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Okkrjä (Gout)
INTRODUCTION
In the very ancient classics the Vatarakta disease as an individual
entity is not formed well established but in scattered form the nearly
same signs, symptoms and the treatment of the Vatarakta disease are
found. It means in those time, the lifestyle was very near to nature and
with full of physical exercise, so the causative factors of Vatarakta
were not made up. The word Vatarakta is made up of two words Vata
& Rakta. The Vata is the chief (King) without which no any disease
may take place, the Rakta is also a very important d hatu which gives
nutrition to each & every body tissues & maintains them normal by
eliminating toxins – malas (waste products) through the natural
orifices of the body. Vatarakta (Gout) is a variety of Vataroga (Group of
diseases caused by Vayu). The disease which is caused by excessively
aggravated Vayu (Vata) & vitiated blood (Rakta) is called Vatarakta.
Vatarakta is also known as-Khuda roga, Vata-balasa, Vatashra & Adhya
vata. Vatarakta is correlated with Gout in modern medical science.
Gout is the true crystal deposition disease characterized by pain &
swelling of I St Metatarsophalengeal joint initially followed by other
joints with an abnormal elevation of Urate level in the body either due
to over production or under excretion or sometimes both. Itcan also
be defined as the pathological reaction of the joint or periarticular
tissues to the presence of non sodium urate monohydrate crystals,
clinically this may present as inflammatory arthritis, bursitis,
tenosynovitis, cellulitis or as a nodular tophaceous crystal deposits.
Although prolonged hyperuriceamia is necessary but is alone not
sufficient for development of Gout.
Defination
Gout is a true crystal deposit metabolic disease. Generally it doesn’t materially
shorten the life span, but it may impair the quality of life.

It is defined as the pathological reaction of the joint or periarticular tissues to the

presence of monosodium urate monohydrate (MSU) crystals which deposits in
peripheral connective tissues in and around synovial joints, initially favouring lower
rather than upper limbs and especially targeting the first MTP (Metatarsophalangeal)
joint and small joints of feet and hands. MSU crystals take months or years to grow to
a detectable size, implying a long asymptomatic phase.

Gout is manifested by the following features, occurring singly or in combination:

1. Increased serum uric acid (SUA) concentration (hyperuricaemia >7 mg/dL

which represents the upper limits of solubility of MSU in serum at 37 oC at
blood pH).
2. Recurrent attacks of characteristic type if acute & chronic arthritis in which
crystals of MSU exhibits in leucocytes present in the synovial fluid.
3. Aggregated deposits of MSU (tophi means large aggregates of urate crystals)
in and around the joints of the extremities.
4. Renal disease involving interstitial tissue and blood vessels.
5. Uric acid nephrolithiasis.
Facts & Prevalence
Data from a number of countries suggest that gout is becoming more prevalent
(Table). In the USA, the National Health Interview Surveys asked participants
about members of their household having gout within the preceding year. The
one-year period prevalence of self-reported gout increased from 4.8/1000 in
1969 to 7.8/1000 in 1976, increasing further to 8.3/1000 in 1980 . Since then,
the prevalence has remained fairly stable at 8.4–9.9/1000 , with the most
recently published estimate being 9.4/1000 in 1996 . Similarly, the National
Health and Nutrition Examination Survey (NHANES) found that the self-
reported lifetime prevalence of physician-diagnosed gout increased from
26.4/1000 in NHANES III (1988–1994) to 37.6/1000 in NHANES 2007–2010 .
Furthermore, serum uric acid level (the key causal precursor of gout and
primary end-point by the FDA for gout drug approval) has increased over the
interval between the two NHANES studies. Gout-related claims in an
administrative claims database increased from 2.9/1000 in 1990 to 5.2/1000 in
1999.

Table
Prevalence of gout

Country Author Year Data Source Gout definition Prevalence

estimate

United Wallace et 1990 Medical claims Claim for gout or ULT in one year 2.9/1000
States al database

1999 5.2/1000
Country Author Year Data Source Gout definition Prevalence
estimate

Lawrence et 1969 National Health Self-reported one-year period 4.8/1000

al Interview Surveys prevalence

1976 7.8/1000

1980 8.3/1000

1983 to 9.9/1000
1985

1988 8.5/1000

1992 8.4/1000

1996 9.4/1000

Juraschek et 1988– NHANES III Self-reported lifetime physician- 26.4/1000

al 1994 diagnosis

2007– NHANES 2007–2010 Self-reported lifetime physician- 37.6/1000

2010 diagnosis
Country Author Year Data Source Gout definition Prevalence
estimate

UK Currie 1975 GP records GP diagnosis (lifetime prevalence) 2.6/1000

Steven 1987 GP records GP diagnosis (lifetime prevalence) 3.4/1000

(Scotland)

Harris et al 1993 GP records (England) GP diagnosis (lifetime prevalence) 9.5/1000

Mikuls et al 1999 General Practice GP diagnosis (one-year consultation 13.9/1000

Research Database prevalence)

Annemans 2000– IMS Disease GP diagnosis (5.5-year consultation 14.0/1000

et al 2005 Analyser prevalence)

Elliott et al 2001 RCGP weekly returns GP diagnosis (one-year consultation 4.3/1000

service prevalence)

2002 4.2/1000

2003 4.9/1000

2004 4.7/1000
Country Author Year Data Source Gout definition Prevalence
estimate

2005 4.8/1000

2006 4.9/1000

2007 4.7/1000

New Lennane et 1958 Random community Personal interview and examination European
Zealand al sample (lifetime prevalence) 3/1000
Maori 27/1000

Prior and 1966 Random community Personal interview and examination European
Rose sample (lifetime prevalence) 9/1000
Maori 60/1000

Klemp et al 1992 Random community Personal interview and examination, European

sample ARA criteria 29/1000
(lifetime prevalence) Maori 64/1000

Winnard et 2009 Aotearoa New Hospital discharge records (1988– European

al Zealand Health 2009) or 32/1000

Tracker (ANZHT) prescription for Maori 61/1000

Country Author Year Data Source Gout definition Prevalence
estimate

allopurinol/colchicine (2001–2009)

Pacific 71/1000

China Nan et al 2002 Random community Interview and questionnaire, self- 3.6/1000
sample report, confirmed
in medical record

Miao et al 2004 Random community Interview, questionnaire and 5.3/1000

sample examination, ARA
criteria

ARA, American Rheumatism criteria; GP, General practitioner; NHANES, National Health and Nutrition Examination
Survey; RCGP, Royal College of General Practitioner; ULT, urate-lowering therapy; UK, United Kingdom

In the UK, the estimated lifetime prevalence of gout was 2.6/1000 in 1975, 3.4/1000
in 1987 and 9.5/1000 in 1993 . In the General Practice Research Database (GPRD),
the one-year consultation prevalence of gout was 13.9/1000 in 1999 . A similar
consultation prevalence of 14.0/1000 was seen in the IMS Disease Analyzer between
2000 and 2005 . Subsequently, the Royal College of General Practitioners Weekly
Returns Service (RCGP-WRS) found that the annual prevalence appeared to increase
slightly from 4.3/1000 in 2001 to 4.7/1000 in 2007 .
Comparison of data from successive surveys undertaken in New Zealand using
similar methods shows a marked increase in the prevalence of gout in both European
and Maori subjects . Lifetime prevalence estimates in 1958, 1966 and 1992 were
3/1000, 9/1000 and 29/1000 in European subjects respectively. Corresponding
estimates in Maori subjects were 27/1000, 60/1000 and 64/1000 respectively. More
recently, a nationwide study that used different methods of sampling and case
ascertainment showed similar prevalence estimates (i.e. 32/1000 for European
subjects and 61/1000 for Maori subjects) .
Data from China also suggest that gout is becoming more prevalent. Successive
random population surveys in the city of Qingdao, found the prevalence of gout to be
3.6/1,000 in 2002 increasing to 5.3/1,000 in 2004 .
There is notable variation in the prevalence of gout obtained in these studies. This is
likely explained by a combination of differing methods used for sampling and case
ascertainment and definition, different time-periods for prevalence estimation (i.e.
confined-period prevalence vs. lifetime prevalence), demographics, and differences in
genetic, lifestyle, and co-morbid risk factor profiles in different geographical
populations. However, comparison of estimates within the same countries and within
the same datasets reduces the impact of this methodological and clinical
heterogeneity, and provides sufficient evidence that gout has become increasingly
more common over the past few decades.

Incidence of gout
There are fewer studies examining the incidence of gout. In the USA, the John
Hopkins Precursors Study recruited 1216 male medical students (mean age 22.2
years) between 1948 and 1964, following them for a mean period of 29 years . Sixty
men developed gout, corresponding to an incidence of 1.73 per 1000 person-years.
The Health Professionals Follow-Up Study (HPFS) followed 47,150 male health
professionals for 12 years, identifying 730 cases of incident gout (incidence, 1.50 per
1,000 person-years, using the ACR survey criteria ). In an analysis nested within the
Framingham Heart Study, 1951 men and 2476 women who were aged between 29
and 62 years and free of gout at recruitment in 1947 were followed-up for a median
of 28 years . Incidence of gout per 1000 person-years was 4.0 in men and 1.4 in
women. Serial investigations of computerized medical records from the Rochester
Epidemiology Project showed that the incidence of gout without diuretic exposure
(using the ACR survey criteria ) doubled from 20.2/100,000 in 1977/78 to
45.9/100,000 in 1995/96, whereas the proportion of gout associated with diuretic use
decreased significantly during this period .
In contrast to the Rochester Epidemiology Project, data from three primary care
consultation database studies in the UK do not suggest that the incidence of gout is
changing. Gout incidence remained fairly stable in the GPRD in the 1990s, ranging
from 11.9 per 10,000 person-years in 1991 to 18.0 per 10,000 person-years in 1994,
before decreasing back to 13.1 per 10,000 person-years in 1999 . A study using the
Health Improvement Network (THIN) UK primary care database followed 1,775,505
individuals, aged 20 to 89 years and free of gout at baseline, for an average of 5.2
years between January 2000 and December 2007 . 24,768 cases of incident gout were
identified, equating to a crude incidence rate of 2.68 per 1,000 person-years
(incidence per 1,000 person-years was 4.42 in men and 1.32 in women), and
incidence remained stable over the study period (2000-1: 2.67 per 1,000 person-
years, 2006-7: 2.52 per 1,000 patient-years). Although the incidence of gout appears
to be higher in the later THIN study than the earlier GPRD study, data from the
RCGP-WRS found the mean annual incidence of gout to be 12.4 cases per 10,000
person-years between 1994 and 2007, without evidence of changing incidence over
this period .

Hyperuricaemia
It has been well-established that hyperuricemia is the key causal precursor in the
development of gout. Population studies have demonstrated and quantified a direct
positive (linear to exponential) relation between serum urate levels and a future risk
of gout, as summarized here. The Normative Aging Study followed 2,046 healthy
male veterans aged 21 to 81 years over a period of 14.9 years, identifying 84 new
cases of acute gouty arthritis [26]. The incidence of gout per 1,000 person-years in
people with serum urate levels <6.0mg/dl, 6.0–6.9mg/dl, 7.0–7.9mg/dl, 8.0–8.9mg/dl,
9.0–9.9mg/dl and ≥10.0mg/dl was 0.8, 0.9, 4.1, 8.4, 43.2, and 70.2 respectively. In
the Framingham Heart Study, there was a similar marked dose-dependent increase in
both incidence and relative risk (RR) of developing gout with serum urate level
(Figure 1) . A study from Italy undertaken in the Health Search/Longitudinal Patient
Primary Care database also found a dose-response relationship between serum urate
levels at baseline and incident gout . Compared to those with a serum urate level
<6mg/dl, the odds of incident gout were 1.75 (95%CI 1.44, 2.12) with serum urate 6–
7mg/dL, rising to 6.20 (95%CI 5.32, 7.24) and 15.31 (95%CI 12.51, 18.75) in those
with serum urate 7–9mg/dl and ≥9mg/dl respectively. In the Kinmen Study from
Taiwan, 42 out of 223 men with hyperuricaemia but no history of gout at baseline in
1991 had developed gout when re-examined in 1996/7, corresponding to a five-year
cumulative incidence of 18.8%. The five-year cumulative incidence was 10.8% in
those with a serum urate level of 7.0–7.9mg/dl, 27.7% with a serum urate 8.0–
8.9mg/dl, and 61.1% with a serum urate ≥9.0mg/dl. These studies, together with the
fact that effective management of hyperuricemia prevents gout, provide convincing
evidence that hyperuricaemia is a necessary casual component for the development of
gout.
Figure 1
Increasing incidence of gout in men and women with serum urate level

Figure 2
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Dietary factors
Although an association between gout and dietary factors, particularly purine-rich
foods and alcoholic beverages, has been recognised for centuries, it is only recently
that robust epidemiological evidence of such have emerged (Table 2). The most
comprehensive assessment of the association between gout and diet has been
undertaken in the HPFS. In this large, prospective study, a semi-quantitative food
frequency questionnaire was administered to 51,529 male health professionals at
baseline and at four- and eight-year follow-up. Over a 12-year period, 730 incident
cases of gout were identified. In addition to confirming the historical observations
that excessive consumption of purine-rich foods and alcoholic drinks are independent
risk factors for gout, evidence has been provided for more novel dietary associations:
namely, that fructose and sugar-sweetened soft-drinks increase the risk of developing
gout whereas dairy products, coffee, and vitamin C appear to be protective against the
development of gout.

Table 2
Dietary factors and risk of incident gout

Dietary factor Study Exposure group Referent group Multivariate risk

estimate
(95% confidence
interval)

Total Meat HPFS Highest quintile Lowest quintile RR 1.41 (1.07, 1.86)

Seafood HPFS Highest quintile Lowest quintile RR 1.51 (1.17, 1.95)

Purine-rich vegetables HPFS Highest quintile Lowest quintile RR 0.96 (0.79, 1.19)

Dairy products HPFS Highest quintile Lowest quintile RR 0.56 (0.42, 0.74)

Low-fat dairy HPFS Highest quintile Lowest quintile RR 0.58 (0.45, 0.76)

High-fat dairy HPFS Highest quintile Lowest quintile RR 1.00 (0.77, 1.29)

Coffee HPFS ≥6 cups/day None RR 0.41 (0.19, 0.88)

Nurses’ Health Study ≥4 cups/day None RR 0.43 (0.30, 0.61)

Decaffeinated coffee HPFS ≥4 cups/day None RR 0.73 (0.46, 1.17)

Dietary factor Study Exposure group Referent group Multivariate risk
estimate
(95% confidence
interval)

Nurses’ Health Study >1 cups/day None RR 0.77 (0.63, 0.95)

Tea HPFS ≥4 cups/day None RR 0.82 (0.38, 1.75)

Nurses’ Health Study ≥4 cups/day None RR 1.55 (0.98, 2.47)

Total caffeine HPFS Highest quintile Lowest quintile RR 0.83 (0.64, 1.08)

Nurses’ Health Study Highest quintile Lowest quintile RR 0.52 (0.41, 0.68)

Sugar-sweetened soft HPFS ≥2 servings/day <1 RR 1.85 (1.08, 3.16)

drinks serving/month

Nurses’ Health Study ≥2 servings/day <1 RR 2.39 (1.34, 4.26)

serving/month

Diet soft drinks HPFS ≥2 servings/day <1 RR 1.12 (0.82, 1.52)

serving/month
Dietary factor Study Exposure group Referent group Multivariate risk
estimate
(95% confidence
interval)

Nurses’ Health Study ≥2 servings/day <1 RR 1.18 (0.87, 1.58)

serving/month

Free fructose HPFS Highest quintile Lowest quintile RR 2.02 (1.49, 2.75)

Nurses’ Health Study Highest quintile Lowest quintile RR 1.62 (1.20, 2.19)

Vitamin C HPFS >1500mg/day <250mg/day RR 0.55 (0.38, 0.80)

Alcohol ARIC “High” alcohol Not defined HR 2.00 (1.42, 2.82)

intake

THIN >42 units/week None OR 3.00 (2.66, 3.38)

HPFS >50g/day None RR 2.53 (1.73, 3.70)

Framingham Heart >7oz/week 0-1oz/week RR 2.21 (1.56, 3.14)

(men)
Dietary factor Study Exposure group Referent group Multivariate risk
estimate
(95% confidence
interval)

Framingham Heart >7oz/week 0-1oz/week RR 3.10 (1.69, 5.68)

(women)

Beer HPFS >2 servings/day <1 RR 2.51 (1.77, 3.55)

serving/month

Spirits HPFS >2 servings/day <1 RR 1.60 (1.19, 2.16)

serving/month

Wine HPFS >2 servings/day <1 RR 1.05 (0.64, 1.72)

servingmonth

ARIC, Atherosclerosis Risk in Communities; HPFS, Health Professionals Follow-up Study; HR, hazards ratio; OR,
odds ratio; RR, relative risk; THIN, The Health Improvement Network

Purine-rich foods theoretically predispose to gout by providing exogenous substrate

for purine metabolism, the end-product of which is uric acid in humans (Figure ).
Compared with men in the lowest quintile, men in the highest quintiles of total meat
and seafood intake had an increased risk of incident gout of 41% and 51%
respectively, adjusting for age, energy intake, body mass index (BMI), diuretic use,
hypertension, renal failure, and dietary factors including alcohol . Consumption of
purine-rich vegetables was not a risk factor for incident gout. Men in the highest
quintile of consumption of dairy products, particularly low-fat dairy, had almost half
the risk of risk of incident gout compared to those in the lowest quintile. High-fat
dairy consumption had no protective effect. The multivariate RRs per additional daily
serving were 1.21 (95%CI 1.04, 1.41) for total meat, 1.07 (95% CI 1.01, 1.12) for
seafood, 0.82 (95% CI 0.75, 0.90) for total dairy, and 0.79 (95%CI 0.71, 0.87) for
low-fat dairy. A recent randomized control trial (RCT) has found that intact milk
intake has an acute uricosuric urate-lowering effect . Proteins contained in milk, such
as casein, lactoalbumin, and orotic acid may exert their uricosuric effects without the
concomitant purine load contained in other animal protein sources such as meat and
seafood .
Another RCT has suggested that skimmed milk powder derivatives have anti-inflammatory effects
against acute gout flares among patients with pre-existing gout .

Figure

Proposed mechanism of action of lifestyle factors in the aetiology of hyperuricaemia and gout

Excessive consumption of purine-rich foods has been shown to trigger recurrent gout
attacks in a novel internet-based case-crossover study in which each participant acts
as their own control, thereby allowing the effect of transient exposures on an acute
event to be studied whilst eliminating confounding due to individual characteristics
that do not change during the study period . In an analysis of 1,247 recurrent gout
attacks occurring over a one-year period in 633 participants, the multivariate OR for
recurrent gout attacks for each increasing quintile of purine consumption were 1.17
(95%CI 0.88, 1.55), 1.38 (95%CI 1.02, 1.87), 2.21 (95%CI 1.62, 3.01) and 4.76
(3.37, 6.74) respectively, compared with the lowest quintile over a two-day period
and adjusted for use of alcohol, diuretics, allopurinol, colchicine and non-steroidal
anti-inflammatory drugs.
Coffee is thought to reduce serum uric acid levels by a number of mechanisms
(Figure 2). It is rich in anti-oxidants, such as the phenol chlorogenic acid, which are
thought to increase insulin sensitivity and in turn enhance renal urate excretion .
Caffeine is itself a methyl xanthine and may therefore be a competitive inhibitor of
xanthine oxidase , the major enzyme in purine metabolic pathways. In a subsequent
HPFS analysis, a dose-dependent inverse relationship between the number of cups of
coffee consumed per day and incident gout was seen (0 cups, RR 1.00 referent; <1
cup, RR 0.97, 95%CI 0.78, 1.20; 1–3 cups, RR 0.92, 95%CI 0.75, 1.11; 4–5 cups, RR
0.60, 95%CI 0.41, 0.87; ≥6 cups, RR 0.41, 95%CI 0.19, 0.88) . A similar more
modest inverse association was seen between consumption of decaffeinated coffee
and incident gout whereas no association was seen for either tea consumption or total
caffeine intake. The association between coffee consumption and incident gout in
women has been examined in the Nurses’ Health Study . 89,433 female nurses who
were gout-free prior to baseline were followed-up for 26 years, during which 896
incident gout cases occurred. A similar inverse relationship was found between
coffee consumption and risk of gout. Compared with women who drank no coffee,
women who drank ≥948mls of coffee per day had less than half the risk of incident
gout, after adjustment for age, total energy intake, BMI, menopause, use of hormonal
replacement, diuretic use, hypertension and dietary factors (Table 3). As with men in
the HPFS [37], there was a modest inverse relationship with decaffeinated coffee and
no association with tea. In contrast to men in the HPFS, there was a negative
association between total caffeine intake and incident gout. Women consuming 359–
497mg/day and ≥498mg/day had 23% and 48% reduced risk respectively, compared
with women consuming ≤131mg/day (Table 3).
Fructose acts as a substrate for uric acid production by enhancing degradation of
purine nucleotides (Figure 2) [39]. Consumption of sugar-sweetened soft drinks has
also been shown to increase the risk of incident gout in a dose-dependent manner in
the HPFS [40]. Compared to men who consumed sugar-sweetened soft-drinks less
frequently than once per month, the multivariate RR of incident gout was 1.29
(95%CI 1.00, 1.68) in those consuming 5–6 servings per week, 1.45 (95%CI 1.02,
2.08) with once daily consumption, and 1.85 (95%CI 1.08. 3.16) in those consuming
2 or more servings per day. Consumption of diet soft-drinks was not a risk factor for
incident gout. A positive dose-dependent relationship was also seen between free
fructose intake and incident gout (quintile 1 referent; quintile 2, RR 1.29, 95%CI
1.02, 1.64; quintile 3, RR 1.41, 95%CI 1.09, 1.82; quintile 4, RR 1.84, 95%CI 1.40,
2.41; quintile 5, RR 2.02, 95%CI 1.49, 2.75). In the Nurses’ Health Study, women
drinking one serving of sugar-sweetened soft drinks per day and ≥2 servings per day
were at a 74% and 139% higher risk of incident gout respectively, compared to those
consuming <1 serving per month (Table 3) [41]. Compared to women in the lowest
quintile of free fructose intake, the multivariate RRs of incident gout in the highest
and second highest quintiles were 1.62 (95%CI 1.20, 2.19) and 1.34 (95%CI 1.01,
1.76) respectively.
Vitamin C has recognised uricosuric properties (Figure 2) [42] and high vitamin C
intake has been shown to be protective against the development of gout in the HPFS
[43]. The multivariate RR of incident gout was 0.97 (95%CI 0.85, 1.12) for total
vitamin C consumption of 250–499mg/day, 0.83 (95%CI 0.71, 0.97) for 500–
999mg/day, 0.66 (95%CI 0.52, 0.86) for 1000–1499mg/day, and 0.55 (95%CI 0.38,
0.80) for ≥1500mg/day, compared with those consuming less than 250mg per day.
Cherries and cherry extract have recognised urate-lowering properties and hence have
attracted much interest as a potential treatment for gout. However, epidemiological
evidence of the association between cherry consumption and gout is sparse. In the
internet-based case-crossover study described above, intake of cherries (multivariate
OR 0.65; 95% CI 0.50, 0.85) and cherry extract (OR 0.55; 95% CI 0.30, 0.98) over
the preceding two-day period both appeared to be protective against recurrent gout
attacks [44].
Go to:

Alcohol consumption
Several studies have examined the long-recognised observation that alcohol
consumption is a risk factor for the development of gout . Alcohol consumption is
thought to predispose to gout by providing substrate for purine metabolism in the
form of guanosine (particularly beer), enhancing nucleotide turnover, and impairing
renal urate excretion via lactic acidosis. The Atherosclerosis Risk in Communities
(ARIC) study was a population-based prospective cohort study which recruited
15,792 individuals aged 45–64 years between 1987 and 1989. In a sub-analysis
undertaken in 10,872 participants who did not have gout prior to baseline, 274 people
developed gout over the nine-year follow-up period. Those who fulfilled an
unspecified definition of “high” alcohol intake had twice the risk of incident gout,
adjusted for sex, race, BMI, alcohol intake, and estimated glomerular filtration rate.
In a case-control study nested within the THIN primary care database study, 24,768
people with incident gout were compared to 50,000 control subjects without gout
who were frequency-matched for age, gender and calendar year [25]. There was a
dose-response relationship between incident gout and prior alcohol consumption.
Compared with those who did not drink alcohol, the multivariate ORs of incident
gout in those drinking 1–9, 10–24, 25–42 and >42 units of alcohol per week were
1.06 (95%CI 1.01, 1.11), 1.56 (95%CI 1.49, 1.65), 2.45 (95%CI 2.27, 2.63) and 3.00
(95%CI 2.66, 3.38) respectively, adjusting for age, calendar year, GP visits, BMI,
ischaemic heart disease, hypertension, hyperlipidemia, diabetes, chronic renal failure
and use of diuretics (1 unit = 10mls of pure ethanol or 8g of alcohol). In the HPFS,
increasing alcohol intake was associated with increasing risk of incident gout [47].
Compared with men who did not drink alcohol, the multivariate RRs were 1.09
(95%CI 0.85, 1.40) for daily alcohol consumption 0.1–4.9g, 1.25 (95%CI 0.95, 1.64)
for 5.0–9.9g, 1.32 (95%CI 0.99, 1.75) for 10.0–14.9g, 1.49 (95%CI 1.14, 1.94) for
15.0–29.9g, 1.96 (95%CI 1.48, 2.60) for 30.0–49.9g, and 2.53 (95%CI 1.73, 3.70) for
≥50g. The multivariate RR per 10g increase in daily alcohol consumption was 1.17
(95%CI 1.11, 1.22). Compared to men drinking each type of drink less than once per
month, those imbibing ≥2 drinks per day had 2.5 times the risk of incident gout for
beer, 1.6 times for spirits and no increased risk associated with wine (Table 3). The
multivariate RR per serving per day was 1.49 (95%CI 1.32, 1.70) for beer, 1.15
(95%CI 1.04, 1.28) for spirits and 1.04 (95%CI 0.88, 1.22) for wine. The
Framingham Heart Study has shown excessive alcohol consumption to be an
independent risk for gout in both women and men [23]. Women who drank ≥7oz of
alcohol per week had over three times the risk of incident gout and men drinking this
amount over twice the risk, compared to those who drank less than 0–1oz per week
(Table 3). Moderate consumption (2–6oz per week) was not associated with incident
gout in either gender. In the internet-based case-crossover study described above
[48], alcohol consumption was found to trigger recurrent gout attacks (multivariate
OR 2.5; 95% CI 1.1, 5.9; ≥7 alcoholic drinks consumed in the previous two days,
compared with no consumption; adjusted for purine intake and diuretic use).
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Obesity and the metabolic syndrome

Gout is very commonly associated with comorbidity, including the metabolic syndrome. In a large
cross-sectional study undertaken in NHANES-III, the prevalence of the metabolic syndrome in
people with gout was 62.8% compared with 25.4% amongst people without gout (odds ratio (OR)
3.05; 95%CI 2.01, 4.61; adjusted for age and gender) [49].
Several individual components of the metabolic syndrome have been shown to be independent risk
factors for the development of gout (Table 4). A dose-dependent effect between increasing BMI and
risk of incident gout has been demonstrated in several large prospective epidemiological studies. In
the THIN database case-control study, individuals with a BMI between 25–29kg/m2 had an
multivariate OR of 1.62 (95% CI 1.55, 1.70) for incident gout and those with BMI of ≥30kg/m2 an
OR of 2.34 (95% CI 2.22, 2.47) compared to those with a BMI 20–24kg/m2 [25]. In the HPFS,
compared to those with a BMI 21–22.9kg/m2, the multivariate RR of incident gout in men was 0.85
in those with a BMI <21kg/m2, increasing to 1.40 with BMI 23–24.9kg/m2, 1.95 with BMI 25–
29.9kg/m2, 2.33 with BMI 30–34.9kg/m2and 2.97 with BMI ≥35 kg/m2 [50]. Furthermore, risk of
incident gout was increased in men who had gained 20–29lbs (multivariate RR1.57; 95%CI 1.15,
2.14) and ≥30lbs (RR 2.47; 95%CI 1.86, 3.28) in weight since the age of 21 years compared with
those whose weight was stable. In contrast, weight loss of 10lbs or more since baseline reduced the
risk of incident gout by 39% (multivariate RR 0.61; 95%CI 0.40, 0.92).

Table 4
Medical conditions and risk of incident gout
An analysis undertaken in the ARIC study provides similar data for women (Table 4) [51]. A total
of 6,263 women aged 45–64 years with no history of gout prior to baseline were followed-up for 9
years, identifying 106 cases of incident gout. Compared to women with a BMI<25kg/m2 at baseline,
the adjusted RR of incident gout was 1.63 (95%CI 0.84, 3.18) with a BMI 25–29.9 kg/m2, 2.76
(95%CI 1.40, 5.44) with a BMI 30–34.9kg/m2, and 3.90 (95%CI 1.95, 7.82) with a BMI ≥35kg/m2.
In women with BMI 25–29.9 kg/m2 and BMI ≥30kg/m2 at age 25 years, the multivariate RRs for
incident gout were 3.36 (95%CI 2.09, 5.41) and 2.84 (1.33, 6.09) respectively, compared to those
with BMI<25 kg/m2 at age 25 years. Women with the highest tertile of weight gain (≥16.3kg) from
age 25 years to baseline had twice the risk of incident gout compared with individuals in the lowest
tertile (multivariate RR 2.05; 95%CI 1.06, 3.96).
Evidence of a dose-dependent effect of increasing BMI on risk of incident gout in men and women
is provided by the Framingham Heart Study (Table 4) [23]. Compared to those with a
BMI<25kg/m2, the multivariate RR of incident gout was 1.44 (95%CI 0.88, 2.37) in women with a
BMI 25–29.9kg/m2, rising to 2.74 (95%CI 1.65, 4.58) in those with a BMI≥30kg/m2. In men, the
corresponding RRs were 1.76 (95%CI 1.22, 2.54) and 2.90 (95%CI 1.89, 4.44) respectively.
Increasing BMI has also been found to be an independent risk factor for gout flare in the THIN
database (BMI 15–19kg/m2, men hazards ratio (HR) 0.77, women 0.79; BMI 25–29kg/m2, men HR
1.07, women 1.10; BMI ≥30kg/m2, men 1.12, women 1.43) compared to those with a BMI in the
range 20–24kg/m2 [52].
Several large prospective epidemiological studies have examined the association between
hypertension and gout (Table 4). Hypertension was found to be an independent risk factor for
incident gout in the THIN database case-control study although the magnitude of increased risk was
small [25]. In contrast, in both HPFS and ARIC, the risk of incident gout in those with hypertension
was twice that of those without hypertension [46,50]. The findings of two studies suggest that
hypertension has a greater effect on risk of incident gout in women than men. In the Framingham
Heart Study, the multivariate RR of incident gout associated with hypertension was 1.59 (95% 1.12,
2.24) in men and 1.82 (95%CI 1.06, 3.14) in women, although there was considerable overlap of the
confidence intervals [23]. However, in the THIN database, narrower confidence intervals suggest
that hypertension has a greater influence on gout flares in women (multivariate RR 1.45; 95%CI
1.30, 1.62) than men (RR 1.08; 95%CI 1.02, 1.13) [52].
Although hyperglycaemia and insulin resistance are recognised components of the metabolic
syndrome, the role of diabetes mellitus as a risk factor for the development for gout has received
relatively little attention. Interestingly, in the THIN database case-control study, individuals with
diabetes had a 33% lower risk of developing gout than those without diabetes (multivariate RR
0.67; 95%CI 0.63, 0.71) [53]. This finding was more marked in men than women (Table 4). The
risk of developing gout reduced with increasing duration of diabetes: duration 0–3 years RR 0.81
(95%CI 0.74, 0.90), 4–9 years RR 0.67 (95%CI 0.61, 0.73), and 10 years or longer RR 0.52 (95%CI
0.46, 0.58). Risk was also less with type I than type II diabetes (Table 4). Although these findings
may seem counter-intuitive, the predisposition to hyperuricaemia and gout induced by
hyperinsulinaemia and insulin resistance in the pre-diabetic state is thought to be reversed by the
uricosuric effects of glycosuria once frank diabetes develops [54–56].
A less well-established putative risk factor for gout is obstructive sleep apnoea which is commonly
associated with both components of the metabolic syndrome and hyperuricaemia [57–59]. Hypoxia
enhances nucleotide turnover thereby generating purines which are metabolised to uric acid [60,61],
providing a biologically plausible mechanism by which obstructive sleep apnoea might predispose
to gout. In a small cross-sectional study undertaken in a GP consultation database, gout was
associated with sleep disorders (OR 1.39; 95%CI 1.06, 1.81; adjusted for age, gender, practice,
diabetes, hypertension, diuretic use and ischaemic heart disease) [62].There was no association with
obstructive sleep apnoea although the study was under-powered. Larger prospective
epidemiological studies are required to examine this proposed association in more detail.
Go to:

Medications
A number of medications and substances have been implicated in the aetiology of gout [63],
however, diuretics have received the greatest attention. A recent systematic review examined the
risk of gouty arthritis in patients using diuretics [64], identifying two RCTs and 11 epidemiologic
studies. In one RCT, the rate ratio of gout for use of bendrofluazide vs placebo was 11.8, whereas
the other RCT found a rate ratio of 6.3 for use of hydrochlorothiazide plus triamterene vs placebo.
Three cohort studies [28,50,65] and four case-control studies [66–69] found an increased of gout in
diuretic users. The two largest cohort studies identified by this systematic review adjusted for
medications [65], comorbidities [50,65] and life-style factors [50] finding RRs of 1.77 for incident
gout in the HPFS (95%CI 1.42, 2.20) [50] and 1.99 for initiation of anti-gout medication (95%CI
1.21, 3.26) [65]. The Framingham Heart Study was not included in this review but reported
multivariate RRs for diuretic use of 2.39 (95%CI 1.53, 3.74) in women and 3.41 (95%CI 2.38, 4.89)
in men [23]. In the THIN case-control study, the RR for incident gout amongst those currently using
diuretics was 2.36 (95%CI 2.21, 2.52) in people with hypertension and 3.01 (95%CI 2.72, 3.33)
amongst those without hypertension, after adjustment for GP visits, BMI, alcohol use, ischaemic
heart disease, hypertension, hyperlipidaemia, renal failure, and use of other anti-hypertensive drugs
[70]. Furthermore, amongst current diuretic users, the risk of developing gout increased with both
the duration of diuretic therapy and increased dosage, providing evidence of a dose-dependent
effect. Finally, the aforementioned internet-based case-crossover study has also showed consistent
findings for the risk of recurrent gout [67]. These studies collectively confirm the well-recognized
clinical entity of diuretic-induced gout, also known as secondary gout.
Aspirin has long-been recognised to have effects on renal tubular urate handling. In the 1950s, high-
dose aspirin was found to be uricosuric whilst low-doses were urate-retaining [71]. However, only
very recently has epidemiological evidence of the clinical significance of this association come to
light. In the internet-based case-crossover study, use of low-dose aspirin (≤325 mg/day) in the prior
two consecutive days was associated with an increased risk of recurrent gout attacks (OR 1.81;
95%CI 1.30, 2.51) [72]. Interestingly, concurrent use of allopurinol removed the increased risk of
recurrent gout attacks associated with low-dose aspirin (adjusted OR 0.89; 95%CI 0.55, 1.44)
suggesting that urate-lowering therapy may mitigate the risk of recurrent acute gout exacerbated by
use of low-dose aspirin.
Several classes of anti-hypertensive drugs are known to influence serum urate levels. Β-blockers
increase serum urate levels whereas both calcium-channel blockers and losartan have urate-
lowering properties [63,73]. In addition to examining the risk of gout associated with diuretic use,
the THIN primary care database case-control study described above also investigated the risk of
incident gout conferred by a wide-range of anti-hypertensive drugs including calcium-channel
blockers, losartan, β-blockers, angiotensin-converting-enzyme (ACE) inhibitors, and non-losartan
angiotensin-II (AII) receptor blockers [70]. Amongst those with hypertension, current use of β-
blockers (RR 1.48; 95%CI 1.40, 1.57), ACE-inhibitors (RR 1.24; 95%CI 1.17, 1.32), and non-
losartan AII-receptor blockers (RR 1.29; 95%CI 1.16, 1.43) was more common in those with
incident gout whereas current use of calcium-channel blockers (RR 0.87; 95%CI 0.82, 0.93) and
losartan (RR 0.81; 95%CI 0.70, 0.94) was less common.
Go to:

Renal Disease
The association between gout and renal disease is complex and could be bi-directional, i.e. although
renal disease predisposes to the development of gout, gout and its treatment are thought themselves
to lead to renal impairment and chronic kidney disease. Such associations have been recognised for
many years yet early studies were undertaken in specialist secondary care populations [74–76]
which may not representative of the majority of patients with gout who are managed exclusively in
primary care. More recently, two population-based epidemiological studies have provided
convincing evidence that renal disease is a risk factor for gout. In the HPFS, the multivariate RR of
incident gout in men with chronic renal failure compared to those without chronic renal failure was
3.61 (95%CI 1.60, 8.14) [50]. In the THIN case-control study, prior history of chronic renal failure
was strongly associated with incident gout (OR 2.48; 95%CI 2.19, 2.81) [25]. Renal failure was also
associated with risk of gout flare (HR 1.33; 95%CI 1.20, 1.48) [52]. Furthermore, in the ARIC
study, participants with a low estimated glomerular filtration rate (<60ml/min) had twice the risk of
incident gout as those with a normal estimated glomerular filtration rate (>90ml/min) (multivariate
HR 2.43; 95%CI 1.50, 3.94) [46].
Go to:

Osteoarthritis
Although hyperuricaemia is a very strong risk factor for gout, many hyperuricaemic individuals do
not develop gout. It is not fully understood why some people with hyperuricaemia appear to form
and deposit MSU crystals more readily than others, however, it is thought that MSU crystals may
deposit more easily in osteoarthritic cartilage [77]. This hypothesis has also been suggested to
explain the striking predilection of gout for the first metatarsophalangeal joint, which is also a target
joint for OA [78]. Both radiographic and clinical cross-sectional studies have shown that attacks of
gout occur at joints already affected by OA. A hospital-based study of 262 subjects with gout found
a significant correlation between the occurrence of acute attacks of gout and radiographic OA at the
first MTP joints, tarsal joints and knees [79]. More recently, a community-based study of 164
subjects with gout found a strong association between sites of acute attacks of gout and the presence
of clinical OA (multivariate OR 7.94; 95%CI 6.27, 10.05), adjusted for age, gender, BMI and
diuretic use [80]. However, nodal OA was no more frequent in gout subjects than in 656 control
subjects without gout [81]. Such cross-sectional studies cannot determine causality or temporal
aspects of this association, hence further prospective studies are required.

Epidemiology:-
 Prevalence of gout varies between populations with a strong male
predominance (>5:1).
 It is the most common inflammatory arthritis in men and in older women.
 Prevalence increases with increasing serum uric acid (SUA) and with age.
 SUA levels are higher in men (from the age of 20) than women (after the
menopause) positively correlate with obesity and vary according to ethnicity
(highest in New Zealand).
 Only a minority of hyperuricaemic people develop gout.
 Man is the only mammal to spontaneously develop hyperuricaemia & gout, as
only human lack uricase the enzyme responsible for the degradation of uric
acid in other mammals.
P a g e | 26

Aetiology:-
Primary gout-
 About 1/3rd of the body uric acid pool is derived from dietary sources and 2/3 rd
from endogenous purine metabolism.
 The concentration of uric acid in body fluids depends on the balance between
its synthesis and elimination by the kidneys (2/3rd) and gut (1/3rd).
 Purine nucleotide synthesis and degradation are regulated by a network of
enzyme pathways; xanthine oxidase catalyses the end conversion of
hypoxanthine to xanthine and then xanthine to uric acid.
 Some primary gout patients are intrinsic ‘over producers’ of uric acid
 <1% there may be an inherited defect in purine metabolism, which should be
suspected if gout develops > 25 years of age, in patient with uric acid renal
calculi, or if there is a strong family history of early onset gout.
 Risk factors and associations for primary gout include metabolic syndrome-
high alcohol intake and diets relatively high in red meat or fructose or
relatively low in vitamin C or coffee.

Secondary gout-
  It results from hyperuricaemia due to renal impairment or chronic diuretics use.
In diuretic induced gout, nodal generalised OA is a further risk factor,
especially in elderly women. Lead poisoning is a rare cause of hyperuricaemia
& secondary gout.

Types and pathogenesis-

Hyperuricaemia and gout may be classified into 2 types:

Metabolic and Renal, each of which may be primary or secondary.

Primary refers to cases in which underlying biochemical defect causing
hyperuricaemia is not known, while secondary denotes cases with known causes of
hyperuricaemia.

P a g e | 15

1. Hyperuricaemia of metabolic origin-

 Uric acid is the end product of purine metabolism. This type comprises about
10% cases which are characterised by overproduction of uric acid (increased
nucleic acid turnover - as in cancer, psoriasis, and during tumor lysis induced
by chemotherapy ) and reduced excretion on the remainder.
 The cause of primary metabolic gout includes a number of specific enzyme
defect in purine metabolism which may either of unknown cause or are inborn
errors of metabolism (eg. Complete HGPRT deficiency).
 The secondary metabolic gout is due to either increased purine biosynthesis or
a deficiency of glucose-6-phosphatase.

2. Hyperuricaemia of renal origin-

 About 90% cases of gout are the result of reduced renal excretion of uric acid.
 Plasma levels of uric acid are governed by a four-part renal transport system
that involves glomerular filtration, reabsorption, secretion and post secretory
reabsorption. Approximately 90% of the filtered urate is reabsorbed, and the
urate transporter I gene (URAT I) has an important role in the reabsorption
process. Altered renal excretion could be due to reduced glomerular filtration
of uric acid, enhanced tubular reabsorption or decreased secretion underlies
most cases of primary gout.
  The cause of gout of renal origin include diuretic therapy, drug induced (e.g.
aspirin, pyrazinamide, nicotinic acid, ethambutol and alcohol), adrenal
insufficiency, starvation, diabetic ketosis, and disorders of parathyroid and
thyroid.
 Renal disease rarely causes secondary hyperuricaemia such as polycystic
kidney disease and leads to urate nephropathy.
 Gout in young females caused by decreased renal urate clearance and renal
insufficiency. Premenopausal gout is rare. Most women with gouty arthritis are
postmenopausal and elderly have OA and arterial hypertension that cause mild
renal insufficiency and usually are receiving diuretics.

P a g e | 16

Two pathways are involved in purine synthesis:

(1) A de novo pathway in which purines are synthesised from non-purine precursors.

(2) A salvage pathway in which free purine bases derived from the breakdown of
nucleic acid of endogenous or exogenous organ are recaptured (salvaged).

Deficiency of hypoxanthine guanine phosphoribosyl transferase (HGPRT) enzyme

leads to increased synthesis of purine nucleotides through the do novo pathway and
hence increased production of uric acid. A complete lack of HGPRT occurs in the
uncommon X-linked Lesch-Nyhan syndrome, seen only in males and characterized by
hyperuricaemia, severe neurologic deficits with mental retardation, self-mutilation,
and in some cases gouty arthritis.

Solubility of MSU crystals in a joint is modulated by temperature (the lower the less
soluble) and by the intra-articular concentration of urate and cations. Crystallization
depends on the presence of nucleating agents such as insoluble collagen fibres,
chondroitin sulphate, proteoglycans, cartilage fragments, and other crystals. Since
synovial fluid is a poorer solvent for MSU than plasma, urates in the joint fluid
becomes supersaturated more easily, particularly in peripheral joints (ankles and
toes), where temperature is as low as 20 oC. With prolonged hyperuricaemia, crystals
& microtophi of urates develops in synovium. Some events nd trauma causes release
of crystals in synovial fluid which initiates cascade of events. MSU crystals are
phagocytosed by macrophages and through an incompletely understood mechanism
activate the NALP3 inflammasome, a multiprotein complex that includes the
protease caspase 1. The inflammasome activated caspase 1,in turn, cleaves and
activates several cytokines, most notably IL-1β and IL-18. IL-1β induces the
expression of adhesion molecules and the synthesis of neutrophil chemokine CXCL8,
which is essential for the localization of neutrophils at the site of acute inflammation.

The neutrophils pour fuel on the fire by releasing toxic free radicals, leukotrienes
(LT-B4), and lysosomal enzymes. Thus comes about an acute arthritis, which
typically remits spontaneously in days to weeks.

Repeated attacks of acute arthritis leads to chronic arthritis and the formation of tophi
in the inflamed synovial membranes and periarticular tissues. In time severe damage
to the cartilage develops and the function of the joints is compromised.
P a g e | 17

Factors contributing the conversion of asymptomatic hyperuricaemia into primary

gout:-
 Age (20 to 30 years) and duration of the hyperuricaemia.
 Genetic predisposition- X-linked abnormalities of HGPRT.
 Heavy alcohol consumption predisposes to attack of gouty arthritis.
 Obesity increases the risk of asymptomatic gout.
 Certain drugs (e.g. thiazides) reduce excretion of urate and predispose to the
development of gout.
 Lead toxicity

MORPHOLOGICAL/ CLINICAL FEATURES-

1. Acute gouty arthritis-

 Inflamed Heberden’s or Bouchard’s nodes may be a first manifestation of

gouty arthritis.
 The first MTP joint is affected in over 50% of cases-‘podagra’ (seizing of
foot). Other common sites are in order of decreasing frequency are : the instep,
ankles, heels, knees, wrists, fingers and elbows. It is elf limiting over 5-14
days, with complete return to normality

Typical attacks have the following characteristics:-

  Initially there is monoarticular involvement accompanied with intense pain, but
later it becomes polyarticular along with symptoms like fever, malaise and
even confusion, especially if a large joint such as the knee is involved.
 Severe pain, often described as the ‘worst pain ever’
 Extreme tenderness: the patient is unable to wear socks
 There is joint effusion containing numerous polymorphs, macrophages and
microcrystals of urates. The mechanism of acute inflammation appears to
include phagocytosis of crystals by leucocytes, activation of the kallikrein
system, activation of the complement system and urate- mediated disruption of
lysosomes within the leucocytes leading to release of lysosomal products in the
joint effusion.
 Milder episodes lasting just a few days (‘petite attacks’).
 Some have attacks in more than one joint a few days later (‘cluster attacks’).
P a g e | 18
 Marked synovitis (large/ tense effusion, warmth, restricted movement with
stress pain) triggered by precipitation of sufficient amount of long,
selender/needle shaped crystals of MSU from serum or synovial fluid.
 There is dense neutrophilic infiltration that permeates the synovium and
synovial fluid. The MSU crystals are frequently found in the cytoplasm of the
neutrophils & are arranged in small clusters in the synovium.
 The synovium is oedematous and congested, and also contains scattered
lymphocytes, plasma cells urate crystals and macrophages.

2. Recurrent and chronic gout-

 After an acute attack, some people never have a second attack, in others the
next episode occurs within 1 year and the frequency of attacks gradually
increases with time. Later attacks are more likely to involve several joints and
be more severe.
 The interval between the first attack and the development of chronic symptoms
is variable but averages around 10 years. The main determinant is the SUA; the
higher it is, the earlier and more extensive the development of joint damage
and MSU deposits.
 The urates may heavily encrusts the articular surfaces and from visible deposits
in the synovium.
  The synovium becomes hyperplastic, fibrotic, and thickened by inflammatory
cells and forms a pannus that destroys the underlying articular cartilage leading
to juxta-articular bone erosions. In severe cases, fibrous or bony ankylosis
ensues resulting in partial to complete loss of joint function.

3. Chronic tophaceous gout-

 A tophus (meaning a porous stone) is mass of MSU crystals measuring a few

millimetres to a few centimetres in diameter. Tophi are the pathognomonic
hallmark of gout.
They are formed by large aggregation of MSU crystals surrounded by an
intense inflammatory reaction of macrophages, lymphocytes, fibroblasts and
large foreign body giant cells, which may have completely or partially
engulfed masses of crystals.
P a g e | 19
 Tophi may appear in the extensor surfaces of fingers, hands, forearm, elbows,
articular cartilage of joints and in the periarticular ligaments, tendons and soft
tissues, including the olecranon and patellar bursae, Achilles tendons, and
earlobes. Less frequently they may occur in the kidneys, nasal cartilages or
elsewhere.
 The white color of MSU crystals may be evident and permits distinction from
rheumatoid nodules. Nodules may appear surprisingly rapidly in under 1 year,
in patients with chronic renal failure.

4. Gouty nephropathy/Renal and urinary tract manifestation/Renal

lesions-

 Uric acid (not MSU) stones cause renal colic in around 10% of gout patients.
The incidence is higher in hot climates and favoured by purine overproduction,
uricosuric drugs, and defects in tubular reabsorption of uric acid, dehydration
and lowering urine pH (e.g. chronic diarrhoea or ileostomy). Hyperuricaemia
and gout also predisposes to the calcium oxalate, calcium phosphate or mixed
stones.
 Progressive renal diseases (intratubular precipitations, free uric acid crystals,
production of uric acid renal stones, urinary obstructions) are the important
complication confined to untreated severe chronic tophaceous gout. This
 results from MSU crystal deposition in the interstitium of the medulla and
pyramids with consequent chronic inflammation, giant cell reaction, fibrosis
and secondary pyelonephritis.
 Chronic gouty arthritis frequently involves the kidneys. There are three types
of renal lesions:
1. Acute urate nephropathy - is attributes to the intratubular deposition of MSU
crystals resulting in acute obstructive uropathy.
2. Chronic urate nephropathy - refers to the deposition of urate crystals in the
renal interstitial tissue.
3. Uric acid nephrolithiasis - is related to hyperuricaemia resulting in
hyperuricaciduria.

P a g e | 20
Cardiovascular diseases including atherosclerosis and hypertension are common
in individuals with gout. Renal manifestations sometimes appear in form of renal
colic associated with the passage of gravel and stones and may proceed to chronic
gouty nephropathy. About 20% of those with chronic gout die of renal failure.

Laboratory diagnosis-

 Presumptive diagnosis should be confirmed by needle aspiration of acutely or

chronically involved joints or tophaceous deposits.
 In acute gout, synovial fluid shows increased turbidity due to the greatly
elevated cell count (> 90% neutrophils); chronic gouty fluid is more variable
but occasionally appears white due to the high crystal load.
 During acute gouty attacks needle shaped MSU crystals typically are seen both
intracellularly and extracellularly.
 Synovial fluid leukocyte counts are elevated from 2000-60,000/μL.
 Large amount of crystals occasionally produce a thick pasty or chalky joint
fluid; if there is any suspicion of septic arthritis, joint fluid must be cultured.
 Arthrocentesis of these joints is a useful technique to establish the diagnosis of
gout between attacks.
 SUA levels can be normal or low at the time of an acute attack, as
inflammatory cytokines can be uricosuric and effective initiation of
hypouricaemic therapy can be precipitate attacks.
  A 24 hour urine collection for uric acid on a low purine diet can be useful in
assessing the risk of stones, elucidating over-production or under-excretion of
uric acid and deciding whether it may be appropriate to use a uricosuric
therapy.
 Excretion of >800 mg of uric acid per 24 hour on a regular diet suggests that
causes of over-production of purine should be considered.
 Assessment of renal function (serum creatinine, urinalysis), hypertension, and
blood glucose and serum lipid profile, haemoglobin, WBC count, LFT should
be undertaken because of possible pathologic sequelae of gout.
 During an attack, an elevated CRP and neutrophilia are usual; the ESR is often
modestly raised in tophaceous gout.
 Ultrasound, CT and MRI are likely to become more sensitive for early changes
& can detect subclinical microtophi and MSU deposits within cartilage of the
first MTP joint, even at first clinical presentation.
P a g e | 21
 X-rays can assess the degree of joint damage. In early disease they are usually
normal, but changes of OA may develop in affected joints with time, or be
present as a predisposing factor in secondary gout. Gouty ‘erosions’ (bony
tophi) are a less common.

Calcium Pyrophosphate Dihydrate (CPPD) crystal deposition

(Pseudogout)-
CPPD also known as pseudogout and chondrocalcinosis is one of the more common
disorders associated with intra-articular crystal formation in hyaline and
fibrocartilage of joints. It is usually occurs in individuals over 50 years of age and
becomes more common with increasing age.

The sexes and the races are equally affected. CPPD is divided into sporadic
(idiopathic), hereditary, and secondary/metabolic types. In the hereditary type the
crystals develops relatively early in life and are associated with severe OA. The
autosomal dominant form of the disease is caused by germline mutations in the
ANKH gene, which encodes a transmembrane pyrophosphate transport channel. The
secondary/metabolic form is associated with various disorders like:
(haemochromatosis, hypomagnesaemia, hypothyroidism, hyperparathyroidism,
hypophosphatasia, ochronosis diabetes, gout, Wilson’s disease) hereditary, familial
occurrence, RA, and OA.
The knee (hyaline cartilage and menisci) is but far the most common site, followed
by the wrist (triangular fibrocartilage) and pelvis (symphysis pubis). It is often
clinically occult, but can cause acute self-limiting synovitis or occur as a chronic
arthritis showing a strong association/overlap with OA, especially at the knee.

Clinical features-
 The joint involvement may last from several days to weeks and may be
monoarticular or polyarticular; the knees (most common site) followed by the
wrists, shoulders, elbows, and ankles are most commonly affected.
 CPPD is frequently asymptomatic; however, it also can produce acute,
subacute, or chronic arthritis that can be confused with OA or RA.

P a g e | 22
 Triggering factors include direct trauma and intercurrent illness or surgery
(especially parathyroidectomy).
 The typical attack resembles acute gout and develops rapidly, with severe pain,
stiffness and swelling.
 Overlying erythema is common and examination reveals a very tender joint
held in the flexed position .
 Low grade fever and temperature as high as 40 oC is common and the patient
may appear confused and ill. The attack is self limiting .
 Induction of peculiar form of OA.
 Production of symmetric synovitis (large/ tense effusion, warmth, restricted
movement with stress pain) that is clinically similar to RA.
 Spinal stenosis (most commonly seen in elderly).
 Intervertebral disc and ligament calcification with restriction of spine mobility
that mimics ankylosing spondylitis.
 Rarely periarticular tophus like nodules.

Laboratory diagnosis-
 Radiographs reveal punctate or linear radiodense deposits in fibrocartilaginous
joint menisci or articular hyaline cartilage (chondrocalcinosis).
  Definitive diagnosis requires demonstration of typical rhomboid or rode like
crystals in synovial fluid or articular tissues.
 In the absence of joint effusion or indications to obtain a synovial biopsy,
chondrocalcinosis is presumptive of CPPD deposition.
 Synovial fluid analysis with microbial culture is essential to rule out the
possibility of infection.
 The leukocyte count can range from several thousand to 100,000 cells/μL, with
the mean being about 24,000 cells/μL and the predominant cell being the
neutrophil.

Differential Diagnosis-
The most important differential diagnosis in gout is septic arthritis. This
should be considered in those with signs of infection or those who do not
improve with treatment. To help with diagnosis, a synovial fluid Gram
stain and culture may be performed. Other conditions that can look similar
include pseudogout, rheumatoid arthritis, psoriatic arthritis, and reactive
arthritis. Gouty tophi, in particular when not located in a joint, can be
mistaken for basal cell carcinoma or other neoplasms.

Prognosis-
Without treatment, an acute attack of gout usually resolves in five to seven
days; however, 60% of people have a second attack within one year. Those
with gout are at increased risk of hypertension, diabetes
mellitus, metabolic syndrome and kidney and cardiovascular disease and
thus are at increased risk of death. This may be partly due to its association
with insulin resistance and obesity, but some of the increased risk appears
to be independent.
Without treatment, episodes of acute gout may develop into chronic gout
with destruction of joint surfaces, joint deformity and painless tophi. These
tophi occur in 30% of those who are untreated for five years, often in
the helix of the ear, over the olecranon processes, or on the Achilles
tendons. With aggressive treatment, they may dissolve. Kidney stones also
frequently complicate gout, affecting between 10 and 40% of people and
occur due to low urine pH promoting the precipitation of uric acid. Other
forms of chronic kidney dysfunction may occur.
Complications-
Complications of gout can include small lumps forming under the skin
(tophi), joint damage and kidney stones. These are more likely to
occur if gout is left untreated.
Tophi
Gout is caused by a chemical called uric acid forming small crystals in and
around the joints. These crystals also often build up under the skin and
form small white or yellow lumps known as tophi.
Tophi are usually painless, but they can form in awkward places, such as
at the ends of your fingers and around your toes. Sometimes they can
make everyday tasks such as preparing food or getting dressed difficult.
They can also can become inflamed and produce a toothpaste-like
discharge.
Tophi can develop anywhere in the body, but usually form on the:

 toes
 heels
 knees
 fingers
 ears
 forearms
 elbows
It normally takes several years after the first attack of gout for tophi to
develop, but some people develop them even before experiencing an
attack. They're usually a sign of severe gout and a good reason to
start treatment to reduce the level or uric acid in your body.
Successful treatment will prevent the tophi from getting any bigger, and
long term treatment often gradually shrinks them.
If you have very large or painful tophi, they may have to be surgically
removed.
Joint damage
Without treatment, gout attacks may become more frequent and prolonged,
and your likelihood of developing permanent joint damage will increase.
In the most serious cases, surgery may be required to repair or replace a
damaged joint.
Kidney stones
Occasionally, high levels of uric acid can lead to the formation of kidney
stones.
Some kidney stones interfere with the flow of urine, resulting in pain when
you pass urine, and can make you feel that you need to pass urine more
often.
Some kidney stones interfere with the flow of urine, resulting in pain when
you pee, and can make you feel that you need to pee more often.
You may be prescribed medication to make your urine less acidic, which
should help dissolve any kidney stones that have developed. Read more
about treating kidney stones.
Psychological and emotional effects
Gout can also affect your mood, work and home life. The severe pain that
gout causes can make it difficult to do everyday tasks and to get around,
which in turn can lead to feelings of depression or anxiety.

Treatment
Treatment for gout includes pain relief to help you cope with a gout
attack, as well as medication and lifestyle changes to prevent further
attacks.
Pain relief for a gout attack
What to do during an attack
You should:
 take any medication you've been prescribed as early as possible after
you notice an attack (see below) – this should start to have an effect
within two or three days
 rest and raise the limb

 avoid knocking or damaging the affected joint

 keep the joint cool – remove surrounding clothing and apply an ice
pack, such as a bag of frozen peas wrapped in a towel
 ensure you're well hydrated

Apply the ice pack to your joint for around 20 minutes. Don't apply ice
directly to your skin and don't apply it for more than 20 minutes at a time
because this could damage the skin.
If necessary, you can keep reapplying an ice pack to your skin during an
attack, but you should wait until your skin has returned to a normal
temperature first.

NSAIDs
Non-steroidal anti-inflammatory drugs (NSAIDs) are usually
recommended as the first treatment for gout. They work by reducing pain
and inflammation during an attack.
NSAIDs used to treat gout include naproxen, diclofenac and etoricoxib.
If you've been prescribed NSAIDs, it's a good idea to have them with you
at all times so you can use them at the first sign of a gout attack. Continue
to take your medication throughout the attack and for 48 hours afterwards.
Your GP may also prescribe a medication called a proton pump inhibitor
(PPI), to take alongside your NSAID. This reduces the risk of the NSAID
causing indigestion, stomach ulcers and bleeding from the stomach.
Colchicine
If you're unable to take NSAIDs or if NSAIDs are ineffective, a medicine
called colchicine can be used instead.
Colchicine reduces some of the swelling and pain associated with a gout
attack.
It's best to have it with you at all times so you can use it at the first sign of
a gout attack. Your GP will tell you how long to take it for and how often.
When taken in high doses, side effects of colchicine include feeling sick,
abdominal (tummy) pain and diarrhoea.
Corticosteroids
Corticosteroids are sometimes used to treat severe cases of gout if other
treatments don't work or you're unable to take an NSAID or colchicine.
A short course of steroid tablets often provides relief, but they can't be
used long-term in high doses as they cause side effects, including:
 weight gain

 thinning of the bones (osteoporosis)

 easy bruising

 muscle weakness

Corticosteroids can also be given by injection to provide rapid pain relief.

This can be either into a muscle, a vein or directly into the affected joint.
Medication and lifestyle changes to prevent further attacks
You can reduce your chances of having further gout attacks by taking
medication and making lifestyle changes to reduce the level of uric acid in
your body.
Medication
Medication to reduce uric acid levels – known as urate-lowering therapy
(ULT) – is usually recommended if you have recurrent attacks of gout or
you have complications of gout.
Most people with gout will eventually need to have ULT, so you may want
to discuss the advantages and disadvantages of this treatment with your
doctor as soon as you've been diagnosed with gout.
They should explain that while ULT can significantly reduce your risk of
having further attacks, the medication needs to be taken on a daily basis
for the rest of your life and there's a small risk of side effects.
If you decide to start ULT, a medicine called allopurinol is usually tried
first. If this isn't suitable or doesn't work, other medications may be used
instead. These medications are described below.
Allopurinol
Allopurinol helps reduce the production of uric acid. It can help prevent
gout attacks, although it won't help relieve symptoms during an attack.
Allopurinol is a tablet taken once a day. When you first start taking it, your
dose will be adjusted to make sure the level of uric acid in your blood is
low enough. Regular blood tests will be needed to monitor this until
the most effective dose is found.
Allopurinol can sometimes cause a gout attack soon after you start taking
it and it can take up to a year or two before no further attacks occur. It's
important to persevere with treatment even if you do have attacks during
this time.
To help relieve attacks, your doctor will prescribe one of the pain relieving
medications described above to take alongside your allopurinol at first.
Most people taking allopurinol won't experience any significant side
effects. However, side effects can include:
 a rash – this is usually mild and goes away on its own, but it can be a
sign of an allergy; if you develop a rash, stop taking the medication
immediately and contact your GP for advice
 indigestion
 headaches
 diarrhoea

Febuxostat
Like allopurinol, febuxostat is a medication taken once a day that reduces
the body's production of uric acid. It's often used if allopurinol isn't
suitable or causes troublesome side effects.
As with allopurinol, febuxostat can make your symptoms worse when you
first start taking it. Your doctor will initially prescribe one of the pain
relieving medications described in case you experience attacks.
Side effects of febuxostat can include:
 diarrhoea

 feeling sick

 headaches

 a rash

Other medications
Less commonly used ULT medications include benzbromarone and
sulfinpyrazone.
These types of medication tend to only be used if people are unable to take
allopurinol or febuxostat. They need to be prescribed under the supervision
of a specialist.
Lifestyle changes
Certain lifestyle changes can also help reduce your risk of experiencing
further attacks of gout, including:
 avoiding foods containing high levels of purine (the chemical
involved in the production of uric acid), such as red meat, offal, oily
fish, seafood and foods containing yeast extract – see the gout and
diet leaflet (PDF, 1Mb) produced by the UK Gout Society
 avoiding sugary drinks and snacks – these are associated with an
increased risk of gout
 maintaining a healthy weight – follow a balanced diet; don't crash
diet or try high-protein, low-carbohydrate diets
 taking regular exercise – try activities that don't put too much strain
on your joints, such as swimming
 drinking plenty of water – keeping yourself well hydrated will
reduce the risk of crystals forming in your joints
 cutting down on alcohol – avoid beer and spirits in particular and
don't binge drink
There's some evidence to suggest that taking regular vitamin
Csupplements can reduce gout attacks, although the effect may only be
small. Talk to your GP first if you're thinking about taking vitamin C
supplements, as they aren't suitable or safe for everyone.

okrjä
Ikfjp;&
 okrjä O;kf/k eas okr dh o`f) vkSj jä dh nqf’V LorU= :i ls
gksrh gS] rFkk nksuksa dh lEewPNZuk ls O;kf/k dh
mRifÙk gksrh gSA blfy, O;kf/k dks ^okrjä^ uke fn;k
gSA
 vkpk;Z pjd us LorU= v/;k; ^^okr”kksf.kr
fpfdfRlra^^ esa okrjä dk o.kZu fd;k gSA
 vkpk;Z lqJqr us ^^okrO;kf/kfunku^^ v/;k; ds vUrxZr
gh okrjä dk o.kZu fd;k gSA
  vkpk;Z okXHkÍ us Hkh LorU= v/;k; ^^okr”kksf.kr
funkua^^ esa okrjä dk o.kZu fd;k gSA

fu#fä&
i. okrjäkH;ka tfurks O;kf/k% okrjäaA
¼pñfpñ 29@1 ij pØikf.k½
ii. okrL;kojs.k cyeRL;feu~ “kksf.kr bfr okrcykl%A

i;k;Z&
i. okr”kksf.kr ¼pjd] y?kq okXHkͽ
ii. [kqM ¼pjd] y?kq okXHkͽ &[kqM “kCn dk vFkZ lfU/k
gSA [kqM “kCn {kqnz ;k y?kq ds vFkZ eas Hkh iz;ksftr
gksrk gSA okrjä esa y?kqq lfU/k;ksa esa foÑfr gksrh
gksrh gS] blfy, [kqM dgrs gSaA
iii. okrcykl ¼pjd] y?kq okXHkͽ & okr ds vkoj.k ls jä
vf/kd nq’V gks tkrk gS] ftlls cyoku O;kf/k jäfiÙk dh
mRifÙk gksrh gS] blfy, okrcykl dgrs gSaA
iv. vk<+;okr ¼pjd½@vk<+;jksx ¼y?kq okXHkͽ &
Jhear ¼/kuh½ yksxksa eas ;g O;kf/k vf/kd ik;h tkrh gSA
vk<+; dk vFkZ Jhear@/kuh gksrk gS] blfy,
vk<+;okr@vk<+;jksx dgk gSA

funku&
yo.kkEydVq{kkjfLuX/kks’.kth.kZHkkstuS%A
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vp³~Øe.k”khykuka dqI;rs okr”kksf.kre~A
¼på fpå 29@5&8½
 ¼ekå fuå

23@1&3½

¼Hkkå izå iwoZå

29@1&3½
Page |2

I. vkgkjt&
 yo.k] vEy] dVq] {kkj] fLuX/k] m’.k vkSj vth.kZ gksus ij
Hkh Hkkstu djukA
 fDyé] ”kq’d] vEcqt ekal] vkuwi ekal] fi.;kd¼fry dh
[kyh½] ewyd¼ewyh@ewy”kkd dk lsou½A
 dqyRFk] ek’k] fu’iko¼lse “kkd½ ”kkdkfn] iyy ¼ekal½]
b{kq dk lsouA
 nf/k] vkjuky¼dk°kh½] lkSohj ¼fljdk½] rØ] lqjk] vklo dk
vfr lsouA
 e/kqj vkgkj dk lq[kiwoZd Hkkstu djuk
 fo:)k”ku] v/;”kuA
II. fogkjt&
 Øks/k] fnokLoIu] Átkxj¼jkf=tkxj.k½] vp³~Øe.k”khyA
III. izÑfr&
 izk;% lqdqekj] lq[kh ,oa LFkwy O;fä¼vkå ek/ko o
HkkofeJ½ esa okr vkSj jä dqfir gksdj okrjä dks mRié
djrss gSaaA

izk;”k% lqdqekjk.kka feF;k··gkjfogkfj.kke~A

“kksdkPp izenke|O;k;keSúkkfrihM+ukr~AA
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vO;ok;s rFkk LFkwys okrjäa izdqI;frAA
¼lqå fuå 1@40&41½

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 feF;kgkj] _rqfoijhr vkgkj] lkRE;foijhr vkgkj] e|iku]
Lusgkfn dk vuqfpr iz;ksxA
 II. fogkjt&
 feF;kfogkj] “kksd] vfrO;k;ke] vO;ok;] izenk ¼O;ok; vf/kd
djuk½A
III. izÑfr&
 lqdqekj] LFkwy O;fä okrjä ls dqfir gksrss gSaaA

fonkáéa fo:)a p rÙPpkl`Diznw’ke~A

Hktrka fof/kghua p LoIutkxjeSFkque~AA
izk;s.k lqdqekjk.kkep³~~Øe.k”khfyuke~A
¼vå âå fuå 16@1&2½
Page |3
I. vkgkjt&
 fonkgh ,oa fo:) vé] jäiznw’kd vkgkj
II. fogkjt&
 fof/kiwoZd funzk] tkxj.k] eSFkqu u djuk ,oa
vp³~Øe.k”khy
III. izÑfr&
 lqdqekj O;fä

lEizkfIr&
vfHk?kkrkn”kq);k p iznq’Vs”kksf.krs u`.kke~AA
d’kk;dVqfräkYi:{kkgkjknHkkstukr~A
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ok;qfoo`)ks o`)su jäsuokfjr% ifFk%AA
ÑRlua lanw’;snzäa rTKs;a okr”kksf.kre~A
[kqMa okrcyklk[;ek<;okra p ukefHk%AA
¼på fpå 29@8&11½
vfHk?kkrkn”kq)súk u`.kkel`ft nwf’krsAA
okryS% “khrySokZ;qoZ`)% Øq)ks foekxZe%A
rkn`”kSokl`tk :)% izkänso iznw’k;sr~AA
vk<;jksxa [kqMa okrcykla okr”kksf.kre~A
rnkgqukZefHk%------------------AA
¼vå âå fuå 16@2&4½

 vfHk?kkr ls ;k “kjhj dh oeu&fojspu vkfn }kjk “kqf) u

djus ls “kjhj esa jä nwf’kr gks tkrk gSA
 d’kk;] dVq] frä jlksa rFkk vYi] :{k ¼okrdkjd rFkk “khry½
vkgkj dk lsou djus lsA
 v”o] m’Vª ij p<+us ls] ty eas ØhMk djus ls iouya?
ku¼dwnus½ lsA
 m’.kdky ds fnuksa esa vR;f/kd fo’ke jkLrk pyus ls] vf/kd
O;ok; djus ls] osx /kkj.k djus lsA
 mijksä dkj.kksa ls ok;q vf/kd c<+ tkrh gS rFkk
foekxkZeh gks tkrh gS] ,slh n”kk esa c<+s gq, nwf’kr
jä ds }kjk ok;q dk ekxZ vo:) gks tkrk gSA
 :dh gqbZ ok;q iqu% lEiw.kZ jä dks nwf’kr dj nsrh gSA bl
izdkj nwf’kr okrjä dks
okr”kksf.kr@[kqM@okrcykl@vk<;okr@vk<;jksx ukeksa
ls tkuk tkrk gSA
Page |4
gLR;”okS’VSªxZPNrks·U;S”p ok;q% dksia ;kr% dkj.kS
% lsforS% LoS%A
rh{.kks’.kkEy{kkj”kkdkfnHkksT;S% lUrkik|SHkZw;lk
lsforSúkAA
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la:.k);k”kq ;kr%A
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nw’k;snzäek”kqAA
rr~ lai`äa ok;quk nwf’krsu rRizkcY;knqP;rs okrjäe~A
r}r~ fiÙka nwf’krsukl`tk··äa “ys’ek nq’Vks
nwf’krsukl`tk··ä%AA ¼lqå fuå 1@42&44½

gLR;”oks’VªSxZPNrúkk”urúk fonkáéa l
fonkgk·”kuL;AA
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rRlEi`äa ok;quk nwf’krsu rRizkcY;knqP;rs okrjäe~A
¼Hkkoå izå 29@4&5½

¼ekå fuå 23@4½

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izdqfir gks tkrh gSA
 rh{.k] m’.k] vEy] {kkj] “kkdkfn HkksT; inkFkksaZ ds
lsou ls] lUrkikfn ds lsou lsA
 fonkgh vé dk vf/kd lsou djus okys euq’; ds Hkkstu dk
fonX/k ifjikd lEiw.kZ jä dks fonX/k ;k nwf’kr dj nsrk gSA
 mijksä dkj.kkasa ls “kh?kz gh jä nwf’kr gks tkrk gS]
rFkk og nwf’kr jä “kh?kz lapj.k djds ok;q ds ekxZ dk
vojks/k dj nsrk gSA
 og nq’V jä f[klddj uhps iSjksa esa ,d= gks tkrk gS vkSj
vius dkj.kksa ls izdqfir ok;q ls la;qä gkssdj jksx mRié
djrk gSA
 bl rjg ls nwf’kr ok;q ls feyk gqvk og jä ok;q dh izcyrk
gksus ds dkj.k okrjä dgykrk gSA
 blh rjg ls nwf’kr fiÙkokr }kjk nwf’kr jä ds lkFk la;qä
gksdj rFkk nwf’kr “ys’eokr }kjk nwf’kr jä ds lkFk la;qä
gksdj rFkk ok;q dh izcyrk ds dkj.k ;g jksx okrjä dgykrk
gSA

fo”ks’k lEizkfIr&
lkS{E;kr~ loZljRokPpiouL;kl`tLrFkkA
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¼på fpå 29@13&15½

 ok;q lw{e vkSj lEiw.kZ lfU/k;ksa esa ;k ekxksaZ eas

QSyus okyk gksrk gS rFkk jä nzo vkSj lEiw.kZ lzksrksa
 eas QSyus okyk gksrk gSA bu nksuksa xq.kksa ds dkj.k
dqfir gqvk okr vkSj jä fljkekxksasZ ls lEiw.kZ “kjhj esa
xeu djrk gSA
Page |5
 xeu djrs gq, lfU/k;ksa ds oØ ¼Vs<+s½ gksus ls
ogk¡ okr&jä dh xfr eas vojks/k gksrk gS vkSj og {kqC/k
gkssdj ogha :d tkrk gSA
 fiÙkkfn nks’kksa ls ;qä gksdj mu lfU/k;ksa eas :dk gqvk
okrjä fHké&fHké izdkj ls osnukvksa dks mRié djrk gSA
vr% mUgha :dh gqbZ lfU/k;ksa esa nq%[k dks mRié
djrk gSA
 bl izdkj lfU/k izns”k esa :dk gqvk okrjä euq’;ksa ds “kjhj
esa vR;Ur dfBu la;qDr nks’k ds vuqlkj osnukvksa dks
mRié djrk gSA

okrjä dk LFkku&
rL; LFkkua djkSiknko¯qY;%loZlU/;%A
ÑRok··nkS gLrikns rq ewya nsgs fo/kkofrAA
¼på fpå 29@12½
 okrjä dj] ikn] v¡xqfy;kas vkSj lHkh lfU/k;kas eas LFkku
cukrk gSA loZizFke dj vkSj ikn eas viuk ewy LFkku
cukdj iúkkr lEiw.kZ “kjhj eas QSy tkrk gSA

------------------rPp iwoZa iknkS iz/kkofrAA

fo”ks’kk|ku;kuk|S izyEckS----------------
¼vå âå fuå 16@4½
 ;g jksx izFke iSjksa eas mRié gksrk gS] fo”ks’k :i ls ?
kksM+s vkfn dh lokjh djus ij iSjksa dks yVdkus ls ;g
jksx izFke iSjkas eaas gksrk gSA

ikn;kseZwyekLFkk; dnkfp)Lr;ksjfiA
vk[kksfoZ’kfeo Øq)a rn~nsgeuqliZfrAA
¼lqå fuå 1@48½
ikn;kseZwyekLFkk; dnkfp)Lr;ksjfiA
vk[kksfjo fo’ka Øq)a d`RLua nsga fo/kkofrAA
¼vå âå fuå 16@7&8½
ikn vFkok gLr ds ewy dk vkJ; ysdj dqfir gksdj vk[kksfo’k
¼pwgs ds fo’k½ ds leku lkjs nsg esa QSy tkrk gSA

iwoZ:i&
Losnks·R;FkZa u ok dk’.;Za Li”kkZKRoa {krs·fr:d~A
lfU/k”kSfFkY;ekyL;a lnua fiMdksåe%AA
tkuqt«ks:dV;algLriknk¯lfU/k’kqA
fuLrksn% LQqj.ka Hksnks xq:Roa lqfIrjso pAA
d.Mw% lfU/k’kq :XHkwRok HkwRok u”;fr pklÑr~A
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¼på fpå 29@16&18½

¼ekå fuå

23@5&7½

¼Hkkå izå

29@6&8½
Page |6
 Losn dk vf/kd vkuk vFkok loZFkk vHkko gksuk] “kjhj
eas Ñ”krk mRié gksuk] Li”kZKku dk u gksuk] “kjhj esa
{kr gksus ij vf/kd osnuk@ihM+k gksukA
 lfU/k;kas eas f”kfFkyrk gksuk] vkyL;] “kjhj eas volkn
gksuk] fifMdkvksa dk gksukA
 tkuq] ta?kk] Å:] dfV] val] gLr] iknkaxksa dh lfU/k;kas
esa rksn&LQqj.k&Hksnu&xq:rk&”kwU;rk&d.Mw gksrh
gSSA
 ckj ckj lfU/k;ksa eas osnuk mRié gksdj u’V gks tkrh gSA
 “kjhj esas foo.kZrk&e.My dk gksukA

izkxzwis f”kfFkykS fLoékS “khrykS lfoi;Z;kSA

oSo.;ZrksnlqIrRoxq:RokS’klefUorkSAA
¼lqå fuå 1@47½
 nksuksa ikn f”kfFky] Losn;qDr] “khry rFkk dHkh dHkh
foi;Z; ;qDr gksrs gSaA mueas foo.kZrk] rksn] lqIrrk]
xq:rk] vks’k ¼nkg½ gksrk gSA
--------------rL; y{k.ke~A
Hkfo’;r% dq’Blea rFkk lkn% “yFkk¯rkAA
tkuqt«ks:dV;algLriknk¯lfU/k’kqA
d.MwLQqj.kfuLrksnHksnxkSjolqIrrk%AA
HkwRok HkwRok iz.k”;fUr eqgqjkfoHkZofUr pA
¼vå âå fuå 16@5&7½
 dq’B ds iwoZ:i ds leku tSls%& ¼vfr”y{.k ;k
vfrlj@vfrddZ”k Li”kZ] vfrLosn ;k Losn dk u vkuk]
foo.kZrk] nkg] d.Mw] Ropk esa laKkuk”k ;k rksn]
dksBksa dk mér gksuk] Je@Fkdku] oz.kksa dk tYnh
mRié gksuk vkSj nsj rd cus jguk] oz.kksa esa osnuk
vf/kd gksuk rFkk Hkj tkus ij Hkh :{krk] FkksM+s dkj.k ls
Hkh dqfir gksuk ¼iqu% gks tkuk½ jksekøk vkSj jä dk
dkyk gks tkuk½A
 vaxksa dk vius dk;kZsa esa vlkeF;Z] vaxksas esa
f”kfFkyrk rFkk tkuq] ta?kk] Å:] dfV] val] gkFk iSj vkSj
lfU/k;kas esa
d.Mw&LQqj.k&rksn&Hksnu&xq:rk&laKkuk”k ;s ckj ckj
izdV gksdj u’V gks tkrs gSa vkSj fQj vk tkrs gSaA

Hksn ,oa y{k.k& Okrjä ds

Hksn
vkJ; ds vk/kkj ij nks’k ds vk/kkj ij

mÙkku okrjä
4 Hksn 8 Hksn
xEHkhj okrjä
Okkrt okrjDr Okkrt okrjDr

mHk;fefJr okrjDr
fiÙkt okrjDr jät okrjDr

“ys’et okrjDr fiÙkt okrjDr

 I. vkJ; ds vk/kkj ij&
a. mÙkku okrjä&
mÙkueFk xEHkhja f}fo/ka rr~ izp{krsA
Ro³~eklkJ;eqÙkkua-------------
¼på fpå 29@19½
Ro³~{kklkJ;eqÙkkua rRiwoZa tk;rs rr%AA
¼vå âå fuå 16@8½
 tks Ropk vkSj ekal esa vfJr gksrk gSA
Page |7

d.Mwnkg:xk;kerksnLQqj.kdqøkuS%A
vkfUork “;kojäk RoXckás rkezk rFks’;rsAA

¼på fpå 29@20½

d.M~okfnla;qrksÙkkus Roäkezk “;koyksfgrkAA

lk;kek Hk`”knkgks’kk------------
¼vå âå fuå 16@9½
 d.Mw] nkg ,oa Å’kk] ihM+k] vk;ke ¼f[kapko½] rksn]
LQqj.k] dqøku ¼vaxksa esa V<+kiu½] Ropk dk o.kZ
rkez@”;ko@yksfgr ¼jä½ gks tkrk gSA

b. xEHkhj okrjä&
-------------------------xEHkhja RoUrjkJ;e~AA
¼på fpå 29@19½
dkykUrjs.k xEHkhja lokZu~ /kkrwufHknzor~A
¼vå âå fuå 16@9½

xEHkhjs “o;Fkq% LrC/k% dfBuks·UrHkZ`”kkfrZeku~A

“;koLrkezks·Fkok nkgrksnLQqj.kikdoku~AA
¼på fpå 29@21½
 vkpk;Z pjd ds vuqlkj tks okrjä jä] ekal] esnk vkfn Hkhrjh
/kkrqvksa esa vkfJr gksrk gS] og xEHkhj dgykrk gSA
 vkpk;Z y?kq okXHÍ ds vuqlkj mÙkku okrjä gh dkykUrj
esa lHkh /kkrqvkas esa izlfjr gksrk gqvk xEHkhj cu tkrk
gSA
 dfBu “o;Fkq ¼”kksFk½] LrC/krk ¼tdM+kgV½] “kksFk
ds Hkhrjh Hkkx esa vR;f/kd ihM+k] Ropk dk o.kZ “;ko ;k
rkez gks tkrk gS] lfU/k;k¡ nkg&rksn&LQqj.k&ikd ;qä gks
tkrh gSaA

xEHkhjs·f/kdiwoZ:d~A
“o;FkqxzkZfFkr% ikdh ok;q% lU/;kfLFkeTtklqAA
fNUnféo pjR;UroZØhdqoZaúk osxoku~A
djksfr [k°ka i¯qa ok “kjhjs loZrúkju~AA
¼vå âå fuå 16@10&11½

 xEHkhj okrjDr esa izFke vf/kd osnuk gksdj xzfFkr

¼mÙkf.Mr½ rFkk idus okyk “kksFk gksrk gS] lfU/k]
vfLFk vkSj eTtk esa ok;q dkVrh gqbZ ,oa cyoku gksus ls
 Vs<+k djrh gqbZ fopjrh gSA leiw.kZ “kjhj esa fopjrh
gqbZ “kjhj esa [k°krk ;k i¯qrk mRié djrh gSA

Page |8
c. mHk;fefJr okrjDr&
#fXonkgkfUorks·Hkh{k.ka ok;q lU/;kfFkeTtlqA
fNUnféo pjR;UroZØhdqoZaúk osxokuAA
djksfr [k°ka ia¯q ok “kjhjs loZr”pju~A
losZfy¯Súk foKs;a okrkl`xqHk;kJ;e~AA
¼på fpå 29@22&23½

 ihM+k] fonkg] osxokyh ok;q lfU/k&vfLFk vkSj eTtk esa

ckj&ckj dkVus dh rjg ihM+k mRié djrh gS] vFkok lfU/k
vkfn dks Hkhrj ls Vs<k xeu djrh gSA
 leiw.kZ “kjhj esa xeu djrh gqbZ osx okyh ok;q [akt
¼yaxM+kiu½ vFkok ia¯q jksx dks mRié djrh gSA
 lHkh mÙkku vkSj xEHkhj okrkDr ds y{k.k ;fn ,d jksxh
esa fey tk,a rks mldks mHk;fefJ okrjDr le>uk pkfg,A

II. nks’k ds vk/kkj ij&

i. pkj Hksn ¼vkpk;Z lqJqr erkuqlkj½&
a. Li”kksZf}Xuks rksnHksniz”kks’kLokiksisrkS
okrjDrsu iknkSA ¼lqå fuå 1@45½
 okr vkSj jDr dh nqf’V dh iz/kkurk ls nkuksa iSjksa esa
Li”kZ dh rhoz vlfg’.kqrk] rksn] Hksnuor~ ihM+k] “kks’k
rFkk Li”kZ Kku dh deh izrhr gksrh gSA

b. fiÙkkl`XH;keqxznkgkS HkosrkeR;FksZ’.kkS
jDr”kksQkS e`nw pAA ¼lqå fuå 1@45½
  fiÙk vkSj jDr dh nqf’V dh iz/kkurk ls nkuksa iSjksa esa
mxz nkg] vf/kd m’.krk] ykyjax] l`tu rFkk e`nqrk mRié
gksrh gSA

c. d.MweUrkS “osr”khrkS l”kksQkS ihuLrC/kkS]

“ys’enq’Vs rq jDrsA ¼lqå fuå 1@46½
 dQ dh nqf’V ds ;qDr okrjDr esa nkuksa iSjksa esa d.Mw]
“osrrk] “khrrk] “kksFk] rFkk LrC/krk ¼dBksjrk½ mRié
gks tkrh gSA

d. losZnZq’Vs “kksf.krs pkfi nks’kk% Loa Loa :ia

ikn;ksnZ”kZ;fUrAA ¼lqå fuå 1@46½
 loZ nks’kksa ls ;qDr okrjDr esa fofo/k nks’k vius&vius
y{k.kksa dks iSjksa esa izdV djrs gSaA

Page |9

ii. vkB Hksn&

a. okrt okrjä&
fo”ks’kr% fljk;ke”kwyLQqj.krksnue~A
“kksFk;L; dk’.;aZ jkS{;a p “;korko`f)gkuk;%A
/keU;¯qfylU/khuka l³~dkspks·¯xzgks·fr:d~A
dqøkuLrEHkus “khriz}s’kúkkfuys·f/kdsAA
¼på fpå 29@25&26½

okrs·f/kds·f/kda r= “kwyLQqj.krksnue~A
“kksQL; jkS{;a Ñ’.kRo”;korko`f)gkuk;%AA
/keU;¯qfylU/khuka l³~dkspks·¯xzgks·fr:d~A
“khr}s’kkuqi”k;kS LrEHkosiFkqlqIr;% AA
¼vå âå fuå 16@12&13½
 ¼Hkkå izå

29@9&10½

¼ekå fuå

23@8&9½
 fo”ks’k :i ls fljkvksa esa ruko@f[kapko] “kwy] LQqj.k
vkSj rksn] “kksFk dk o.kZ Ñ’.k&”;ko rFkk :{k gksrk
gS] ;g ?kVrk&c<+rk jgrk gSA
 /keuh] vaxqfy;kas vkSj lfU/k;ksa esa ladksp gks tkrk
gS] vaxksa eaas LrC/krk o osnuk vf/kd gksrh gSA
 “khr ls }s’k] LrEHku] dEiu] Li”kZ laKkuk”kA
 vkpk;Z ek/ko ,oa HkkofeJ us “kksQ ds LFkku ij “kksFk
“kCn dk iz;ksx fd;k gSA
b. jät okrjä&
ðk;FkqHkZ`”k:d~ rksnLrezkfúkfefpek;rsA
fLuX/k:{kS% “kea uSfr d.MwDysnkfUorks·l`ftAA
¼på fpå 29@27½
jäs “kksQks·fr:äksnLrezkfúkfefpek;rsA
fLuX/k:{kS% “kea uSfr d.MwDysnkfUor%AA
¼vå âå fuå 16@14½

¼ekå fuå 23@10½

¼Hkkå izå

29@11½
 “kksFk rhoz osnuk vkSj rksn ;qDr gksrk gS] rkez o.kZ
dk gksrk gS] fpefpekgV gksrh gS] “kksFk d.Mw vkSj
Dysn ;qä jgrk gSA
 fLuX/k vkSj :{k nzO;kas ds lsou ls jksx dh “kkfUr ugha
gksrh gSA
 vkpk;Z ek/ko ,oa HkkofeJ us “kksQ ds LFkku ij “kksFk
“kCn dk iz;ksx fd;k gSA
P a g e | 10
c. fiÙkt okrjä&
fonkgks osnuk ewPNkZ LosnLr`’.kk enks Hkze%A
jkx% ikdúk Hksnúk “kks’kúkksDrkfu iSfÙkdsAA
¼på fpå 29@28½

fiÙks fonkg% lEeksg% Losnks ewPNkZ en% lr`V~A

Li”kkZ{keRoa :x~jkx% “kksQ% ikdks Hk`”kks’erkAA
¼vå âå fuå 16@15½

fiÙks-------------------------------
”kkZlgRoa :xzkx% “kksFk% ikdks Hk`”kks’erkAA
¼ekå fuå 23@11½

fiÙks---------------------------------------------------------
enLr`’kkA
Li”kkZlgRoa :xnkg% “kksFk% ikdh Hk`”kks’.krkAA
¼Hkkå izå 29@12½

 fonkg] osnuk] ewPNkkZ vfrLosn] vfr`’.kk] en] Hkze] jkx]

ikd] Hksnuor~ ihM+k] lEeksg ¼lKka gkfu½ Li”kZklgRo]
“kskQ rFkk vR;f/kd m’.kk gksrh gSA

d. dQt okrjä&
LrSfeR;a xkSjoa Lusg% lqfIreZUnk p :d~ dQsA
¼på fpå 29@29½

dQS LrSfeR;xq:rklqfIrfLuX/kRo”khrrk%A
d.MweZUnk p :d~----------------------------
¼vå âå fuå 16@16½

¼Hkkå izå

29@13½

¼ekå fuå

23@12½
 LrSfeR; ¼xhys diM+s ls “kjhj dk <dk gqvk izrhr gksuk½
“kjhj esa xq:rk] fLuX/krk] “khryrk] ”kwU;rk] d.Mw vkSj
eUn osnukk gksrh gSA
e. f. g. h. }U}t ,oa f=nks’kt&
 gsrqy{k.klalxZf}+++++++++++++++++|
kn~ }U}f=nks’kte~AA ¼på fpå

29@29½

}U}loZfy¯ p l³~djs AA ¼vå âå

fuå 16@16½

¼Hkkå izå

29@13½

¼ekå fuå 23@12½

 }U} ladj ¼nks&nks nks’kksa dh vf/kdrk okys okrjDr esa
}U}ksa ds y{k.k jgrs gSaA okr fiÙkt] okr&dQt]
fiÙkt&dQt okrjä ds y{k.k jgrs gSaA
 lcds ladj ¼f=nks’kt okrjä½ esa rhuksa nks’kksa ds
y{k.k jgrs gSaA
P a g e | 56

lk/;kl/;rk&
,dnks’kkuqxa lk/;a uoa ;kI;a f}nks’kte~A
f=nks’ktuelk/;a L;k|L; p L;q:inzok%AA
¼på fpå 29@30½

¼Hkkå izå

29@18½

¼ekå fuå 23@18½

,dnks’kkuqxa----------------------------
f=nks’kta R;tsRlzkfo LrC/kecqZndkfj pAA
¼vå âå fuå 16@17½
 ,d nks’kt rFkk uohu okrjDr&lk/;
 f}nks’kt okrjDr] ,d o’kZ iqjkuk gks&;kI;
 f=nks’kt minzo lfgr lzko;qDr fu”py vkSj vcqZn ds lelu
mBk gqvk&vlk/;
laizlzkfo foo.kZa p LrC/kecZqnÑøk ;r~AA
otZ;sPpSo ladkspdjfefUnz;rkiue~A
vÑRLuksinzoa ;kI;a lk/;a L;kfé:inzoe~AA
¼på fpå 29@33&34½
 oz.k ls lzko gks] LrC/krk gks] vcZqn dh mRifÙk gks x;h
gks]
tks vaxksa eas ladksp mRié djrk gks]
tks bfUnz;ksa esa rki mrié djrk gks & vlk/; ,oa oT;Z
 ftl okrjä easa lEiw.kZ minzo u gks & ;kI;
 ftlesa minzo u gks@loZFkk vHkko gks & lk/;

vtkuqLQqfVra ;Pp izfHkéa izlqra p ;r~A

minzoSúk ;Ttq’Va izk.kekal{k;kfnfHk%AA
“kksf.kra rn~lk/;a L;k|kI;a laoRljksfRFkre~A
¼lqå fuzå 1@49½

vtkuq-----------------------------------
minzoSúk---------------------------------------
okr~jäelk/;a L;k|kI;a laoRljksfRFkre~A
¼Hkkå izå 29@19½

¼ekå fuå

23@14&15½
 ftl okrjä eas tkuqi;Zar LQqVu gks tk;s] ekalkafn fofn.kZ
gks tk;s rFkk mlls lzko gksus yxs] izk.k¼cy½ vkSj ekal
{k;kfn minzoksa ls ;qä gks & vlk/;
 ,d o’kZ iqjkuk gks & ;kI;
P a g e | 12
okrjä ds minzo&
vLoIukjkspdðkklekaldksFkf”kjksxzgk%A
ewPNkZ;en:d~r`’.kkTojeksgizosdk%AA
fgDdkik¯qY;ohliZikdrksnHkzeDyek%A
v¯qyhoØrk LQksVk nkgeeZxzgkcZqnk%AA
,rS:inzoSoZT;aZr eksguSdsu ok·fi ;r~A
¼på fpå 29@31&33½

vLoIu-----------------------------------------------
vÑRLuksinzoa ;kI;a lk/;a L;kfé:inzoe~ A
¼Hkkå izå 29@15&17½

¼ekå fuå

23@15&17½

 fuækuk”k] v:fp] “okl] ekaldksFk ¼ekal dk lM+uk½]

f”kjksxzg ¼f”kj esa “kwy o tdM+kgV½] r`’.kk] en]
osnuk] Toj] eksg] dEi] fgDdk] i¯qrk ¼vaxqyh dk Vs<+k
gksuk½] filiZ] ikd] rksn] Hkze] Dye] vaxqyhodzrk]
LQksV] nkg] eeZLFkkuksa esa tdM+kgV] vcZqnA
 mijksDr minzokas ls ;qDr okrjä& vlk/;
 ;fn bu minzoksa esa ,d gh eksg minzo iz/kku gks rks
Hkh& vlk/;
 mi;ZqDr lEiw.kZ minzo u jgus ij@vYi minzo gks& ;kI;
¼Hkkå iz] ekå fuå½
 minzoksa ds iw.kZr;k jfgr gksus ij& lk/; ¼Hkkå iz] ekå
fuå½

vlk/;rk@?kkrdrk dk dkj.k&
jDrekxZa fugUR;k”kq “kk[kklfU/k”kq ek:r%A
fufo”;ku;ksU;ekok;Z osnukfHkgZjsn~lwu~AA
¼på fpå 29@35½

¼vå âå fuå

16@18½
 ok;q “kk[kk vkSj lfU/k;ksa esa izos”k djds jä ds ekxZ
dks nq’V ¼vojks/k½ dj nsrh gS vkSj c<+k gqvk jä Hkh
ok;q ds ekxkZsa dk vojks/k dj nsrk gSA
 bl izdkj ok;q vkSj jä nksuksa ijLij ,d nwljs ds ekxZ dks
jksddj osnuk dks mRié djrs gSa vkSj ml osnuk ls izk.kh
dk izk.k fudy tkrk gSA

fpfdRlk lw=
तत्रमुञ्चेदसृक्शृङ्गजलौकःसूच्यलाबुभिःaA
प्रच्छनैर्वासिराभिर्वायथादोषंयथाबलम्AA ३६ A
रुग्दाह शूल तोदार्तादसृक् स्राव्यं जलौकसाA
शृङ्गैस्तुम्बैर्हरेत्सुप्तिकण्डूचिमिचिमायनात्A
A ३७ AA
देशाद्देशं व्रजत् स्राव्यं सिराभिः प्रच्छनेन
वाaaA अङ्गग्लानौ न तु स्राव्यं रूक्षेवातोत्तरे च
यत्AA ३८ AA गम्भीरं श्वयथुं स्तम्भं कम्पं स्नायु
सिरामयान्A
ग्लानिं चापि स सङ्कोचां
कुर्याद्वायुरसृक्क्षयात्AA ३९ AA

1&okrjDr jksx esa J`x] tykSdk] lwph] vykcw]

iz{kku o f”kjkos/k }kjk dqfir nks’k ds vuqlkj ;k
jksx&jksxh ds cykuqlkj jDreks{k.k djkuk pkfg;sA
2&okrksYo.k okrjDr esa jDreks{k.k djkuk fuf’k}
gSA jDreks{k.k ds iwoZ Lusgu] e`nq fojspu rFkk
ofLr }kjk leqfpr iwoZdeZ djkuk pkfg;sA vH;ax]
lsd] iznsg] ysi] vUu] Lusg bR;kfn }kjk mi;qDr cfg
%ifjektZu djk;saA

mRrku vkSj xEHkhj okrjDr fpfdRlk

lw+=&
 बाह्यमालेपनाभ्यङ्ग परिषेकोपनाहनैः|विरेकास्थापन
स्नेहपानै र्गम्भीरमाचरेत्AA ४३ AA

mRrku okrjDr esa vkysiu] vH;ax] ifjlspu] vkSj

miukg ds iz;ksx }kjk fpfdRlk djuh pkfg,A
xEHkhj okrjDr esa fojspu] fu#gcfLr] vkSj Lusgiku
ds }kjk fpfdRlk djuh pkfg,A

BIBLIOGRAPHY
1. Charaka Samhita; With ‘Vidyotini’ Hindi commentary by Sastri narayana satya; reprint
edition; Vol. 1; Chaukhambha Bharati Academy; Varanasi 221001; India;2013; Page no.
820-824
2. Susruta Samhita; With ‘Ayurveda Tattva Sandipika’ Hindi commentary by Shastri Kaviraja
Ambikadutta; reprint edition; Vol. 1; Chaukhambha Sanskrit Sansthan; Varanasi 221001;
India; 2014; Page no. 299-301
3. Astanga Hrdayam; With ‘Vidyotini’ Hindi commentary by Gupta Kaviraja Arideva; reprint
edition; Chaukhambha Prakashan; Varanasi 221001; India; 2012; Page no. 381-382
4. Bhawaprakasa; ‘Vidyotini’ Hindi commentary by Misra Brahma Sankara; reprint edition;
vol 2; Chaukhamnha Sanskrit Bhawan; Varanasi 221001; India; 2012; page no. 295-302
5. Madhava Nidanam; With ‘Vidyotini’ Hindi commentary by Yadunandana Upadhyaya;
reprint edition; Vol. 1; Chaukhambha Prakashan; Varanasi 221001; India; 2013; Page no.
498-505
6. Sharma K Ajay; Roga Vijnana evam vikriti Vijnanareprint edition; Vol. 2; Chaukhambha
Visvabharati; Varanasi 221001; India; 2013; Page no. 266-276
7. Colledge R Nicki et al; Davidson’s Principles and Practice of Medicine; ed. 21 st; Churchill
Livingstone Elsevier; 2010; Page no. 1096-1101
8. Longo L Ian et al; Harrison’s Principles of Internal Medicine; Vol. 2; ed. 18 th; The Mc Grew
Hill Company; 2012; Page no. 2837-2840
9. Robbins and Cotran; Kumar Vinay et al; ed. 8th; Saunders Elsevier; 2013; Page no. 1242-
1246
10. Mohan Harsh; Textbook of pathology; reprint ed. 6 st; Jaypee Bothers Medical Publishers;
Daryaganj, New Delhi 110002; India; 2013; Page no. 853-855
 11. World Journal of Pharmacy and Pharmaceutical Sciences, Volume 4, Issue 1,976-989,
Research Article ISSN 2278-4357. Author Dr. Rohit Ranjan.
12. www.ncbi.nlm.nih.gov/pmclarticles/PMC41197921
13. www.nhs.uk
14. wikipedia

*******

Pathogenesis of acute gouty arthritis

Hyperuricaemia

Precipitation of urate crystals in joints

Activation of compliment and kinin system

Phagocytosis by macrophages

Release of IL-1β, other cytokines

Neutrophil chemotaxis

Release of LTB4, prostaglandins, free radicals

Phagocytosis of crystals by neutrophils

Release of crystals
Lysis of neutrophils

Release of lysosomal enzymes

Release of protease

Tissue injury and inflammation

Pathogenesis of acute gouty arthritis

 Classification of gout
Primary Gout (90% cases) Secondary Gout (10% cases)

Overproduction of uric acid Overproduction of uric acid with increased urinary excreti
Diet Increased nucleic acid turnover (e.g. leukemias & other ag
Unknown enzyme defects (80-90%) Inborn errors of metabolism (e.g. complete HGPRT deficie
Known enzyme defects (e.g. partial HGPRT deficiency,
Reduced
rare)
excretion of uric acid with normal production
Reduced excretion of uric acid with normal production
Chronic renal disease

Factors that predispose to chronic hyperuricaemia and gout

Diminished renal excretion (common) Increased production of uric acid (uncommon)

Inherited isolated renal tubular defect (under excretors)Increased purine turnover

Renal failure Chronic myeloproliferative or lymphoproliferative disord
Chronic drug therapy (Thaizide & Loop diuretics, low dose aspirin,
Increased Cyclosporine,
de novo pyrazinamide)
synthesis (Over producers)which reduc
Lead toxicity (e.g. in ‘moonshine’ drinkers) Unidentified abnormality (most common)
Lactic acidosis (alcohol) Specific enzyme defect (rare)
Hypoxanthine - guanine phosphoribosyl transferase defi
Phosphoribosyl pyrophosphate synthetase over activity
unkn unkn
Glucose 6 phosphatase deficiency
 funku lsou

okr izdksid funku jä izdksid funku

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fo:)k”ku] v/;”ku dqyRFk] ek’k] “kkd] b{kq dk lsou
feF;kgkj] _rqfoijhr ,oa lkRE;foijhr vkgkj
fonkgh vé dk vfrlsou] e?kiku
fogkjt& feF;kgkj] _rqfoijhr vkgkj] lkRE;foijhr vkgkj
gfLr] v”o] m’Vª dh lokjh fogkjt&
tydzhMk] iouya?ku vfHk?kkr
“kksd] vfrO;k;ke] vfrO;ok;] vO;ok; “kjhj dh oeu&fojspukfn }kjk “kqf) u gksuk
m’.kdky esa vR;f/kd fo’ke jkLrk pyus dzks/k]
ls lUrkikfn dk lsou
osx/kkj.k] iztkxj ¼jkf=tkxj.k½

okr izdksi jä izdksi

vkSj lEiw.kZ lfU/k;kas@ekxksaZ esajäQSyus okyk
nzo vkSj gksrklzksrkas
lEiw.kZ gSA esa QSyus okyk gksrk

izdqfir okr ds lkFk jä dk lEiw.kZ “kjhj dh fljkekxZ esa lapj.k@ xeu

odz lfU/k;kas esa okr rFkk jä dh xfr dk vojks/k

odz lfU/k;kas esa LFkkulaJ;

nks’kksa ls ;qä gksdj mu lfU/k;kas eas :ds gq, okrjä }kjk fHké&fHké izdkj dh

O;kf/k LoHkko ls loZizFke iknewy esa LFkkulaJ;

okrjä
Okrjä dh lEizkfIr