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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient reported here presented with first symptoms at the age of 10 showing an abnormal gait, calf hypertrophy and winged scapulae. She was diagnosed with eosinophilic myositis after muscle biopsy. A second muscle biopsy at the age of 20 and subsequent genetic testing, however, revealed the underlying condition of a primary gamma-sarcoglycanopathy, or LGMD2C. To our knowledge, this is the first LGMD2C patient reported who initially presented with eosinophilic myositis. Eosinophilia has been reported previously in patients with Calpainopathy and Becker Muscular Dystrophy and might be an early, but transient feature of a wider range of muscular dystrophies.
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PMID:Eosinophilic myositis as presenting symptom in gamma-sarcoglycanopathy. 1916 90

A 68-year-old woman with a 4 year history of bronchial asthma developed marked myalgia in the extremities following exercise to which she was unaccustomed. Examination on admission, 11 days after onset, revealed myalgia, muscular weakness and cutaneous hemorrhagic bullae. Blood tests revealed eosinophilia (9160/mm(3)) and elevation of creatinine kinase and C-reactive protein. Muscle biopsy in the quadriceps femoris showed small vessel vasculitis and eosinophilic infiltration. Skin biopsy revealed leukocytoclastic vasculitis with neutrophilic and eosinophilic infiltration and fibrinoid necrosis. We diagnosed her as having Churg-Strauss syndrome (CSS). Corticosteroid treatment relieved her symptoms and resulted in normalization of the laboratory test results. Myositis is rare as an initial manifestation of CSS. The previous studies on immunological changes after eccentric exercise suggest that unaccustomed exercise could induce an increase in the serum level of interleukin-6 and trigger the onset of CSS.
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PMID:Churg-Strauss syndrome presenting as myositis following unaccustomed exercise. 1949 52

THE RESULTS OF THIS INVESTIGATION MAY BE SUMMARIZED AS FOLLOWS: 1. The inhalation of formaldehyde gas in even small quantities is followed by bronchitis and pneumonia. Pneumonia is due to the inhalation of the gas and not to secondary infection. 2. Formalin belongs to that rare group of poisons which are capable of producing death suddenly when swallowed. 3. The introduction of formalin into the stomach is followed by the production of a gastritis which varies greatly in character. The duodenum and upper jejunum may also be involved in the inflammatory process. 4. Intraperitoneal injections of formalin cause peritonitis of a fibrino-haemorrhagic character. A definite reaction is obtained when very dilute formalin (1-1000) is employed. In the peritoneal cavity formalin exercises a destructive action upon all organs (pancreas, liver, peritoneal fat, Fallopian tubes, etc.) with which it comes in contact and causes inflammation in these organs. 5. The lethal dose of formalin when injected intraperitoneally into guinea pigs is approximately 2 cc. of 1-1000 formalin for each 100 grm. of body weight. 6. The injection of formalin into the lungs is followed by pneumonia and bronchitis. 7. The inflammation which follows subcutaneous injections of formalin is characterized by intense exudation. 8. The injection of formalin into the muscles produces myositis. 9. The injection of formalin into the anterior chamber of the eye causes the accumulation of an exudate containing leucocytes and fibrin. When formalin is dropped into the conjunctival sac iritis follows and may be severe enough to destroy the eye. 10. Formalin in whatever way introduced into the body is absorbed, and is then capable of producing lesions in the parenchymatous organs. 11. Changes in the liver after absorption of formalin consist of mild or severe grade of cloudy swelling accompanied by vacuolation of the protoplasm, changes in the nuclei and leucocytic infiltration. Focal necrosis may result. Similar changes follow the inhalation of formaldehyde. 12. The injection of formalin or the inhalation of the vapors of formaldehyde produces cloudy swelling of the parenchyma of the kidney. Focal necrosis may result. 13. Pneumonia and bronchitis are found in all animals after the injection of formalin. 14. The leucocytic infiltration which follows the introduction of formalin into an organ has these general characteristics: The eosinophiles are the first leucocytes to appear; these are followed by the other polynuclear leucocytes; last appear the large and small mononuclear leucocytes. Similar phenomena occur in the trachea, bronchi and lungs of animals subjected to formaldehyde inhalations. 15. Formalin is, directly or indirectly, chemiotactic for leucocytes. The tissues which are not infiltrated with leucocytes after the injection of formalin are those which have been so injured by the chemical that an inflammatory reaction is impossible. 16. Animals subjected to chronic poisoning with formalin administered by intraperitoneal injection develop fibrinous peritonitis, associated with marked eosinophilia. The changes in the kidneys and liver consist of cloudy swelling, fatty degeneration, focal necrosis and leucocytic infiltration.
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PMID:THE TOXIC EFFECTS OF FORMALDEHYDE AND FORMALIN. 1986 82

We report a novel case of eosinophilic orbital myositis associated with Churg-Strauss syndrome. A 56-year-old man with a 20-year history of chronic sinusitis and seasonal allergic rhinitis was admitted because of fever, swelling of cheeks and extremities, diplopia, and eosinophilia. With findings from gadolinium-enhanced FST1WI of the orbits and a muscle biopsy of the skeletal muscle, the diagnosis was made. He was treated with oral corticosteroid, and his symptoms rapidly improved.
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PMID:A case of eosinophilic orbital myositis associated with CSS. 1993 60

The granules of eosinophiles are cytotoxic to Trypanosoma cruzi trypomastigote and amastigote forms and to several cell types of the host, revealing their role in either parasite elimination or the production of tissue lesions. In this study, we evaluated the biological characteristics of T. cruzi infection that are responsible for the increase in tissue eosinophile levels in mice previously immunized with a bat isolated T. cruzi-like strain that does not infect mice. Nonisogeneic mice were divided into 24 groups that received from zero to three inoculations of T. cruzi-like RM1 strain, with or without adjuvant, followed by challenge with T. cruzi VIC or JG strains. Uni- and multivariate comparisons were performed comparing the tissue eosinophile levels with the parasitemia peak, severity of myositis in skeletal muscle, phase of infection, and the immunization strategies induced by the T. cruzi-like strain (adjuvant, number of reinoculations, and parasites). Although the severity of inflammation was higher in the acute phase, the score of tissue eosinophiles was similar in the acute and chronic phases of infection. In addition, there was a positive correlation among eosinophile levels and parasitemia peak. In the chronic phase, a greater eosinophile count was accompanied by an augmentation of myositis. Regardless of the phase of infection, we observed a positive correlation between the intensity of eosinophile infiltration and the number of sensitizations with T. cruzi-like strain. The multivariate analysis showed that the peak of parasitemia, number of inoculations with the T. cruzi-like strain, and severity of myositis were associated with greater tissue eosinophilia, in comparison with adjuvant, T. cruzi strains used in the challenge or tissue parasitism. Therefore, tissue eosinophile levels proved to be an important parameter in the pathogenesis of experimental Chagas disease in the acute and chronic phases of infection and might be related to reinfections, parasite multiplication ability, and severity of inflammatory process.
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PMID:Immunization of mice with a Trypanosoma cruzi-like strain isolated from a bat: predictive factors for involvement of eosinophiles in tissue damage. 2045 82

Eosinophilic fasciitis is a rare disease, but it must be considered in patients with adult myalgia. Here, we report the case of 32-year-old man who presented with a 4-month history of bilateral myalgia of the lower limbs, which subsequently spread to the upper limbs. There was no specific medical history, no trauma, and no intense activity. Physical examination revealed induration of the skin with irreducible flexion of the fingers as observed in scleroderma. Laboratory examination showed peripheral eosinophilia associated with moderate elevation of both the erythrocyte sedimentation rate and C-reactive protein. No infectious, neoplastic, hemopathic, or immunological abnormality was detected. Magnetic resonance imaging (MRI) showed thickening of the muscular fascias of the thigh in high signal intensity on T2-weighted images, slightly enhanced after contrast agent injection on T1 images, without myositis. MRI-guided muscle biopsy demonstrated fascia infiltration characterized by mononuclear inflammatory cells and polynuclear eosinophils. A diagnosis of eosinophilic fasciitis was confirmed and the patient received prednisolone. One month later, he reported improvements in general health, pain, motion, joint mobility, and skin induration associated with normalization of both hypereosinophilia and biologic inflammation. After 12 months, clinical MRI and laboratory parameters were normal and the patient was considered to be in clinical remission.
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PMID:From diagnosis to remission: place of MRI in eosinophilic fasciitis. 2122 85

Infectious myositis is defined as an infection of a skeletal muscle. Infectious myositis is most commonly caused by bacteria; however, a variety of viral, parasitic, and fungal agents may also cause myositis. The pathogenesis of nonbacterial infectious myositis is via direct or hematogenous infection of the musculature or immune mechanisms. Symptoms typically include muscular pain, tenderness, swelling, and/or weakness. The diagnosis of the specific microbe is often suggested by the presence of concordant clinical signs and symptoms, a detailed medical and travel history, and laboratory data. For example, immunocompromised hosts have a heightened risk of fungal myositis, whereas the presence of a travel history to an endemic location and/or eosinophilia may suggest a parasitic cause. Definitive diagnosis requires detecting the organism by specific laboratory testing including serologies, histopathology, and/or cultures. Treatment entails antimicrobial agents against the pathogen, with consideration for surgical drainage for focal purulent collections within the musculature.
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PMID:Nonbacterial myositis. 2130 20

Trichinellosis is a zoonosis acquired by the ingestion of insufficiently cooked pork meat containing the encapsulated larvae of Trichinella spiralis. Trichinellosis is presented with myalgia which affects various muscle groups; its intensity is usually related to the severity of the disease and may cause restriction of joint movement. However, joint pain in the course of trichinellosis could not be explained entirely by myositis. This study investigated the other possible causes of restricted movements of joints in animal model. We found that the histopathological changes in the joints of T. spiralis infected rats were in the form of inflammatory cellular infiltrates and ulceration in the synovial membrane with degeneration and ulceration of the articular cartilage. Immunohistochemical examination of the joints revealed the presence of T. spiralis local antigen or immune complex deposited in the synovial membrane. Leukocytosis and eosinophilia were observed throughout the experimental period but eosinophil level declined slowly but still elevated. In conclusion, the restricted movements during the course of trichinellosis seem to be not only due to direct invasion of muscles by the encapsulated T. spiralis larvae but also due to immune complex deposition in the joints.
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PMID:Pathogenesis of restricted movements in trichinellosis: an experimental study. 2162 63

Human trichinellosis is an important food-borne zoonosis caused by a nematode worm, Trichinella. The symptoms of the disease vary widely depending on the infection load, stage of infection and host immunity and include nausea, vomiting, abdominal pain, fever, facial edema and muscle pain. The disease is usually characterized by moderate to high eosinophilia. We hereby discuss an atypical case of trichinellosis, which presented with myositis of the thigh muscles but had no eosinophilia and no facial or periorbital edema and was associated with osteomyelitis of the femur. The diagnosis was made by the demonstration of anti-trichinella antibodies and later confirmed by the presence of larvae of Trichinella in the digested muscle biopsy. Physicians must be aware of trichinosis and should include it in their differential diagnosis when examining patients with fever and myositis with or without eosinophilia.
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PMID:Atypical trichinellosis without eosinophilia associated with osteomyelitis. 2183 32

Infectious myositis may be caused by a wide variety of bacterial, fungal, viral, and parasitic agents. Parasitic myositis is most commonly a result of trichinosis, cystericercosis, or toxoplasmosis, but other parasites may be involved. A parasitic cause of myositis is suggested by history of residence or travel to endemic area and presence of eosinophilia. The diagnosis of parasitic myositis is suggested by the clinical picture and radiologic imaging, and the etiologic agent is confirmed by parasitologic, serologic, and molecular methods, together with histopathologic examination of tissue biopsies. Therapy is based on the clinical presentation and the underlying pathogen. Drug resistance should be put into consideration in different geographic areas, and it can be avoided through the proper use of anti-parasitic drugs.
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PMID:Parasitic infections and myositis. 2188 48


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