Osteoarthritis in hip or knee can increase diabetes risk

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Individuals who have osteoarthritis in the hip or knee are significantly more likely to develop diabetes than are people without the condition, according to findings from a population-based cohort study.

The relationship between osteoarthritis (OA) and new-onset diabetes was largely explained by the walking limitations brought on by OA, which was unsurprising to lead author Tetyana Kendzerska, MD, PhD, of the University of Toronto, who presented the study at the annual meeting of the Canadian Rheumatology Association.

Dr. Tetyana Kendzerska of the University of Toronto
Dr. Tetyana Kendzerska
“Given that walking is critical for physical activity, this is not surprising perhaps [because] we know that physical activity is a key preventive measure for all chronic conditions, including diabetes,” Dr. Kendzerska said in an interview.

But Dr. Kendzerska noted that even though “the World Health Organization has determined that osteoarthritis is the fastest growing chronic disease and the single most common cause of disability in older adults [and] the majority of people with OA have at least one other chronic condition – usually diabetes, high blood pressure, [or] heart disease ... few studies have examined the impact of OA on these other conditions, including on the development of diabetes.”

Dr. Kendzerska and her coauthors used existing data to study a population of 16,362 adults aged 55 or older who did not have diabetes at baseline enrollment during 1996-1998 and were then followed until 2014 for a median period of 13 years. The adults’ median age was 68 years and median body mass index was 25.3 kg/m2; 61% were female. Cox regression modeling was used to quantify any association found between osteoarthritis and diabetes.

A total of 1,637 (10%) had hip osteoarthritis, 2,431 (15%) had knee osteoarthritis, and 3,908 (24%) had some type of walking limitation. Over the course of the follow-up period, 3,539 (22%) developed diabetes. The risk for diabetes was significantly elevated in particular for individuals with two hip or knee joints with OA, where the hazard ratio was 1.25 (95% CI, 1.08-1.44; P = .003) for hips and 1.16 (95% CI, 1.04-1.29; P = .008) for knees, after adjustment for baseline age, sex, income, body mass index, preexisting hypertension and cardiovascular disease, and prior primary care exposure. However, further adjustment to the comparisons for walking limitation attenuated the relationships so that they were no longer statistically significant.

The next steps for research may be to assess the impact of evidence-based osteoarthritis care on mobility and metabolic derangements, she said.

Previous “studies have been limited by a number of methodological limitations, [such as] cross-sectional design or failure to control for other factors that may explain a relationship. Our study has addressed these limitations and thus provides important evidence to suggest that osteoarthritis-related difficulty walking contributes causally to the development of diabetes [but] now we need studies to show if effective treatment of hip and knee osteoarthritis can reduce diabetes risk.”

The Canadian Institutes of Health Research funded the study. Dr. Kendzerska did not report any relevant financial disclosures.

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Individuals who have osteoarthritis in the hip or knee are significantly more likely to develop diabetes than are people without the condition, according to findings from a population-based cohort study.

The relationship between osteoarthritis (OA) and new-onset diabetes was largely explained by the walking limitations brought on by OA, which was unsurprising to lead author Tetyana Kendzerska, MD, PhD, of the University of Toronto, who presented the study at the annual meeting of the Canadian Rheumatology Association.

Dr. Tetyana Kendzerska of the University of Toronto
Dr. Tetyana Kendzerska
“Given that walking is critical for physical activity, this is not surprising perhaps [because] we know that physical activity is a key preventive measure for all chronic conditions, including diabetes,” Dr. Kendzerska said in an interview.

But Dr. Kendzerska noted that even though “the World Health Organization has determined that osteoarthritis is the fastest growing chronic disease and the single most common cause of disability in older adults [and] the majority of people with OA have at least one other chronic condition – usually diabetes, high blood pressure, [or] heart disease ... few studies have examined the impact of OA on these other conditions, including on the development of diabetes.”

Dr. Kendzerska and her coauthors used existing data to study a population of 16,362 adults aged 55 or older who did not have diabetes at baseline enrollment during 1996-1998 and were then followed until 2014 for a median period of 13 years. The adults’ median age was 68 years and median body mass index was 25.3 kg/m2; 61% were female. Cox regression modeling was used to quantify any association found between osteoarthritis and diabetes.

A total of 1,637 (10%) had hip osteoarthritis, 2,431 (15%) had knee osteoarthritis, and 3,908 (24%) had some type of walking limitation. Over the course of the follow-up period, 3,539 (22%) developed diabetes. The risk for diabetes was significantly elevated in particular for individuals with two hip or knee joints with OA, where the hazard ratio was 1.25 (95% CI, 1.08-1.44; P = .003) for hips and 1.16 (95% CI, 1.04-1.29; P = .008) for knees, after adjustment for baseline age, sex, income, body mass index, preexisting hypertension and cardiovascular disease, and prior primary care exposure. However, further adjustment to the comparisons for walking limitation attenuated the relationships so that they were no longer statistically significant.

The next steps for research may be to assess the impact of evidence-based osteoarthritis care on mobility and metabolic derangements, she said.

Previous “studies have been limited by a number of methodological limitations, [such as] cross-sectional design or failure to control for other factors that may explain a relationship. Our study has addressed these limitations and thus provides important evidence to suggest that osteoarthritis-related difficulty walking contributes causally to the development of diabetes [but] now we need studies to show if effective treatment of hip and knee osteoarthritis can reduce diabetes risk.”

The Canadian Institutes of Health Research funded the study. Dr. Kendzerska did not report any relevant financial disclosures.

 

Individuals who have osteoarthritis in the hip or knee are significantly more likely to develop diabetes than are people without the condition, according to findings from a population-based cohort study.

The relationship between osteoarthritis (OA) and new-onset diabetes was largely explained by the walking limitations brought on by OA, which was unsurprising to lead author Tetyana Kendzerska, MD, PhD, of the University of Toronto, who presented the study at the annual meeting of the Canadian Rheumatology Association.

Dr. Tetyana Kendzerska of the University of Toronto
Dr. Tetyana Kendzerska
“Given that walking is critical for physical activity, this is not surprising perhaps [because] we know that physical activity is a key preventive measure for all chronic conditions, including diabetes,” Dr. Kendzerska said in an interview.

But Dr. Kendzerska noted that even though “the World Health Organization has determined that osteoarthritis is the fastest growing chronic disease and the single most common cause of disability in older adults [and] the majority of people with OA have at least one other chronic condition – usually diabetes, high blood pressure, [or] heart disease ... few studies have examined the impact of OA on these other conditions, including on the development of diabetes.”

Dr. Kendzerska and her coauthors used existing data to study a population of 16,362 adults aged 55 or older who did not have diabetes at baseline enrollment during 1996-1998 and were then followed until 2014 for a median period of 13 years. The adults’ median age was 68 years and median body mass index was 25.3 kg/m2; 61% were female. Cox regression modeling was used to quantify any association found between osteoarthritis and diabetes.

A total of 1,637 (10%) had hip osteoarthritis, 2,431 (15%) had knee osteoarthritis, and 3,908 (24%) had some type of walking limitation. Over the course of the follow-up period, 3,539 (22%) developed diabetes. The risk for diabetes was significantly elevated in particular for individuals with two hip or knee joints with OA, where the hazard ratio was 1.25 (95% CI, 1.08-1.44; P = .003) for hips and 1.16 (95% CI, 1.04-1.29; P = .008) for knees, after adjustment for baseline age, sex, income, body mass index, preexisting hypertension and cardiovascular disease, and prior primary care exposure. However, further adjustment to the comparisons for walking limitation attenuated the relationships so that they were no longer statistically significant.

The next steps for research may be to assess the impact of evidence-based osteoarthritis care on mobility and metabolic derangements, she said.

Previous “studies have been limited by a number of methodological limitations, [such as] cross-sectional design or failure to control for other factors that may explain a relationship. Our study has addressed these limitations and thus provides important evidence to suggest that osteoarthritis-related difficulty walking contributes causally to the development of diabetes [but] now we need studies to show if effective treatment of hip and knee osteoarthritis can reduce diabetes risk.”

The Canadian Institutes of Health Research funded the study. Dr. Kendzerska did not report any relevant financial disclosures.

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Key clinical point: Osteoarthritis in the hip or knee puts individuals at increased risk of diabetes, largely because of walking limitations.

Major finding: The risk for diabetes was significantly elevated for individuals with two hip or knee joints with OA, where the hazard ratio was 1.25 (95% CI, 1.08-1.44; P = .003) for hips and 1.16 (95% CI, 1.04-1.29; P = .008) for knees.

Data source: Population-based cohort study of 16,362 individuals without diabetes at baseline.

Disclosures: The Canadian Institutes of Health Research funded the study. Dr. Kendzerska did not report any relevant financial disclosures.

Familial and sporadic ankylosing spondylitis differ in small ways

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While differences do exist between familial and sporadic ankylosing spondylitis, key similarities suggest that the two conditions can be treated the same way, according to a new study presented at the annual meeting of the Canadian Rheumatology Association.

“AS [ankylosing spondylitis] patients with a family history of AS are not very different from patients without any family history,” Nigil Haroon, MD, of the University Health Network in Toronto, explained in an interview. “They have similar disease activity as measured by markers of inflammation [and] similar disease severity as assessed by radiographic scoring for spinal damage.”

Dr. Haroon, along with his coinvestigators – including Bruce Sheng, MD,of the same institution, who presented the study at the meeting – prospectively followed AS patients satisfying the New York criteria for a period of 15 years, collecting data on 888 eligible subjects who were eventually included in the study. Of the subjects included, 74% were male, the average age was 45.6 years (standard deviation, 13.7 years), and average disease duration was 15 years (SD, 11.5 years).

Dr. Nigil Haroon of University Health Network Toronto.
Dr. Nigil Haroon


The investigators found some similarities between the 177 (20%) patients with familial AS who had at least one first- or second-generation relative with the disease and the 711 with sporadic AS. Anti–tumor necrosis factor (anti-TNF) treatment failed in 23.1% of familial AS patients and 23.6% of sporadic disease patients based on the lack of a “sustained clinical effect” for more than 1 year. There were also no differences found between the groups in clinical and radiographic severity of disease.

However, patients with familial AS did record earlier onset of disease (22.5 years vs. 24.3 years; P = .016), longer disease duration (17.4 years vs. 14.3 years; P = .003), and higher HLA-B27 positivity (90% vs. 65%; P less than .001), along with higher rates of uveitis, psoriatic arthritis, and inflammatory bowel disease.

“Some of the findings are expected, including the higher prevalence of HLA-B27 due to gene sharing in the family. ... The higher B27 sharing may also affect the uveitis prevalence as well in familial AS,” Dr. Haroon explained. “The similar radiographic progression rates and treatment responses are interesting findings.”

In terms of the ramifications of these findings, Dr. Haroon stated that clinicians should reevaluate how they prescribe drugs to their AS patients.

“The high likelihood of uveitis in familial AS patients – 43% versus 29% – may affect the choice of treatment as all drugs are not equally effective in uveitis,” he said. “As the family history of extra-articular manifestations is high in familial AS, it remains to be seen if a lower threshold for investigating symptoms suggestive of IBD/uveitis will decrease delays in diagnosis of these conditions in individuals with a family history of AS.”

Moving forward from here, Dr. Haroon called for family studies, especially those including families with multiple individuals affected with AS, as these can help identify genetic risk factors that may be contribute to the development of AS.

“There is paucity of data on familial AS,” Dr. Haroon said. “The strength of this study is the large dataset.”

The study was funded by the Canadian Rheumatology Association’s Summer Research Program, which supported Dr. Sheng. Dr. Sheng and Dr. Haroon did not report any other relevant financial disclosures.
 

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While differences do exist between familial and sporadic ankylosing spondylitis, key similarities suggest that the two conditions can be treated the same way, according to a new study presented at the annual meeting of the Canadian Rheumatology Association.

“AS [ankylosing spondylitis] patients with a family history of AS are not very different from patients without any family history,” Nigil Haroon, MD, of the University Health Network in Toronto, explained in an interview. “They have similar disease activity as measured by markers of inflammation [and] similar disease severity as assessed by radiographic scoring for spinal damage.”

Dr. Haroon, along with his coinvestigators – including Bruce Sheng, MD,of the same institution, who presented the study at the meeting – prospectively followed AS patients satisfying the New York criteria for a period of 15 years, collecting data on 888 eligible subjects who were eventually included in the study. Of the subjects included, 74% were male, the average age was 45.6 years (standard deviation, 13.7 years), and average disease duration was 15 years (SD, 11.5 years).

Dr. Nigil Haroon of University Health Network Toronto.
Dr. Nigil Haroon


The investigators found some similarities between the 177 (20%) patients with familial AS who had at least one first- or second-generation relative with the disease and the 711 with sporadic AS. Anti–tumor necrosis factor (anti-TNF) treatment failed in 23.1% of familial AS patients and 23.6% of sporadic disease patients based on the lack of a “sustained clinical effect” for more than 1 year. There were also no differences found between the groups in clinical and radiographic severity of disease.

However, patients with familial AS did record earlier onset of disease (22.5 years vs. 24.3 years; P = .016), longer disease duration (17.4 years vs. 14.3 years; P = .003), and higher HLA-B27 positivity (90% vs. 65%; P less than .001), along with higher rates of uveitis, psoriatic arthritis, and inflammatory bowel disease.

“Some of the findings are expected, including the higher prevalence of HLA-B27 due to gene sharing in the family. ... The higher B27 sharing may also affect the uveitis prevalence as well in familial AS,” Dr. Haroon explained. “The similar radiographic progression rates and treatment responses are interesting findings.”

In terms of the ramifications of these findings, Dr. Haroon stated that clinicians should reevaluate how they prescribe drugs to their AS patients.

“The high likelihood of uveitis in familial AS patients – 43% versus 29% – may affect the choice of treatment as all drugs are not equally effective in uveitis,” he said. “As the family history of extra-articular manifestations is high in familial AS, it remains to be seen if a lower threshold for investigating symptoms suggestive of IBD/uveitis will decrease delays in diagnosis of these conditions in individuals with a family history of AS.”

Moving forward from here, Dr. Haroon called for family studies, especially those including families with multiple individuals affected with AS, as these can help identify genetic risk factors that may be contribute to the development of AS.

“There is paucity of data on familial AS,” Dr. Haroon said. “The strength of this study is the large dataset.”

The study was funded by the Canadian Rheumatology Association’s Summer Research Program, which supported Dr. Sheng. Dr. Sheng and Dr. Haroon did not report any other relevant financial disclosures.
 

 

While differences do exist between familial and sporadic ankylosing spondylitis, key similarities suggest that the two conditions can be treated the same way, according to a new study presented at the annual meeting of the Canadian Rheumatology Association.

“AS [ankylosing spondylitis] patients with a family history of AS are not very different from patients without any family history,” Nigil Haroon, MD, of the University Health Network in Toronto, explained in an interview. “They have similar disease activity as measured by markers of inflammation [and] similar disease severity as assessed by radiographic scoring for spinal damage.”

Dr. Haroon, along with his coinvestigators – including Bruce Sheng, MD,of the same institution, who presented the study at the meeting – prospectively followed AS patients satisfying the New York criteria for a period of 15 years, collecting data on 888 eligible subjects who were eventually included in the study. Of the subjects included, 74% were male, the average age was 45.6 years (standard deviation, 13.7 years), and average disease duration was 15 years (SD, 11.5 years).

Dr. Nigil Haroon of University Health Network Toronto.
Dr. Nigil Haroon


The investigators found some similarities between the 177 (20%) patients with familial AS who had at least one first- or second-generation relative with the disease and the 711 with sporadic AS. Anti–tumor necrosis factor (anti-TNF) treatment failed in 23.1% of familial AS patients and 23.6% of sporadic disease patients based on the lack of a “sustained clinical effect” for more than 1 year. There were also no differences found between the groups in clinical and radiographic severity of disease.

However, patients with familial AS did record earlier onset of disease (22.5 years vs. 24.3 years; P = .016), longer disease duration (17.4 years vs. 14.3 years; P = .003), and higher HLA-B27 positivity (90% vs. 65%; P less than .001), along with higher rates of uveitis, psoriatic arthritis, and inflammatory bowel disease.

“Some of the findings are expected, including the higher prevalence of HLA-B27 due to gene sharing in the family. ... The higher B27 sharing may also affect the uveitis prevalence as well in familial AS,” Dr. Haroon explained. “The similar radiographic progression rates and treatment responses are interesting findings.”

In terms of the ramifications of these findings, Dr. Haroon stated that clinicians should reevaluate how they prescribe drugs to their AS patients.

“The high likelihood of uveitis in familial AS patients – 43% versus 29% – may affect the choice of treatment as all drugs are not equally effective in uveitis,” he said. “As the family history of extra-articular manifestations is high in familial AS, it remains to be seen if a lower threshold for investigating symptoms suggestive of IBD/uveitis will decrease delays in diagnosis of these conditions in individuals with a family history of AS.”

Moving forward from here, Dr. Haroon called for family studies, especially those including families with multiple individuals affected with AS, as these can help identify genetic risk factors that may be contribute to the development of AS.

“There is paucity of data on familial AS,” Dr. Haroon said. “The strength of this study is the large dataset.”

The study was funded by the Canadian Rheumatology Association’s Summer Research Program, which supported Dr. Sheng. Dr. Sheng and Dr. Haroon did not report any other relevant financial disclosures.
 

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Key clinical point: Familial and sporadic ankylosing spondylitis patients have a similar response to TNF inhibitors.

Major finding: Anti-TNF treatment failed in 23.1% of familial AS patients and 23.6% of sporadic disease patients based on the lack of a “sustained clinical effect” for more than 1 year.

Data source: Prospective cohort study of 888 patients with AS over 15 years.

Disclosures: Funded by the Canadian Rheumatology Association’s Summer Research Program. No other relevant disclosures were reported.