introduction about hyperuricemia / Gout and its etiological factors

2. Introduction
• Hyperuricemia is an excess of uric acid in the blood. Uric acid passes through the liver,
and enters to the bloodstream. Most of it is excreted in the urine, or passes through
intestines to regulate "normal" levels.
• Also important to blood uric acid levels are purines. Purines are nitrogen-containing
compounds, which are made inside the cells of our body (endogenous), or come from
outside of our body, from foods containing purine (exogenous). Purine breaks down into
uric acid.
• Increased levels of uric acid from excess purines may accumulate in tissues, and form
crystals. This may cause high uric acid levels in the blood.
• The amount of urate in the body depends on the balance between the amount
of purines eaten in food, the amount of urate synthesised within the body (e.g.,
through cell turnover), and the amount of urate that is excreted in urine or through the
gastrointestinal tract.

3. • Normal uric acid blood levels varies between genders, 2.4 - 6.0 mg/dL for
women and 3.4 - 7.0 mg/dL for men.
• The upper limit lies at 7.0 mg/dL where any higher puts us at risk for
developing hyperuricemia.
• The cause of hyperuricemia is divided into three categories:
uric acid underexcretion,
uric acid overproduction or
combined causes.
What Causes Hyperuricemia?

4. Underexcretion
Underexcretion makes up most cases of hyperuricemia. Urate, a salt of
uric acid, is filtered by the kidneys and undergoes a process that ends in
the urate leaving the body through the urine. One misstep in this process
can result in renal insufficiency and subsequently a poor rate of uric acid
excretion.

5. Underexcretion or poor kidney function can be caused by the following:
• Renal insufficiency. In the case of renal failure, uric acid remains in the blood as
the kidneys are unable to properly perform the excretion process or other organic
compounds compete for clearance.
• Metabolic syndrome. Other health complications such as hypertension, obesity and
insulin resistance can contribute to the decreased excretion of urate by the kidneys.
• Medications. Diuretics, low-dose salicylates, cyclosporine and nicotinic acid have
been linked to causing poor excretion performance by the kidneys.
• Genetics. While considered rare, patients with this condition experience progressive
renal failure that results in a lower rate of uric acid excretion.
• Hypertension. High blood pressure and the associated medications have been
known to cause hyperuricemia.

6. CONTINUE….
• Acidosis. Conditions that increase acidity in the blood such as alcoholic
ketoacidosis, diabetic ketoacidosis, lactic acidosis and starvation acidosis can
cause poor kidney function and hyperuricemia.
• Pre-eclampsia and eclampsia. These conditions are often associated to elevated
uric acid levels which can cause hyperuricemia.
• Lead exposure (chronic): Clinical studies have shown that occupational or
prolonged exposure to lead can affect kidney function.
• Other conditions: Hypothyroidism, hyperparathyroidism, sarcoidosis, and
trisomy 21.

7. Overproduction
Overproduction occurs in a minority of patients who have hyperuricemia. Hyperuricemia induced by
overproduction may be caused by external factors like high purine diet or internal factors like
increased purine breakdown. Overproduction of uric acid can be caused by the following:
• Diet. A diet that majorly consists of high-purine meats, organ foods and legumes can contribute to
the overproduction of uric acid.
• Lesch-Nyhan syndrome. Processes involved in this syndrome contribute to the overproduction of
uric acid. Patients with this syndrome are also more likely to develop gout.
• Kelley-Seegmiller syndrome. Processes involved in this syndrome contribute to the
overproduction of uric acid. Patients with this syndrome are also more likely to develop gout.
• Increased nucleic acid turnover. Processes involved in this syndrome contribute to the
overproduction of uric acid. Patients with this syndrome are also more likely to develop gout and
kidney stones.
• Tumor lysis syndrome. This syndrome is known to produce the most serious complications of
hyperuricemia.
• Other conditions: Glycogenoses (III, V, and VII) and exposure to organic pollutants.

8. Combination Causes
A combination of overproduction and underexcretion can provide to be a problematic cause
of hyperuricemia. The combination of both mechanisms can put patients at greater risks of
developing complications. Combination causes can be a result of the following:
• Alcohol Consumption. Alcohol increases the production of uric acid and also produces
competing compounds that lead to the decrease of uric acid excretion by the kidneys.
• Fructose Foods and Drinks. Fructose increases uric acid levels by increasing purine
metabolism. Additionally, studies have found that fructose also plays a hand in decreasing
kidney function and uric acid excretion.
• Rapid Weight Loss. The enhanced breakdown of tissue from unhealthy or rapid weight
loss may produce more uric acid and decrease excretion due to the sudden and rapid
change in urate levels.
• Deficiency of aldolase B. This is a common genetic disorder, patients with this deficiency
are likely to develop gout.
• Glucose-6-phosphatase deficiency. This disorder can also lead to kidney complications or
failure.

9. PERFORMA

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