Hypertension is one of the most common comorbidities of
gout. Studies have shown that the presence of hypertension is independently
associated with the risk of incident gout through reduced renal blood flow with
increased renal and systemic vascular resistance and decreased renal excretion
of urate.
Hypertension is the term used to describe high blood pressure. Blood pressure
is a measurement of the force against the walls of your arteries as your heart
pumps blood through your body. Gout is a kind of arthritis that occurs when
uric acid builds up in blood and causes joint inflammation. Acute gout is a
painful condition that typically affects one joint. Chronic gout is repeated
episodes of pain and inflammation, which may involve more than one joint.
To study the risk of incident gout among patients with hypertension and
antihypertensive drugs a study was conducted in United Kingdom between January
2000 and December 2007 in which the data was collected from the health
improvement network database containing the computerized medical records
entered by general practitioners in the United Kingdom. Patients free of gout
and cancer were included in the study.
The potential impact of antihypertensive drugs by class: diuretics, β blockers,
calcium channel blockers, angiotensin converting enzyme inhibitors, losartan,
and non-losartan angiotensin II receptor blockers were evaluated. Dose of
antihypertensive drugs were classified into three groups: medium or low
(recommended starting doses or lower), high (higher than recommended starting
doses), and unknown. From the database data was collected on personal characteristics
and lifestyle factors such as alcohol use, smoking, and body mass index, as
well as comorbidities such as ischaemic heart disease, hypertension,
hyperlipidaemia, renal failure, and heart failure.
The study denoted that in both groups gout was associated with an increased
number of visits to a general practitioner, alcohol use, adiposity, ischaemic
heart disease, hyperlipidemia, and renal failure. As compared with no use of
calcium channel blockers, current use among people with hypertension was
associated with a lower risk of developing gout.
The relative risks for individual calcium channel blockers were 0.79 or
amlodipine, 0.87 for nifedipine, and 0.86 (0.75 to 0.99) for diltiazem. The
relative risks for calcium channel blockers according to duration of use among
those with hypertension were 1.04 for less than one year, 0.89 for 1-1.9 years,
and 0.77 for two or more years.
In this large general practice cohort representative of the UK population,
it was found that use of calcium channel blockers and losartan was associated
with a moderately lower risk of incident gout among patients with hypertension.
An increased risk of developing gout among those with hypertension was found to
be associated with the use of diuretics, β blockers, angiotensin converting
enzyme inhibitors, and non-losartan angiotensin II receptor blockers. The
longer one uses these antihypertensives the risk of developing gout also
increases, except for β blockers, and non-losartan angiotensin II receptor blockers.
Calcium channel blockers could increase the glomerular filtration rate and
consequently the clearance rates of uric acid and creatinine. These inverse
associations were stronger with both a longer duration and a higher dose of
use.
From a public health perspective it is concluded that the high comorbidity
burden of gout and hypertension can be reduced by using the urate lowering
antihypertensive drugs like calcium channel blockers which increase the
glomerular filtration rate and consequently the clearance rates of uric acid
and creatinine.
Reference: Antihypertensive drugs and risk of incident gout among patients with
hypertension: population based case-control study; Hyon et al; BMJ 2012.