What is pulmonary osteoarthropathy?

  Hypertrophic osteoarthropathy was first reported by Maric in 1889. There are primary and secondary forms. Primary hypertrophic osteoarthropathy has a family history, the cause is unknown, and it is genetically related. Pulmonary hypertrophic osteoarthropathy (PHO) is the most common secondary type, often preceding pulmonary symptoms by several months or years, and is easily misdiagnosed as a simple osteoarthropathy, ignoring the diagnosis of lung cancer. Pulmonary hypertrophic osteoarthropathy is not rare, and is often combined with lung cancer, bronchiectasis, and abscess chest.  The pathogenesis of hypertrophic osteoarthropathy is not well understood, but it is well established that hypertrophic osteoarthropathy is a specific response to certain disease states. There are several hypotheses: (1) humoral theory: under normal conditions the lung can remove or inactivate a factor from the patient’s organs or tissues, but in the case of lung lesions health search, the lung can not remove or inactivate this factor, so that it enters the circulation, causing characteristic bone and soft tissue hyperplasia, but so far the existence of this factor has not been confirmed. The recent discovery of multiple tumor-derived growth-promoting peptide factors provides a point of support for the development of this doctrine.  (2) Neurological theory: It is believed that the diseased organ transmits an impulse through the vagus nerve, which causes vasodilatation and pestle change at the fingertip via a reflex mechanism, and when the vagus nerve is cut, pain and signs can be relieved, along with a decrease in blood flow to the affected area.  (3) Receptor theory: In recent years, it has been found that the glucocorticoid receptor and epidermal growth factor receptor in patients with hypertrophic osteoarthropathy increase the level of epidermal growth factor in urine. It was also found that the changes in glucocorticoid receptors and epidermal growth factor receptors are related to the characteristic skin changes of the disease, while the increase in urinary epidermal growth factor content may be related to systemic changes such as subperiosteal new bone formation.  The most prominent clinical manifestation is the pestle finger, which has a “wobbly feeling” when the nail is palpated. In the late stage, the skin thickens, the nails become curved, cyanotic, and produce a drumstick-like deformity. Some patients have non-sunken edema in the lower extremities, resembling rubbery leg changes. In general, skin changes in primary hypertrophic osteoarthropathy are more prominent and more frequently present. Secondary hypertrophic osteoarthropathy has less frequent skin changes and milder signs and symptoms. About half of the patients have painful swollen joints and joint effusion. The knee and ankle joints are most commonly involved, and the elbow, wrist, metacarpophalangeal and metatarsophalangeal joints are usually asymmetrically painful, mainly at night, with mild joint pain or even severe pain. Signs include localized redness, warmth, tenderness and swelling, joint effusion and limitation of motion, or painless joint effusion. In the areas without a lot of muscle coverage, due to the formation of new bone in the long bone periosteum, can lead to increasing thickening of the forearm or calf, and the wrist and ankle joints are also correspondingly thick. In addition to the above-mentioned manifestations, patients with hypertrophic osteoarthropathy may also have weakness, gynecomastia feminization pubic hair female-like distribution bone marrow fibrosis gastrointestinal proliferative lesions and chromosomal abnormalities.  3, treatment For hypertrophic osteoarthropathy there is no exact health search therapy. For pain symptoms, non-steroidal anti-inflammatory drugs or analgesics can be applied. For excessive sweating can be treated with beta-blockers or sympathectomy. When facial skin growths affect the appearance and function, plastic surgery is feasible. All treatments cannot change the course of the disease. For secondary hypertrophic osteoarthropathy, aggressive treatment of the primary disease is required, such as removal of lung tumors or correction of cardiovascular malformations can lead to remission of hypertrophic osteoarthropathy. If the pestle finger has been present for more than a few months, the connective tissue changes may not be restored.  4, prevention (1) eliminate and reduce or avoid the onset of factors, improve the living environment space, develop good living habits, prevent infection, pay attention to dietary hygiene reasonable dietary allocation. Avoid cold and humidity.  (2) Pay attention to exercise, increase the body’s ability to resist disease, do not overwork, overexertion, quit smoking and alcohol. Maintain a balanced psychology and overcome anxiety and tension.  (3) Early detection, early diagnosis and early treatment, establish confidence in overcoming the disease and adhere to treatment.