What are differential diagnosis for gout?
Differential Diagnosis of Acute Gout
| Diagnosis | Joint distribution | Synovial fluid findings |
|---|---|---|
| Gram stain/culture | ||
| Pseudogout (calcium pyrophosphate deposition disease) | Knee, wrist, or first metatarsophalangeal | Negative |
| Septic arthritis | Knee is most commonly involved (may be any joint distribution) | Positive |
What is pathophysiology of gout?
Gout refers to disease that occurs in response to the presence of monosodium urate (MSU) crystals in joints, bones, and soft tissues. It may result in an acute arthritis (a gout flare), chronic arthritis (chronic gouty arthritis), or tophi (tophaceous gout) [1,2].
What crystals cause gout?
Gout occurs when urate crystals accumulate in your joint, causing the inflammation and intense pain of a gout attack. Urate crystals can form when you have high levels of uric acid in your blood.
Is gout a metabolic disease?
Gout is both an inflammatory and a metabolic disease. With further investigation of urate’s role, the possibility of proper gout management additionally mitigating metabolic syndrome is an evolving and important question. Keywords: Diabetes; Fructose; Gout; Hypertension; Metabolic syndrome; Uric acid.
How can you tell the difference between gout and rheumatoid arthritis?
Gout is an inflammatory disorder, but it is not an autoimmune condition. Gout is caused by high blood levels of uric acid that the body cannot excrete properly. These uric acid crystals can deposit in the synovial tissues, causing inflammation and pain. RA is an autoimmune inflammatory condition.
What is difference between gout and pseudogout?
In pseudogout, or CPPD, crystals of pyrophosphate dihydrate form in your joints causing pain. Gout, on the other hand, is caused by the formation of monosodium urate crystals due to high levels of uric acid. The crystals form around your joints, causing pain.
What are the four stages of gout?
The 4 Stages of Gout Progression (and How to Stop Gout from Getting Worse)
- Stage 1: High Uric Acid Levels.
- Stage 2: Acute Gout.
- Stage 3: Intercritical Gout.
- Stage 4: Chronic Gout.
- How to Know If Your Gout Is Progressing.
- What Makes Gout Get Worse.
- How Gout Treatment Prevents Disease Progression.
- Can Gout Be Cured?
What is the main cause of gout?
Gout is caused by a condition known as hyperuricemia, where there is too much uric acid in the body. The body makes uric acid when it breaks down purines, which are found in your body and the foods you eat.
How does metabolic syndrome cause gout?
Serum urate levels also depend on the degree of excretion by the kidneys, and low excretion is the main factor contributing to high urate levels. Hyperuricemia increases the risk of gout from monosodium urate crystal formation, which can occur spontaneously at a concentration of 6.8 mg/dL.
What is disorders of purine metabolism?
Gout is an inherited disorder of purine metabolism that causes hyperuricemia in humans, particularly men. The term “gout” in general use refers to a form of arthritis.
What are the signs and symptoms of LCHAD deficiency?
Signs and symptoms of LCHAD deficiency typically appear during infancy or early childhood and can include feeding difficulties, lack of energy (lethargy), low blood sugar (hypoglycemia), weak muscle tone ( hypotonia ), liver problems, and abnormalities in the light-sensitive tissue at the back of the eye ( retina ).
When does long chain CoA dehydrogenase deficiency occur?
Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency is a rare condition that prevents the body from converting certain fats to energy, particularly during periods without food (fasting).
What kind of fatty acid oxidation disorder is LCHAD?
LCHAD deficiency is a severe fatty acid oxidation disorder that is fatal if untreated. [ 2]
Where is the HADHA gene located in LCHAD deficiency?
This enzyme complex metabolizes long-chain fatty acids, and LCHAD activity is specific for compounds of C12-C16 chain length. The genes for the alpha and beta subunits have been localized to chromosome 2. The HADHA gene has been cloned, and a common mutation, c. 1528G>C, has been identified in the mutant alleles of LCHAD deficiency. [ 1]