Spasms and pain in fingers (toes) and calves
Introduction
Introduction Hemorrhoids and pain in the fingers and calves are one of the clinical symptoms of Caschin-Beck disease. Kaschin-Beck disease, Kaschin-Beck disease, is a kind of endemic cartilage and joint deformity disease, which is a deformed osteoarthrosis with cartilage necrosis.
Cause
Cause
(1) Causes of the disease
The etiology of Kashin-Beck disease mainly involves the following three types of factors: low selenium in the ecological environment of the ward; organic pollution in drinking water; mycotoxins.
1. The ecological environment of the ward is low in selenium: Originally, the former Soviet scholars proposed that the disease was caused by too much, insufficient or unbalanced one or several elements. In the early days, it was thought to be related to less water, more calcium, more sputum, and more sputum. Later, it was claimed that the disease caused by excessive phosphorus and manganese in the water and soil and main and non-staple foods in the ward. None of these have found the exact basis from the patient or in the experimental study.
Chinese scientists have found that Kaschin-Beck disease is closely related to environmentally low selenium:
1 The distribution of the diseased area in China is generally consistent with the low-selenium soil zone. The total selenium content of most of the diseased areas is below 0.15mg/kg, and the grain selenium content is less than 0.02mg/kg;
2 The selenium content of blood, urine and hair in the ward is lower than that in the non-disease area, and a series of metabolic changes associated with low selenium can be detected in the patient;
3 When the level of selenium in the hair of the ward is rising, the condition is reduced;
4 selenium supplementation can reduce the new incidence of Kashin-Beck disease and promote the repair of metaphyseal lesions.
But there are also some important facts that do not support low selenium is the cause of this disease:
1 Some areas have low selenium and do not have Kaschin-Beck disease, such as Yulin and Luonan in Shaanxi and some Keshan disease areas in Sichuan and Yunnan. In some areas, selenium is not very low, but this disease occurs, such as Qingzhou in Shandong. Zuoquan, Huo County of Shanxi, Ankang of Shaanxi, Banma of Qinghai, etc.;
2 after selenium supplementation can not completely control the new development of the disease;
3 cell culture showed that chondrocyte growth has no special need for selenium;
4 Low selenium animal experiments can not cause cartilage necrosis similar to this disease.
At present, more people tend to think that low selenium is only a conditional factor in the onset of this disease.
2. Organic pollution in drinking water: In many wards in China, folks have long attributed the cause of this disease to poor water quality. Japanese scholar Yan Ze and others studied the relationship between plant organic matter in drinking water and Kashin-Beck disease, and believed that ferulic acid or hydroxycinnamic acid in organic matter may be a causative factor.
In our country from 1979 to 1982, the scientific investigation of Kaschin-Beck disease in Yongshou County and other areas, it was found that the total amount of humic acid and hydroxyhumic acid in water was positively correlated with the prevalence of Kashin-Beck disease, and the selenium content was negative. Correlation; humic acid content in the ward is generally higher than that in non-disease areas. The isolation and identification of organic matter in the drinking water of the ward showed that there was no significant difference in the core part of the humic acid structure between the ward and the non-disease area. Small molecular organics such as phenolphthalein, thiophene and nitrogen-containing benzothiazoles were in the ward. More appeared in the middle. Electron spin resonance (ESR) was used to detect the free radical signal in the drinking water of the ward, and its concentration was significantly higher than that of the control non-disease area. The concentration of free radicals in the drinking water was linearly related to the humic acid content. Some researchers believe that organic matter contamination in drinking water produces exogenous free radicals (semi-anthraquinone free radicals), and increased free radicals entering the body can damage chondrocytes.
So far, the relationship between organic matter pollution in drinking water and the incidence of Kashin-Beck disease has not been supported by sufficient epidemiological and experimental research data.
3. Mycotoxins: As early as 1943 to 1945, the former Soviet scholars proposed that the ward cereals were contaminated with some Fusarium bacteria and formed heat-resistant toxic substances, and residents were sick of eating foods containing the poisons. After the 1960s, Chinese scholar Yang Jianbo and others have done a lot of work in this area. In recent years, the following major advances have been made in the T-2 toxin:
1 ELISA method was used to detect T-2 toxin in the main food flour and corn flour of the diseased patients, and the content was found to be significantly higher than that of non-disease commercial flour and corn flour; the granular foods such as rice, millet and yellow rice collected from all places were collected. No or only trace amount of T-2 toxin detected;
2 Inoculate the non-disease corn with Fusarium graminearum to prepare the bacterial grain, and mix the normal feed with 10% proportion. The chicks were fed with cartilage banded necrosis of the knee joint for 5 weeks. The T-2 toxin was used directly, and the chicks were fed with the feed at 100 g/kg body weight for 5 weeks, and the degenerative changes of the knee cartilage appeared.
Other units in the country have also carried out some work on the relationship between mycotoxins and Kashin-Beck disease. At present, the dominant fungi in the grains of different wards are different, and there is also a lack of consistent pathogenic fungi and their strains. The detection results of mycotoxins in food are not consistent. In addition, due to technical limitations, T-2 toxins and their metabolites have not yet been detected from patients with Kashin-Beck disease.
4. Experimental animal model research: In order to explore the etiology and pathogenesis, many scholars at home and abroad have devoted themselves to the study of experimental animal models of this disease. Chinese researchers generally use cartilage damage as a basic morphological indicator for determining animal models. However, in the past experiments with rats or dogs, most of the see-up of the epiphyseal chondrocyte necrosis, matrix degeneration, and small cell-free areas were observed in the tarsal plate and articular cartilage, and the control group Compared to the lack of qualitative differences, it is difficult to judge its value. In recent years, the experiments have been carried out in the food and water of the gorges in the rhesus monkeys. After 6 months or 18 months of feeding the water or grain in the ward, a series of secondary changes occurred in the deep layers of articular cartilage and epiphyseal cartilage in most monkeys after focal, banded necrosis and necrosis.
The pathological development process and major pathological features of Kashin-Beck disease are basically reproduced. The experimental results indicated that there were pathogenic factors in the water and grain of the ward; the pathogenic effect of such pathogenic factors on the experimental animals did not decrease with the disease condition of the ward.
It has not been proven to date that there is a naturally occurring Kashin-Beck disease in the animal kingdom. In the past, the joints of livestock or dogs in the ward were swollen and cautious, which were far from human Kaschin-Beck disease. Two foreign countries mentioned that they can compare with this disease:
1 Osteoochondrosis of livestock: This disease is similar to Kaschin-Beck disease in the development of articular cartilage and epiphyseal cartilage necrosis and development of secondary osteoarthrosis, but the most typical change is chondrocyte differentiation. Obstruction and accumulation of local hypertrophic chondrocytes. Although Kaschin-Beck disease can be seen with uneven thickness of the tarsal plate, the existing materials have not proved that before the cartilage necrosis, the accumulation of hypertrophic chondrocytes is the basis.
2 Birds of tibial dysplasia (tibial dyschondroplasia): The basic lesion is that the epiphyseal cartilage matrix can not be calcified, and the cartilage internalization bone stops. Although it is sometimes considered to be equivalent to osteochondrosis of livestock, since there is no cartilage necrosis and the articular cartilage is not tired, it has nothing in common with human KBD.
(two) pathogenesis
1. A large number of T-2 toxins (Fusarium oxysporum toxin) were detected directly from wards, patients, and locally marketed grains (corn and wheat). Chicks were fed with normal feed of T-2 toxin at a dose of 100 g/d. The cartilage of the chicks was cartilage necrosis, and cartilage joint disease occurred. The lesion characteristics were similar to those of mammalian cartilage joint disease. The disease mainly occurs in young animals, selective necrosis of articular cartilage and epiphyseal cartilage, separation of osteochondritis, and subsequent deformation of cartilage joints. It has been elucidated that the mechanism of action of T-2 toxin on various tissues and organs of the body is to inhibit the synthesis of proteins and DNA, leading to osteonecrosis of bone cells. Experimental pathological studies have shown that the degeneration of articular cartilage caused by T-2 toxin is in the transition zone of rapid growth of cell growth and hypertrophy, which is essentially the same as the deep layer of cartilage cartilage seen in human large bone lesions. Chondrocyte damage caused by T-2 toxin is mainly caused by damage of cell membrane system, mitochondrial swelling, and endoplasmic reticulum expansion. This is due to the change of membrane permeability, the imbalance of intracellular ions and water, and the edema of cells.
Mitochondrial damage necessarily affects its energy supply function, thus impeding cell metabolism. Chondrocyte membrane damage is the main feature of early ultrastructural changes before chondrocyte necrosis, and further damage will lead to chondrocyte necrosis. According to this theory, the causative agent of Kashin-Beck disease is the T-2 toxin produced by Fusarium, which is contaminated by food in the disease area. The carrier is wheat (flour) and corn in the ward, not rice, and the related factors are diseases. The unique natural, social and living environment of the district.
Whether it is from macroscopic or microscopic chemical environment, the population of Kaschin-Beck disease is in a low selenium ecological environment, that is, the selenium content of ecological substances in the ward, from water, soil, grain to human hair and blood, is significantly lower than Non-ward area. Supplementation of selenium can effectively correct the selenium nutrition level of children in the ward and promote the repair of dry lesions. Selenium and its compounds are antioxidants, selenium-containing glutathione peroxidase, which catalyzes the reductive decomposition of lipid hydroperoxides and hydrogen peroxide, prevents damage to cell membranes, and maintains cell membrane integrity. And stability. The selenium deficiency in the tissue reduces the antioxidant capacity. In addition to causing oxidative damage to the cell membrane system, it can also cause free radical damage of proteins, nucleic acids, etc., resulting in decreased tissue enzyme activity, collagen denaturation, and reduced DNA amount. The reduction of plasma sulfhydryl groups (ie, total plasma sulfhydryl groups, non-protein sulfhydryl groups, and protein-bound sulfhydryl groups) is associated with a deficiency in selenium, suggesting impaired antioxidant defense systems in children. Studies have shown that selenium has an antagonistic effect on T-2 toxins (including other Fusarium toxins), which can reduce lipid peroxidation damage.
Because selenium is a component of glutathione peroxidase, it can participate in many biological processes and protect the body from a range of foreign compounds. The anti-oxidation effect of selenium is mainly manifested in the inhibition of peroxidation, the decomposition of peroxides to eliminate harmful free radicals, and the repair of cell membrane molecules. In addition, T-2 toxin mainly affects the ATP content of hepatocytes, and selenium has a protective effect on the reduction of ATP in the liver caused by T-2 toxin, which can protect liver cell mitochondrial membrane, microsomal membrane and lysosomal membrane from damage. The role still needs to be confirmed by in-depth research. The relationship between low selenium and Kashin-Beck disease is still controversial. The investigation found that there are non-disease points in the low selenium area, and there are disease points in the high selenium area.
On the one hand, it was found that there was a significant dose-effect relationship between the degree of early lesions and selenium levels, and on the other hand, selenium was administered in three different types (ie, moderately active, mildly active, and relatively stationary). In the year, there are 1% of new cases of dry ward disease and 4% of new cases of osteophytes, and the content of selenium is not directly related to X-ray metaphyseal lesions. Judging from the effect of selenium control for many years, the net improvement rate of the selenium group compared with the control group was mostly 10% to 30%. Therefore, it cannot be said that the disease is caused by simple selenium deficiency. This disease is also related to the deficiency of various elements such as manganese, phosphorus and zinc, which needs further research and confirmation.
When switching to deep wells and drinking water, the incidence of Kashin-Beck disease is significantly reduced. Changing water can prevent the occurrence of Kaschin-Beck disease and reduce or relatively stabilize the patient's condition. The activity of alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, etc. in children in the affected area decreased after water change, which was significant compared with that before water change. Therefore, it is believed that Kaschin-Beck disease is related to organic poisoning in water. It has also been suggested that the occurrence of Kashin-Beck disease is not related to drinking water, so further research is needed.
2. Mechanism of cartilage damage: Chinese researchers mainly have the following three kinds of insights:
One opinion is that the biochemical basis of cartilage damage in this disease is a disorder of sulfur metabolism. Chondroitin sulfate (Chs) is an important component of the cartilage matrix. Researchers with this knowledge found that the excretion of Chs in the urine of patients with this disease increased, the degree of sulfation decreased, the molecular weight became smaller, and the proportion of various amino polysaccharides in urine was imbalanced. . They believe that these changes suggest a sulphur utilization barrier. The sulfation of Chs in the body is regulated by the sulfation factor (SF) produced by the liver and kidney organs. They found that the serum SF activity of children with this disease is significantly lower than that of the local healthy control children, and the latter is lower than the non-ward control children. . They believe that sulphur metabolism disorder is the result of reduced SF activity. The pathogenic factor of this disease is caused by a series of cartilage damage by interfering with the biological function of SF.
Another suggestion is that the membrane defect state of cells is the biochemical basis for the pathogenesis of this disease. They found that the phospholipids of the erythrocyte membrane lipid composition decreased, the molecular ratio of cholesterol/phospholipid increased, and the phosphatidylcholine (PC) decreased in phospholipids, and the sphingomyelin (SM) changes little, SM/ The molecular ratio of PC is elevated. These changes mean the aging of biofilms. The above situation is also seen in the cartilage analysis of the autopsy material of this patient. They believe that the combination of low temperature, low selenium and monotonic food (insufficient intake of phospholipids) leads to a weak membrane system and reduced antioxidant capacity.
There is also a view that exogenous free radicals can cause both chondrocyte necrosis and abnormal chondrocyte metabolism. The latter will synthesize and secrete an abnormal matrix rich in type I collagen, and cause abnormal mineralization with rapid speed, small particle size and low crystallinity, thereby causing pathological chemical processes of the disease. The mice were fed with ward and water, and the type I collagen in the cartilage matrix was increased, and the ratio of type I/II was increased.
The above changes in aminoglycans, collagen and cell membrane systems provide useful clues for exploring the mechanism of cartilage damage, but there is still a large distance to explain how the cause selectively acts on specific parts of cartilage and initiates a series of characteristic changes. .
3. Pathology: This disease is mainly caused by invasion of the bone and joint system. Other tissues and systems such as muscle tissue, endocrine gland, digestive system and circulatory system may also be involved. The nature of the lesions generally becomes dominant with malnutrition degeneration. It mainly invades the hyaline cartilage part of the cartilage internalized bone type bone (such as the limb bone). The lesions are symmetrical, the joints are thickened, and the limbs are deformed. The joints that are usually negative and have more activity are the most affected. There are two main pathological changes in cartilage tissue:
(1) Basic pathological changes of cartilage: firstly, the epiphyseal cartilage plate is invaded, and secondly, the articular cartilage is involved, and the osteophyte is bent, the thickness is uneven, the chondrocytes are not aligned, the ossification is disordered, the growth is delayed, and the pause is stopped. The capillaries of the bone marrow invade the deep layer of the cartilage plate, often separating or dividing part of the cartilage band into cartilage islands, which is a characteristic of this disease. Calcification may sometimes occur in the matrix of a portion of the cartilage band to form a transverse trabecular bone. These phenomena can cause bone growth to pause or delay. The cartilage matrix of the epiphyseal cartilage plate is also softened. The chondrocytes can disappear completely, and the nearby chondrocytes gather together.
This disease mainly involves the bones of the cartilage osteogenesis, especially the bones of the limbs, which are characterized by degeneration and necrosis of hyaline cartilage and accompanying absorption and repair changes. Chondrocytes often have coagulative necrosis. After the nucleus is pyknotic, fragmented, and dissolved, the red-stained cell shadow remains. Then the residual image disappears and the matrix is red-stained, which becomes a foci-like, band-shaped cell-free zone. The necrotic area can be further disintegrated and liquefied. The chondrocytes that survive around the necrotic foci often have reactive hyperplasia, forming groups of chondrocytes of varying sizes. In the adjacent bone tissue, pathological calcification can occur in the necrotic site; the blood vessels and connective tissue of the primary bone marrow invade the necrotic foci, appearing to be mechanized and ossified, and finally the cartilage necrosis of the bone tissue to involve the mature chondrocytes (hypertrophic chondrocytes) Mainly, showing a near-bone distribution. When necrosis is enlarged, it also affects other levels of chondrocytes. Necrotic lesions are often multiple, varying in size, in a punctate, flaky or banded manner.
(2) tarsal cartilage lesions: the necrosis of the epiphyseal cartilage mainly occurs in the mast cell layer, and the severe one can penetrate the entire layer of the tarsal plate. After the necrosis occurs in the deep layer of the tarsal plate, the blood vessels from the metaphysis can not be invaded, and the normal cartilage osteogenesis stops. However, the proliferating layer of chondrocytes that survive above the necrotic foci can continue to proliferate and differentiate, resulting in the tarsal plate. A partial thickening. Degenerative calcification often occurs at the proximal edge of the necrotic foci, and bone can be deposited along the metaphyseal end of the necrotic foci, forming an irregular bone or transverse beam, indicating that the normal ossification process is paused. The osteogenesis of other parts of the tarsal plate continues, resulting in uneven thickness of the tarsal plate and uneven ossification lines.
When the necrotic foci runs through the entire tarsal plate, the absorption, mechanization and ossification of the necrosis in both directions of the nucleus and the metaphysis end finally lead to the early closure of the tarsal plate, and the longitudinal growth of the tubular bone is stopped early, resulting in Short finger (toe) or short limb deformity.
Due to the rich blood vessels in the metaphysis, the absorption, mechanization and ossification of the epiphyseal cartilage after necrosis are more rapid, so the X-ray image can be significantly aggravated or improved in a short period of time (months to 1 year).
(3) Articular cartilage lesions: Articular cartilage begins with the same dystrophic lesions, and cartilage destruction gradually occurs. The joint surface is rough and uneven, and cartilage ulcer often occurs, which affects joint activity and induces pain. Part of the cartilage can fall off to form a "articular rat." In severe cases, the edge of the articular cartilage proliferates and is discoided, and often has bones, so the joints become thicker. The synovial membrane also has a villous proliferation. The fluff can be detached as a free body. The synovial membrane around the cartilage is also often hypertrophy, which can constitute cartilage and tibia, and the bone end is enlarged and the edge is irregular. In addition, bone is often loose, trabecular bone destruction, absorption, can form vacuoles and cyst-like structures, and can be accompanied by hyperplastic changes. The bone is obviously thinner and can be loose and spongy. The marrow cavity is dilated, and necrotic foci and vacuoles often appear in the marrow. Muscles, organs, and endocrine glands are accompanied by lesions that are degraded by dystrophic degeneration.
Like the necrotic foci of the epiphyseal cartilage, the lesions of the articular cartilage are also near-bone, that is, the cartilage cells in the deep maturation are first involved, often forming a typical banded necrosis. Because the absorption of necrotic substances in this part is slow and the necrosis exists for a long time, the proliferating chondrocyte mass in the peripheral part of the necrotic foci is often more noticeable. In a large necrotic foci, when the necrotic material disintegrates and liquefies, a fissure or a cystic cavity is formed. Under the mechanical action of gravity and friction, the surface cartilage tissue is easy to peel off (separate osteochondritis), forming a joint free body (articular rat), while the local articular surface leaves ulcers of different sizes. In the severe lesions, the articular cartilage can disappear completely in the whole layer, causing a large piece of bone to be exposed. At the edge of the articular surface, there is often a cartilage hyperplasia reaction with cartilage necrosis, resulting in thickening of the edge of the joint and ossification to form a bony marginal growth. As a result, the patient's bone end is enlarged, joint deformation and activity are limited.
Late joint synovial connective tissue hyperplasia, calcification and ossification, and more serious joints. The process of degeneration, necrosis, disintegration and repair of hyperplasia of articular cartilage is repeated, so that advanced cases show changes in deformed joint disease. But bone joint stiffness has never been seen. Monoclonal immunohistochemistry showed that type II collagen expression in the surface of articular cartilage was decreased, type I collagen was increased, and hyperplastic chondrocyte group was expressed in type I, II, III and VI collagen.
The absorption mechanism of articular cartilage necrosis can only start from the normal gap of the bone plate shell, the repair reaction is relatively weak, and the lesion development is slow. Therefore, the lesions on the articular surface (bone end) under the X-ray are often developed later than the lesions at the metaphysis, and the repair process develops slowly, with little change over a long period of time.
Examine
an examination
Related inspection
Joint examination of limbs and joint movement
It can occur all year round, but it has the most incidence in spring, and the symptoms are heavier, followed by autumn and winter. The incidence is not related to gender, and it occurs mostly in children and adolescents whose bones are not closed, but adults can also develop the disease. The youngest age is 3 to 8 months, and the most is 6 to 18 years old.
The onset and development of this disease are slow, and only about 3% of patients with acute or subacute procedures. Light patients or lesions often have no obvious symptoms in the early stage, sometimes they feel tired and the activities of the limbs are not flexible, especially in the morning, often need to be active to exercise as usual. Deafness and dullness appear on the toes and calves, which is a precursor to the disease. During the examination, the fingers, wrists, elbows, knees, ankle joints may have tenderness and irregular hair-like rubbing sounds, and the distal end of the fingers are gently curved to the palm side, especially in the index finger.
Symptoms and signs: The disease often starts unconsciously. The patient may be consciously fatigued at the beginning, limb weakness, skin sensation (such as ants walking, numbness, etc.), muscle soreness, pain, etc. These symptoms are often not constant and are not obvious. Its main and typical clinical manifestations are closely related to osteochondral damage and joint function.
1. Early manifestations, early symptoms and signs are lacking in characteristics before the joints become significantly larger and short finger (toe) deformity occurs. According to a large number of investigations and follow-up observations, the following performances deserve attention.
(1) joint pain: often multiple, symmetrical, often appear in the large amount of knuckles and large weight of the knee, ankle joint. The patient feels pain, soreness or "stomach pain."
(2) refers to the bending of the distal section: that is, the distal knuckles of the 2nd, 3rd, and 4th fingers are bent toward the palm of the hand, often greater than 15°. This is the earliest sign of the disease, and it has certain significance in the early diagnosis of the diseased area. However, a small number of children in non-patient areas may also have a lesser degree (less than 15 °) bending of the fingertips; adolescents with no bending in the ward may also develop this disease. The bending of the fingertips often coincides with the deviation of the fingers. The skew is more common with the index finger, followed by the middle finger and the ring finger.
(3) Arched fingers: the fingers are bowed to the volar side.
(4) Suspected knuckles thickening: generally occurs in the middle section.
2. After the development of the disease, after the disease progresses, in addition to the early manifestations of joint pain and other factors continue to increase, the main symptoms and signs appear:
(1) joint thickening: the most common is the multiple, symmetrical interphalangeal joint thickening, often first appeared in the first interphalangeal joint of the second, third, and fourth fingers. Generally, the thickening of the right finger joint is more obvious than that of the left hand, and the joint of the mechanically injured joint or the thimble wearing the thimble is thicker and heavier.
(2) joint movement disorder: the performance of the morning feels the fist is stiff, the fist is not tight, the fingertips can not touch the palm horizontal stripes, the fist can not quickly stretch. The elbow joint is limited in flexion and extension and is flexed and contracted. When the shoulder joint is involved, the patient can't touch the opposite side of the ear with his hands, and even wash his face without washing his forehead. Knee inversion or eversion, O-leg or X-leg. Due to the flexion and deformation of the knee and hip joints, the patient has difficulty in squatting, the lumbar spine is compensatory lordosis, and the hips are kyphosis. When walking, the stride is small, and there is a swing or abduction, which is a "duck gait." Ankle joint flexion and extensional obstruction. The patient's pain and movement disorders often manifest as aggravation after a break or morning, and a slight reduction in activity. After many patients in the morning, they need to step on the bed to "slip" and then take a step.
(3) Joint friction sound: ranging from small cymbal sounds to rough friction sounds. Due to factors such as uneven joint surface, hyperplasia and shedding of synovial villi in joint capsule.
(4) Free joints of the joints: they can be derived from exfoliated articular cartilage fragments, or from the proliferating synovial villi, which are mostly small rice granules. The movement of the free body in the joint cavity may be stuck, causing a joint lock and causing severe pain; the loose body is relieved as the joint activity loosens.
(5) Skeletal muscle atrophy: The muscles of the limbs of the disease, especially the flexor muscles of the lower leg and forearm, are often atrophied, sometimes even before the joint changes significantly. In the later stage of the disease, due to the limitation of pain and joint activities, more disabling factors were involved, resulting in more serious atrophy.
(6) Short finger (toe) malformation: knuckle development is shorter than ordinary people, hand small square. Or because of the different degree of developmental disorders of each finger (toe), the length of their fingers loses normal proportional relationship with each other.
(7) short limb deformity, short stature: the degree of developmental instability of each tubular bone is often uneven. In some patients, the early growth of the tibia is stopped, the ulna is relatively long, the ulnar styloid is displaced to the lower dorsal side, and the hand is tilted to the temporal side, causing Madelung's deformity. The age of onset is small and the lesions may form a Kaschin-Beck diseased dwarf. The limbs of the patient are not proportional to the head and trunk. Generally, the upper arm is significantly shorter than the forearm, the calf is significantly shorter than the thigh, and the trunk is close to normal.
3. The staged division of the disease is based on the severity of the disease, the disease can be divided into early, I degree, II degree, III degree. According to a retrospective survey of patients with Kashin-Beck disease for more than 15 years, it is found that some patients may become normal, and some may evolve to I degree, II degree or even III degree, but none of the patients after the age of 7 become III. degree. Early clinical signs are reversible, and patients above 1 degree can remain unchanged or continue to increase. Therefore, the treatment of early patients is extremely important.
The main demarcation point between early and working degree is whether there are multiple knuckles thickening; the main dividing point of I degree and II degree is whether there is short finger deformity; the main dividing point of II degree and III degree is whether there is short limb deformity ,short and small.
The condition progressed further, the patient became fatigued, joint pain in the limbs, and pain in the calf and forearm after work or walking. The joint movement of the extremities is more inflexible. It can be seen that the finger joints or the ankle joints are slightly thickened, which is common in the first interphalangeal joints of the hands 2, 3, and 4 fingers. Fingers, wrists, elbows, knees, and ankles have difficulty in stretching and flexing. The elbows cannot be fully extended, mostly 170°. Significant and constant burst-like rubbing sounds appear in the joints of the extremities. The hand, forearm and calf muscles are slightly atrophied. At this time, the height of the body is still normal, and it can afford general physical labor. The patient may have a flat foot. This is the first degree of the disease.
When the disease progresses to the second degree, the patient's mental and physical strength is worse, and walking is inconvenient, especially when going downhill, it is very difficult and can only be used for light labor. Finger, wrist, elbow, knee, ankle joint activities are limited, accompanied by severe pain, knee and ankle pain is more common. In this period, the patient may have a certain degree of short-finger deformity, and the fingers may be difficult to flex, and the fingers may not touch the palm when making a fist. Elbow flexion of the elbow joint can form a clear angle, the forearm pronation is a significant obstacle, and the muscles of the limbs are obviously atrophied. Frequent pain in the joint is often caused by the formation of joint small bodies in the joint. Flat feet are heavier.
The disease progresses to the third degree, the patient's activity is difficult, the typical duck step appears when walking, there is a very obvious short-finger deformity, and the short stature can become a dwarf with a height of only about 1 meter. The hands can't make a fist, the elbow flexion is very obvious, and can't stretch to 150°. The muscles of the extremities are extremely atrophied, and there is a significant lumbar spine compensatory anterior curvature. Labor capacity is extremely diminished, and even labor is lost. But the mental development is normal.
If the patient is from a prevalent area of the disease, it is obviously chronic, symmetrical joint deformation, short stature, diagnosis is not difficult. In the epidemic area, if the child's joint pain, lack of activity, convulsions or frictional sounds are found, the disease should be thought of first, and X-ray examination of the bones and joints, especially the X-ray of the fingers, can be further performed to determine the diagnosis early. Laboratory tests have only an auxiliary diagnostic effect on this disease.
Based on years of research and practical experience, China developed the diagnostic criteria for this disease in 1995.
1. Principle of diagnosis
According to the contact history, symptoms and signs of the ward and the X-ray film of the hand bone, the multiple symmetry depression, hardening, destruction and deformation of the finger, wrist joint surface, metaphyseal temporary calcification zone and nucleus can be diagnosed. The disease. X-ray refers to multiple symmetry changes at the distal end of the bone.
2. Diagnostic and grading standards
(1) Severity diagnosis:
1 early:
Children who have not completely healed with dryness have the following four items: A., C. or B., C. or B., D. or only C., diagnosed as early.
A. The hand, wrist or ankle, knee joint activity is mildly restricted, and pain.
B. Multiple symmetry of the end of the finger flexion.
C. The hand and wrist X-ray films have various degrees of depression, hardening, destruction and deformation of the temporary calcification zone or the sacral nucleus of the osteoarticular surface or the metaphysis.
D. The serum enzyme activity is increased, and the content of creatinine, hydroxyproline, and mucopolysaccharide is increased.
2I degree: On the basis of early changes, there are multiple symmetry of the fingers or other limbs, thickening of the joints, limited flexion and extension activities, pain, mild atrophy of the muscles, and different degrees of X-ray changes in the metaphysis or bone ends.
3II degree: On the basis of I degree, symptoms and signs are aggravated, short finger (toe) deformity occurs, and X-ray changes appear early and early closure of the sacral line.
4III degree: On the basis of II degree, symptoms, signs, and X-ray changes are aggravated, and short limbs and short deformities appear.
(2) Active and inactive diagnosis: Children with Kashin-Beck disease who have not fully healed, have any of the following diagnostic activities, otherwise they are inactive.
1 hand, wrist X-ray film showed a temporary calcification of the metaphysis, widening, hardening, deep depression.
2 serum enzyme activity increased, urine creatinine, hydroxyproline, mucopolysaccharide content increased.
Diagnosis
Differential diagnosis
Stinging or numbness in the fingers or arms: Patients with cervical spinal stenosis complained that there are fingers (mostly at the fingertips) or pain and numbness in the arm when the disease is first developed, especially tingling.
The index finger and middle finger are stiff and painful: it is one of the symptoms of cervical hyperplasia. The patient's symptoms are mainly caused by a sudden or severe pain, severe pain or numbness in the neck occipital or neck and shoulders, and along the direction of the affected nerve roots, to the place where the nerve root is distributed; On the side of the ground, the upper limbs, the back of the hand, the fingers, etc. can also have radioactive pain and numbness. The pain is burnt or knife cut, accompanied by acupuncture or over-the-counter string; when the neck is active or coughing, hitting When sneezing or exerting force, the pain and stringy feeling can be aggravated. The patient does not dare to laugh when joking. The site of radiation pain is related to the segment of cervical lesion. In addition, there may be appearances such as upper limbs sinking, soreness, weak grip, falling objects, and even the pen can not hold, and it is difficult to hold other things. In the evening, the neck, shoulders and upper limbs may be more painful, unable to fall asleep, and it is prone to numbness and numbness after suffering from limb compression.
Finger pain or tenderness: It is a clinical manifestation of peripheral neuropathy syndrome or enteric dermatitis. Toe pain, abnormal limbs, poor coordination of legs and feet, fingertip pain or tenderness, hyperalgesia/limited limb pain, leg pain, hyperactive legs, feeling dull, paresthesia, numb fingers.
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