METHODS: We conducted a cross-sectional study on 140 hypertensive patients attending outpatient follow-up in two primary care clinics in Sungai Buloh, Malaysia, using a convenient sampling method. SUA levels were measured and divided into four quartiles. Two radiologist specialists performed B mode ultrasonography to assess the thickness of the right and left carotid intima media in all participants.
RESULTS: Participants' mean SUA level was 355.75 ± 0.13. Their mean age was 53.44 (± 9.90), with a blood pressure control of 137.09 ± 13.22/81.89 ± 8.95. Elevated CIMT taken at ≥75th percentile was 0.666 for the left and 0.633 for the right common carotid arteries. By using a hierarchical method of multiple logistic regression, compared with the first quartile of the SUA level as reference group, the odd of elevated CIMT in quartile 4 in the common carotid artery was (OR = 2.00; 95% CI = 0.64-6.27, P = .576) for the right and (OR = 0.62; 95% CI = 0.20-2.00, P = .594) for the left. Waist circumference (P = .001), body mass index (P = .013), triglycerides (P
MATERIALS AND METHODS: A content development team which consisted of three consultant rheumatologists developed the booklet. Content validation was performed by a panel of evaluators consisted of eleven physicians (four consultant rheumatologists, two clinical specialists, and five medical officers), who were involved in gout management. Face validation was performed by ten patients with gout.
RESULTS: Item-Content Validity Index ranged from 0.9 to 1 with regards to relevancy, clarity, ambiguity and simplicity. Side effects of uricosuric agents were added to the draft based on an evaluator's comment. Item-Face Validity Index was 1, which indicated that all patients were in 100% agreement with all items.
CONCLUSION: We developed and validated our Gout Treat-to- Target booklet. There was high agreement in I-FVI and I-CVI among physicians and patients.
Methods: This cross-sectional study included all gout patients who attended the rheumatology clinic from January 2013 to June 2018 and had received febuxostat as a second-line ULT. Analysis focused on the proportion of gout patients who achieved target serum urate (sUA) of <360 μmol/L, duration taken to achieve target sUA, and febuxostat dosage at achievement of target sUA. Safety assessments included comparison of serum creatinine, estimated glomerular filtration rate (eGFR), and serum alanine aminotransferase (ALT) at baseline, at achievement of target sUA, and at 12-monthly intervals.
Results: Majority (90.9%) of patients achieved target sUA. Median duration required to achieve target sUA was 5.5 months with IQR (interquartile range) of 8.5. Five (22.7%) patients achieved target sUA within one month of therapy with febuxostat 40 mg per day. Eleven (55%) patients achieved target sUA within six months and 16 (80%) by 12 months. Equal proportion of patients achieved target sUA with febuxostat 40 mg per day and 80 mg per day, respectively. There was no significant difference in the changes in serum creatinine level, eGFR and ALT from baseline and at achievement of target sUA, nor at 12-monthly intervals throughout the duration of febuxostat therapy. Apart from three patients who developed hypersensitivity reactions to febuxostat, no other adverse events were reported.
Conclusion: A significant proportion of gout patients with CKD managed to achieve target sUA with a lower dose of febuxostat at 40 mg per day and it is reasonable to maintain this dose for up to six months before considering dose escalation.
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.