Hypertrophic osteoarthropathy was first reported by Maric in 1889. There are two types of hypertrophic osteoarthropathy: primary and secondary. Primary hypertrophic osteoarthropathy has a family history, the cause is unknown, and it is genetically related, and is often combined with lesions of the lungs or pleura, heart, liver, blood, mediastinal barrier, etc. It is also called “pulmonary hypertrophic osteoarthropathy” and is a common type. Pulmonary hypertrophic osteoarthropathy (PHO) is the most common type of secondary disease, often preceding pulmonary symptoms by months or years, and is easily misdiagnosed as a simple osteoarthropathy, ignoring the diagnosis of lung cancer. Pulmonary hypertrophic osteoarthropathy is not uncommon and is often combined with lung cancer, bronchiectasis, and abscess chest.
I. Pathogenesis
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. Body fluid theory
Under normal conditions the lungs can remove or inactivate a factor from the patient’s organs or tissues, but in the case of a diseased lung health search, the lungs cannot remove or inactivate this factor, allowing it to enter the circulation and cause the characteristic bone and soft tissue hyperplasia, but the presence of this factor has not been confirmed to date. 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 by reflex mechanism. When the vagus nerve is cut, pain and signs can be relieved, and blood flow to the affected area is also reduced.
3.The 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. And found that 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 new bone formation under the periosteum.
It has also been found that the increased blood flow at the lesion site in secondary hypertrophic osteoarthropathy is thought to be due to increased blood supply and increased concentration of deoxygenated hemoglobin, resulting in relative tissue hypoxia and causing periosteal hyperplasia and ossification in hypertrophic osteoarthropathy, whereas the slow blood flow and local hypoxia at the lesion site in primary hypertrophic osteoarthropathy is significantly different from the changes in secondary hypertrophic osteoarthropathy, but the lesions are the same and the mechanism is the same. It is unclear how the mechanism of the same lesion.
It is thought that the two should be classified as separate diseases.
Pathology The skin changes are epidermal hypertrophy, mild papilloma-like changes, dermal collagen fiber hyperplasia hair follicle and sebaceous gland hyperplasia, hypertrophy, small amount of surrounding inflammatory cell infiltration fibroblast hyperplasia, subcutaneous soft tissue edema, increased collagen tissue, extraperiosteal small artery wall thickening with predominantly mid-layer thickening, small vessel bruising and lymphocyte infiltration in surrounding tissues Health search bone changes include periosteal edema, inflammatory cell infiltration, followed by Periosteal thickening, osteoid matrix deposition, mineralization, new bone formation, and thickening of the bone cortex because it is connected to the periosteal new bone.
Synovial changes were nonspecific inflammatory, with congestion, edema, mild lining cell hyperplasia, inflammatory cell infiltration, occasional small vessel thickening with fibrosis, and joint opacity formation. Electron microscopy showed electron-dense material deposited under the intima of synovial tissue. The application of immunohistochemical techniques did not reveal any basis for immune-mediated vascular damage.
Clinical manifestations
Pestle finger is one of the most prominent clinical manifestations, and the nail has a “wobbly feeling” on palpation. In advanced stages, the skin thickens, the nails become curved and cyanotic, producing a drumstick-like deformity. Some patients have non-sunken edema in the lower extremities, resembling rubbery leg changes. In general, skin changes are more prominent and more frequent in primary hypertrophic osteoarthropathy. 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, swelling, joint effusion, and limitation of motion, or painless joint effusion. In addition to these signs, patients with hypertrophic osteoarthropathy may also have weakness, feminization of the gynecomastia, feminine distribution of pubic hair, myelofibrosis, gastrointestinal proliferative lesions and chromosomal abnormalities.
Third, 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.
IV. Prevention
1. Eliminate and reduce or avoid the onset 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 and early diagnosis and treatment, establish confidence in overcoming the disease, and adhere to treatment.