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Uric acid induces liver fibrosis through activation of inflammatory mediators and proliferating hepatic stellate cell in mice

Sari DCR, Soetoko AS, Soetoko AS, Romi MM, Tranggono U, Setyaningsih WAW, et al.

Med J Malaysia, 2020 05;75(Suppl 1):14-18.
PMID: 32471964

INTRODUCTION: Uric acid is associated with cardiometabolic risk factor and severity of liver damage. The mechanism of uric acid inducing liver damage is still elusive. This study elucidates the development of liver fibrosis under hyperuricemia.
METHODS AND MATERIALS: Hyperuricemia model was performed in male Swiss Webster mice. Intraperitoneally injection of uric acid (125mg/kg body weight) was done for 7 and 14 days (UA7 and UA14 groups). Meanwhile, the UAL groups were injected with uric acid and followed by the administration of allopurinol (UAL7 and UAL14 groups). On the due date, mice were sacrificed, and liver was harvested. Uric acid, SGOT, SGPT, and albumin level were measured from the serum. The mRNA expression of TLR4, MCP1, CD68, and collagen1 were assessed through RT-PCR. Liver fibrosis was quantified through Sirius red staining, while the number of hepatic stellates cells (HSCs) and TLR4 were assessed through IHC staining.
RESULTS: Uric acid induction for 7 and 14 days stimulated an increase of both SGOT and SGPT serum levels. Followed by enhanced inflammatory mediators: Toll-like receptor-4 (TLR- 4), Monocyte Chemoattractant Protein-1 (MCP-1) and Cluster of Differentiation 68 (CD68) mRNA expression in the liver (p<0.05). The histological findings showed that the UA7 and UA14 groups had higher liver fibrosis scores (p<0.05), collagen I mRNA expression (p<0.05), and the number of HSCs (p<0.05) compared to Control group. Administration of allopurinol showed amelioration of uric acid and liver enzymes levels which followed by inflammatory mediators, liver fibrosis and collagen1, and hepatic stellate cells significantly.
CONCLUSION: Therefore, uric acid augmented the liver fibrosis by increasing the number of hepatic stellate cells.

Matched MeSH terms: Uric Acid/metabolism*
Tophaceous gout in young patients with systemic lupus erythematosus

Veerapen K, Schumacher HR, van Linthoudt D, Neilson EG, Wang F

J Rheumatol, 1993 Apr;20(4):721-4.
PMID: 8496872

Systemic lupus erythematosus (SLE) and gout have been associated infrequently. We describe 3 young adults with SLE who developed tophaceous gout relatively early in the course of their disease. All were underexcretors of uric acid but were studied after the development of renal disease; 2 were treated with diuretics. In 2 cases, gout became obvious while lupus was quiescent.

Matched MeSH terms: Uric Acid/metabolism*
Fulltext Molybdenum cofactor deficiency in a Malaysian child

Ngu LH, Afroze B, Chen BC, Affandi O, Zabedah MY

Singapore Med J, 2009 Oct;50(10):e365-7.
PMID: 19907877

Molybdenum cofactor deficiency is a rare autosomal recessive disorder with devastating neurological manifestations, characterised by neonatal-onset encephalopathy mimicking hypoxic-ischaemic insult, intractable seizure, and feeding and respiratory difficulties. It is often fatal in the early life. We report an affected 8-year-old boy, who presented with severe neurological manifestations since birth, but without clinically-significant seizure. Molybdenum cofactor deficiency must be included in the differential diagnosis of patients presenting with unexplained encephalopathy in the newborn period, and whose neuroimaging findings are consistent with hypoxic ischaemic encephalopathy. The classic laboratory hallmark of this disorder is low serum uric acid, positive urine sulphite dipstick test, and elevated urinary S-sulphocysteine, hypoxanthine and xanthine.

Matched MeSH terms: Uric Acid/metabolism
The effect of control and self-medication of chronic gout in a developing country. Outcome after 10 years

Darmawan J, Rasker JJ, Nuralim H

J Rheumatol, 2003 Nov;30(11):2437-43.
PMID: 14677190

OBJECTIVE: We describe a 10 year observation of the effect of control of hyperuricemia compared with self-medication alone in patients with chronic gout.
METHODS: We studied 299 consecutively self-referred Malayo-Polynesian men with chronic gout, mean age 35 +/- 14.3 SD years. Subjects comprised 228 cases with chronic gout without tophi or urolithiasis (Group 1) and 71 with those complications (Group 2). Attacks of acute gouty arthritis were treated with nonsteroidal antiinflammatory drugs (NSAID) and/or corticosteroids. After acute arthritis had settled, urate-lowering drugs were instituted in both groups combined with low dose colchicine and/or low dose NSAID for at least 0.5-2 years. Urate levels were maintained longterm at a mean of < 5 mg/dl. After 10 years, the dropouts were traced and evaluated for comparison with baseline and those who remained in the study. In Group 2 the urate-lowering drugs were continued.
RESULTS: Control of gout and hyperuricemia was achieved in all patients who remained under control: 91.6% of the 299 patients for at least 2 years (short-term), up to 5 years in 87.5% (medium term), and up to 10 years in 79.6% (longterm). In Group 1 (chronic gout without complication) only 36.8% had no attacks during 8 years, after they had tapered urate-lowering drug after the first 2 years of the study. In the 61 dropouts the intermittent symptomatic treatment and/or self-medication without longterm control of hyperuricemia resulted after 1 decade in chronic gout with more complications and associated conditions leading to increased morbidity, disability, and comorbidity, and 3 early mortalities.
CONCLUSION: By controlling hyperuricemia, improvement of the prognosis of chronic gout, comorbidity, and early death was achieved compared with self-medication alone. Self-medication in a developing country if continued unchecked may become a public health problem in a population with a high prevalence rate of gout.

Matched MeSH terms: Uric Acid/metabolism*