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Neurologic Clinics Feb 2000Myoglobinuria refers to an abnormal pathologic state in which an excessive amount of myoglobin is found in the urine, imparting a cola-like hue, usually in association... (Review)
Review
Myoglobinuria refers to an abnormal pathologic state in which an excessive amount of myoglobin is found in the urine, imparting a cola-like hue, usually in association with myonecrosis and a clinical picture of weakness, myalgias, and edema. Myoglobinuria is produced by multiple causes: any condition that accelerates the use or interferes with the availability of oxygen or energy substrates to muscle cells can result in myoglobinuria, as can events that produce direct muscle injury, either mechanical or chemical. Acute renal failure is the most serious complication, which can be prevented by prompt, aggressive treatment. In patients surviving acute attacks, recovery of muscle and renal function is usually complete.
Topics: Biopsy; Diagnosis, Differential; Energy Metabolism; Humans; Kidney Tubular Necrosis, Acute; Kidney Tubules; Muscle, Skeletal; Muscular Diseases; Myoglobinuria; Oxygen Consumption
PubMed: 10658177
DOI: 10.1016/s0733-8619(05)70187-0 -
Current Neurology and Neuroscience... Oct 2015One large group of hereditary myopathies characterized by recurrent myoglobinuria, almost invariably triggered by exercise, comprises metabolic disorders of two main... (Review)
Review
One large group of hereditary myopathies characterized by recurrent myoglobinuria, almost invariably triggered by exercise, comprises metabolic disorders of two main fuels, glycogen and long-chain fatty acids, or mitochondrial diseases of the respiratory chain. Differential diagnosis is required to distinguish the three conditions, although all cause a crisis of muscle energy. Muscle biopsy may be useful when performed well after the episode of rhabdomyolysis. Molecular genetics is increasingly the diagnostic test of choice to discover the underlying genetic basis.
Topics: Adenosine Triphosphate; Glycogen; Humans; Mitochondria; Muscular Diseases; Myoglobinuria; Renal Dialysis
PubMed: 26319173
DOI: 10.1007/s11910-015-0590-9 -
The Netherlands Journal of Medicine Oct 2009Rhabdomyolysis is a potentially life-threatening syndrome that can develop from a variety of causes; the classic findings of muscular aches, weakness and tea-coloured... (Review)
Review
Rhabdomyolysis is a potentially life-threatening syndrome that can develop from a variety of causes; the classic findings of muscular aches, weakness and tea-coloured urine are non-specific and may not always be present. The diagnosis therefore rests upon the presence of a high level of suspicion of any abnormal laboratory values in the mind of the treating physician. An elevated plasma creatine kinase (CK) level is the most sensitive laboratory finding pertaining to muscle injury; whereas hyperkalaemia, acute renal failure and compartment syndrome represent the major life-threatening complications. The management of the condition includes prompt and aggressive fluid resuscitation, elimination of the causative agents and treatment and prevention of any complications that may ensue. The objective of this review is to describe the aetiological spectrum and pathophysiology of rhabdomyolysis, the clinical and biological consequences of this syndrome and to provide an appraisal of the current data available in order to facilitate the prevention, early diagnosis and prompt management of this condition.
Topics: Acute Kidney Injury; Arrhythmias, Cardiac; Compartment Syndromes; Creatine Kinase; Disseminated Intravascular Coagulation; Humans; Hypovolemia; Muscle Weakness; Muscles; Myoglobin; Myoglobinuria; Prognosis; Rhabdomyolysis; Risk Factors; Syndrome
PubMed: 19841484
DOI: No ID Found -
Ryoikibetsu Shokogun Shirizu 2001
Review
Topics: Alcoholism; Antiviral Agents; Cocaine; Diagnosis, Differential; HIV Infections; Humans; Myoglobinuria; Opportunistic Infections; Prognosis
PubMed: 11555907
DOI: No ID Found -
The Medical Clinics of North America Nov 1972
Topics: Adolescent; Adult; Aged; Child; Female; Heroin; Humans; Hypokalemia; Male; Malignant Hyperthermia; Middle Aged; Muscular Dystrophies; Myoglobinuria; Physical Exertion; Recurrence
PubMed: 5085857
DOI: 10.1016/s0025-7125(16)32319-7 -
The American Journal of the Medical... Jun 1971
Topics: Biopsy; Dermatomyositis; Diagnosis, Differential; Female; Hemoglobinuria; Humans; Middle Aged; Muscles; Muscular Diseases; Myoglobinuria; Pigments, Biological; Porphyrias; Prednisone
PubMed: 5149898
DOI: 10.1097/00000441-197106000-00006 -
Advances in Pediatrics 1990Recurrent heritable childhood myoglobinuria is a potentially fatal entity (mortality up to 35%) in which prompt diagnosis and treatment are critical. Sixty childhood... (Review)
Review
Recurrent heritable childhood myoglobinuria is a potentially fatal entity (mortality up to 35%) in which prompt diagnosis and treatment are critical. Sixty childhood cases have been reported between 1910 to 1988, most with undiagnosed etiologies. We have studied an additional 40 cases referred to CPMC (1980-1988), suggesting that this condition is largely underdiagnosed or unreported. We have found important differences between the childhood and adult-onset cases. Of 77 cases of adult-onset recurrent myoglobinuria, 45% have been diagnosed biochemically. In contrast, only 30% of the 60 childhood cases from the literature have been diagnosed; 11 with CPT deficiency and 7 with various glycolytic defects, and only 5 of our 40 childhood cases have been diagnosed, all with CPT deficiency. The 100 combined childhood cases can be divided into an exertional group (type I) with exertion as the leading precipitating factor (46 literature and 10 CPMC cases), a toxic group (type II) with infection and/or fever as the primary precipitant (14 literature and 23 CPMC cases), and 7 undefined cases. The type I group resembles the adult-onset group in which exercise is also the leading precipitating factor. There is a slight female predominance (male/female = 1:1.3) in the toxic group vs. a marked male predominance in the exertional and adult groups (4:1). Only 4 of 37 cases (11%) of the toxic group are diagnosed (all with CPT deficiency) vs. 19 of 56 cases (34%) of the exertional group (12 CPT, 7 glycolytic) and 45% of the adult group. The toxic group is also differentiated by a higher mortality rate and by the presence of additional clinical features, including ictal bulbar signs (8 of 18), encephalopathy (4 of 19), and seizures (2 of 7), as well as persistent cardiac abnormalities, developmental delay (4 of 17), and dysmorphic features (2 of 9). These clinical characteristics clearly differentiate the childhood from the adult cases and suggest the presence of more generalized disease processes and different biochemical etiologies. A study of the heritable causes of myoglobinuria is important because identification of the biochemical defect may elucidate the pathogenetic mechanism of the myoglobinuria and facilitate the development of rational treatment strategies aimed at circumventing or correcting the metabolic block.
Topics: Adolescent; Adult; Child; Female; Humans; Male; Myoglobinuria; Recurrence
PubMed: 2264536
DOI: No ID Found -
Clinical Laboratory May 2021In professional soccer players (n = 27), confounders of quantitative myoglobinuria following physical training were assessed in order to improve interpretation of...
BACKGROUND
In professional soccer players (n = 27), confounders of quantitative myoglobinuria following physical training were assessed in order to improve interpretation of post-exercise myoglobinuria.
METHODS
Urine samples were collected in the morning before training sessions, 48 to 72 hours following a game. Urine myoglobin was assayed using immunoturbidimetry. Blood was drawn 48 hours following training session. Creatinine was assayed using a Jaffe method. Creatine kinase (CK) activity was assayed according to the IFCC reference method. Serum myoglobin was assayed using the same assay as the one used for urine. Hp polymorphism was assessed on hemoglobin supplemented serum. Serum Hp concentration was assayed nephelometrically. Training intensity was assessed using a wearable GPS tracking system. Physical load monitoring included the covered total distance, the distance at different speed zones, and the number of sprints/accelerations/decelerations/jumps. Multiple regression analysis was used to detect the determinants of post-exercise myoglobinuria.
RESULTS
Myoglobinuria negatively correlated with serum haptoglobin (Hp) concentration. Athletes presented with Hp values, which were lower than the Hp phenotype reference ranges, which can be explained by depletion of circulating Hp stores. Myoglobinuria was most pronounced in players carrying a Hp 2-2 phenotype, which is associated with the lowest Hp reference range. Myoglobin clearance was inversely correlated with Hp 2-2 concentration. Correlation between myoglobinuria and biomarkers of muscle damage was weak. Neither age nor glomerular filtration rate were found to be confounders of myoglobinuria. When comparing myoglobinuria with training intensity, the number of sprints, average acceleration speed, and maximal speed were determining factors for predicting exercise-induced myoglobinuria.
CONCLUSIONS
In athletes, plasma myoglobin binding capacity is depleted. Moderate myoglobinuria not only should be regarded as a muscle damage marker, but also should be interpreted as an indicator for Hp depletion. Apart from its significance as a biomarker for muscle damage and rhabdomyolysis, myoglobinuria in athletes should be a warning that the heme binding capacity of plasma Hp is depleted, indicating an exhausted defense against Fenton chemistry induced free radicals. Fenton chemistry is associated with free radical formation, which is to be avoided because of the causative relationship with inflammatory processes and tissue damage.
Topics: Creatinine; Exercise; Haptoglobins; Humans; Myoglobin; Myoglobinuria; Rhabdomyolysis
PubMed: 33978364
DOI: 10.7754/Clin.Lab.2020.200855 -
The Veterinary Clinics of North... Nov 2004
Review
Topics: Animals; Cat Diseases; Cats; Dog Diseases; Dogs; Humans; Muscular Diseases; Myoglobinuria; Rhabdomyolysis
PubMed: 15474684
DOI: 10.1016/j.cvsm.2004.05.020 -
Wiadomosci Lekarskie (Warsaw, Poland :... May 1994General data is presented on myoglobin structure and function, the pathomechanism of myoglobinuria and on its main causes. Attention was also paid to the most serious... (Review)
Review
General data is presented on myoglobin structure and function, the pathomechanism of myoglobinuria and on its main causes. Attention was also paid to the most serious result of massive rhabdomyolysis-acute renal failure, taking into account the mechanism of its development. Apart from traumatic causes of myoglobinuria and myoglobinaemia, where the usefulness of these determinations is unquestionable, certain other diseases were compared in which the determination of the concentration of this haemoprotein is of important practical aspect.
Topics: Humans; Myoglobin; Myoglobinuria
PubMed: 7817595
DOI: No ID Found