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Journal of Advanced Research Dec 2023Crush syndrome (CS) is a kind of traumatic and ischemic injury that seriously threatens life after prolonged compression. It is characterized by systemic inflammatory... (Review)
Review
BACKGROUND
Crush syndrome (CS) is a kind of traumatic and ischemic injury that seriously threatens life after prolonged compression. It is characterized by systemic inflammatory reaction, myoglobinuria, hyperkalemia and acute kidney injury (AKI). Especially AKI, it is the leading cause of death from CS. There are various cell death forms in AKI, among which ferroptosis is a typical form of cell death. However, the role of ferroptosis has not been fully revealed in CS-AKI.
AIM OF REVIEW
This review aimed to summarize the evidence of ferroptosis in CS-AKI and its related molecular mechanism, discuss the therapeutic significance of ferroptosis in CS-AKI, and open up new ideas for the treatment of CS-AKI.
KEY SCIENTIFIC CONCEPTS OF REVIEW
One of the main pathological manifestations of CS-AKI is renal tubular epithelial cell dysfunction and cell death, which has been attributed to massive deposition of myoglobin. Large amounts of myoglobin released from damaged muscle deposited in the renal tubules, impeding the normal renal tubules function and directly damaging the tubules with oxidative stress and elevated iron levels. Lipid peroxidation damage and iron overload are the distinguishing features of ferroptosis. Moreover, high levels of pro-inflammatory cytokines and damage-associated molecule pattern molecules (HMGB1, double-strand DNA, and macrophage extracellular trap) in renal tissue have been shown to promote ferroptosis. However, how ferroptosis occurs in CS-AKI and whether it can be a therapeutic target remains unclear. In our current work, we systematically reviewed the occurrence and underlying mechanism of ferroptosis in CS-AKI.
Topics: Humans; Acute Kidney Injury; Cell Death; Crush Syndrome; Ferroptosis; Myoglobin
PubMed: 36702249
DOI: 10.1016/j.jare.2023.01.016 -
BMJ Case Reports Dec 2023Cefiderocol is a novel siderophore cephalosporin antibiotic. In the present case report, a woman in her 70s presented with a 1-week history of altered mental status and...
Cefiderocol is a novel siderophore cephalosporin antibiotic. In the present case report, a woman in her 70s presented with a 1-week history of altered mental status and progressive purulent discharge from a non-healing diabetic foot ulcer on her right heel. MRI of the right foot revealed chronic osteomyelitis of the calcaneum. Surgical debridement was performed, and the tissue cultures grew extensively drug resistant (XDR) , XDR and The patient received ampicillin-sulbactam and cefiderocol. The antibiotic treatment course was complicated by brown urine discolouration. Investigations were unrevealing for haemoglobinuria, myoglobinuria and bilirubinuria. A side effect from cefiderocol was suspected and subsequently discontinued. Her urine colour returned to its normal colour within 3 days of discontinuation of cefiderocol.
Topics: Female; Humans; Cefiderocol; Anti-Bacterial Agents; Cephalosporins; Pseudomonas Infections; Microbial Sensitivity Tests; Drug Resistance, Multiple, Bacterial
PubMed: 38103906
DOI: 10.1136/bcr-2023-258207 -
Diagnostics (Basel, Switzerland) Sep 2023Crush syndrome (CS), also known as traumatic rhabdomyolysis, is a syndrome with a wide clinical spectrum; it is caused by external compression, which often occurs in... (Review)
Review
Crush syndrome (CS), also known as traumatic rhabdomyolysis, is a syndrome with a wide clinical spectrum; it is caused by external compression, which often occurs in earthquakes, wars, and traffic accidents, especially in large-scale disasters. Crush syndrome is the second leading cause of death after direct trauma in earthquakes. A series of clinical complications caused by crush syndrome, including hyperkalemia, myoglobinuria, and, in particular, acute kidney injury (AKI), is the main cause of death in crush syndrome. The early diagnosis of crush syndrome, the correct evaluation of its severity, and accurate predictions of a poor prognosis can provide personalized suggestions for rescuers to carry out early treatments and reduce mortality. This review summarizes various methods for the diagnostic and predictive evaluation of crush syndrome, including urine dipstick tests for a large number of victims, traditional and emerging biomarkers, imaging-assisted diagnostic methods, and developed evaluation models, with the aim of providing materials for scholars in this research field.
PubMed: 37835777
DOI: 10.3390/diagnostics13193034 -
Revue Medicale de Liege Sep 2023Rhabdomyolysis is a clinical syndrome related to the damage of skeletal muscle. The symptomatology is often poor, but it classically includes muscle weakness, myalgia...
Rhabdomyolysis is a clinical syndrome related to the damage of skeletal muscle. The symptomatology is often poor, but it classically includes muscle weakness, myalgia and red-brown urine. The causes may be multiple but are most frequently traumatic : the so-called "crush syndrome". The diagnosis is based on the increase in serum creatine kinase, which is sometimes associated with myoglobinuria. Rhabdomyolysis may cause severe complications, such as ionic disorders or acute kidney injury which can lead to the death of the patient.
Topics: Humans; Rhabdomyolysis; Acute Kidney Injury; Muscle Weakness; Syndrome
PubMed: 37712164
DOI: No ID Found -
Disease Models & Mechanisms Sep 2023Rhabdomyolysis is a clinical emergency characterized by severe muscle damage, resulting in the release of intracellular muscle components, which leads to myoglobinuria...
Rhabdomyolysis is a clinical emergency characterized by severe muscle damage, resulting in the release of intracellular muscle components, which leads to myoglobinuria and, in severe cases, acute kidney failure. Rhabdomyolysis is caused by genetic factors linked to increased disease susceptibility in response to extrinsic triggers. Recessive mutations in TANGO2 result in episodic rhabdomyolysis, metabolic crises, encephalopathy and cardiac arrhythmia. The underlying mechanism contributing to disease onset in response to specific triggers remains unclear. To address these challenges, we created a zebrafish model of Tango2 deficiency. Here, we demonstrate that the loss of Tango2 in zebrafish results in growth defects, early lethality and increased susceptibility of skeletal muscle defects in response to extrinsic triggers, similar to TANGO2-deficient patients. Using lipidomics, we identified alterations in the glycerolipid pathway in tango2 mutants, which is critical for membrane stability and energy balance. Therefore, these studies provide insight into key disease processes in Tango2 deficiency and have increased our understanding of the impacts of specific defects on predisposition to environmental triggers in TANGO2-related disorders.
Topics: Animals; Zebrafish; Rhabdomyolysis; Muscle, Skeletal; Mutation; Energy Metabolism
PubMed: 37577943
DOI: 10.1242/dmm.050092