Could Joint Pain In The Feet And Ankles Be Symptoms Of Gout?

Content

• What Can Be Mistaken For Uric Acid Collection In Gout?
• Allopurinol
• Information From Your Family Doctor
• Symptoms Of Pseudogout
• Who Can Get Gout?
• What Is Gout?

Gout is the most common crystal arthropathy and is frequently diagnosed and managed by primary care physicians. Point-of-care ultrasound is a valuable tool to aid in the diagnosis of gout via the identification of the double contour sign, aggregates of crystals, tophi, and erosions. In addition, POCUS can aid in the management of gout by recognizing early signs of gout, monitoring the effectiveness of urate-lowering therapy, and guiding aspiration and corticosteroid injection. If joint fluid analysis is not possible, tentative diagnosis may be made based on the person's medical history, symptoms, a physical examination, and urine and blood tests to assess uric acid levels. Overall, purine restriction generally reduces serum uric acid levels by no more than 1 mg/mL, with modest impact, and diets with very low purine content are not palatable.

By 6 months, the primary endpoint—a serum uric acid level of less than 6.0 mg/dL—was achieved in 45% of subjects on febuxostat 40 mg/day, 67% on febuxostat 80 mg/day, and 42% on allopurinol. In subjects with renal impairment, the primary endpoint was achieved in 50% of subjects on febuxostat 40 mg/day, 72% on febuxostat 80 mg/day, and 42% on allopurinol. Adverse GI effects are uncommon with this dosage, occurring in only 4% of patients. This stands in contrast to the 80% risk of adverse GI effects with the classic hourly colchicine regimen for the treatment of acute gout. Avoiding the use of medications that elevate uric acid in patients with gout is prudent. Thus, in patients with hypertension, other agents are preferable to a thiazide diuretic, provided that blood pressure can be managed easily with a single drug.

What Can Be Mistaken For Uric Acid Collection In Gout?

Gouty tophi are usually whitish in color and have the appearance of cottage cheese. Their presence can cause added pressure around the areas, as well as lead to joint arthritis . With acute attacks, the affected joint can become red, hot, swollen, and painful.

The hallmark clinical feature of intrahepatic cholestasis of pregnancy is pruritus. Jaundice can occur, and laboratory findings reveal the typical features of cholestasis, including elevated levels of serum bile acids, alkaline phosphatase, and total bilirubin. UDCA has been used in ICP to relieve pruritus, and it appears to be safe for mother and fetus.43 Symptoms resolve within several days of delivery but can recur during subsequent pregnancies. Evaluation should begin with a careful history including, for example, risk factors for HIV, exposure to tuberculosis, or exposure to farm animals, which presents a risk for brucellosis and Q fever.

Allopurinol

Intrahepatic cholestasis is often seen in patients who have sepsis.33 Circulatory endotoxins associated with sepsis induce cytokine production, including tumor necrosis factor α, interleukin-1, and interleukin 6, which results in impaired bile acid transport. The cholestasis of infection is often seen in severely ill hospitalized patients, often in the intensive care unit . Other factors can contribute to the cholestasis, including medications and total parenteral nutrition.

RA can later spread to larger joints like the wrists, elbows, knees, ankles, shoulders, and hips as the disease progresses. A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. Patients with gout should avoid excess ingestion of alcoholic drinks, particularly beer, because alcohol use elevates uric acid levels and thus can precipitate attacks of gout. Indeed, heavy drinkers are much more likely to have recurrent gout attacks, even with allopurinol therapy. Moderate wine intake is not associated with increased development of incident gout, but excesses of any form of alcohol in gout patients are associated with acute gout flares. Because allopurinol, febuxostat, and probenecid change serum and tissue uric acid levels, they may precipitate acute attacks of gout.

However, gout patients appear to be less responsive to such a low dose of ascorbate. Vitamin C treatment should be avoided in patients with nephrolithiasis, urate nephropathy, or cystinuria. In 2010, a polyethylene-glycol–conjugated uricase was approved by the FDA for gout.

The patient should see a primary care physician who determines if a specialist consult (i.e., rheumatology, orthopedist) is required. A comprehensive history and physical exam, laboratory tests, and imaging studies are sufficient to determine the etiology of arthritis. The mainstay of treatment is by medications, but sometimes surgery is also required if a foreign body is involved, or there is internal damage to the joint. In addition to the identification of MSU crystal deposition by DECT and imaging evidence of gout-related joint damage by plain radiographs, the double contour sign by ultrasound is included in the ACR/EULAR consensus guidelines for gout classification criteria .

This can lead to early recognition of subclinical gout and lead to measures like dietary modification and urate-lowering therapy to prevent disease progression. There are many practical advantages in the use of ultrasound for the evaluation of gout compared to the previously mentioned imaging modalities. These include ultrasound’s ready availability at the bedside, low operational costs and time, real-time information for clinicians, and the ability to perform a rapid examination of multiple locations [22-24]. The increase of skilled clinician sonographers and of ultrasound equipment makes POCUS an ideal bedside tool for the assessment of the patient with crystal arthropathy.

Calculous or acalculous cholecystitis or biliary obstruction is often a concern in this setting. Therapy for sepsis-induced cholestasis consists of treating the underlying infection. Outcomes usually are dictated more by the patient’s underlying disease than by the cholestasis itself. Most cholestatic hepatic injury resolves with withdrawal of the offending medication. A small subgroup of patients develop progressive liver disease, resulting in biliary cirrhosis and liver failure.

Patients with recurrent attacks of gout have a longer duration of illness and are more likely to have polyarthric disease. Joint involvement in polyarthric attacks appears to have an ascending, asymmetric pattern. In addition to the great toe, other areas affected include the insteps, heels, ankles, knees, fingers, wrists and elbows. .4 Several medications increase the serum uric acid concentration through modification of the filtered load of uric acid or one of the tubular transport processes. JEFFREY A. ALLOWAY, M.D., is a rheumatologist at Wilford Hall USAF Medical Center at Lackland Air Force Base and assistant professor of medicine at the USUHS F. Edward Hébert School of Medicine.

He has extensively published his research in peer-reviewed journals such as the American Journal of Medicine, Current Medical Research and Opinion, and Postgraduate Medicine. He has authored articles for numerous websites on topics such as sleep disorders, gout, rheumatoid arthritis , biology of leg disorders, depression, chronic pain, health literacy, and diabetes. He is a co-author of the textbook Clinical Management of Insomnia, now in its second edition.

The most common prophylactic regimen is a combination of methotrexate and cyclosporine. In general, the more severe the skin, liver, or gut involvement, the less favorable the outcome. Colchicine is another treatment option but does not provide analgesia and is less effective if given beyond 72 to 96 hours after symptoms begin. It should be used with caution in patients with hepatic or renal impairment, and side effects include nausea, vomiting, and diarrhea. Another second-line treatment for those who cannot tolerate NSAIDs is corticosteroids.Caution is necessary when using corticosteroids with patients with diabetes mellitus as it can alter there blood glucose levels. Treatment of monoarticular arthritis depends on the etiology and severity of the condition.

Allopurinol blocks xanthine oxidase and thus reduces the generation of uric acid. Approximately 3-10% of patients taking allopurinol develop symptoms of intolerance, such as dyspepsia, headache, diarrhea, or pruritic maculopapular rash. Allopurinol should immediately be discontinued in patients who develop pruritus or a rash consistent with allopurinol hypersensitivity. Responses may also occur in patients with pseudogout, sarcoid arthropathy, psoriatic arthritis, or calcific tendonitis. Your doctor may examine your blood and fluid from the joint to be sure. • Synovial fluid analysis should also be performed when the clinical situation is uncertain and a probability of infection exists.

The diagnostic standard for acute gout is joint aspiration with synovial fluid analysis for monosodium urate crystals; however, many patients are seen in a primary care or emergency medicine situation where synovial fluid analysis is rarely performed. The American College of Physicians has developed a guideline for diagnosing adults with joint inflammation suspected to be gout. Risk factors of gout include male sex; obesity; hypertension; alcohol intake; and a diet rich in meat, seafood, and fructose-rich food and beverages. Gout is characterized by swelling, pain, or tenderness in a peripheral joint or bursa. Colchicine, nonsteroidal anti-inflammatory drugs, and corticosteroids all relieve pain in acute episodes.

The only moderate sensitivity is likely due to difficulty visualization and poor acoustic windows at small joints such as those of the hands . Most people with elevated blood levels of uric acid will never develop podagra and gout, and gout is not always associated with elevated uric acid blood levels. The condition can also occur despite there being normal levels of uric acid at the point in time when blood levels are measured.