large U.S.-based administrative claims database for the years 2001-2009. The investigators used a validated algorithm to identify cases of upper and lower GI perforation and to determine predictive factors. The median follow-up was 2.5 years.

Older age was found to be a predictor of GI perforation, with adjusted relative risks of 1.6 and 2.1 for people aged 40-64 years and 65 years, respectively, compared with RA patients younger than 40 years. The mean age of the 142,737 patients who did not have a GI perforation was 57.6 years, and the mean age of the 696 patients who did was 62 years (P less than .01).

Diverticulitis and diverticulosis without diverticulitis were also significantly more common in patients who experienced a GI perforation than in those who did not, although the incidence was still low, with rates of 2.9% vs. 0.3% and 1.4% vs. 0.4%, respectively (both P less than .01). Diverticulitis but not diverticulosis was a significant risk factor for perforation.

The main risk factors among the RA medication groups of most relevance were the use of oral glucocorticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), not biologics and not really the disease-modifying antirheumatic drugs (DMARDs), Dr. Curtis said in the interview. Indeed, the incidence of GI perforation was highest in patients who used glucocorticoids in combination with DMARDs other than methotrexate (3.03 per 1,000 patient years).

Steroid monotherapy carried an incidence of 2.86 per 1,000 patient-years. Steroids used in combination with methotrexate and biologics also increased the risk of the GI complications (2.24 and 1.87 per 1,000 patient-years, respectively).

The rates of GI perforations in patients treated with biologics, methotrexate, or other DMARDs without steroids were 1.02, 1.08, and 1.71 per 1,000 patient-years, respectively. NSAID use was associated with an incidence rate of 1.68 per 1,000 patient-years.

"In contrast to about 10 years ago, when there was a lot more GI bleeding with perforation in the upper GI tract, there are population studies now suggesting that we need to be more worried about perforations of the lower GI tract," Dr. Curtis said.

In the study, 80% of the perforations seen were in the lower GI tract, so the use of gastroprotective medications may not be that useful.

"I think that the relative contribution of NSAIDs [to GI perforation] is probably diminished, just because we are seeing more lower now than upper."

Although still important, upper GI bleeding and peptic ulcer disease are perhaps less critical than antecedent diverticulitis and its associated complications.

Minimization of NSAID and steroid use is probably warranted in higher-risk patients, Dr. Curtis advised. "In somebody with a history of diverticulitis, I would be very cautious," he noted.

Dr. Curtis disclosed research and consulting relationships with Abbot, Amgen, BMS, Centocor, CORRONA, Crescendo, Pfizer, Roche, and UCB.

LONDON – Although a potentially serious complication, perforation of the gastrointestinal tract is rare, judging from the findings of an analysis of more than 140,000 patients with rheumatoid arthritis.

Upper or lower GI tract perforation occurred in 696 (0.5%) of patients, with an overall, unadjusted incidence rate of 1.7 cases per 1,000 person-years, according to a report by Dr. Jeffrey Curtis.

"For [most of] the rheumatoid arthritis patients someone has in their practice, [GI perforation] is going to be very uncommon; I think that should be reassuring," Dr. Curtis said during an interview at the annual European Congress of Rheumatology.

"We also observed that there were cases [of GI perforation] for every biologic group," added Dr. Curtis, a rheumatologist, epidemiologist, and associate professor of medicine at the University of Alabama at Birmingham. This should help dispel any concerns that the adverse event might occur with certain biologic agents used to treat RA, he suggested.

In a retrospective study, Dr. Curtis and his associates analyzed records of 143,433 RA patients from a large U.S.-based administrative claims database for the years 2001-2009. The investigators used a validated algorithm to identify cases of upper and lower GI perforation and to determine predictive factors. The median follow-up was 2.5 years.

Older age was found to be a predictor of GI perforation, with adjusted relative risks of 1.6 and 2.1 for people aged 40-64 years and 65 years, respectively, compared with RA patients younger than 40 years. The mean age of the 142,737 patients who did not have a GI perforation was 57.6 years, and the mean age of the 696 patients who did was 62 years (P less than .01).

Diverticulitis and diverticulosis without diverticulitis were also significantly more common in patients who experienced a GI perforation than in those who did not, although the incidence was still low, with rates of 2.9% vs. 0.3% and 1.4% vs. 0.4%, respectively (both P less than .01). Diverticulitis but not diverticulosis was a significant risk factor for perforation.

The main risk factors among the RA medication groups of most relevance were the use of oral glucocorticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), not biologics and not really the disease-modifying antirheumatic drugs (DMARDs), Dr. Curtis said in the interview. Indeed, the incidence of GI perforation was highest in patients who used glucocorticoids in combination with DMARDs other than methotrexate (3.03 per 1,000 patient years).

Steroid monotherapy carried an incidence of 2.86 per 1,000 patient-years. Steroids used in combination with methotrexate and biologics also increased the risk of the GI complications (2.24 and 1.87 per 1,000 patient-years, respectively).

The rates of GI perforations in patients treated with biologics, methotrexate, or other DMARDs without steroids were 1.02, 1.08, and 1.71 per 1,000 patient-years, respectively. NSAID use was associated with an incidence rate of 1.68 per 1,000 patient-years.

"In contrast to about 10 years ago, when there was a lot more GI bleeding with perforation in the upper GI tract, there are population studies now suggesting that we need to be more worried about perforations of the lower GI tract," Dr. Curtis said.

In the study, 80% of the perforations seen were in the lower GI tract, so the use of gastroprotective medications may not be that useful.

"I think that the relative contribution of NSAIDs [to GI perforation] is probably diminished, just because we are seeing more lower now than upper."

Although still important, upper GI bleeding and peptic ulcer disease are perhaps less critical than antecedent diverticulitis and its associated complications.

Minimization of NSAID and steroid use is probably warranted in higher-risk patients, Dr. Curtis advised. "In somebody with a history of diverticulitis, I would be very cautious," he noted.

Dr. Curtis disclosed research and consulting relationships with Abbot, Amgen, BMS, Centocor, CORRONA, Crescendo, Pfizer, Roche, and UCB.

LONDON – Although a potentially serious complication, perforation of the gastrointestinal tract is rare, judging from the findings of an analysis of more than 140,000 patients with rheumatoid arthritis.

Upper or lower GI tract perforation occurred in 696 (0.5%) of patients, with an overall, unadjusted incidence rate of 1.7 cases per 1,000 person-years, according to a report by Dr. Jeffrey Curtis.

"For [most of] the rheumatoid arthritis patients someone has in their practice, [GI perforation] is going to be very uncommon; I think that should be reassuring," Dr. Curtis said during an interview at the annual European Congress of Rheumatology.

"We also observed that there were cases [of GI perforation] for every biologic group," added Dr. Curtis, a rheumatologist, epidemiologist, and associate professor of medicine at the University of Alabama at Birmingham. This should help dispel any concerns that the adverse event might occur with certain biologic agents used to treat RA, he suggested.

In a retrospective study, Dr. Curtis and his associates analyzed records of 143,433 RA patients from a large U.S.-based administrative claims database for the years 2001-2009. The investigators used a validated algorithm to identify cases of upper and lower GI perforation and to determine predictive factors. The median follow-up was 2.5 years.

Older age was found to be a predictor of GI perforation, with adjusted relative risks of 1.6 and 2.1 for people aged 40-64 years and 65 years, respectively, compared with RA patients younger than 40 years. The mean age of the 142,737 patients who did not have a GI perforation was 57.6 years, and the mean age of the 696 patients who did was 62 years (P less than .01).

Diverticulitis and diverticulosis without diverticulitis were also significantly more common in patients who experienced a GI perforation than in those who did not, although the incidence was still low, with rates of 2.9% vs. 0.3% and 1.4% vs. 0.4%, respectively (both P less than .01). Diverticulitis but not diverticulosis was a significant risk factor for perforation.

The main risk factors among the RA medication groups of most relevance were the use of oral glucocorticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), not biologics and not really the disease-modifying antirheumatic drugs (DMARDs), Dr. Curtis said in the interview. Indeed, the incidence of GI perforation was highest in patients who used glucocorticoids in combination with DMARDs other than methotrexate (3.03 per 1,000 patient years).

Steroid monotherapy carried an incidence of 2.86 per 1,000 patient-years. Steroids used in combination with methotrexate and biologics also increased the risk of the GI complications (2.24 and 1.87 per 1,000 patient-years, respectively).

The rates of GI perforations in patients treated with biologics, methotrexate, or other DMARDs without steroids were 1.02, 1.08, and 1.71 per 1,000 patient-years, respectively. NSAID use was associated with an incidence rate of 1.68 per 1,000 patient-years.

"In contrast to about 10 years ago, when there was a lot more GI bleeding with perforation in the upper GI tract, there are population studies now suggesting that we need to be more worried about perforations of the lower GI tract," Dr. Curtis said.

In the study, 80% of the perforations seen were in the lower GI tract, so the use of gastroprotective medications may not be that useful.

"I think that the relative contribution of NSAIDs [to GI perforation] is probably diminished, just because we are seeing more lower now than upper."

Although still important, upper GI bleeding and peptic ulcer disease are perhaps less critical than antecedent diverticulitis and its associated complications.

Minimization of NSAID and steroid use is probably warranted in higher-risk patients, Dr. Curtis advised. "In somebody with a history of diverticulitis, I would be very cautious," he noted.

Dr. Curtis disclosed research and consulting relationships with Abbot, Amgen, BMS, Centocor, CORRONA, Crescendo, Pfizer, Roche, and UCB.