Calcium Pyrophosphate Deposition Disease Article

Content

• Rheumatoid Arthritis
• Gout And Calcium Pyrophosphate Deposition Disease
• Complications Of Pseudogout

The condition is self-limiting and usually resolves in a few weeks. Pseudogout can be differentiated from gout by examining the specific crystals deposited in the inflamed joints. Non-steroidal anti-inflammatory drugs reduce symptoms and joint swelling in most individuals with CPPD and may be sufficient to treat the majority of patients. Ibuprofen , naproxen , and indomethacin are commonly used NSAIDs but increase the risk for damage to the stomach, potentially leading to ulcers in certain patients at risk. This risk is reduced when using COX-2 selective NSAIDs such as celecoxib or valdecoxib as well as the partially COX-2 selective drug meloxicam .

Rheumatoid Arthritis

NSAIDs have limited efficacy on joint involvement of oxalosis, while colchicine and steroids have not been assessed either. The use of nitisinone for ochronotic arthropathy is still much debated, but it could provide beneficial effects on joint involvement. The effects of copper chelators have not been assessed either in the joint involvement of Wilson’s disease. NSAIDs should be avoided because of the liver affection they may worsen.

Unfortunately, no treatment can get rid of the crystal deposits that cause pseudogout. Taking low doses of colchicine may help to reduce your risk of future attacks. Your doctor can talk to you about the risks and benefits of taking this medicine. Pseudogout develops when deposits of calcium pyrophosphate dihydrate crystals build up in the cartilage of a joint. Pseudogout (SOO-doe-gout) is a form of arthritis caused by calcium pyrophosphate crystal deposits in a joint, most commonly the knee. It is characterized by sudden and intense redness, warmth, pain, and swelling in one or more joint.

Gout And Calcium Pyrophosphate Deposition Disease

It is believed that the presence of the calcium crystals more rapidly strips away the lining of the cartilage. In many, it may be difficult to determine if the calcium deposits are causing any damage in the joint or are simply present by coincidence. Again, the knee is commonly affected, just as we see in those with ordinary OA.

A meta-analysis found an independent association between gout and cardiovascular mortality as well as all-cause mortality. In the United States in 2015–16, the overall prevalence of gout in adults was 3.9%, corresponding to a total affected population of 9.2 million. Prevalence is approximately 20% in patients with a family history of gout. It is estimated that more than 2 million people in the United States take medication to decrease serum uric acid levels. In particular, 3 genes are noted to have a strong association with hyperuricemia. The locus with the strongest evidence of association is the glucose transporter 9 gene, commonly referred to as the solute carrier 2A9 , the product of which alters the renal excretion of uric acid.

Inflammatory Arthritis

About 90% of patients with gout develop excess urate stores because of an inability to excrete sufficient amounts of uric acid in the urine . Most of the remaining patients either overconsume purines or produce excessive amounts of uric acid endogenously . A gout attack may be triggered either by release of crystals or by precipitation of crystals in a supersaturated microenvironment . In either situation, it is believed, naked urate crystals then interact with intracellular and surface receptors of local dendritic cells and macrophages, triggering a danger signal to activate the innate immune system.

There are various imaging features for common crystal-related deposition diseases including monosodium urate, calcium pyrophosphate dihydrate as well as hydroxyapatite depositional diseases. Pseudogout, also known as calcium pyrophosphate deposition disease , is caused by the formation of calcium pyrophosphate dihydrate crystals in the synovial fluid of the joints. Crystal-induced arthropathies are diseases in which tiny crystals form in joint spaces, causing inflammation and joint damage.

Complications Of Pseudogout

Do not take aspirin with these drugs because it blocks their effects on the kidneys. Read the labels of any prescription or over-the-counter medicines you take to be sure they don't contain aspirin. All of these drugs are powerful so you need to understand why you are taking them, what side effects may occur and what to do if you have any problems.

How can you tell the difference between gout and pseudogout?

While gout is caused by uric acid crystals; pseudogout is caused by calcium pyrophosphate dehydrate crystals (CPPD). And though the two have similar symptoms, treatment is somewhat different. Pseudogout causes sudden attacks of joint pain, swelling, and warmth. The attacks can last for days to weeks.

The CPP crystals that produce pseudogout comprise a combination of inorganic pyrophosphate and calcium. Urate initially precipitates in the form of needlelike crystals. The light-retarding (phase-shifting) characteristics of urate crystals allow them to be recognized by polarizing microscopy . Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled . Merck & Co., Inc., Kenilworth, NJ, USA is a global healthcare leader working to help the world be well.

What Is Cppd?

Oral steroids are given as prednisone or methylprednisolone; they work best for patients with severe polyarticular attacks. Oral CS can also exacerbate pre-existing diabetes by promoting hyperglycemia. In a prospective study performed on 14 patients who presented with an acute flare of pseudogout, intra-muscular triamcinolone injection provided an effective treatment to the patients.

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The disease may cause lasting arthritis that may be mistaken for osteoarthritis, rheumatoid arthritis or gout. Another important diagnostic tool for this CPPD is plain X-ray. X-ray can detect calcifications in the cartilage and also reveal the extent of damage in the joint . Other radiographic features that can be visualized are osteophytes, the narrowing of joint space and subchondral cysts . Additional radiographic modalities, such as ultrasound, MRI and CT can be useful in patients with atypical sites of CPP crystal deposition, e.g., atlanto-occipital joint and spine (Crowned dens syndrome; Figure 2) .

Changing or stopping medications associated with hyperuricemia may also help. Having a diet high in purines, which the body breaks down into uric acid. Purine-rich foods include red meat, organ meat, and some kinds of seafood, such as anchovies, sardines, mussels, scallops, trout, and tuna. Calcific tendinosis is most commonly seen in the shoulder in the distal supraspinatus tendon insertion at the greater tuberosity of the humerus. Less common locations may include tendons of infraspinatus, subscapularis, and deltoid, wrist, elbow, gluteus maximus, knee, and neck. Rarely erosion of bone adjacent to calcification at the insertion site of the tendons can be visualized.

In addition, resting painful joints is also important to relieve symptoms. Genetic factors are also held responsible for the development of CPPD in a few cases. Once the crystals reach the joint space, a cascade of inflammatory reactions is initiated; which ultimately cause the painful symptoms. Chronic form – The chronic form progresses slowly and causes degenerative changes which take several months to resolve. This form resembles rheumatoid arthritis, and radiological examination will be necessary to differentiate the two.

What Is Calcium Pyrophosphate Crystals Deposition Cppd?

But even if your sample doesn't show uric acid crystals, you still may have gout. Crystals don't always form in the synovial fluid during a gout attack. Identification of synovial fluid crystals assumes ability to successfully obtain synovial fluid. Patients may initially decline arthrocentesis but may be more willing if made aware that diagnosis can be wrong up to 20% of the time without proof of crystal presence and identity . Large bulging effusions at knees may be relatively easy to aspirate but accurate and successful needle placement in knees may be achieved less often than many suspect. Confirmation by X-ray contrast injection has been used to study accuracy of injections .