IL-17, neutrophil activation and muscle damage following endurance exercise. (41/86)

The T-cell subset Th17 is induced partly by interleukin (IL)-6 and activated by IL-23, and produces a proinflammatory cytokine IL-17. Since IL-6 increases dramatically following long-lasting endurance exercise, this response may also stimulate the induction of IL-17 and IL-23 after exercise. The aim of this study was to clarify the dynamics of IL-17 in association with endurance exercise-induced muscle damage and inflammatory responses. Fourteen male triathletes participated in a duathlon race consisting of 5 km of running, 40 km of cycling and 5 km of running. Venous blood and urine samples were collected before, immediately after 1.5 h and 3 h after the race. Plasma and urine were analyzed using enzyme-linked immunosorbent assays (ELISA). Haematological and biochemical variables such as neutrophil activation marker (myeloperoxidase: MPO), muscle damage marker (myoglobin: Mb) and soluble receptor activator of nuclear factor (NF)-KB ligand (sRANKL) were also determined to estimate the biological and pathological significance. Plasma concentrations oflL-6 (+26.0x), MPO (+3.2x) and Mb (+4.9x) increased significantly immediately after the race and IL-17 and IL-23 tended to increase. Furthermore, plasma concentrations of IL-12p40 and sRANKL increased significantly after the race. The measured parameters related to Thl 7 cytokines in the urinary output were closely correlated with each other and muscle damage marker. These findings suggest that IL-17 induced by IL-6 and activated by IL-23 or other IL-17 producing-cells and IL-23 might promote neutrophil activation and muscle damage following prolonged endurance exercise.  (+info)

Severe falciparum malaria with dengue coinfection complicated by rhabdomyolysis and acute kidney injury: an unusual case with myoglobinemia, myoglobinuria but normal serum creatine kinase. (42/86)

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Myoglobinuria: the importance of reaching a firm diagnosis--a patient with defective fatty acid oxidation. (43/86)

A 52 year old man presented with myoglobinuria-induced acute renal failure requiring dialysis. Despite renal biopsy, the cause of the myoglobinuria was not established until he re-presented a year later with a milder episode. At this stage investigations, including a muscle biopsy, demonstrated a defect in fatty acid oxidation amenable to dietary and lifestyle advice. This report emphasizes the importance of reaching a definitive diagnosis in myoglobinuria.  (+info)

Bacillus cereus septicemia associated with rhabdomyolysis and myoglobinuric renal failure. (44/86)

A patient with acute myeloblastic leukemia (AML) developed septicemia due to Bacillus cereus with subsequent rhabdomyolysis and myoglobinuric renal failure. He died despite intensive care. Postmortem examination revealed diffuse muscle necrosis with infiltration of Gram-positive bacilli and widespread bacterial microthrombi in various organs. Septicemia associated with rhabdomyolysis has been described in 12 cases. This case represents the first reported case of B. cereus septicemia associated rhabdomyolysis. Renal failure and shock were considered to be the most important prognostic factors, and either direct infiltration or toxin of the bacteria was suggested to be the mechanism of rhabdomyolysis in sepsis. B. cereus can be one of the lethal organisms in immunocompromised patient such as the present case. Rhabdomyolysis should be considered when a patient with septicemia complains of muscle pain. Prompt hydration and correction of acidosis are important to prevent renal failure and shock.  (+info)

Rhabdomyolysis and concomitant neurological lesions after intravenous heroin abuse. (45/86)

Seven cases of rhabdomyolysis in heroin addicts are presented. All patients showed concomitant neurological symptoms suggesting mononeuropathy, incomplete plexus lesions or myelopathy. In most cases rhabdomyolysis occurred without preceding trauma to the muscles (for example tissue compression or coma). Five patients had a history of recently resumed heroin abuse after prolonged abstinence. An allergic or toxic reaction to heroin or adulterants seems to be more likely than trauma in the pathogenesis of these complications. Severe rhabdomyolysis can occur without visible muscular swelling. Routine screening of creatine kinase is recommended in heroin addicts with neurological complications, as rhabdomyolysis may lead to fatal renal failure and may easily fail to be diagnosed.  (+info)

Amphetamine-induced myoglobinuric acute renal failure. (46/86)

A 36-year-old man was admitted because of sopor and dark urine after intravenous amphetamine injection. He subsequently developed myoglobinuria and acute renal failure. Serum myoglobin value was remarkably elevated to 83,000 ng/ml, and urine myoglobin was 400,000 ng/ml. Renal biopsy revealed tubular degeneration and tubular obstruction with myoglobin casts by immunofluorescence examination. Amphetamine-induced rhabdomyolysis was suspected to cause myoglobinuric acute renal failure.  (+info)

A review of exertional rhabdomyolysis in wild and domestic animals and man. (47/86)

Exertional rhabdomyolysis is a condition arising in several species of newly captured wild animals after some form of physical exertion and stress. It is characterized by muscle necrosis and myoglobinuria. Death may result from secondary renal failure, acute or chronic heart failure and progressive emaciation.  (+info)

Increased serum lactate dehydrogenase isoenzyme 1 and "flipped" LD-1/LD-2 ratio in myopathy associated with partial carnitine palmitoyltransferase deficiency. (48/86)

We describe a case of a limb-girdle myopathy presenting with myoglobinuria. A partial deficiency of muscle carnitine palmitoyltransferase (EC 2.3.1.21) may also have been present. All "muscle-type" serum enzymes were markedly increased (to between 30- and 400-fold their respective upper reference limits) and creatine kinase (EC 2.7.3.2) isoenzyme 2 (CK-MB) was increased 130-fold but was still less than 2% of the total creatine kinase activity. The isoenzyme pattern of lactate dehydrogenase (EC 1.1.1.27) in serum was "anodic," with isoenzyme 1 greater than isoenzyme 2--an unusual pattern for myopathies. The possible physiological basis for such a finding is discussed.  (+info)