Denise Napoli

Major Finding: Joint space narrowing significantly corresponded with increasing disability in patients with rheumatoid arthritis.

Data Source: Pooled data from several clinical trials of patients in remission from rheumatoid arthritis.

Disclosures: Data were provided by Abbott, Amgen, Centocor, Sanofi-Aventis, and Wyeth (later acquired by Pfizer). None of the authors disclosed financial conflicts of interest in relation to this study.

When it comes to disability in rheumatoid arthritis, it is cartilage loss – not bone damage – that seems to have the greater effect.

Accordingly, therapeutic interventions that aim to reduce patients' disability should focus on cartilage preservation, “since even relatively little cartilage degradation can lead to significant impairment of physical functioning,” wrote Dr. Daniel Aletaha of the division of rheumatology at the Medical University of Vienna and his colleagues.

The authors looked at data from a pool of 4,602 participants in various clinical trials of adalimumab, methotrexate, infliximab, and leflunomide.

“To separate the reversible, RA activity–related component of disability from the irreversible component, we identified patients who achieved clinical remission during the trials [that is, a state of absence of significant RA activity and thus the absence of a reversible disability component],” Dr. Aletaha and his colleagues wrote (Ann. Rheum. Dis. 2011;70:733–9).

Remission was defined as an SDAI (Simplified Disease Activity Index) score of 3.3 or less.

In all, 748 patients were included in the current analysis.

Patient data were assessed at the first visit in which a patient was in remission, and that visit's corresponding HAQ-DI (Health Assessment Questionnaire–Disability Index) score was used as “the best estimate of the patient's irreversible functional disability” for the current study, the investigators wrote.

The HAQ-DI scale has a 0–3 range, with 0 indicating no difficulty in the activities of daily living, and 3 indicating complete disability.

Patients were divided into tertiles according to the degree of both joint space narrowing (JSN), which is a function of cartilage loss, and bone erosion (ERO).

As was expected, in the univariate analysis, the mean scores on the HAQ-DI increased – indicating greater disability – as the JSN/ERO tertiles increased (0.21, 0.24, and 0.35, respectively, for the first, second, and third tertiles; P less than .0001).

“Likewise and even to a numerically greater extent, with increasing tertiles by JSN, residual (irreversible) HAQ-DI scores increased,” wrote the authors, with a mean of 0.18, 0.24, and 0.38 for the first, second, and third tertiles, respectively (P less than .0001).

To assess the independent disability contribution of erosion vs. narrowing, the authors then looked at the effects of higher erosion tertiles within each of the JSN tertiles. In other words, within each tertile of JSN, patients were further stratified into tertiles of ERO, and the HAQ-DI scores were compared.

“In the first and second tertiles formed according to JSN, higher degrees of erosive changes did not contribute at all to irreversible disability,” such that HAQ-DI scores did not differ significantly between ERO tertiles (P = .99 and .77, respectively), they said.

Although patients in the third quartiles of both JSN and ERO did have significantly greater HAQ-DI scores than did patients with less-severe bone erosion (0.417; P = .07), this was an expected finding, wrote the authors, as this group includes patients with severe joint damage.

However, when patients were first divided into ERO tertiles, and then further subdivided according to JSN severity within each tertile, the authors did find a significant effect on disability according to the HAQ-DI.

Indeed, within all three ERO strata, increasing JSN significantly corresponded with increasing HAQ-DI scores (P less than .05, P = .19, and P less than .001 for the first, second, and third ERO tertiles, respectively).

Despite the fact that bony erosion is considered “prototypic for RA,” whereas joint space narrowing (which occurs in other disorders) is considered less characteristic of the disease, “in the present study we have been able to show that the clinical impact of joint destruction cartilage loss seems to be of much higher relevance than damage to the bone,” Dr. Aletaha and his coauthors wrote.

“The data presented here provide sufficient evidence for developing, and further testing of, the hypothesis that cartilage damage, rather than bone destruction, may constitute the pivotal cause of physical functional impairment in RA,” they concluded.

Major Finding: Joint space narrowing significantly corresponded with increasing disability in patients with rheumatoid arthritis.

Data Source: Pooled data from several clinical trials of patients in remission from rheumatoid arthritis.

Disclosures: Data were provided by Abbott, Amgen, Centocor, Sanofi-Aventis, and Wyeth (later acquired by Pfizer). None of the authors disclosed financial conflicts of interest in relation to this study.

When it comes to disability in rheumatoid arthritis, it is cartilage loss – not bone damage – that seems to have the greater effect.

Accordingly, therapeutic interventions that aim to reduce patients' disability should focus on cartilage preservation, “since even relatively little cartilage degradation can lead to significant impairment of physical functioning,” wrote Dr. Daniel Aletaha of the division of rheumatology at the Medical University of Vienna and his colleagues.

The authors looked at data from a pool of 4,602 participants in various clinical trials of adalimumab, methotrexate, infliximab, and leflunomide.

“To separate the reversible, RA activity–related component of disability from the irreversible component, we identified patients who achieved clinical remission during the trials [that is, a state of absence of significant RA activity and thus the absence of a reversible disability component],” Dr. Aletaha and his colleagues wrote (Ann. Rheum. Dis. 2011;70:733–9).

Remission was defined as an SDAI (Simplified Disease Activity Index) score of 3.3 or less.

In all, 748 patients were included in the current analysis.

Patient data were assessed at the first visit in which a patient was in remission, and that visit's corresponding HAQ-DI (Health Assessment Questionnaire–Disability Index) score was used as “the best estimate of the patient's irreversible functional disability” for the current study, the investigators wrote.

The HAQ-DI scale has a 0–3 range, with 0 indicating no difficulty in the activities of daily living, and 3 indicating complete disability.

Patients were divided into tertiles according to the degree of both joint space narrowing (JSN), which is a function of cartilage loss, and bone erosion (ERO).

As was expected, in the univariate analysis, the mean scores on the HAQ-DI increased – indicating greater disability – as the JSN/ERO tertiles increased (0.21, 0.24, and 0.35, respectively, for the first, second, and third tertiles; P less than .0001).

“Likewise and even to a numerically greater extent, with increasing tertiles by JSN, residual (irreversible) HAQ-DI scores increased,” wrote the authors, with a mean of 0.18, 0.24, and 0.38 for the first, second, and third tertiles, respectively (P less than .0001).

To assess the independent disability contribution of erosion vs. narrowing, the authors then looked at the effects of higher erosion tertiles within each of the JSN tertiles. In other words, within each tertile of JSN, patients were further stratified into tertiles of ERO, and the HAQ-DI scores were compared.

“In the first and second tertiles formed according to JSN, higher degrees of erosive changes did not contribute at all to irreversible disability,” such that HAQ-DI scores did not differ significantly between ERO tertiles (P = .99 and .77, respectively), they said.

Although patients in the third quartiles of both JSN and ERO did have significantly greater HAQ-DI scores than did patients with less-severe bone erosion (0.417; P = .07), this was an expected finding, wrote the authors, as this group includes patients with severe joint damage.

However, when patients were first divided into ERO tertiles, and then further subdivided according to JSN severity within each tertile, the authors did find a significant effect on disability according to the HAQ-DI.

Indeed, within all three ERO strata, increasing JSN significantly corresponded with increasing HAQ-DI scores (P less than .05, P = .19, and P less than .001 for the first, second, and third ERO tertiles, respectively).

Despite the fact that bony erosion is considered “prototypic for RA,” whereas joint space narrowing (which occurs in other disorders) is considered less characteristic of the disease, “in the present study we have been able to show that the clinical impact of joint destruction cartilage loss seems to be of much higher relevance than damage to the bone,” Dr. Aletaha and his coauthors wrote.

“The data presented here provide sufficient evidence for developing, and further testing of, the hypothesis that cartilage damage, rather than bone destruction, may constitute the pivotal cause of physical functional impairment in RA,” they concluded.

Major Finding: Joint space narrowing significantly corresponded with increasing disability in patients with rheumatoid arthritis.

Data Source: Pooled data from several clinical trials of patients in remission from rheumatoid arthritis.

Disclosures: Data were provided by Abbott, Amgen, Centocor, Sanofi-Aventis, and Wyeth (later acquired by Pfizer). None of the authors disclosed financial conflicts of interest in relation to this study.

When it comes to disability in rheumatoid arthritis, it is cartilage loss – not bone damage – that seems to have the greater effect.

Accordingly, therapeutic interventions that aim to reduce patients' disability should focus on cartilage preservation, “since even relatively little cartilage degradation can lead to significant impairment of physical functioning,” wrote Dr. Daniel Aletaha of the division of rheumatology at the Medical University of Vienna and his colleagues.

The authors looked at data from a pool of 4,602 participants in various clinical trials of adalimumab, methotrexate, infliximab, and leflunomide.

“To separate the reversible, RA activity–related component of disability from the irreversible component, we identified patients who achieved clinical remission during the trials [that is, a state of absence of significant RA activity and thus the absence of a reversible disability component],” Dr. Aletaha and his colleagues wrote (Ann. Rheum. Dis. 2011;70:733–9).

Remission was defined as an SDAI (Simplified Disease Activity Index) score of 3.3 or less.

In all, 748 patients were included in the current analysis.

Patient data were assessed at the first visit in which a patient was in remission, and that visit's corresponding HAQ-DI (Health Assessment Questionnaire–Disability Index) score was used as “the best estimate of the patient's irreversible functional disability” for the current study, the investigators wrote.

The HAQ-DI scale has a 0–3 range, with 0 indicating no difficulty in the activities of daily living, and 3 indicating complete disability.

Patients were divided into tertiles according to the degree of both joint space narrowing (JSN), which is a function of cartilage loss, and bone erosion (ERO).

As was expected, in the univariate analysis, the mean scores on the HAQ-DI increased – indicating greater disability – as the JSN/ERO tertiles increased (0.21, 0.24, and 0.35, respectively, for the first, second, and third tertiles; P less than .0001).

“Likewise and even to a numerically greater extent, with increasing tertiles by JSN, residual (irreversible) HAQ-DI scores increased,” wrote the authors, with a mean of 0.18, 0.24, and 0.38 for the first, second, and third tertiles, respectively (P less than .0001).

To assess the independent disability contribution of erosion vs. narrowing, the authors then looked at the effects of higher erosion tertiles within each of the JSN tertiles. In other words, within each tertile of JSN, patients were further stratified into tertiles of ERO, and the HAQ-DI scores were compared.

“In the first and second tertiles formed according to JSN, higher degrees of erosive changes did not contribute at all to irreversible disability,” such that HAQ-DI scores did not differ significantly between ERO tertiles (P = .99 and .77, respectively), they said.

Although patients in the third quartiles of both JSN and ERO did have significantly greater HAQ-DI scores than did patients with less-severe bone erosion (0.417; P = .07), this was an expected finding, wrote the authors, as this group includes patients with severe joint damage.

However, when patients were first divided into ERO tertiles, and then further subdivided according to JSN severity within each tertile, the authors did find a significant effect on disability according to the HAQ-DI.

Indeed, within all three ERO strata, increasing JSN significantly corresponded with increasing HAQ-DI scores (P less than .05, P = .19, and P less than .001 for the first, second, and third ERO tertiles, respectively).

Despite the fact that bony erosion is considered “prototypic for RA,” whereas joint space narrowing (which occurs in other disorders) is considered less characteristic of the disease, “in the present study we have been able to show that the clinical impact of joint destruction cartilage loss seems to be of much higher relevance than damage to the bone,” Dr. Aletaha and his coauthors wrote.

“The data presented here provide sufficient evidence for developing, and further testing of, the hypothesis that cartilage damage, rather than bone destruction, may constitute the pivotal cause of physical functional impairment in RA,” they concluded.

Major Finding: For every 0.6-point increase on the DAS28, there was a corresponding 4% increase in outpatient infections; for every 5 points on the CDAI, there was a 14% increase, for all CDAI scores less than 10.

Data Source: More than 2,000 infections that were registered through the CORRONA database between March 2002 and December 2007.

Disclosures: Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients' mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785–91).

“To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy” (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti rheumatic drug over three consecutive visits spanning at least 6 months), they said.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were outpatient.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10–22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity compared with low activity, 1.19; 95% confidence interval, 1.06–1.34; IRR for high activity, 1.07; 95% CI 0.90–1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84–3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection. Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, they said.

Indeed, they added, the “continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections.”

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Major Finding: For every 0.6-point increase on the DAS28, there was a corresponding 4% increase in outpatient infections; for every 5 points on the CDAI, there was a 14% increase, for all CDAI scores less than 10.

Data Source: More than 2,000 infections that were registered through the CORRONA database between March 2002 and December 2007.

Disclosures: Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients' mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785–91).

“To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy” (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti rheumatic drug over three consecutive visits spanning at least 6 months), they said.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were outpatient.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10–22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity compared with low activity, 1.19; 95% confidence interval, 1.06–1.34; IRR for high activity, 1.07; 95% CI 0.90–1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84–3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection. Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, they said.

Indeed, they added, the “continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections.”

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Major Finding: For every 0.6-point increase on the DAS28, there was a corresponding 4% increase in outpatient infections; for every 5 points on the CDAI, there was a 14% increase, for all CDAI scores less than 10.

Data Source: More than 2,000 infections that were registered through the CORRONA database between March 2002 and December 2007.

Disclosures: Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients' mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785–91).

“To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy” (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti rheumatic drug over three consecutive visits spanning at least 6 months), they said.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were outpatient.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10–22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity compared with low activity, 1.19; 95% confidence interval, 1.06–1.34; IRR for high activity, 1.07; 95% CI 0.90–1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84–3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection. Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, they said.

Indeed, they added, the “continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections.”

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Major Finding: Among 8,295 patients with resistant office hypertension, 63% had ambulatory 24-hour blood pressure values greater than or equal to 130 mm Hg systolic and/or 80 mm Hg diastolic and were diagnosed as true resistant hypertension, whereas 37% showed 24-hour BP values below this limit and therefore were considered to have white-coat resistant HT.

Data Source: An analysis of data on more than 68,000 patients in the Spanish Ambulatory Blood Pressure Monitoring (ABPM) Registry.

Disclosures: The Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories. The authors disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring (ABPM) Registry, which included 68,045 patients with good-quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra's criteria for resistant hypertension (RH): office BP greater than or equal to 140 mm Hg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at “appropriate” doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA. 110.168948]).

White-coat RH patients were slightly but significantly older (65 vs. 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% vs. 10%), to be diabetic (35% vs. 28%), and to have cardiovascular disease (19% vs. 16%), compared with the white-coat RH patients. Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on an electrocardiogram, vs. 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 vs. 72 micromol/L), higher urinary albumin excretion (11 vs. 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% vs. 20%).

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, “thus possibly overestimating the true prevalence of RH.”

And despite the findings of significant differences in clinical characteristics between groups, “their discriminating value in clinical practice is probably low,” cautioned the authors.

Major Finding: Among 8,295 patients with resistant office hypertension, 63% had ambulatory 24-hour blood pressure values greater than or equal to 130 mm Hg systolic and/or 80 mm Hg diastolic and were diagnosed as true resistant hypertension, whereas 37% showed 24-hour BP values below this limit and therefore were considered to have white-coat resistant HT.

Data Source: An analysis of data on more than 68,000 patients in the Spanish Ambulatory Blood Pressure Monitoring (ABPM) Registry.

Disclosures: The Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories. The authors disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring (ABPM) Registry, which included 68,045 patients with good-quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra's criteria for resistant hypertension (RH): office BP greater than or equal to 140 mm Hg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at “appropriate” doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA. 110.168948]).

White-coat RH patients were slightly but significantly older (65 vs. 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% vs. 10%), to be diabetic (35% vs. 28%), and to have cardiovascular disease (19% vs. 16%), compared with the white-coat RH patients. Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on an electrocardiogram, vs. 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 vs. 72 micromol/L), higher urinary albumin excretion (11 vs. 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% vs. 20%).

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, “thus possibly overestimating the true prevalence of RH.”

And despite the findings of significant differences in clinical characteristics between groups, “their discriminating value in clinical practice is probably low,” cautioned the authors.

Major Finding: Among 8,295 patients with resistant office hypertension, 63% had ambulatory 24-hour blood pressure values greater than or equal to 130 mm Hg systolic and/or 80 mm Hg diastolic and were diagnosed as true resistant hypertension, whereas 37% showed 24-hour BP values below this limit and therefore were considered to have white-coat resistant HT.

Data Source: An analysis of data on more than 68,000 patients in the Spanish Ambulatory Blood Pressure Monitoring (ABPM) Registry.

Disclosures: The Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories. The authors disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring (ABPM) Registry, which included 68,045 patients with good-quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra's criteria for resistant hypertension (RH): office BP greater than or equal to 140 mm Hg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at “appropriate” doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA. 110.168948]).

White-coat RH patients were slightly but significantly older (65 vs. 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% vs. 10%), to be diabetic (35% vs. 28%), and to have cardiovascular disease (19% vs. 16%), compared with the white-coat RH patients. Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on an electrocardiogram, vs. 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 vs. 72 micromol/L), higher urinary albumin excretion (11 vs. 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% vs. 20%).

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, “thus possibly overestimating the true prevalence of RH.”

And despite the findings of significant differences in clinical characteristics between groups, “their discriminating value in clinical practice is probably low,” cautioned the authors.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Increasing disease activity in rheumatoid arthritis is associated with a higher risk for both outpatient infections and more serious infections requiring hospitalization in patients receiving stable therapy.

Moreover, this finding was true even among patients with mild disease activity, according to Dr. Karen Au of the division of rheumatology at the University of California, Los Angeles.

In a study published in the May issue of Annals of the Rheumatic Diseases, Dr. Au and her colleagues looked at 6,246 patients with RA who were listed on the CORRONA (Consortium of Rheumatology Researchers of North America) registry, which includes data contributed by 80 academic and private practices across the United States.

The patients’ mean age was 60 years; 75% were women. CDAI (Clinical Disease Activity Index) scores were available for 6,020 patients. DAS28 (disease activity score based on a 28-joint count) was calculated throughout the study period for 3,666 patients (Ann. Rheum. Dis. 2011;70:785-91).

"To minimize confounding related to recent changes in disease-modifying medications on the rate of infections, we limited the study to RA patients on stable therapy" (defined as no change in the dose of either methotrexate, TNF (tumor necrosis factor) inhibitor, corticosteroid, or any other disease-modifying anti-rheumatic drug over three consecutive visits spanning at least 6 months), according to the researchers.

Overall, 2,282 infections were reported during the study period, from March 2002 to December 2007; 1,382 patients had one or more outpatient infections and 50 patients had serious infections that required hospitalization.

Most of the infections tallied (2,223 of the total 2,282) were of an outpatient nature.

When outpatient infections alone were considered, researchers found that for all patients with CDAI scores less than 10 of a possible 76 (corresponding to the mildest class of disease), there was a 14% increase in outpatient infections for each 5-point increase in score, after the researchers controlled for covariates including body mass index, smoking, disease duration, therapy, and coexisting cardiovascular disease (incidence rate ratio, 1.14; P = .003).

And although no further linear relationship was noted, patients with moderate (CDAI scores of 10-22) and high (CDAI scores greater than 22) disease activity had increased infections, compared with patients with mild disease activity, although only the moderate category was statistically significant (IRR for moderate activity, compared with low activity, 1.19; 95% confidence interval, 1.06-1.34; IRR for high activity, 1.07; 95% CI 0.90-1.27).

Among patients for whom DAS28 data were available, there was a 4% increase in outpatient infections for each 0.6-point increase in the score, which persisted throughout the entire DAS28 spectrum (IRR, 1.04; P = .03).

A history of infections increased the likelihood of having an outpatient infection (IRR, 2.84-3.15; P less than .001), as did use of methotrexate, use of TNF inhibitors, and poorer functional class.

Although infections requiring hospitalization were much less frequent among the study participants, the authors were able to identify that for every 0.6-point increase in the DAS28, there was a corresponding significant 25% increase in the rate of infections that required hospitalization.

On the CDAI scale, there was no significant trend between an increasing score and inpatient infections on multivariate analysis, likely because of the small number of inpatient infections observed, according to the authors.

Prednisone use of 7.5 mg daily or more was also independently associated with infections that required hospitalization, as was a history of infection, they noted.

Previous studies have shown that RA patients have a twofold increased risk of developing infections, compared with patients who do not have RA, and they are also at higher risk of serious infections requiring hospitalization, the researchers said.

Indeed, they added, the "continued increased mortality observed in RA patients compared with the general population can be explained partly by a higher susceptibility to infections."

However, until now, the "independent contribution of RA disease activity and associated systemic inflammation is unclear."

The strength of this study, they pointed out, lies in the size and quality of the prospectively collected clinical data in the CORRONA database.

Several of the authors reported contracts and professional affiliations with the CORRONA database. Several also reported financial relationships with multiple pharmaceutical companies, including Amgen, Centocor, Pfizer, Roche/Genentech, and UCB.

Daily atorvastatin use had no significant impact on atherosclerosis progression among systemic lupus erythematosus patients, compared with placebo.

Indeed, among SLE patients without hyperlipidemia, nonstatin interventions "should be considered for the accelerated atherosclerosis of SLE," noted Dr. Michelle Petri, professor of medicine and director of the lupus center at Johns Hopkins University, Baltimore, in the May issue of the Annals of the Rheumatic Diseases.

Dr. Petri and colleagues looked at 200 patients with SLE. To be included in the analysis, patients could not have a history of atherosclerotic events, chronic liver disease, or statin use in the 3 months prior to the study. Patients were also excluded if they had baseline triglyceride levels greater than 500 mg/dL, levels of LDL cholesterol greater than 190 mg/dL, creatinine kinase levels greater than 1.5 times the upper limit of normal, or liver-function test findings greater than two times the upper limit of normal (Ann. Rheum. Dis. 2011;70:760-5).

Patients’ mean age was 48 years, and 92% were female. Roughly two-thirds of patients were white, and the remaining one-third were black.

Patients were randomized to receive either 40 mg daily of atorvastatin or an identical placebo; they underwent helical CT scans and carotid duplex scans at baseline and 2 years.

At baseline, the mean total cholesterol was 186 mg/dL, and 34% of patients had total cholesterol levels greater than 200 mg/dL. The mean LDL cholesterol was 103 mg/dL, with 48% having LDL levels in excess of 100 mg/dL.

Also at baseline, 57% of participants had no coronary artery calcium; 22% had an Agatston score of 0-10; 12% scored 11-99; and 8% scored 100 or greater. The carotid intima-media thickness (IMT) was 0.4-0.5 mm in 23% of patients, 0.5-0.6 mm in 46%, 0.6-0.7 mm in 19%, and 0.7-1.0 mm in 12%.

Overall, 17% of patients had carotid plaque at baseline.

According to Dr. Petri, by 2 years there were no statistically significant differences between groups with respect to changes in coronary artery calcium score or carotid IMT. Both groups did have a statistically significant change in carotid IMT by 2 years (0.07 mm between baseline and study end for the treatment group vs. 0.09 mm for the placebo group; P less than 0.0001 for both groups) but this was not significant between groups.

Overall, among the patients treated with statin, 48% showed improved carotid IMT (defined as better than 10% change); 6% stayed the same, and 46% got worse. Among the placebo group, 29% of patients improved, whereas 4% remained the same and 67% of patients had worse measurements after 2 years.

The difference between patients who improved was a statistically significant difference (P = .014).

Among statin patients who had no carotid plaque at baseline, 25% were found to have plaque at 2 years, compared with 23% among placebo patients (P = .77).

Looking at laboratory values, the only significant difference between groups was seen in levels of total cholesterol. Among atorvastatin patients, this measure dropped more than 30 points over the study period, from 181.6 mg/dL to 150.7 mg/dL; for placebo patients, it rose 5.5 points, from 190.1 mg/dL to 195.6 mg/dL (P less than 0.0001).

Meanwhile, 51% in the atorvastatin group had abnormal ALT levels during follow-up, compared with 31% in the placebo group (P = .01); creatine kinase values did not differ between groups.

The authors conceded that 2 years of follow-up may not have been sufficient to observe any benefit in SLE; they added that an 80-mg dose (vs. the 40 mg used in this study) may have proved more efficacious. However, "it would not have been possible for us to have done our study with 80 mg, given the high frequency" of abnormal liver function tests with 40-mg atorvastatin, they wrote.

"Although statins may have some benefit for the disease activity of rheumatoid arthritis or multiple sclerosis, we found no evidence of a beneficial effect on SLE activity," concluded the authors.

Nevertheless, "patients with SLE with hyperlipidemia ... should continue to be treated with statins and other antihyperlipidemic medications if they meet the National Cholesterol Education Program guideline thresholds for treatment," they added.

Dr. Petri disclosed being a former member of the Pfizer advisory board and participating in a Pfizer speakers bureau unrelated to atorvastatin. Pfizer is the maker of atorvastatin, marketed as Lipitor.

None of the other authors had any other competing interests to disclose.

Daily atorvastatin use had no significant impact on atherosclerosis progression among systemic lupus erythematosus patients, compared with placebo.

Indeed, among SLE patients without hyperlipidemia, nonstatin interventions "should be considered for the accelerated atherosclerosis of SLE," noted Dr. Michelle Petri, professor of medicine and director of the lupus center at Johns Hopkins University, Baltimore, in the May issue of the Annals of the Rheumatic Diseases.

Dr. Petri and colleagues looked at 200 patients with SLE. To be included in the analysis, patients could not have a history of atherosclerotic events, chronic liver disease, or statin use in the 3 months prior to the study. Patients were also excluded if they had baseline triglyceride levels greater than 500 mg/dL, levels of LDL cholesterol greater than 190 mg/dL, creatinine kinase levels greater than 1.5 times the upper limit of normal, or liver-function test findings greater than two times the upper limit of normal (Ann. Rheum. Dis. 2011;70:760-5).

Patients’ mean age was 48 years, and 92% were female. Roughly two-thirds of patients were white, and the remaining one-third were black.

Patients were randomized to receive either 40 mg daily of atorvastatin or an identical placebo; they underwent helical CT scans and carotid duplex scans at baseline and 2 years.

At baseline, the mean total cholesterol was 186 mg/dL, and 34% of patients had total cholesterol levels greater than 200 mg/dL. The mean LDL cholesterol was 103 mg/dL, with 48% having LDL levels in excess of 100 mg/dL.

Also at baseline, 57% of participants had no coronary artery calcium; 22% had an Agatston score of 0-10; 12% scored 11-99; and 8% scored 100 or greater. The carotid intima-media thickness (IMT) was 0.4-0.5 mm in 23% of patients, 0.5-0.6 mm in 46%, 0.6-0.7 mm in 19%, and 0.7-1.0 mm in 12%.

Overall, 17% of patients had carotid plaque at baseline.

According to Dr. Petri, by 2 years there were no statistically significant differences between groups with respect to changes in coronary artery calcium score or carotid IMT. Both groups did have a statistically significant change in carotid IMT by 2 years (0.07 mm between baseline and study end for the treatment group vs. 0.09 mm for the placebo group; P less than 0.0001 for both groups) but this was not significant between groups.

Overall, among the patients treated with statin, 48% showed improved carotid IMT (defined as better than 10% change); 6% stayed the same, and 46% got worse. Among the placebo group, 29% of patients improved, whereas 4% remained the same and 67% of patients had worse measurements after 2 years.

The difference between patients who improved was a statistically significant difference (P = .014).

Among statin patients who had no carotid plaque at baseline, 25% were found to have plaque at 2 years, compared with 23% among placebo patients (P = .77).

Looking at laboratory values, the only significant difference between groups was seen in levels of total cholesterol. Among atorvastatin patients, this measure dropped more than 30 points over the study period, from 181.6 mg/dL to 150.7 mg/dL; for placebo patients, it rose 5.5 points, from 190.1 mg/dL to 195.6 mg/dL (P less than 0.0001).

Meanwhile, 51% in the atorvastatin group had abnormal ALT levels during follow-up, compared with 31% in the placebo group (P = .01); creatine kinase values did not differ between groups.

The authors conceded that 2 years of follow-up may not have been sufficient to observe any benefit in SLE; they added that an 80-mg dose (vs. the 40 mg used in this study) may have proved more efficacious. However, "it would not have been possible for us to have done our study with 80 mg, given the high frequency" of abnormal liver function tests with 40-mg atorvastatin, they wrote.

"Although statins may have some benefit for the disease activity of rheumatoid arthritis or multiple sclerosis, we found no evidence of a beneficial effect on SLE activity," concluded the authors.

Nevertheless, "patients with SLE with hyperlipidemia ... should continue to be treated with statins and other antihyperlipidemic medications if they meet the National Cholesterol Education Program guideline thresholds for treatment," they added.

Dr. Petri disclosed being a former member of the Pfizer advisory board and participating in a Pfizer speakers bureau unrelated to atorvastatin. Pfizer is the maker of atorvastatin, marketed as Lipitor.

None of the other authors had any other competing interests to disclose.

Daily atorvastatin use had no significant impact on atherosclerosis progression among systemic lupus erythematosus patients, compared with placebo.

Indeed, among SLE patients without hyperlipidemia, nonstatin interventions "should be considered for the accelerated atherosclerosis of SLE," noted Dr. Michelle Petri, professor of medicine and director of the lupus center at Johns Hopkins University, Baltimore, in the May issue of the Annals of the Rheumatic Diseases.

Dr. Petri and colleagues looked at 200 patients with SLE. To be included in the analysis, patients could not have a history of atherosclerotic events, chronic liver disease, or statin use in the 3 months prior to the study. Patients were also excluded if they had baseline triglyceride levels greater than 500 mg/dL, levels of LDL cholesterol greater than 190 mg/dL, creatinine kinase levels greater than 1.5 times the upper limit of normal, or liver-function test findings greater than two times the upper limit of normal (Ann. Rheum. Dis. 2011;70:760-5).

Patients’ mean age was 48 years, and 92% were female. Roughly two-thirds of patients were white, and the remaining one-third were black.

Patients were randomized to receive either 40 mg daily of atorvastatin or an identical placebo; they underwent helical CT scans and carotid duplex scans at baseline and 2 years.

At baseline, the mean total cholesterol was 186 mg/dL, and 34% of patients had total cholesterol levels greater than 200 mg/dL. The mean LDL cholesterol was 103 mg/dL, with 48% having LDL levels in excess of 100 mg/dL.

Also at baseline, 57% of participants had no coronary artery calcium; 22% had an Agatston score of 0-10; 12% scored 11-99; and 8% scored 100 or greater. The carotid intima-media thickness (IMT) was 0.4-0.5 mm in 23% of patients, 0.5-0.6 mm in 46%, 0.6-0.7 mm in 19%, and 0.7-1.0 mm in 12%.

Overall, 17% of patients had carotid plaque at baseline.

According to Dr. Petri, by 2 years there were no statistically significant differences between groups with respect to changes in coronary artery calcium score or carotid IMT. Both groups did have a statistically significant change in carotid IMT by 2 years (0.07 mm between baseline and study end for the treatment group vs. 0.09 mm for the placebo group; P less than 0.0001 for both groups) but this was not significant between groups.

Overall, among the patients treated with statin, 48% showed improved carotid IMT (defined as better than 10% change); 6% stayed the same, and 46% got worse. Among the placebo group, 29% of patients improved, whereas 4% remained the same and 67% of patients had worse measurements after 2 years.

The difference between patients who improved was a statistically significant difference (P = .014).

Among statin patients who had no carotid plaque at baseline, 25% were found to have plaque at 2 years, compared with 23% among placebo patients (P = .77).

Looking at laboratory values, the only significant difference between groups was seen in levels of total cholesterol. Among atorvastatin patients, this measure dropped more than 30 points over the study period, from 181.6 mg/dL to 150.7 mg/dL; for placebo patients, it rose 5.5 points, from 190.1 mg/dL to 195.6 mg/dL (P less than 0.0001).

Meanwhile, 51% in the atorvastatin group had abnormal ALT levels during follow-up, compared with 31% in the placebo group (P = .01); creatine kinase values did not differ between groups.

The authors conceded that 2 years of follow-up may not have been sufficient to observe any benefit in SLE; they added that an 80-mg dose (vs. the 40 mg used in this study) may have proved more efficacious. However, "it would not have been possible for us to have done our study with 80 mg, given the high frequency" of abnormal liver function tests with 40-mg atorvastatin, they wrote.

"Although statins may have some benefit for the disease activity of rheumatoid arthritis or multiple sclerosis, we found no evidence of a beneficial effect on SLE activity," concluded the authors.

Nevertheless, "patients with SLE with hyperlipidemia ... should continue to be treated with statins and other antihyperlipidemic medications if they meet the National Cholesterol Education Program guideline thresholds for treatment," they added.

Dr. Petri disclosed being a former member of the Pfizer advisory board and participating in a Pfizer speakers bureau unrelated to atorvastatin. Pfizer is the maker of atorvastatin, marketed as Lipitor.

None of the other authors had any other competing interests to disclose.

Daily atorvastatin use had no significant impact on atherosclerosis progression among systemic lupus erythematosus patients, compared with placebo.

Indeed, among SLE patients without hyperlipidemia, nonstatin interventions "should be considered for the accelerated atherosclerosis of SLE," noted Dr. Michelle Petri, professor of medicine and director of the lupus center at Johns Hopkins University, Baltimore, in the May issue of the Annals of the Rheumatic Diseases.

Dr. Petri and colleagues looked at 200 patients with SLE. To be included in the analysis, patients could not have a history of atherosclerotic events, chronic liver disease, or statin use in the 3 months prior to the study. Patients were also excluded if they had baseline triglyceride levels greater than 500 mg/dL, levels of LDL cholesterol greater than 190 mg/dL, creatinine kinase levels greater than 1.5 times the upper limit of normal, or liver-function test findings greater than two times the upper limit of normal (Ann. Rheum. Dis. 2011;70:760-5).

Patients’ mean age was 48 years, and 92% were female. Roughly two-thirds of patients were white, and the remaining one-third were black.

Patients were randomized to receive either 40 mg daily of atorvastatin or an identical placebo; they underwent helical CT scans and carotid duplex scans at baseline and 2 years.

At baseline, the mean total cholesterol was 186 mg/dL, and 34% of patients had total cholesterol levels greater than 200 mg/dL. The mean LDL cholesterol was 103 mg/dL, with 48% having LDL levels in excess of 100 mg/dL.

Also at baseline, 57% of participants had no coronary artery calcium; 22% had an Agatston score of 0-10; 12% scored 11-99; and 8% scored 100 or greater. The carotid intima-media thickness (IMT) was 0.4-0.5 mm in 23% of patients, 0.5-0.6 mm in 46%, 0.6-0.7 mm in 19%, and 0.7-1.0 mm in 12%.

Overall, 17% of patients had carotid plaque at baseline.

According to Dr. Petri, by 2 years there were no statistically significant differences between groups with respect to changes in coronary artery calcium score or carotid IMT. Both groups did have a statistically significant change in carotid IMT by 2 years (0.07 mm between baseline and study end for the treatment group vs. 0.09 mm for the placebo group; P less than 0.0001 for both groups) but this was not significant between groups.

Overall, among the patients treated with statin, 48% showed improved carotid IMT (defined as better than 10% change); 6% stayed the same, and 46% got worse. Among the placebo group, 29% of patients improved, whereas 4% remained the same and 67% of patients had worse measurements after 2 years.

The difference between patients who improved was a statistically significant difference (P = .014).

Among statin patients who had no carotid plaque at baseline, 25% were found to have plaque at 2 years, compared with 23% among placebo patients (P = .77).

Looking at laboratory values, the only significant difference between groups was seen in levels of total cholesterol. Among atorvastatin patients, this measure dropped more than 30 points over the study period, from 181.6 mg/dL to 150.7 mg/dL; for placebo patients, it rose 5.5 points, from 190.1 mg/dL to 195.6 mg/dL (P less than 0.0001).

Meanwhile, 51% in the atorvastatin group had abnormal ALT levels during follow-up, compared with 31% in the placebo group (P = .01); creatine kinase values did not differ between groups.

The authors conceded that 2 years of follow-up may not have been sufficient to observe any benefit in SLE; they added that an 80-mg dose (vs. the 40 mg used in this study) may have proved more efficacious. However, "it would not have been possible for us to have done our study with 80 mg, given the high frequency" of abnormal liver function tests with 40-mg atorvastatin, they wrote.

"Although statins may have some benefit for the disease activity of rheumatoid arthritis or multiple sclerosis, we found no evidence of a beneficial effect on SLE activity," concluded the authors.

Nevertheless, "patients with SLE with hyperlipidemia ... should continue to be treated with statins and other antihyperlipidemic medications if they meet the National Cholesterol Education Program guideline thresholds for treatment," they added.

Dr. Petri disclosed being a former member of the Pfizer advisory board and participating in a Pfizer speakers bureau unrelated to atorvastatin. Pfizer is the maker of atorvastatin, marketed as Lipitor.

None of the other authors had any other competing interests to disclose.

Daily atorvastatin use had no significant impact on atherosclerosis progression among systemic lupus erythematosus patients, compared with placebo.

Indeed, among SLE patients without hyperlipidemia, nonstatin interventions "should be considered for the accelerated atherosclerosis of SLE," noted Dr. Michelle Petri, professor of medicine and director of the lupus center at Johns Hopkins University, Baltimore, in the May issue of the Annals of the Rheumatic Diseases.

Dr. Petri and colleagues looked at 200 patients with SLE. To be included in the analysis, patients could not have a history of atherosclerotic events, chronic liver disease, or statin use in the 3 months prior to the study. Patients were also excluded if they had baseline triglyceride levels greater than 500 mg/dL, levels of LDL cholesterol greater than 190 mg/dL, creatinine kinase levels greater than 1.5 times the upper limit of normal, or liver-function test findings greater than two times the upper limit of normal (Ann. Rheum. Dis. 2011;70:760-5).

Patients’ mean age was 48 years, and 92% were female. Roughly two-thirds of patients were white, and the remaining one-third were black.

Patients were randomized to receive either 40 mg daily of atorvastatin or an identical placebo; they underwent helical CT scans and carotid duplex scans at baseline and 2 years.

At baseline, the mean total cholesterol was 186 mg/dL, and 34% of patients had total cholesterol levels greater than 200 mg/dL. The mean LDL cholesterol was 103 mg/dL, with 48% having LDL levels in excess of 100 mg/dL.

Also at baseline, 57% of participants had no coronary artery calcium; 22% had an Agatston score of 0-10; 12% scored 11-99; and 8% scored 100 or greater. The carotid intima-media thickness (IMT) was 0.4-0.5 mm in 23% of patients, 0.5-0.6 mm in 46%, 0.6-0.7 mm in 19%, and 0.7-1.0 mm in 12%.

Overall, 17% of patients had carotid plaque at baseline.

According to Dr. Petri, by 2 years there were no statistically significant differences between groups with respect to changes in coronary artery calcium score or carotid IMT. Both groups did have a statistically significant change in carotid IMT by 2 years (0.07 mm between baseline and study end for the treatment group vs. 0.09 mm for the placebo group; P less than 0.0001 for both groups) but this was not significant between groups.

Overall, among the patients treated with statin, 48% showed improved carotid IMT (defined as better than 10% change); 6% stayed the same, and 46% got worse. Among the placebo group, 29% of patients improved, whereas 4% remained the same and 67% of patients had worse measurements after 2 years.

The difference between patients who improved was a statistically significant difference (P = .014).

Among statin patients who had no carotid plaque at baseline, 25% were found to have plaque at 2 years, compared with 23% among placebo patients (P = .77).

Looking at laboratory values, the only significant difference between groups was seen in levels of total cholesterol. Among atorvastatin patients, this measure dropped more than 30 points over the study period, from 181.6 mg/dL to 150.7 mg/dL; for placebo patients, it rose 5.5 points, from 190.1 mg/dL to 195.6 mg/dL (P less than 0.0001).

Meanwhile, 51% in the atorvastatin group had abnormal ALT levels during follow-up, compared with 31% in the placebo group (P = .01); creatine kinase values did not differ between groups.

The authors conceded that 2 years of follow-up may not have been sufficient to observe any benefit in SLE; they added that an 80-mg dose (vs. the 40 mg used in this study) may have proved more efficacious. However, "it would not have been possible for us to have done our study with 80 mg, given the high frequency" of abnormal liver function tests with 40-mg atorvastatin, they wrote.

"Although statins may have some benefit for the disease activity of rheumatoid arthritis or multiple sclerosis, we found no evidence of a beneficial effect on SLE activity," concluded the authors.

Nevertheless, "patients with SLE with hyperlipidemia ... should continue to be treated with statins and other antihyperlipidemic medications if they meet the National Cholesterol Education Program guideline thresholds for treatment," they added.

Dr. Petri disclosed being a former member of the Pfizer advisory board and participating in a Pfizer speakers bureau unrelated to atorvastatin. Pfizer is the maker of atorvastatin, marketed as Lipitor.

None of the other authors had any other competing interests to disclose.

Daily atorvastatin use had no significant impact on atherosclerosis progression among systemic lupus erythematosus patients, compared with placebo.

Indeed, among SLE patients without hyperlipidemia, nonstatin interventions "should be considered for the accelerated atherosclerosis of SLE," noted Dr. Michelle Petri, professor of medicine and director of the lupus center at Johns Hopkins University, Baltimore, in the May issue of the Annals of the Rheumatic Diseases.

Dr. Petri and colleagues looked at 200 patients with SLE. To be included in the analysis, patients could not have a history of atherosclerotic events, chronic liver disease, or statin use in the 3 months prior to the study. Patients were also excluded if they had baseline triglyceride levels greater than 500 mg/dL, levels of LDL cholesterol greater than 190 mg/dL, creatinine kinase levels greater than 1.5 times the upper limit of normal, or liver-function test findings greater than two times the upper limit of normal (Ann. Rheum. Dis. 2011;70:760-5).

Patients’ mean age was 48 years, and 92% were female. Roughly two-thirds of patients were white, and the remaining one-third were black.

Patients were randomized to receive either 40 mg daily of atorvastatin or an identical placebo; they underwent helical CT scans and carotid duplex scans at baseline and 2 years.

At baseline, the mean total cholesterol was 186 mg/dL, and 34% of patients had total cholesterol levels greater than 200 mg/dL. The mean LDL cholesterol was 103 mg/dL, with 48% having LDL levels in excess of 100 mg/dL.

Also at baseline, 57% of participants had no coronary artery calcium; 22% had an Agatston score of 0-10; 12% scored 11-99; and 8% scored 100 or greater. The carotid intima-media thickness (IMT) was 0.4-0.5 mm in 23% of patients, 0.5-0.6 mm in 46%, 0.6-0.7 mm in 19%, and 0.7-1.0 mm in 12%.

Overall, 17% of patients had carotid plaque at baseline.

According to Dr. Petri, by 2 years there were no statistically significant differences between groups with respect to changes in coronary artery calcium score or carotid IMT. Both groups did have a statistically significant change in carotid IMT by 2 years (0.07 mm between baseline and study end for the treatment group vs. 0.09 mm for the placebo group; P less than 0.0001 for both groups) but this was not significant between groups.

Overall, among the patients treated with statin, 48% showed improved carotid IMT (defined as better than 10% change); 6% stayed the same, and 46% got worse. Among the placebo group, 29% of patients improved, whereas 4% remained the same and 67% of patients had worse measurements after 2 years.

The difference between patients who improved was a statistically significant difference (P = .014).

Among statin patients who had no carotid plaque at baseline, 25% were found to have plaque at 2 years, compared with 23% among placebo patients (P = .77).

Looking at laboratory values, the only significant difference between groups was seen in levels of total cholesterol. Among atorvastatin patients, this measure dropped more than 30 points over the study period, from 181.6 mg/dL to 150.7 mg/dL; for placebo patients, it rose 5.5 points, from 190.1 mg/dL to 195.6 mg/dL (P less than 0.0001).

Meanwhile, 51% in the atorvastatin group had abnormal ALT levels during follow-up, compared with 31% in the placebo group (P = .01); creatine kinase values did not differ between groups.

The authors conceded that 2 years of follow-up may not have been sufficient to observe any benefit in SLE; they added that an 80-mg dose (vs. the 40 mg used in this study) may have proved more efficacious. However, "it would not have been possible for us to have done our study with 80 mg, given the high frequency" of abnormal liver function tests with 40-mg atorvastatin, they wrote.

"Although statins may have some benefit for the disease activity of rheumatoid arthritis or multiple sclerosis, we found no evidence of a beneficial effect on SLE activity," concluded the authors.

Nevertheless, "patients with SLE with hyperlipidemia ... should continue to be treated with statins and other antihyperlipidemic medications if they meet the National Cholesterol Education Program guideline thresholds for treatment," they added.

Dr. Petri disclosed being a former member of the Pfizer advisory board and participating in a Pfizer speakers bureau unrelated to atorvastatin. Pfizer is the maker of atorvastatin, marketed as Lipitor.

None of the other authors had any other competing interests to disclose.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients published online March 28 in Hypertension.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona, and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring Registry (ABPM), which included 68,045 patients with good quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

"Valid registries had to fulfill a series of pre-established criteria, including greater than or equal to 80% of systolic BP (SBP) and diastolic BP (DBP) successful recordings during the daytime and nighttime periods, 24-hour duration, and at least one BP measurement per hour," wrote the authors.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra’s criteria for resistant hypertension: office BP greater than or equal to 140 mmHg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at "appropriate" doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA.110.168948]).

White-coat RH patients were slightly but significantly older (65 versus 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% versus 10%), to be diabetic (35% versus 28%), and to have cardiovascular disease (19% versus 16%), compared with the white-coat RH patients.

Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on electrocardiogram, versus 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 versus 72 micromol/L), higher urinary albumin excretion (11 versus 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% versus 20%).

Circadian BP patterns also showed slight differences between groups, with a higher proportion of risers – who have an increase in BP during nighttime – among the true RH cohort, based on either systolic (22% versus 18%) or diastolic (12% versus 10%) measurements.

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, "thus possibly overestimating the true prevalence of RH."

And despite the findings of significant differences in clinical characteristics between groups, "their discriminating value in clinical practice is probably low," cautioned the authors.

The authors disclosed that the Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories, which makes valsartan. The authors also disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients published online March 28 in Hypertension.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona, and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring Registry (ABPM), which included 68,045 patients with good quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

"Valid registries had to fulfill a series of pre-established criteria, including greater than or equal to 80% of systolic BP (SBP) and diastolic BP (DBP) successful recordings during the daytime and nighttime periods, 24-hour duration, and at least one BP measurement per hour," wrote the authors.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra’s criteria for resistant hypertension: office BP greater than or equal to 140 mmHg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at "appropriate" doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA.110.168948]).

White-coat RH patients were slightly but significantly older (65 versus 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% versus 10%), to be diabetic (35% versus 28%), and to have cardiovascular disease (19% versus 16%), compared with the white-coat RH patients.

Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on electrocardiogram, versus 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 versus 72 micromol/L), higher urinary albumin excretion (11 versus 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% versus 20%).

Circadian BP patterns also showed slight differences between groups, with a higher proportion of risers – who have an increase in BP during nighttime – among the true RH cohort, based on either systolic (22% versus 18%) or diastolic (12% versus 10%) measurements.

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, "thus possibly overestimating the true prevalence of RH."

And despite the findings of significant differences in clinical characteristics between groups, "their discriminating value in clinical practice is probably low," cautioned the authors.

The authors disclosed that the Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories, which makes valsartan. The authors also disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients published online March 28 in Hypertension.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona, and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring Registry (ABPM), which included 68,045 patients with good quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

"Valid registries had to fulfill a series of pre-established criteria, including greater than or equal to 80% of systolic BP (SBP) and diastolic BP (DBP) successful recordings during the daytime and nighttime periods, 24-hour duration, and at least one BP measurement per hour," wrote the authors.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra’s criteria for resistant hypertension: office BP greater than or equal to 140 mmHg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at "appropriate" doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA.110.168948]).

White-coat RH patients were slightly but significantly older (65 versus 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% versus 10%), to be diabetic (35% versus 28%), and to have cardiovascular disease (19% versus 16%), compared with the white-coat RH patients.

Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on electrocardiogram, versus 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 versus 72 micromol/L), higher urinary albumin excretion (11 versus 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% versus 20%).

Circadian BP patterns also showed slight differences between groups, with a higher proportion of risers – who have an increase in BP during nighttime – among the true RH cohort, based on either systolic (22% versus 18%) or diastolic (12% versus 10%) measurements.

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, "thus possibly overestimating the true prevalence of RH."

And despite the findings of significant differences in clinical characteristics between groups, "their discriminating value in clinical practice is probably low," cautioned the authors.

The authors disclosed that the Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories, which makes valsartan. The authors also disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients published online March 28 in Hypertension.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona, and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring Registry (ABPM), which included 68,045 patients with good quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

"Valid registries had to fulfill a series of pre-established criteria, including greater than or equal to 80% of systolic BP (SBP) and diastolic BP (DBP) successful recordings during the daytime and nighttime periods, 24-hour duration, and at least one BP measurement per hour," wrote the authors.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra’s criteria for resistant hypertension: office BP greater than or equal to 140 mmHg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at "appropriate" doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA.110.168948]).

White-coat RH patients were slightly but significantly older (65 versus 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% versus 10%), to be diabetic (35% versus 28%), and to have cardiovascular disease (19% versus 16%), compared with the white-coat RH patients.

Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on electrocardiogram, versus 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 versus 72 micromol/L), higher urinary albumin excretion (11 versus 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% versus 20%).

Circadian BP patterns also showed slight differences between groups, with a higher proportion of risers – who have an increase in BP during nighttime – among the true RH cohort, based on either systolic (22% versus 18%) or diastolic (12% versus 10%) measurements.

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, "thus possibly overestimating the true prevalence of RH."

And despite the findings of significant differences in clinical characteristics between groups, "their discriminating value in clinical practice is probably low," cautioned the authors.

The authors disclosed that the Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories, which makes valsartan. The authors also disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients published online March 28 in Hypertension.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona, and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring Registry (ABPM), which included 68,045 patients with good quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

"Valid registries had to fulfill a series of pre-established criteria, including greater than or equal to 80% of systolic BP (SBP) and diastolic BP (DBP) successful recordings during the daytime and nighttime periods, 24-hour duration, and at least one BP measurement per hour," wrote the authors.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra’s criteria for resistant hypertension: office BP greater than or equal to 140 mmHg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at "appropriate" doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA.110.168948]).

White-coat RH patients were slightly but significantly older (65 versus 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% versus 10%), to be diabetic (35% versus 28%), and to have cardiovascular disease (19% versus 16%), compared with the white-coat RH patients.

Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on electrocardiogram, versus 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 versus 72 micromol/L), higher urinary albumin excretion (11 versus 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% versus 20%).

Circadian BP patterns also showed slight differences between groups, with a higher proportion of risers – who have an increase in BP during nighttime – among the true RH cohort, based on either systolic (22% versus 18%) or diastolic (12% versus 10%) measurements.

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, "thus possibly overestimating the true prevalence of RH."

And despite the findings of significant differences in clinical characteristics between groups, "their discriminating value in clinical practice is probably low," cautioned the authors.

The authors disclosed that the Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories, which makes valsartan. The authors also disclosed having attended meetings funded by Lacer.

Up to 37% of resistant office hypertension is actually white-coat hypertension, according to an analysis of ambulatory blood pressure monitoring data from more than 8,000 patients published online March 28 in Hypertension.

Meanwhile, the remaining 63% who are truly resistant have a starkly worse clinical profile than do their white-coat counterparts, including significantly higher likelihoods of smoking, and having diabetes, left ventricular hypertrophy, microalbuminuria, and cardiovascular disease.

Dr. Alejandro de la Sierra of the University of Barcelona, and colleagues, looked at 2009 data from the Spanish Ambulatory Blood Pressure Monitoring Registry (ABPM), which included 68,045 patients with good quality office BP data, ambulatory BP data, and information about prescribed antihypertensives, including at least one diuretic.

Ambulatory BP measurements were acquired using an automated, noninvasive oscillometric device placed by a physician, and which registered BP at 20-minute intervals over a 24-hour period.

"Valid registries had to fulfill a series of pre-established criteria, including greater than or equal to 80% of systolic BP (SBP) and diastolic BP (DBP) successful recordings during the daytime and nighttime periods, 24-hour duration, and at least one BP measurement per hour," wrote the authors.

Patients returned the following day to their doctors for removal of the device.

Overall, 12% of participants in the registry (8,295 patients; 51% male, mean age 64 years) met Dr. de la Sierra’s criteria for resistant hypertension: office BP greater than or equal to 140 mmHg systolic and/or 90 mm Hg diastolic while being treated with three or more antihypertensive agents at "appropriate" doses.

ABPM patients were classified in two groups: 5,182 patients (62.5%) had ambulatory 24-hour BP values greater than or equal to 130 and/or 80 mm Hg and were diagnosed as true RH, and 3,113 patients (37.5%) showed 24-hour BP values below this limit and were considered as having white-coat RH, wrote the authors (Hypertension 2011 March 28 [doi: 10.1161/HYPERTENSIONAHA.110.168948]).

White-coat RH patients were slightly but significantly older (65 versus 64 years), and more likely to be female (54%).

Truly resistant patients, however, were more likely to be smokers (15% versus 10%), to be diabetic (35% versus 28%), and to have cardiovascular disease (19% versus 16%), compared with the white-coat RH patients.

Moreover, 19% of the true RH patients had left ventricular hypertrophy, as seen on electrocardiogram, versus 14% of white-coat patients.

They also had higher creatinine levels than did their white-coat counterparts (75 versus 72 micromol/L), higher urinary albumin excretion (11 versus 7 mg/g), and a higher percentage of patients with a urinary albumin excretion greater than 30 mg/g (30% versus 20%).

Circadian BP patterns also showed slight differences between groups, with a higher proportion of risers – who have an increase in BP during nighttime – among the true RH cohort, based on either systolic (22% versus 18%) or diastolic (12% versus 10%) measurements.

Body mass index and total cholesterol did not vary significantly between groups.

According to the authors, the study represents the first time that the prevalence of resistant hypertension was assessed in such a large cohort of patients.

However, the researchers pointed to one major weakness of the study: the inability to confirm that patients prescribed antihypertensive drugs were adherent to their medication regimen, "thus possibly overestimating the true prevalence of RH."

And despite the findings of significant differences in clinical characteristics between groups, "their discriminating value in clinical practice is probably low," cautioned the authors.

The authors disclosed that the Spanish ABPM Registry was initiated and is maintained by Lacer Laboratories, which makes valsartan. The authors also disclosed having attended meetings funded by Lacer.