p–ISSN: 2723 - 6609 e-ISSN: 2745-5254

Vol. 5, No. 4 April 2024 http://jist.publikasiindonesia.id/

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1408

Differences The Incidence of Hyperuricemia in Families with

Gouty Arthritis and Families Without Gouty Arthritis in

Buleleng Regional General Hospital, Bali, Indonesian

Larasati A. Wahyu

, Pramarta Y. Dwiputra

Department of Internal Medicine Buleleng Regional General Hospital Bali, Indonesian

Email: [email protected]

*Correspondence

ABSTRACT

Keywords:

Hyperuricemia, Gouty

Arthritis, History of gout.

The most common manifestation of hyperuricemia is gout.

Hyperuricemia is the leading cause of gout. It is about five

times more common than gout. The heritability of

hyperuricemia and gout is about 73%, and 40-50% of

patients have a family history of gout. Indonesia, especially

Bali, has a high prevalence of hyperuricemia in families with

gout at 26.6%. Therefore, we performed this study to look

for differences in the incidence of hyperuricemia in families

with gouty arthritis and families without gouty arthritis.

In an unpaired case-control study, which is the target

population is Balinese, the target population is Balinese

individuals with gouty arthritis who come to the Internal

Medicine Polyclinic of Buleleng Regional General Hospital.

The controls in this study were Balinese individuals without

gouty arthritis; there were 41 samples who made a pedigree

and checked serum uric acid at one time. Of the total 41 case-

control samples used, the incidence of hyperuricemia in

families with gouty arthritis is 65.9%, and in families

without gouty arthritis, is 29.3%, with an Odd Ratio (OR)

value of 2.25 with a 95% confidence interval, p-value =

0.002. There were differences in hyperuricemia incidence in

families with gouty arthritis and families without gouty

arthritis, with a p-value = 0.002. Hyperuricemia in families

with gouty arthritis is 2.25 times (OR) higher than in

families without gouty arthritis.

Introduction

Hyperuricemia is an elevated serum uric acid level, usually greater than 6 mg/dL in

women and 7 mg/dL in men. Hyperuricemia results from increased uric acid production,

decreased excretion, or a combination of both processes10 (Topolyanskaya, Vakulenko,

Semashkova, Kupina, & Dvoretskiy, 2020). Previously, hyperuricemia was more

prevalent in developed countries than in developing countries. The prevalence of

hyperuricemia in the US was 21.4%; in Bangladesh, the prevalence was 9.3% (men vs

women; 8.4% vs 10.2%). However, this presented the fact that hyperuricemia was also

Differences The Incidence of Hyperuricemia in Families with Gouty Arthritis and Families

Without Gouty Arthritis in Buleleng Regional General Hospital, Bali, Indonesian

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1409

common not only in advanced countries but also in developing countries. However, there

was no actual prevalence of hyperuricemia in Indonesia. Several studies were conducted

in urban areas of Indonesia. In Depok City, West Java, the prevalence of hyperuricemia

was 18.6%, while in Bali, the prevalence was 18.2%7 (Dewi & Rini, 2020).

The most common manifestation of hyperuricemia is gout10. Gout is the most

common inflammatory joint disease, impacting morbidity and premature mortality (Nian

& You, 2022). The disease is heritable, as suggested by familial clustering of the disease;

however, the existence of many known risk factors, such as male gender, increasing age,

obesity, chronic renal impairment, hypertension, long-term use of diuretics and specific

diets with high purine and alcohol, also supports a strong environmental contribution8

(ERWIN, 2021). Whatever the cause, the result is elevated serum uric acid, which in some

patients ultimately causes clinical gout9. Hyperuricemia is the leading cause of gout; it is

about five times more common than gout, affecting 43.3 million (21.4%) U.S. 6. Adults

people with higher serum urate levels are at an increased risk for incident gout. They will

also have more frequent flare-ups over time6,10 (Usman, Darmawan, Hamijoyo, &

Wachjudi, 2019).

The heritability of hyperuricemia and gout is about 73%, and 40-50% of patients

have a family history of gout9 (Firsty & Putri, 2021). High heritability of hyperuricaemia,

the main driver of urate crystal deposition and the development of gout, has led to efforts

to identify susceptibility genes8. Several replicated loci are for genes encoding renal urate

transporters or related proteins, whereas others may be involved in metabolic pathways 6

(Kuo et al., 2015).

Indonesia, especially Bali, has a high prevalence of hyperuricemia in families with

gout at 26.6%. In previous studies in Bali, there was a high prevalence of hyperuricemia

in families with a history of gout, particularly among men12 (Sety, 2018). From the

literature which states that hyperuricemia is the leading cause of gouty arthritis and the

role of genes and family history influences gouty arthritis, it is estimated that there are

differences in the incidence of hyperuricemia in families with gouty arthritis and families

without gouty arthritis.

Research Methods

The research design used an unpaired case-control, the target population of Balinese

individuals with gouty arthritis who come to the Internal Medicine Polyclinic of Buleleng

Regional General Hospital. The controls in this study were Balinese individuals without

gouty arthritis. Research to look for differences in the incidence of hyperuricemia in

families with gouty arthritis and families without gouty arthritis.

Larasati A. Wahyu, Pramarta Y. Dwiputra

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1410

Figure 1 The flow of sampling

Sample selection using consecutive random sampling, sample size using the

formula:

n1=n2= (za√2PQ + zb√(P1Q1+P2Q2) )2 = 41 sample

(P1-P2)2

The research procedure is that individuals with gouty arthritis are made pedigree

with identity data and addresses of family members, giving informed consent, and

checking serum uric acid at once. The same procedure was also carried out on family

members of individuals without gouty arthritis. Hyperuricemia was defined as serum uric

acid ≥ 7 mg/dL for male subjects and ≥ 6 mg/dL for female subjects. Results were

analyzed using the Statistical Program for Social Science (SPSS), and the data will be

presented in a figure.

Figure 2 Schematic of Research

Differences The Incidence of Hyperuricemia in Families with Gouty Arthritis and Families

Without Gouty Arthritis in Buleleng Regional General Hospital, Bali, Indonesian

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1411

Results and Discussion

Of the total 41 case-control samples used, the results of the incidence of

hyperuricemia in families with gouty arthritis were 27 people (65.9%), and as many as

14 people (34.1%) did not experience hyperuricemia. Individuals with families without

gouty arthritis experienced hyperuricemia in as many as 12 people (29.3%), and those

who did not experience hyperuricemia in 29 people (70.7%). The incidence of

hyperuricemia in families with gouty arthritis is 65.9%, and in families without gouty

arthritis is 29.3%, with an Odd Ratio (OR) value of 2.25 with a 95% confidence interval,

p-value = 0.002, which is statistically significant (Hati, 2022).

Table 1

Results of the analyzed differences in the incidence of hyperuricemia in families with

gouty arthritis and families without gouty arthritis.

Gout is a common disease caused by purine metabolism disorder, primarily caused

by the accumulation of uric acid crystals in joints and other tissues9. The occurrence of

gout is often significantly correlated with the increase in serum uric acid levels. Genetic

factors can contribute to the high prevalence of hyperuricemia in certain ethnic groups.

Gout can be suffered due to genetic factors4,5. The history of gout in one's family tree

can be a risk factor for gout. Gout is caused by genetics called primary gout. This is

because the gene factor derived from parents who also suffer from gout is genetically

inherited from its predecessor (MAUPE, 2019). Genetic factors in patients with gout

usually begin with a disorder of purine metabolism, which causes excessive gout in the

blood3.

Genes associated with gout fall into four categories: production of uric acid,

reabsorption of uric acid in renal tubule, excretion of uric acid in renal tubule, and others9.

Several common genetic variants are associated with serum urate and gout genome-wide

association studies, such as SLC2A9, ABCG2, SLC22A12, GCKR, and PDZK1, among

Hyperuricemia

(+)

Hyperuricemia (-)

Total

Family

With

Gouty

Arthritis

27 (65,9%)

14 (34,1%)

(100%)

0,002

Family

Without

Gouty

Arthritis

12 (29,3%)

29 (70,7%)

(100%)

Total

39 (47,6%)

43 (52,4%)

(100%)

Larasati A. Wahyu, Pramarta Y. Dwiputra

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1412

others5. Therefore, genetic variants associated with serum urate levels require testing for

association with gout, preferably in sample sets where gout is ascertained by the

American Rheumatology Association clinical classification criteria or the gold-standard

method of microscopic demonstration of MSU crystals4. The result of this study is that

the incidence of hyperuricemia in families with gouty arthritis is 65.9%, and in families

without gouty arthritis is 29.3%. A study in Northern Sulawesi, Indonesia, presented that

genetics is considered as one of the prominent risk factors (OR 14.42 (8.01–26.23) p <

0.0001). Another heritability analytical study for hyperuricemia and gout showed that

hyperuricemia had more vital genetic traits than gout (UTAMA, 2021). The concordance

of hyperuricemia was 53% in monozygotic twin pairs and 24% in dizygotic twin pairs

(p< 0.001)3. Based on a survey by Feti Kumala Dewi (2020), there was a relationship

between genetic and gout arthritis with chi-square results p = 0.0029. Research by Mei

Fransyah (2021) the results showed that of the 40 respondents who suffered from Gout

Arthritis, the majority of respondents who had family members who suffered from Gout

Arthritis were 26 people (65.5%), and those who did not have family members who

suffered from Gout Arthritis were 14 people (35.0%)3. From the results of the research

obtained, researchers assume that gout arthritis sufferers are more dominant in families

who have gouty arthritis because gout arthritis can be inherited from the genes of the

patient's family 13. The risk of gout is increased more by having affected first-degree

relatives than by having affected second-degree relatives, and it appears ‘dose-dependent’

in that the risk increases with the number of affected relatives. These results confirm the

long-held belief that gout clusters within families and supports an essential contribution

of common familial factors in predisposing to the development of gout8.

In addition to the genetic factors outlined herein, several environmental risk factors

contribute to the development of gout, including high intake of purine-rich beverages

such as beer, purine-rich foods such as red meat and seafood, and sugar-sweetened

beverages, including those sweetened with high-fructose corn syrup 1,2. These dietary

factors lead to increased purine synthesis through the hepatic salvage pathways, leading

to increased urate production. High circulating insulin levels in individuals with

metabolic syndrome also promote renal underexcretion of uric acid. Diuretic agents are a

further meaningful environmental; acute urate increases accompanying therapies such as

diuretics may also increase flare risk4.

This study regarding differences in the incidence of hyperuricemia in families with

gouty arthritis and families without gouty arthritis has some limitations; we only

measured serum uric acid at a given point in time. In contrast, the serum uric acid level

in the body may fluctuate over hours. Transient hyperuricemia sometimes occurs in

healthy individuals11; the authors did not examine other family risk factors that could

affect the incidence of hyperuricemia or gouty arthritis.

Conclusion

The study results showed differences in the incidence of hyperuricemia in families

with gouty arthritis and families without gouty arthritis with p-value = 0.002.

Differences The Incidence of Hyperuricemia in Families with Gouty Arthritis and Families

Without Gouty Arthritis in Buleleng Regional General Hospital, Bali, Indonesian

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1413

Hyperuricemia in families with gouty arthritis is 2.25 times (OR) higher than in families

without gouty arthritis.

Larasati A. Wahyu, Pramarta Y. Dwiputra

Indonesian Journal of Social Technology, Vol. 5, No. 4, April, 2024 1414

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