Gout and Corticosteroids Assignment

Running head: GOUT 1
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Title: Gout and Corticosteroids

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Abstract
Gout is a form of arthritis that mostly affects men. Gout leads to sudden and severe pain
at the joints. The pain starts at the tore and spreads to other joints infecting areas around the
joints including the knee, foot and ankle. Scholars claim that men are most vulnerable than
women, with women being 3 times less likely to contact gout compared to men. Its expression
and development is dependent on chronic hyperuricemia, development of monosodium urate
crystals and how inflammatory system interacts with the monosodium urate (MSU) crystals. In
this article, I am going to discuss the pathophysiology and pharmacology of gout and
corticosteroids. This condition is mostly pronounced among men after reaching the age of 40 and
among women after menopause. The review will therefore consider people within the age
bracket of 40 and 60 years.
Gout is influenced by certain factors such as genetic factors and environmental factors.
Age, sex, alcohol, obesity and diet also influence gout and corticosteroids. Presence of gout is
marked by the presence of monosodium urate crystals in synovial fluid. After one has been
diagnosed with this condition some modifiable risk factors such as obesity, diuretic therapy,
alcohol consumption and high purine diet need to be addressed. The signs and symptoms for
gout include intense pain in the joints, lingering discomfort, inflammation and redness on the
affected joints and limited movement. Different diagnosis methods including joint fluid test and
blood test are carried out to find out if one is suffering from this condition. After one is been
diagnosed with gout, different therapies can be applied for treatment. Among these is
administration of different drugs including corticosteroids and colchicine.

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Introduction
Gout is a sudden and a complicated type of arthritis that can attack anyone. It is the
oldest form of arthritis dating back to the 5th century BC (John Hopkins Medicine, 2020). This
condition does not attack a person based on socioeconomic status but it is related to uric acid
metabolism. The characteristic features of gout include swelling, tenderness, redness and pain in
the joints. In most cases gout start from the big tore. The attack of gout occurs abruptly such that
it can wake one from sleep with heat sensation on the big toe. The infected joints start to swell,
feels hot and become so tender that the weight of a bedsheet is unbearable. The signs and
symptoms of this condition may appear and go but there are ways to manage them and prevent
flares.
Pathophysiology
Gout is an inflammatory arthritis belonging to arthropathy group known as crystalline
arthropathies. It is due to an inflammatory response to uric acid crystals which are as a result of
high uric acid levels in the system, a phenomenon known as hyperuricemia. Continuous
accumulation and saturation of uric acid leads to crystals being deposited and accumulating in
tissues and joints which stimulate the body immune system to respond. Uric acid tophi, which
are characteristic features of tophaceou gout, manifest as stone like nodules under the skin and
could lead to considerable discomfort and destruction (Aslam and Michet, 2017). Factors leading
to the formation of these crystals have been identified however they vary from one person to
another. The variability of these factors among different people does not affect in any way the
expression and prevalence of this condition.

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According to Shekelle et al. (2017) different risk factor have been discovered, with the
association between race and obesity, and gout having been appreciated since long. Other risk
factors have been recently discovered while others are yet to be clarified. Elevated levels of uric
acid in the body increases one’s chances of contracting gout. The risk factors for gout include:
plasma urate concentration- the Normative Aging Study carried out on this factor indicated that
cases of gout increased from <1% to 30 percent for plasma urate concentration of <0.42 mmol/L
to >0.60 mmol/L. although acute hyperuricemia does not cause gout due to insufficient time
needed for the formation of the MSU crystal, the patients are at a high risk of uric acid
nephropathy. One’s diet is another risk factor, whereby one eating too much seafood and meat
and taking fructose sweetened beverages lead to rise of uric acid levels in the body.
Alcohol consumption increases levels of uric acid hence increasing the risk of gout.
When one is overweight, there body produces a lot of uric acid hence overworking their kidneys
to eliminate the uric acid. Some medical conditions increases the risk for gout. Untreated blood
pressure, and other chronic infection like diabetes pose a risk of contracting this condition.
Certain medication such as thiazide diuretics, used in the treatment of high blood pressure and
low dose aspirin can alter uric acid levels in the system. Anti-rejection drugs used by individuals
with recent experience of organ transplant are also at risk. Having family members who had this
condition, increases one’s risk of contracting it. Age and sex are also risk factors for gout. This
condition is more prevalent among men because women naturally have low uric levels. Men can
develop this infection earlier (between 30 and 50 years) unlike women whose signs and
symptoms could be seen after menopause (Soskind, Abazia and Bridgeman, 2017). Having
recently undergone surgery or trauma is thought to increase the risk for gout.

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If gout go untreated it could advance to severe conditions. Recurrent gout- some people
after an attack by gout may never experience its signs and symptoms while in others they could
appear severally at different times. There are medication that could be used to prevent recurrent
gout. If left unattended, this condition can erode and destroy the joints. Advanced gout is a
condition whereby urate crystals known as tophi form under the skin. These nodules, though not
painful, swell and become tender when one is attacked by gout (Soskind et al., 2017). Lastly,
kidney stones is a complication of gout, developing as a result collection of urate crystals in the
urinary track among gout patients. Kidney stones can be treated.
Pharmacology
Robinson and Delbeth (2015) claim that there has been a great progress as pertains gout
pharmacotherapy. Scholars have stressed the significance of serum urate therapy for effective
and efficient management of gout. Safe and effective dosing approaches for the previously and
currently used drugs have been identified. New therapeutic agents are being introduced and
approved. These include therapies to lower urate levels and anti-inflammatory treatments for
acute flares (Robinson and Dalbeth, 2015). However, the treatment and management of gout is
faced by different challenges. The major challenge is the quality of care. The strategies drawn to
ensure quality practice need to focus translating last decade’s success and progresses in to
clinical benefits to gout patients.
Different diagnostic methods are carried out on a person suspected to be having gout.
For the joint fluid test, fluid is drawn from the infected area then examined for urate crystals.
Blood test can be carried out to determine the creatinine levels in the blood as well as those of
uric acid. Blood test could however produce misleading results as someone could have elevated
of uric acid in their systems but no gout while others could show signs of gout but uric acid

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levels are normal. X-ray imaging are important to figure out the result joint inflammation.
Musculoskeletal ultrasound is a technique mostly used in Europe in the detection of urate
crystals in a tophus or joint. Dual energy CT scan has the ability to show urate crystals in a joint
despite the joint being inflamed (Qaseem, Harris and Forciea, 2016).
The medications for gout are based on one’s current health and also their preferences.
The medications include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and
corticosteroids. Corticosteroids could be in form of pills or injection to the infected joint.
Corticosteroids are important at relieving symptoms of gout and prevent inflammations. Most
prescribed for patients who cannot use colchicine and NSAIDs.
Pharmacodynamics and pharmacokinetics
Among the corticosteroids used in gout treatment include prednisolone
(Glucocorticoids) which use different mechanisms to prevent the anti-inflammatory effect. These
include stimulating production of lipocortin inhibiting phospholipase A2 and reduce release of
arachidonic acid hence decreased production of inflammatory mediators (Hellmann and
Imboden, 2019). Its generic name is hydrocortisone.
Route of administration
Prednisolone can be administered using intravenous route, orally or the intra-articular
administration. Prednisolone action is within 12 to 36 hours. This medication is 90 percent
plasma protein bound with it binding to corticosteroid-binding globulin. The oral dosage for
Prednisolone is between 40 mm and 60 mg per day or 40mg in a day when intravenously
administered. The metabolism of this drug occurs at hepatic site as well as the extrahepatic sites.

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Indications, contradictions, precautions and side effects
Administration of this drug is accompanied with different side effects including altered
fat distribution in the body, osteoporosis, peptic ulcer, glaucoma, edema and muscle wasting
(Grosser, Smyth and FitzGerald, 2018). Depending on the indication and general situation, some
contradiction could be peptic ulcers, diabetes, hypertension and osteoporosis. The precaution for
this medication is that its dose has to be reduced gradually and discontinued if the therapy exceed
7 days. Insulin dependent diabetics if using this medication would need an increase insulin dose
(Sahai, Sharma, Misra and Dutta, 2018).
Other drug interactions
If the gout treatment is not working, the patient can try alternative medicine, however,
doctor’s advice is needed. Drinking of coffee has been associated with lowering uric acid levels.
Vitamin C supplements can also be considered in reducing uric acid concentrations in the blood.
Studies however indicate that Vitamin C influences the severity and frequency of gout attacks.
Cherries reduce uric acid concentration in the blood. More research is however needed to
confirm the use of coffee and cherries in gout treatment. Medication are the best therapy for
treating and preventing gout (Liu, Zhen, Zhao, Zhai, Liu and Zhang, 2015). However, lifestyle
changes could be of importance. Limiting alcohol intake, fructose sweetened drinks and intake of
high purine content food could help prevent gout. Regular exercise could help in losing weight
and also reduce risk of gout. For the lifestyle changes, one’s doctor plays a role in advising the
patient what to and not to do.
Conclusion

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Gout is a metabolic condition caused by elevated levels of uric acid in the blood hence
one develops gouty arthritis. Both pharmacological and non-pharmacological interventions can
be used in the management of this condition. Life style changes are important to prevent the
occurrence of this condition.

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References
Aslam, F. and Michet, C. (2017). My treatment approach to gout. Mayo Clinic Proceedings, Vol.
92, No. 8, pp. 1234-47. DOI: https://doi.org/10.1016/j.mayocp.2017.05.026
Grosser, T., Smyth, E. M. And FitzGerald, G. A. (2018). Adrenocorticotropic hormone, adrenal
steroids, and the adrenal cortex. In: Dandan RH, Knollmann. Goodman and Gillman’s the
pharmacological basis of therapeutics. United States of America: Mc Graw Hill
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Hellmann, D. B., & Imboden Jr, J. B. (2019). Rheumatologic, immunologic, & allergic disorders.
Current Medical Diagnosis & Treatment.
John Hopkins Medicine. (2020). Gout. https://www.hopkinsarthritis.org/arthritis-info/gout/
Liu, C., Zhen, Y., Zhao, Q., Zhai, J. L., Liu, K. and Zhang, J. X. (2016). Prednisone lowers
serum uric acid levels in patients with decompensated heart failure by increasing renal
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Qaseem, A., Harris, R. P. and Forciea, M. A. (2017). Management of Acute and Recurrent Gout:
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Expert Opin Pharmacother 16(4):533–546. doi:10.1517/14656566.2015.997213

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Soskind, R., Abazia, D. T. and Bridgeman, M. B. (2017). Updates on the treatment of gout,
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