Download GOUT AND ITS COMORBIDITY AMONG NIGERIANS BY DR. S.A.

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Remote ischemic conditioning wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Myocardial infarction wikipedia , lookup

Saturated fat and cardiovascular disease wikipedia , lookup

Coronary artery disease wikipedia , lookup

Cardiovascular disease wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Transcript
GOUT AND ITS COMORBIDITY AMONG NIGERIANS
BY
DR. S.A. OGUNTONA MBChB, FWACP. CERT. RHEUM.
DEPARTMENT OF MEDICINE
OLABISI ONABANJO UNIVERSITY/ OLABISI ONABANJO
UNIVERSITY
TEACHING
HOSPITAL.
SAGAMU. OGUN STATE.
NIGERIA.
CORRESPONDENCE TO : DR. S.A. OGUNTONA
P.O.BOX 231, SAGAMU.
OGUN STATE. NIGERIA.
Mobile- 08035534449
E-mail- [email protected], [email protected]
1
GOUT AND ITS COMORBIDITY AMONG NIGERIANS
ABSTRACT
Background- Gout is a chronic disease associated with excessive high levels of serum
urate (hyperuricaemia) with resultant deposition of monosodium urate crystals in the
tissue. It presents with both articular and non-articular features. Patients with gout
frequently experience a range of co-morbidities which complicates management and
affects long-term prognosis.
Method
Included in the study are patients that met the American College of Rheumatology
criteria for the diagnosis of gout. Serum uric acid level was determined in all patients.
Other relevant investigations as related to the associated comorbid condition were
requested for.
Results
Hypertension was the leading comorbid condition found (62.5%), followed by obesity,
diabetes and chronic renal failure. None of those patients was however found to have
ischaemic heart disease.
Conclusion
Patients with hyperuricaemia and gout should be considered at risk for other comorbid
conditions. Therefore, appropriate and aggressive urate-lowering pharmacotheraphy
should be instituted in a goal-oriented approach to reach a serum uric level within
normal range.
Key words- Gout, comorbidity, South West Nigeria
2
Introduction
Gout is a multi-systemic disease in which metaboloic, excretory, and excessive purine
intake contributes to high level of serum urate (hyperuricaemia) with subsequent
deposition of monosodium urate crystals in the tissues1.
Patients with hyperuricaemia or gout, or both often experience high rates of comorbidity with attendant management challenges2. In many cases, there is clear
evidence that gout may be a consequence of comorbidity. For example, gout occurs
frequently in patients with chronic kidney disease. On the other hand, it is important to
consider the extent to which hyperuricaemia or gout per se may contribute to the
genesis of comorbidity3. In the latter case, both hyperuricaemia and gout are treatable.
An appropriate diagnosis and goal oriented treatment should be carried out in order to
prevent those comorbidity.
Comorbidity with gout can also impair quality of life4. Using a variety of distinct validated
measures, patients with gout have been shown to experience a significant overall
reduction in quality of life4.
3
Materials and methods
This is a prospective study of all gout patients seen over three years (July 2009-June
2012) in a private rheumatology clinic. Both patients with hyperuricaemia and features
of gout with elevated serum uric acid level were enlisted in the study. Serum uric acid
was determined at first consultation in all patients.
Also determined alongside serum uric acid level were body mass index (BMI), fasting
lipid profile, urinalysis, electrolyte, urea and creatinine. Electrocardiogram (ECG),
echocardiogram were demanded where necessary. Also requested for were fasting
blood sugar, HbA1C and plain chest radiographs.
Results
28 cases of hyperuricaemia/gout were seen over the study period, representing 8.3% of
total cases of rheumatology seen. 22 males (78.6%) and 6 females (21.4%) were seen.
Mean age of males at presentation was 42.5years, and mean age of females at
presentation was 63.6years. Serum uric acid ranged between 9.6mg/dl to 15.7mg/dl
and the mean was 12.5mg/dl. Males generally had higher values than females.
Comorbid condition was found in 16 patients (57.1%), 14 males (87.5%) and 2 females
(12.5%).
Treatment with allopurinol was helpful in all patients, with reduction in the serum uric
acid level and symptomatic relieve of arthritic pain.
4
Discussion
The aim of this study is to review some of the comorbid conditions that occur in gout
patients among the people of south west Nigeria, and to determine if
hyperuricaemia/gout may represent modifiable risk factor for the comorbid conditions.
The leading comorbid condition in this study was hypertension (62.5%). This result
agrees with some other earlier studies in African countries where hypertension was
found to be the leading comorbid state with hyperuricaemia/gout. Hypertension
accounted for 39% in the study by Mijinyawa in Togo5, 42% in the study by Mody et al in
South Africa6. Oyoo reported 61.5% in Kenya7, and Adelowo et al reported 49.3% in
Nigeria (in press).
Most earlier studies agreed that most patients with hyperuricaemia and gout frequently
suffer hypertension and therefore concluded that even in the absence of gout,
hyperuricaemia may directly promote hypertension8.
Ouppatham and colleagues conducted a study on more than 5500 members of the Thai
Armed Forces, and they demonstrated that the presence of hyperuricaemia predicts
increased systolic and diastolic blood pressure9.
Feig and coworkers assessed whether hyperuricaemia might affect blood pressure in
humans, by recruiting a group of adolescents with new onset hypertension and relative
hyperuricaemia. As a group, these individuals experienced a reduction of blood
pressure towards or into normal range during treatment with 400mg daily of allopurinol.
This decrease in blood pressure was reversed on discontinuation of allopurinol10.
It is a well-accepted concept that impaired renal function can decrease urate filtration
and consequently hyperuricaemia11. The question of whether hyperuricaemia can
promote kidney disease has been debated for years. Many clinical studies indeed
suggest that hyperuricaemia provides risk for renal disease12. Several recent studies
also provide evidence that lowering urate concentration with allopurinol may slow the
progression of chronic kidney disease13.
It is also well documented that individuals with metabolic syndrome have a higher
incidence of gout, so by extrapolation, it can be inferred that individuals with
hyperuricaemia may also have an increased incidence of insulin resistance. Yoo and
colleagues in one study showed that the incidence of insulin resistance in gout patients
may be increased by as much as 35% over individuals without gout 14. Choi and
colleagues also concluded in their study that gout conveyed 35% to 65% increase in
risk for future incidence of Type 11 diabetes15.
5
Many studies has associated hyperuricaemia with cardiovascular disease 16,17,18. In a
review by Johnson and coworkers, everyone of 14 large population studies identified
hyperuricaemia as a risk factor for cardiovascular disease and 10 of the 14 studies
favoured hyperuricaemia as an independent risk factor19. Similarly, Wheeler and
associates performed a meta-analysis of 15 studies and each demonstrated a modest
overall increased relative risk for cardiovascular disease for patients with
hyperuricaemia20.
Baker and colleagues examined 21 population studies on hyperuricaemia and
cardiovascular disease and concluded that it is possible that hyperuricaemia is a more
important cardiovascular risk factor in patients already at risk for cardiovascular
disease21.
In an analysis of the MRFIT (Multiple Risk Factor Intervention Trial) investigation,
Krisshan and coworkers observed a modest increase for risk of myocardial infarction
(MI) in patients with either hyperuricaemia or gout, and patients with gout appeared to
have an increased risk of MI relative to patients with hyperuricaemia alone 22. These
data was however not analyzed to determine whether the increase in all the gout
patients over the hyperuricaemia ones was statistically significant.
It can therefore be concluded that hyperuricaemia and gout appear to be independent
risk factors for hypertension, renal disease, and cardiovascular disease. Physicians
should therefore consider and look for comorbid conditions in patients with gout and
treat them appropriately and aggressively.
6
Table 1 -SPECTRUM OF RHEUMATOLOGY CASES SEEN OVER 3 YEARS (JULY
2009- JUNE 2012)
Serial No
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Condition
Osteoarthritis
Rheumatoid
arthritis
Cervical
spondylosis
Lunbar
spondylosis
Low back
pain
Gout
SLE
Shoulder
pain
syndrome
Hypermobility
syndrome
Fibromyagia
Polymyalgia
rheumatica
Bursitis
Trigger finger
Sjorgren’s
syndrome
Reiter’s
syndrome
Septic
arthritis
Lateral
epicondylitis
Medial
epicondylitis
Scleroderma
Psoriatic
arthropathy
Plantar
fasciitis
Carpal tunnel
syndrome
Archilis
tendinitis
Number
104
12
Male
32
4
Percentage Female
30.8
72
33.3
8
Percentage
69.2
66.7
36
23
63.9
13
36.1
25
21
56
14
44
48
37
77.1
11
22.9
28
6
12
22
1
4
78.6
16.7
33.3
6
5
8
21.4
83.3
66.7
8
0
0
8
100
6
2
0
0
0
0
6
2
100
100
4
16
1
3
6
0
75
37.5
O
1
10
1
25
62.5
100
1
1
100
0
0
2
0
0
2
100
2
2
100
0
0
2
2
100
0
0
2
1
0
1
0
100
2
0
100
0
7
2
28.6
5
71.4
3
1
33.3
2
66.7
8
1
12.5
7
87.5
336
160
176
7
Table 2
COMORBID CONDITIONS ASSOCIATED WITH GOUT (16 patients had comorbid
conditions)
CLINICAL CONDITION
PERCENTAGE
Hypertension
NUMBER OF PEOPLE
WITH COMORBIDITY OUT
OF TOTAL OF 16
10
Chronic renal failure
3
18.8
Heart failure
1
6.3
Obesity
6
37.5
Diabetes mellitus (type 11)
4
25
Ischaemic heart disease
None
0
Stroke
1
6.3
62.5
Table 3
Comparative characteristics of gout among various African populations (%).
Adapted from Adelowo et al.
Comorbid
condition
Togo
South
Mijinyawa5 Africa
Cassim
et al
South
Africa
Mody
et al6
South
Kenya
Africa
Oyoo7
Tikly et
al
Nigeria
Adelowo
et al (in
press)
Nigeria
Oguntona
(present
study)
Hypertension
39.0
-
42
-
61.5
49.3
62.5
Obesity
38
-
-
-
90.5
12.7
37.5
Diabetes
-
-
10.5
-
7.7
4.1
25 (type
11 DM)
Alcohol
74.0
-
-
-
100
17.8
-
-
-
-
15.4
10.3
-
Osteoarthritis -
8
References
1. Choi HK, Mount DB, Reginato AM. Pathogenesis of Gout. Ann Intern Med 2005;
143: 499-516
2. Riedel AA, Nelson M, Wallace K, et al. Prevalence of comorbid conditions and
prescription medication use among patients with gout and hyperuricemia in a
managed care setting. J Clin Rheumatol. 2004 Dec;10(6):308-314.
3. Sanchez-Lozada LG, Soto V, Tapia E, et al. Role of Oxidative Stress in the
Renal Abnormalities Induced by Experimental Hyperuricemia. Am J Physiol
Renal Physiol. 2008 Oct;295(4):F1134-1141;
4. Roddy E, Zhang W, Doherty M. Is gout associated with reduced quality of life? A
case-control study. Rheumatology (Oxford) 2007;46:1441–1444
5. Mijinyawa M. Gout in patients attending the rheumatology unit of Lome hospital
Br J of Rheum 1995;34:843-846
6. Mody GM, Naidoo PD. Gout in South African Blacks. Ann Rheum Dis
1984;43:394-397
7. Oyoo GO. Gout in patients attending a rheumatology clinic in Nairobi, Kenya
Health Line 2004; 8(4)
8. Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in
hypertension and cardiovascular and renal disease? Hypertension. 2003
Jun;41(6):1183-1190.
9. Ouppatham S, Bancha S, Choovichian P. The relationship of hyperuricemia and
blood pressure in the Thai army population. J Postgrad Med. 2008 OctDec;54(4):259-262.
10. Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of
adolescents with newly diagnosed essential hypertension: a randomized trial.
JAMA. 2008 Aug 27;300(8):924-932.
11. Kang DH, Nakagawa T. Uric acid and chronic renal disease: possible implication
of hyperuricemia on progression of renal disease. Semin Nephrol 2005;25:43-9.
12. Chang HY, Tung CW, Lee PH, et al. Hyperuricemia as an independent risk factor
of chronic kidney disease in middle-aged and elderly population. Am J Med Sci.
2010 Jun;339(6):509-515.
13. Goicoechea M, de Vinuesa SG, Verdalles U, et al. Effect of allopurinol in chronic
kidney disease progression and cardiovascular risk. Clin J Am Soc Nephrol.
2010 Aug;5(8):1388-1393.
14. Yoo HG, Lee SI, Chae HJ, Park SJ, Lee YC, Yoo WH. Prevalence of insulin
resistance and metabolic syndrome in patients with gouty arthritis. Rheumatol Int.
Advance access published December 20, 2009, doi 10.1007/s00296-009-1304x.
15. Choi HK, De Vera MA, Krishnan E. Gout and the risk of type 2 diabetes among
men with a high cardiovascular risk profile. Rheumatology (Oxford). 2008
Oct;47(10):1567-70.
16. Choi HK, Curhan G. Independent impact of gout on mortality and risk for
coronary heart disease. Circulation. 2007 Aug 21;116 (8):894-900.
9
17. Ioachimescu AG, Brennan DM, Hoar BM, et al. Serum uric acid is an
independent predictor of all-cause mortality in patients at high risk of
cardiovascular disease: a preventive cardiology information system (PreCIS)
database cohort study. Arthritis Rheum. 2008 Feb;58 (2):623-630.
18. Niskanen LK, Laaksonen DE, Nyyssonen K, et al. Uric acid level as a risk factor
for cardiovascular and all-cause mortality in middle-aged men: a prospective
cohort study. Arch Intern Med. 2004 Jul 26;164 (14):1546-1551.
19. Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in
hypertension and cardiovascular and renal disease? Hypertension. 2003 Jun;41
(6):1183-90.
20. Wheeler JG, Juzwishin KD, Eiriksdottir G, et al. Serum uric acid and coronary
heart disease in 9,458 incident cases and 155,084 controls: prospective study
and meta-analysis. PLoS Med. 2005 Mar;2 (3):e76.
21. Baker JF, Krishnan E, Chen L, Schumacher HR. Serum uric acid and
cardiovascular disease: recent developments, and where do they leave us? Am J
Med 2005;118: 816–826.
22. Krishnan E, Svendsen K, Neaton JD, et al. Long-term cardiovascular mortality
among middle-aged men with gout. Arch Intern Med. 2008 May 26;168
(10):1104-1110.
10