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ARTERIAL HYPERTENSION IN PATIENTS WITH GOUT AND
SYMPTOMATIC HYPERURICEMIA
Sharapova Nozima Erkinjonovna
Asian International University, Bukhara, Uzbekistan
Currently, gout is a serious medical problem, and the number of patients with
gouty arthritis is constantly growing in all countries with a high standard of living.
Asymptomatic hyperuricemia and the high prevalence of gout (1-3%) among the
population are important risk factors for cardiovascular diseases. The aim of the
study is to assess the association of hyperuricemia with lipid profile disorders in
patients with arterial hypertension, gout, and asymptomatic hyperuricemia.
Nevertheless, the problem of using antihypertensive drugs in gout in Uzbekistan
remains open. Thus, the analysis of the latest literature shows that at present, the
problem of early diagnosis and modern treatment of arterial hypertension in patients
with gout and asymptomatic hyperuricemia remains open.
Key words: gouty arthritis, asymptomatic hyperuricemia, uric acid, arterial
hypertension.
Gout is a systemic disease characterized by the deposition of sodium
monourate crystals in various tissues and inflammation in people with hyperuricemia
(GU) due to environmental or genetic factors [1, 14]. The first big toe joint is usually
affected (50-60%) with the development of acute monoarthritis. In 15-20% of cases,
gout begins with damage to other joints of the feet: II-IV fingers, ankles, knees and,
exceptionally, the joints of the hands. In 5% of cases, the onset of the disease is
observed in polyarticular joints. A number of studies have shown that at least 1-3%
of the population suffers from gout. The incidence of gout has doubled over the past
10–20 years and continues to grow steadily: in various populations, it ranges from 5
to 50 per 1000 men and 0.2 per 1000 women [3, 11, 19, 22]. Asymptomatic elevations
of uric acid (UA) occur in 5–20% of the population, of whom only 5–20% develop
gout. According to the authors, asymptomatic hyperuricemia is observed in
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approximately 2–5% of men in the USA, 17% of the French population, 7% in Spain,
and 19.3% in Russia [14, 16]. A direct relationship has been established between the
level of uricemia and the likelihood of developing gout attacks.
Blood uric acid levels above 8.0 mg/dl (707 μmol/l) are considered a high-
risk group for the development of gout, occurring in 5 to 12% of cases. At the same
time, it has been found that GU occurs 10 times more often than gouty arthritis [5].
The prevalence of gout increases in direct proportion to age and is more than 3% in
people over 75 years of age [2, 21]. The baseline level of gout has been shown to be
significantly related to the level of uric acid. For example, the annual incidence was
4.5% for uric acid levels > 540 mmol/l and only 0.1% for levels below 420 mmol/l.
The 5-year cumulative incidence of gout with uric acid levels > 540 mmol/l was 22%
[6]. There is evidence that the onset of gout is younger [7, 24]. This suggests a close
relationship between gout and hyperuricemia [9]. Several studies have shown that
women and familial gout, nephrolithiasis, and some comorbid conditions common to
gout patients, such as obesity, hypertriglyceridemia, and insulin resistance, are more
likely to develop the disease [16, 19, 25]. The level of CK is higher in postmenopausal
women than in premenopausal women and in urban areas than in rural areas.
Hyperuricemia has recently been considered as a risk factor for cardiovascular
complications. It has been found that a large proportion (about 2/3) of patients with
gout die from cardiovascular disease related to atherosclerosis, and only less than a
quarter die from chronic renal failure [23]. According to the results of various studies,
the frequency of arterial hypertension (AH) in patients with gout ranges from 25 to
52%, with an average of 36-41%, and increases to 72% in patients with metabolic
syndrome [8, 15]. According to R. J. Johnson and co-authors, with an increase in SC
by 1 mg/dl, systolic blood pressure (SBP) increases by 30 mm Hg and glomerular
hypertrophy develops. The specific features of the diurnal blood pressure profile in
young people with Gout are the tendency of the nocturnal decrease in diastolic arterial
pressure (DAP) to invert the diurnal DAP rhythm, as well as an increase in nocturnal
blood pressure variability with an increase in blood pressure. According to D.G.
Shonicheva, the frequency of systolic and diastolic hypertension in young patients
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with impaired purine metabolism is 50%. It is currently believed that more than 10%
of patients with gout are true SK hyperproducers [10, 21]. These include people with
various enzyme disorders, neoplastic diseases, and people taking cytostatics [12, 20].
In the majority of patients with gout (90%) renal excretion of SK is reduced (less than
750 mg per day) [18]. Uricosuric renal function decline can be due to various causes,
including hypertension, chronic renal failure (CRF), organic kidney damage
(polycystic, etc.), and drug exposure.
Epidemiological studies have shown that 15-20% of patients with gout
develop urolithiasis (UT). In patients with primary gout, nephrolithiasis is 1000 times
more common than in the general population [13, 25]. Urolithiasis is detected in 20%
of cases with gout, which is hundreds of times more common than in patients without
gout, and often (40%) precedes the articular manifestations of gout. The causes of the
formation of urate stones are hyperuricemia, increased urine density, and a decrease
in the fraction of excreted uric acid [14]. It is now known that gout occurs under the
influence of a complex of etiological factors, which are influenced by environmental
and genetic factors. Today, most researchers consider gout to be a multi-organ
disease. In addition to damage to the joints and kidneys, the heart and nervous system
can be involved in this process; hypertension, obesity, dermatoses, migraine diseases,
that is, the process affects many organs at the same time and has a systemic nature [4,
16, 19]. According to modern data, there are 3 main phases in the pathogenesis of the
disease: 1) hyperuricemia and accumulation of urate in the div, 2) urate deposition
in the tissues, 3) acute gouty inflammation. Internal factors are of primary
pathological importance. Increased uric acid and impaired excretion can be the result
of a combination of individual disorders. In almost 90% of cases, persistent
hyperuricemia is associated with reduced excretion by the kidneys, and only a small
proportion of patients with gout develop the disease solely as a result of excessive
uric acid formation. Increased urate synthesis may be associated with a primary
genetic defect, and sometimes with an increase in purines, a number of diseases
(lymphoproliferative, hemolysis, diabetic ketoacidosis, pernicious anemia,
sarcoidosis, hyperparathyroidism, hypothyroidism, psoriasis)
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Food purines (beer, meat, bitter tea, caviar, legumes, coffee, cocoa,
chocolate), drugs, in particular nicotinic acid, thiazide and loop diuretics, low-dose
salicylates, are observed in healthy people, and also lead to short-term GU due to the
rapid clearance of SK. In addition, a high-purine diet leads to a slight increase in SK
- approximately 60-129 μmol / l. and a similar decrease in SK levels with a low-purine
diet leads to chronic GU when conditions arise for a constant increase in SK.
The following question is currently becoming increasingly relevant: How
“harmless” is asymptomatic SG? Some researchers believe that an increase in SG can
have a beneficial effect on the div. Some literature has noted that SG can improve
mental and physical performance [13]. Numerous studies in the 1960s and 1970s have
shown that people with SG are more intelligent and sensitive [7, 20]. A number of
authors have suggested that elevated SG may be one of the main plasma antioxidants
and prevent oxidative stress associated with aging, thereby helping to prolong life.
Along with data on some positive effects of SG, many studies have linked SG
to cardiovascular disease and kidney damage.
One of the main visceral manifestations of gout is gouty nephropathy, which
occupies one of the leading places among the extraarticular manifestations of gout.
The concept of gouty nephropathy includes various forms of kidney damage caused
by disorders of purine metabolism and other metabolic and vascular changes
characteristic of gout. Kidney damage develops in 30-50% of patients with gout [16].
The harmful effect of Gout on the kidneys has been proven experimentally, therefore
the term "asymptomatic Gout" reflects the absence of one of the manifestations of
gout - the articular syndrome, but does not exclude the development of urate
nephropathy [18]. Various authors distinguish the following clinical and
morphological variants of kidney damage with impaired uric acid metabolism: acute
uric acid nephropathy (AUN), urate nephrolithiasis, urate nephropathy.
Acute uric acid nephropathy is common but not always diagnosed.
Predisposing factors for UAN include increased urinary uric acid concentration,
decreased urine pH, and decreased extracellular fluid volume. Acute UAN leads to
diffuse intrarenal deposition of uric acid in the distal tubules and collecting ducts,
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where crystal deposition and intrarenal obstruction occur. Urinary tract obstruction
develops as a result of uric acid crystallization in the distal tubules and collecting
ducts, in the renal pelvis, and sometimes in the ureters. The most common
manifestation of acute uric acid nephropathy is the development of acute renal failure,
a characteristic feature of which is hyperuricosuria [11, 18, 24]. Urate nephrolithiasis
According to the literature, 10-20% of patients with primary gout have a history of
urolithiasis. The formation of stones in gout is facilitated by uricosuria of more than
700 mg per day, a decrease in urine pH, oliguria, and risk factors for the development
of uric acid stones are age over 60 years and increased div weight [8, 15]. According
to the literature, attention is paid to the fact that urate nephrolithiasis in patients with
gout may precede articular syndrome. In 40% of patients with gout, the disease begins
with urate nephrolithiasis and is subsequently accompanied by joint damage [3]. Urate
nephropathy is a variant of chronic metabolic tubulointerstitial nephritis (TIN),
characterized by the accumulation of SK crystals in the interstitium with the
development of a secondary inflammatory process [6, 15, 21]. The main
manifestations of urate nephropathy include urinary syndrome (leukocyturia,
moderate proteinuria, microhematuria, hypostenuria), changes in renal tubular
function [22]. According to some authors, with a persistent increase in SK levels >
470 μmol/l, up to 600 μmol/l for women and 780 μmol/l for men, the risk of further
development of renal failure increases by 3-10 times, and every fourth patient with
gout develops end-stage chronic kidney disease. [1, 13]. Therefore, timely diagnosis
of kidney damage in gout is an important prognostic factor.
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