Meeting News

Expert lays out mystery of why some gout is non-inflammatory

William Rigby

SCOTTSDALE, Ariz. — Clinicians know that patients can vary widely by onset, location and serum uric acid levels, but reason for the variance can still be puzzling, according to an expert here at the annual Basic and Clinical Immunology for the Busy Clinician symposium.

“To get inflammation in the joint we usually work from the construct that there are many factors,” said William Rigby, MD, vice chair, department of medicine, Dartmouth Geisel School of Medicine. “No joint inflammation arises spontaneously,” he said, noting the factors that lead to inflammation are genetics, environment and sex predisposition.

Gouty arthritis pathogenesis for genetics is URAT-1, “the environment is alcohol” and there are more men with the disease, he said.

Yet, there is no gouty pneumonitis, no gouty uveitis, and very little gouty dermatitis, he said.

“The question you are all going to have to ask yourself is why — of all the joints and all the different structures in the body — why do you get synovitis,” Rigby said.

More importantly, "why do some people walk into your office with a swollen digit that if you stick a needle into it is going to pull out paste of monosodium uric acid crystals. There is no inflammation, very little symptoms and if you took an X-ray there might be some joint erosion but no inflammatory response,” he said.

Rigby said the contrast is a patient with an intense inflammatory response in the MTP joint and the clinical phenomenon — podagra.

“So, why the variability in onset, why the difference related to location and serum uric acid?” Rigby said.

His conclusions are that first, “our biologics inform our understanding. It is clearly an IL-1 dependent process,” he said.

Research has confirmed that if a patient has a serum uric acid level of >9 for 5 years, only 22% will develop clinical gout, Rigby said. “So there is something else that is regulating this process.” He said it is not the “total body overload of uric acid.”

Rigby said that an interesting research insight was the correlation between higher serum uric acid with the amount of water intake: “it was negatively correlated with water intake. So, hydration, hydration, hydration.”

Clinicians and researchers still do not know why some uric acid deposits are non-inflammatory, he concluded. – by Joan-Marie Stiglich, ELS

Reference:
Rigby W. Translational Advances in Inflammatory Arthritis. Presented at: Seventh Annual Basic and Clinical Immunology for the Busy Clinician; February 15-16, 2019; Scottsdale, Ariz. 

Disclosure: Rigby has previously disclosed relevant relationships with Bristol-Myers Squibb, Pfizer and Roche.

William Rigby

SCOTTSDALE, Ariz. — Clinicians know that patients can vary widely by onset, location and serum uric acid levels, but reason for the variance can still be puzzling, according to an expert here at the annual Basic and Clinical Immunology for the Busy Clinician symposium.

“To get inflammation in the joint we usually work from the construct that there are many factors,” said William Rigby, MD, vice chair, department of medicine, Dartmouth Geisel School of Medicine. “No joint inflammation arises spontaneously,” he said, noting the factors that lead to inflammation are genetics, environment and sex predisposition.

Gouty arthritis pathogenesis for genetics is URAT-1, “the environment is alcohol” and there are more men with the disease, he said.

Yet, there is no gouty pneumonitis, no gouty uveitis, and very little gouty dermatitis, he said.

“The question you are all going to have to ask yourself is why — of all the joints and all the different structures in the body — why do you get synovitis,” Rigby said.

More importantly, "why do some people walk into your office with a swollen digit that if you stick a needle into it is going to pull out paste of monosodium uric acid crystals. There is no inflammation, very little symptoms and if you took an X-ray there might be some joint erosion but no inflammatory response,” he said.

Rigby said the contrast is a patient with an intense inflammatory response in the MTP joint and the clinical phenomenon — podagra.

“So, why the variability in onset, why the difference related to location and serum uric acid?” Rigby said.

His conclusions are that first, “our biologics inform our understanding. It is clearly an IL-1 dependent process,” he said.

Research has confirmed that if a patient has a serum uric acid level of >9 for 5 years, only 22% will develop clinical gout, Rigby said. “So there is something else that is regulating this process.” He said it is not the “total body overload of uric acid.”

Rigby said that an interesting research insight was the correlation between higher serum uric acid with the amount of water intake: “it was negatively correlated with water intake. So, hydration, hydration, hydration.”

Clinicians and researchers still do not know why some uric acid deposits are non-inflammatory, he concluded. – by Joan-Marie Stiglich, ELS

Reference:
Rigby W. Translational Advances in Inflammatory Arthritis. Presented at: Seventh Annual Basic and Clinical Immunology for the Busy Clinician; February 15-16, 2019; Scottsdale, Ariz. 

Disclosure: Rigby has previously disclosed relevant relationships with Bristol-Myers Squibb, Pfizer and Roche.

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