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Effect of caffeinated and decaffeinated coffee on serum uric acid and uric acid clearance, a randomised within-subject experimental study


1, 2, 3, 4, 5, 6, 7

 

  1. Department of Internal Medicine, Faculty of Medicine, Naresuan University, Thailand. puidulian@gmail.com
  2. Department of Pharmaceutical Technology, Faculty of Pharmaceutical Sciences, Naresuan University, Thailand.
  3. Department of Pharmaceutical Chemistry and Pharmacognosy, Faculty of Pharmaceutical Sciences, Naresuan University, Thailand.
  4. Department of Mathematics, Faculty of Science, Naresuan University, Thailand.
  5. Department of Applied Thai Traditional Medicine, Faculty of Public Health, Naresuan University, Thailand.
  6. Department of Internal Medicine, Faculty of Medicine, Naresuan University, Thailand.
  7. Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Thailand.

CER13637
2021 Vol.39, N°5
PI 1003, PF 1010
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PMID: 33025883 [PubMed]

Received: 01/06/2020
Accepted : 02/09/2020
In Press: 01/10/2020
Published: 31/08/2021

Abstract

OBJECTIVES:
The effect of coffee on serum uric acid (SUA) has shown conflicting results. This study was to determine the effects of caffeinated coffee (CC) and decaffeinated coffee (DC) on SUA, serum xanthine oxidase activity (sXOA) and urine uric acid clearance (UAC).
METHODS:
This was a prospective randomised within-subject experimental study design of 51 healthy male participants. Each study period consisted of 3 periods, including a control, an intervention, and washout period for 1, 3 and 1 week, respectively. During the intervention period, the participants received 2, 4 or 6 gram/day of coffee, either CC or DC.
RESULTS:
For DC groups, SUA significantly decreased by 6.5 (±1.1) mg/dL to 6.2 (±1.1) mg/dL during the intervention period (p=0.014). sXOA significantly increased by 0.05 (±0.07) nmol/min/mL to 0.20 (±0.38) nmol/min/mL during the intervention period (p=0.010) of CC. For UAC, there was no significant change with CC or DC. In hyperuricaemic participants, SUA significantly decreased by 7.7 (±0.7) mg/dL to 7.2 (±0.7) mg/dL during the intervention period (p=0.028) of DC. For non-hyperuricaemic, CC significantly increased SUA by 5.9 (±0.7) mg/dL to 6.2 (±0.9) mg/dL during the intervention period (p=0.008) and significantly decreased SUA to 6.0 (±0.8) mg/dL (p=0.049) during the withdrawal period. A significant increase of sXOA according with SUA in CC groups from 0.05 (±0.07) nmol/min/mL to 0.25 (±0.44) nmol/min/mL during the intervention period (p=0.040) was presented in non-hyperuricaemic participants.
CONCLUSIONS:
DC had a significant decrease of SUA during the intervention period. However, in non-HUS participants, SUA significantly increased in CC.

DOI: https://doi.org/10.55563/clinexprheumatol/gd9nia

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