RESUMO
BACKGROUND: Rhabdomyolysis is a serious complication of heat stroke. Unlike that in acute kidney injury, the risk of muscle bleeding in rhabdomyolysis is often ignored and can substantially increase via the widespread use of anticoagulants, leading to the formation of intramuscular hematoma. CASE SUMMARY: During the summer, a middle-aged man and an elderly man were diagnosed with heat stroke, rhabdomyolysis, and acute renal impairment. Low-dose enoxaparin sodium was initiated for prophylaxis of deep vein thrombosis after the disease was stabilized with continuous renal replacement therapy. After that, the patients' hemoglobin decreased progressively, and no obvious intracranial, thoracic, digestive, or skin bleeding tendency was found. However, one of the patients had hip muscle pain, and computed tomography and color ultrasound confirmed that the patients separately had lumbar back and hip intermuscular hematoma. After discontinuation of anticoagulant drugs and monitoring of the steady increase in hemoglobin, the intermuscular hematomas were gradually absorbed. Following the use of prophylactic anticoagulation therapy, the patients' hemoglobin showed a progressive downward trend. Hematoma formation in the lumbosacral and buttock muscles was confirmed after excluding bleeding in typical regions (such as the digestive tract, thoracic cavity, and abdominal cavity). Anticoagulant drugs were discontinued immediately, and nutritional support was increased. Subsequently, the hemoglobin levels gradually increased, and the hematoma volumes gradually decreased. CONCLUSION: Patients with rhabdomyolysis have a risk of muscle bleeding, and inappropriate use of anticoagulants may lead to an increased risk or even to the formation of an intermuscular hematoma. When continuous blood loss is found in the body, the possibility of bleeding in the muscles and more typical sites should be considered.
RESUMO
Zebrafish and human genomes are highly homologous; however, despite this genomic similarity, adult zebrafish can achieve neuronal proliferation, regeneration and functional restoration within 6-8 weeks after spinal cord injury, whereas humans cannot. To analyze differentially expressed zebrafish genes between axon-regenerated neurons and axon-non-regenerated neurons after spinal cord injury, and to explore the key genes and pathways of axonal regeneration after spinal cord injury, microarray GSE56842 was analyzed using the online tool, GEO2R, in the Gene Expression Omnibus database. Gene ontology and protein-protein interaction networks were used to analyze the identified differentially expressed genes. Finally, we screened for genes and pathways that may play a role in spinal cord injury repair in zebrafish and mammals. A total of 636 differentially expressed genes were obtained, including 255 up-regulated and 381 down-regulated differentially expressed genes in axon-regenerated neurons. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment results were also obtained. A protein-protein interaction network contained 480 node genes and 1976 node connections. We also obtained the 10 hub genes with the highest correlation and the two modules with the highest score. The results showed that spectrin may promote axonal regeneration after spinal cord injury in zebrafish. Transforming growth factor beta signaling may inhibit repair after spinal cord injury in zebrafish. Focal adhesion or tight junctions may play an important role in the migration and proliferation of some cells, such as Schwann cells or neural progenitor cells, after spinal cord injury in zebrafish. Bioinformatic analysis identified key candidate genes and pathways in axonal regeneration after spinal cord injury in zebrafish, providing targets for treatment of spinal cord injury in mammals.
