How to detect and treat pyrophosphate arthropathy?


What is arthropathy and how does it happen?

Arthropathy is a secondary disease. A person experiences pain, but neither the shape nor the functionality of the joint is affected. The pathology manifests itself mainly in the joints of the lower extremities, especially with knee pain due to gonarthrosis.

Symptoms include inflammation, swelling, fatigue and difficulty moving. The person experiences paroxysmal pain, and the body temperature may rise. In women, symptoms are complemented by nagging pain in the lower abdomen, discharge, and intermenstrual bleeding.

The acute period lasts up to two months. In a protracted form, arthropathy can last up to a year. If the disease is not treated, it becomes chronic: remissions are followed by relapses. With the right approach to therapy, the symptoms can be eliminated fairly quickly, but the underlying disease will not go away.

Arthropathy can be of the following types:

  • reactive – with endocrine disorders and leukemia, joint tissues react with pain;
  • dystrophic – pain in the hip joint occurs with arthrosis and conditions when the nutrition of the cartilage is insufficient;
  • pyrophosphoric - caused by a violation of the metabolism of salts and calcium in the body, often due to injuries to large joints;
  • allergic – for allergies;
  • psoriatic – for psoriasis;
  • idiopathic – when it is impossible to accurately determine the cause;
  • hereditary - transmitted genetically.

Joint arthropathy is an unpleasant but completely controllable condition

Pyrophosphate arthropathy – approaches to diagnosis

For citation. Shostak N.A. Pyrophosphate arthropathy – approaches to diagnosis // Breast Cancer. 2015. No. 25. pp. 1518–1519.

Pyrophosphate arthropathy (PPA) belongs to a group of microcrystalline arthritis. The disease is characterized by multiple calcification of articular and periarticular tissues, mainly articular cartilage (chondrocalcinosis (CC) due to the deposition of microcrystals of calcium pyrophosphate in them. PFA is a variant of ectopic calcification of hyaline and fibrous cartilage (intervertebral disc (IVD), pubic symphysis, places of attachment of the tendon to the bone ) with the development of inflammation. The disease can occur at a young age (3–4 decades of life) in cases of hereditary (familial) and metabolic forms (with hemochromatosis, hyperparathyroidism, hypomagnesemia, hypophosphatasia, etc.) and debut after 55 years, which is typical for idiopathic forms of PFA. PFA is characterized by damage to almost all joints, but the knee and wrist joints are most often involved in the process. Clinical manifestations of PFA are varied. The classic variant of PFA is acute arthritis with PFA crystals (pseudogout), characterized by sudden development of monoarthritis with subsequent regression of symptoms over a period of time. 3–5 days. In cases of a predominance of persistent “mechanical” pain in the joint with moderately severe synovitis (instrumental or histological examination reveals deposits of PFC crystals), we speak of osteoarthritis (OA) with PFC deposition. The last option is the most common and at the same time – from the point of view of the differential diagnostic approach – complex. In contrast to primary OA, in OA with PFC deposition, more pronounced osteophytosis and extra-articular calcification are observed, as well as involvement of joints that are not typical for OA (wrist, elbow, shoulder). Other clinical variants of PFA have been described: asymptomatic deposition of PFA crystals and chronic arthritis with PFA crystals (pseudoreumatoid). A combination of several clinical forms of PFA in one patient is possible. Comparative characteristics of some clinical forms of PFA are presented in Table 1.

Verification of the diagnosis is carried out taking into account the detection of PFC crystals in the synovial fluid under polarization microscopy and/or a characteristic x-ray picture: chronic menisci and articular cartilage (Table 2).

The diagnostic criteria for PFA are presented below. When determining PPA crystals using polarization microscopy, some difficulties may arise. Thus, PPA crystals have weak refraction, which makes their visualization difficult. An indispensable condition for visualizing PFC crystals is their sufficiently high concentration in the synovial fluid. A low concentration of PPA crystals may lead to a negative result. The concentration threshold for reliable identification of PPA crystals by polarization microscopy is 10–100 μg/ml. In addition, the result depends on the experience of the researcher [2]. HC is diagnosed when typical calcifications are detected in the area of ​​hyaline and fibrocartilage. Most often, HC is detected in the knee, wrist joints (fibrous-cartilaginous complex), pubic symphysis, hip, elbow, temporomandibular, and sternoclavicular joints. The first three localizations occur in more than 90% of patients with PFA. Calcification may develop at the level of the fibrous ring of the IVD, resembling syndesmophytes in ankylosing spondylitis. According to some data, CU is diagnosed before the first clinical symptoms appear in the involved joints. According to other data, when verified by electron microscopy, PFA CC is detected in 25–93% of patients [3]. Radiography is an insensitive method and visualizes calcium only when its concentration in the areas of interest is high and the deposits reach large sizes. To identify smaller deposits, it is rational to use a more sensitive and specific method - ultrasound of the joints. The following ultrasound criteria for verification of PFC deposits have been proposed: • thin hyperechoic ribbons parallel to the surface of hyaline cartilage, similar to the X-ray phenomenon of HC; • stippled deposits (patchy structures), consisting of several small hyperechoic spots (most common in triangular fibrocartilaginous complexes and tendons); • homogeneous hyperechoic nodular or round deposits, often mobile (localized in bursae or articular inversions) [2]. Treatment and prevention of PFA involves the use of non-drug and drug approaches [4]. Pathogenetic therapy for PFA has not yet been developed. Thus, in the case of OA with PFC crystals, rest is required, cold applications, aspiration of synovial fluid and intra-articular administration of glucocorticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs) and low doses of colchicine (1–2 g/day) are used. The asymptomatic variant of PFA (in the presence of only radiological signs) does not require treatment. We present a clinical observation.
Patient K., 61 years old.
Complaints of pain in both knee joints during long walking, swelling in the area of ​​the right knee joint. At the age of 56 years, pain in the right knee joint appeared for the first time during exercise, right-sided gonarthrosis of stage II according to Kellgren was diagnosed, and short-acting (NSAIDs) and delayed-acting symptom-modifying therapy (chondroprotectors) was administered. Over the next 2 years - periodically occurring arthritis of the right knee joint, wrist, ankle joints, regressing while taking NSAIDs for 3-5 days, regarded as an exacerbation of the articular syndrome in OA, the addition of pain of a “mechanical” nature in the left knee joint. 2 days before the present visit - arthritis of the right knee joint with severe pain. The patient suffers from type 2 diabetes mellitus, angina pectoris of functional class 2, hypercholesterolemia, and therefore constantly takes enalapril 10 mg, acetylsalicylic acid 75 mg, simvastatin 10 mg, amlodipine 5 mg/day. On examination: satisfactory condition, increased nutrition (body mass index - 30 kg/m2). The skin is of normal color and moisture. There is no peripheral edema. The tongue is moist, there are no coatings. Deformation of the knee joints, deformation of the right knee joint due to exudative-proliferative changes, with intra-articular crunching when flexed. Using a visual analogue scale, the patient assessed the pain in the knee joint as 75 mm. Other joints are not visually changed, movements in them are not limited. In the lungs there is vesicular breathing, no wheezing. RR 16/min. Heart sounds are sonorous, the rhythm is correct, heart rate is 68/min, blood pressure is 145/80 mm Hg. Art. The abdomen is soft, moderately painful on palpation in the epigastric region. The liver is not enlarged, the spleen is not palpable. The effleurage symptom is negative on both sides. Stool and urination are normal. In a clinical blood test: ESR – 32 mm/h, in a biochemical blood test: an increase in the level of C-reactive protein to 17 mg/l. Parathyroid hormone is normal. Clinical urine analysis is unremarkable. X-rays of the knee joints show pronounced signs of osteoarthritis with subchondral sclerosis, cystic lucencies in the subchondral parts of the femurs on both sides, narrowing of the joint spaces, osteophytes of the patella, calcifications in the projection of the medial joint space. A study of synovial fluid revealed monoclinic crystals of calcium pyrophosphate with positive birefringence. ECG: sinus rhythm, heart rate – 78/min, horizontal position of the EOS, moderate hypertrophy of the left ventricular myocardium. Taking into account the frequent recurrence of articular syndrome with rapid regression of symptoms, involvement of the wrist joints in the process, the presence of inflammatory changes in blood tests, as well as the detection of chondrocalcinosis on radiography and calcium pyrophosphate crystals in the synovial fluid, pyrophosphate arthropathy was diagnosed: osteoarthritis with calcium pyrophosphate crystals, stage III . FN II. To relieve pain and exudative changes, drugs from the NSAID group were used. In order to prevent recurrence of articular syndrome, the patient was recommended to take colchicine 0.5 g 2 times a day for 12 months and continue taking chondroprotectors. Recommendations are given for weight loss, physical therapy, and the use of orthoses. Thus, the frequent recurrence of acute arthritis in a patient with OA, the course of the articular syndrome with pronounced inflammatory changes, the identification of affected joints during X-ray examination of chronic arthritis, and the involvement of joints in the process that are not subject to load are the reason for carrying out differential diagnostic measures in order to identify PFA. Timely diagnosis and correction of therapy will prevent the progression of cartilage destruction associated with calcification.

In what cases should you seek help?

People who put excessive stress on their joints are at risk for developing arthropathy. Also, pathology occurs more often in those who are prone to allergies, abuse alcohol, have problems with metabolism, or are infected with chlamydia. If you are at risk and have discovered alarming symptoms, go for a consultation with an orthopedist, since it is impossible to identify many joint diseases in the early stages.

Some alarming symptoms include:

  • swelling of tissues, tingling in joints;
  • unreasonable increase in body temperature;
  • weakness and unmotivated fatigue;
  • enlarged lymph nodes;
  • limited movement.

At the initial consultation, the doctor will examine you and prescribe tests. The patient will have to undergo laboratory tests, undergo a series of functional tests for the performance of the liver and kidneys, have an ECG and X-ray in several projections. If the diagnosis is confirmed, complex treatment is prescribed.

Is the joint swollen and painful? See an orthopedist

How is arthropathy treated?

By analogy with the treatment of osteoarthritis, the therapy of arthropathy is complex. It combines physiotherapeutic and medicinal methods, and physical therapy is included at the rehabilitation stage. It is important for the patient to follow simple rules:

  • to refuse from bad habits;
  • balance your diet;
  • monitor body weight;
  • take prescribed medications.

For arthropathy, radon baths, electric shock and climatotherapy are most often prescribed. Among the pharmaceutical drugs that are relevant are antibiotics that eliminate the provoking agent, non-steroidal anti-inflammatory drugs that fight visual manifestations and chondroprotectors. The latter promote tissue regeneration, as they enrich the joint with building material.

In advanced cases, surgery may be necessary

Causes of calcium salt deposition

The deposition of calcium salts can be a primary or secondary process. In the secondary form, the provoking factor is always tissue breakdown as a result of traumatic or inflammatory effects. In the resulting cavities, calcium salts are deposited (calcifications occur) or fibrin fibers (cicatricial deformation begins).

The primary form of pyrophosphate arthropathy refers to idiopathic diseases of the human musculoskeletal system. This means that there is no true cause for the occurrence of such a pathology. It is always caused by hereditary genetic disorders. They can be activated as a result of exposure to unfavorable factors of the external and internal environment.

The main reasons for the prerequisites for the deposition of calcium salts in cartilage tissue are as follows:

  1. high level of calcium in the biochemical composition of the blood;
  2. disruption of metabolic processes of bone tissue renewal;
  3. high level of ergocalciferol in the blood;
  4. discharge of the structure of cartilage tissue due to a deficiency in the diet of certain substances, microelements and vitamins.

The pathogenesis of the development of pyrophosphate arthropathy is quite complex. To effectively prevent this process, it is important to monitor your diet, lead an active lifestyle and fight excess weight. There is a theory that suggests that pyrophosphate arthropathy may be associated with the amount of clean water consumed per day. The less a person drinks pure water, the higher the risk of crystals of calcium salts falling out and settling in different organs and systems.

What are the prognosis and can it be prevented?

If arthropathy is left untreated, the pathology progresses over time. The joint may become infected, and mobility will become increasingly limited, leading to immobility and disability. All this can be avoided if you strictly follow the doctor’s recommendations and do not experiment with self-medication.

Since arthropathy is secondary, in order to prevent it, it is necessary to take preventive measures to prevent the development of other diseases. And if they already exist, then treat them in a timely manner. It never hurts to maintain an adequate level of physical activity, eat right, monitor your body weight and give up bad habits.

To minimize the risks of any joint diseases, be it arthropathy, coxarthrosis or salt deposition due to gout, it is necessary to undergo regular preventive examinations, and not to ignore alarming symptoms. Your health is in your hands!

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