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Gout due to deficiency of a protein found in joint fluid.

Gout due to deficiency of a protein found in joint fluid.

A multinational research team discovered a novel molecular route that is thought to be the origin of gout and the path it takes to joint tissue disintegration.

A protein called lubricin, which is present in joint fluid, may represent a unique therapeutic target for the prevention and treatment of gout, according to researchers.

The discovery was made, in part, through research on a lady who had urate crystal formations and joint degradation but low blood urate levels.

Gout, a common kind of inflammatory arthritis, can make joints extremely painful, swollen, and stiff. A punishment for those Gout has often affected one joint at a time since ancient times. Frequently the joint at the base of the big toe.

According to the American College of Rheumatology, the illness affects more than 3 million people in the US. Men. Also, postmenopausal women and persons with kidney problems are more prone to the condition.

An innovative molecular mechanism that causes gout and leads to the erosion of joint tissue has been discovered by an international research team headed by the University of California San Diego School of Medicine. The journal Arthritis & Rheumatology reported the researchers’ findings.

What is Gout?

An extremely painful, swollen, and stiffening form of arthritis known as gout generates these symptoms in the joints. The metatarsophalangeal joint, which is located at the base of the big toe, is typically affected. The body having too much uric acid is its main cause.

More than 3 million Americans suffer from gout, which is the most prevalent kind of inflammatory arthritis in men. Additionally, females are more prone to get gout after menopause despite the fact that disease is generally less likely to harm them.

Gout episodes can start suddenly and may continue to happen over time. This persistent recurrence can be quite painful and gradually destroy the tissue surrounding the inflammation. Obesity, cardiovascular disease, and hypertension are gout risk factors.

Unusual case study on gout

Purines, which are present in the body, meat, and some beverages, are broken down by the body to produce uric acid.

Uric acid crystals may grow inside a joint as a result of hyperuricemia. This is a high quantity of uric acid in the blood and promotes inflammation.

High uric acid levels are also frequently found in the joint fluid of gout sufferers. Although not invariably, gout can be caused by hyperuricemia. Up to 21% of the population may have asymptomatic hyperuricemia, according to one study.

Dr. Robert Terkeltaub is a professor at the University of California San Diego School of Medicine. He is section chief of rheumatology at the Veterans Affairs San Diego Healthcare System. Also, he is the study’s senior author, stated: “There are factors well beyond having a high serum rate to determine who gets gout, who doesn’t get gout.”

Factors that can cause gout

The researchers’ investigation of a 22-year-old lady with an atypical case of gout was included in their report. She had urate crystal formations and joint degradation, but her blood tests did not reveal elevated urate levels.

Researchers employed RNA-sequencing, a technology that gives a quantitative analysis of messenger RNA molecules in a biological sample, and whole genome sequencing, an investigation of an organism’s entire DNA composition, for their study.

In order to pinpoint a molecular route underlying the patient’s condition. They also used quantitative proteomic techniques, a method that enables a thorough examination of proteins. They examined samples from the young woman, her parents, and unrelated individuals.

Finally, scientists discovered a chemical route that had been damaged in the young woman. Their research focused on lubricin, a protein that lubricates joints.

Researchers found that the woman’s joint fluid had many proteins that were lower than those of her parents’ joint fluid. Also, lower than the combined results from four healthy controls.

“We searched for something that would either be tenfold decreased in the sick… related to the mother or father and the control or tenfold increased in the patient relative to the mother or father and the healthy control,” the researcher explained. And we discovered that the patient had roughly a dozen proteins that had significantly lower levels, Terkeltaub added.

Lubricin was one of those proteins. The following analysis focused on 18 individuals who had uncontrolled hyperuricemia and common gout. Five of them also showed low lubricin levels.

Lubricin inhibits inflammation

In a different section of the investigation, scientists employed mice with and without lubricin. Interleukin-1β, an inflammatory cytokine, was administered into the animals’ knee joints.

The main enzyme that really produces uric acid, xanthine oxidase, was enriched in the cells known as macrophages in the joint lining of the mice that didn’t produce lubricin, according to Terkeltaub.

According to the experiment, lubricin prevents urate from crystallising in joints and inhibits the release of xanthine oxidase and urate via stimulating white blood cells.

Dr. Puja Paul Khanna, an associate professor in the department of Internal Medicine at the University of Michigan Medical School. He stated that the study suggests lubricin may function as a biomarker for gout.

“With the mice models, they are observing that even if you did not have a high level of uric acid, but you are already experiencing damage from those small little, you know, monosodium urate crystals. We have identified lubricin as the cause, so we could block that pathway, Khanna added. “The [monosodium urate] crystals have a higher possibility of accumulating and harming that joint if the mice are deficient, meaning [they] lack lubricin. Right? More research on the same is required in people.

Terkeltaub emphasised that the findings demonstrates that lubricin’s function extends beyond just lubricating joint tissues.

In addition to inhibiting the inflammation brought on by the crystals and limiting the formation of new crystals, lubricin is something that is “actually involved in what we term the homeostasis of uric acid in the joint,” according to the expert.

Terkeltaub noted that the individual’s lubricin and other molecule-controlling lubricin gene variations may have an impact on whether or not a person with hyperuricemia develops gout.

The development of gout

This study shows that more can be learned about the pathophysiology of gout, according to Dr. Theodore Fields, a rheumatologist from Weill Cornell Medicine and Hospital for Special Surgery in New York who was not involved in the study.

He stated, “We continue to have big information gaps about why some patients get gout and some don’t, even if both have the same level of serum urate. It makes perfect sense that factors like lubricin deficiency play a role in certain patients.

Further studies by Terkeltaub will focus on lubricin’s potential as a novel therapeutic target for the prevention and treatment of gout as well as gout biomarkers and biomarkers for other inflammatory diseases.


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How metabolic syndrome may increase the risk of Gout?

How metabolic syndrome may increase the risk of Gout?

Obesity, type 2 diabetes, high cholesterol, and cardiovascular disease all seem to be more common in people with metabolic syndrome(MetS). This may make them more likely to develop in tandem.

The syndrome is a group of risk factors that have been linked to an elevated risk of acquiring additional disorders rather than a single, separate disease.

Metabolic syndrome have a higher risk of developing gout, according to research from the Sungkyunkwan University School of Medicine in South Korea. Its a kind of arthritis that causes pain and swelling in the joints.

A recent study as per the journal Arthritis & Rheumatology, examined over 1.3 million men between the ages of 20 and 39 who had health examinations. The relationship between modifications in the participants’ METs and the onset of gout was examined.

They identified those who had gout using a database of diagnoses. Also, they utilised a statistical model to examine the connection between changes in metabolic syndrome and the onset of gout.

They found that males with metabolic syndrome or those who developed MetS had a higher risk of developing gout. Men who had high triglyceride levels and abdominal obesity—two factors associated with MetS—were at a substantially higher risk.

What is metabolic syndrome (MetS)?

A clinician may suspect metabolic syndrome if a patient displays at least three of the following five signs and symptoms:

  • Specifically, a waist size of more than 40 inches for men and more than 35 inches for women is considered central, visceral, abdominal obesity.
  • 100 mg/dL or more for fasting blood sugar.
  • values of 130/85 mm/Hg or above for blood pressure.
  • Blood triglyceride values of 150 mg/dL or higher.
  • levels of high-density lipoprotein (HDL) cholesterol at or below 50 mg/dL for women and 40 mg/dL or less for men.

What is gout?

An extremely painful, inflammatory, and inflexible form of arthritis known as gout causes the joints to become stiff.

The metatarsophalangeal joint, which is situated at the base of the big toe, is typically affected. An excessive buildup of uric acid in the body is the source of the disorder.

Researchers find

18,473 males in the recent study experienced gout. Compared to people having MetS, people having metabolic syndrome had a nearly four-fold increased risk of developing gout.

The researchers also noted that a participant’s probability of developing gout quadrupled if they had MetS. Yet, the likelihood of developing gout was practically cut in half for those who recovered from MetS.

High triglyceride levels and abdominal obesity were found to have the highest associations with gout risk. This is as per reports of metS factors.

Comparison was made for those in their 20s, 30s, and those who were underweight or had a normal weight. People with underweight were more likely to experience a connection between changes in MetS and gout.

This is the first extensive study to look at the relationship between alterations in the metabolic syndrome and the risk of gout. According to the study, young persons’ chance of developing gout can be greatly decreased by avoiding MetS or recovering from it.

Reports as per studies

Recent epidemiologic studies have revealed that, when compared to controls, those with hyperuricemia and gout had a higher prevalence of the metabolic syndrome.

In a cross-sectional research of 21,544 participants who completed work-related health examinations, those with serum urate levels 9 mg/dL had about a five-fold greater chance of developing metabolic syndrome. This is compared to those with serum urate levels 7 mg/dL.

Ford et al used data from the National Health and Nutrition Examination Surveys (NHANES) from 1999 to 2002. They conducted a cross-sectional analysis of 1370 children and adolescents to ascertain the relationship between serum urate and metabolic syndrome.

In the lowest to highest quartiles of serum urate, risk of metabolic syndrome was 1.0%, 3.7%, 10.3%, and 21.1%, respectively. The top quartile of urate had a roughly 15-fold higher risk of metabolic syndrome than the lowest two quartiles.

When comparing data from 1988-1994 to 1999-2006, NHANES also revealed that the prevalence of gout and metabolic syndrome were rising continuously and at comparable rates.

Rashad Barsoum, MD, FRCP, FRCPE, emeritus professor of medicine at Cairo University, and Rheumatology Advisor talked about the epidemiologic link between gout and metabolic syndrome. It is still disputed whether hyperuricemia is a surrogate marker or a confounding risk factor, but the statistical correlation does not suggest causality, he says, despite the significant evidence linking it to the metabolic syndrome.

Action to reduce risks

The findings of this study, according to Mitchell, “should at the very least act as a wake-up call for the children. Diabetes and hypertension are no longer considered “diseases of the elderly.”

“Gout is merely one of the numerous additional hazards that come with these chronic illnesses. In addition to lowering quality of life, early onset of these diseases may also shorten lifespans. This is over the next few decades, according to the expert.

To “promote the findings of this study to the general public and build a gout prevention programme,” Trinh made a number of recommendations, stating that the following actions may be taken:

Make educational materials that describe the connection between MetS and gout, such as pamphlets, posters, and infographics. Also, the information in these materials must to cover lifestyle modifications for managing MetS.

Join up with medical professionals including primary care doctors and endocrinologists to promote gout prevention strategies and share information about the study’s findings.

Use social media: Share information about the study’s findings and encourage healthy lifestyle choices. By using social media sites like Facebook, Twitter, and Instagram, this can be done.

To inform those who have MetS about the connection between the condition and gout and to offer advice on how to treat it with lifestyle changes, hold workshops or webinars for them.

To promote gout prevention practises to a larger audience, work with neighbourhood organisations like wellness centres or municipal health agencies.



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