RESUMO
BACKGROUND: Testicular pain caused by lumbar disease is uncommon in the clinic. Here we reported a case of discogenic low back pain with testicular pain that was successfully cured. CASE SUMMARY: A 23-year-old male patient presented to our department with chronic low back pain. Based on his clinical symptoms, signs and imaging, he was diagnosed with discogenic low back pain. Since conservative treatment for more than half a year did not significantly improve his low back pain, we decided to treat it with intradiscal methylene blue injection. During the course of surgery, we again identified the low back pain as originating from the degenerated lumbar disc by analgesic discography. Interestingly, the patient's low back pain disappeared along with the testicular pain that had been present for more than 3 mo. After the operation, the patient's low back pain improved, and the testicular pain did not reappear. CONCLUSION: Intradiscal methylene blue injection is a convenient and effective surgical intervention for the treatment of discogenic low back pain. Lumbar disc degeneration may also be a possible clinical cause of testicular pain. Methylene blue injection in the diseased disc improved the low back pain, and the accompanying testicular pain was successfully managed.
RESUMO
PURPOSE: Tumor necrosis factor (TNF)-stimulated gene-6 (TSG-6), a secreted protein associated with inflammation, is believed to possess momentous and multiple anti-inflammatory and tissue-protective properties. However, the role and potential mechanism of TSG-6 in cervical disk degeneration (CDD) are still not clear. Hence, we aimed to explore the effect of TSG-6 on CDD. METHODS: Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) or enzyme-linked immunosorbent assay was applied to detect the expression level of TSG-6 and IL-1ß in normal and degenerated nucleus pulposus (NP) tissues. Then, qRT-PCR and western blot were adopted to test the TSG-6 protein expression after IL-1ß treatment (10 ng/mL) in human NP cells (HNPCs). After over-expressing TSG-6, qRT-PCR was also utilized to evaluate the expression of TNF-α, IL-8, and IL-6 and the synthesis of sulfated glycosaminoglycans (sGAGs), western blot to check the expression of extracellular matrix (ECM) proteins [collagen II, aggrecan, and matrix metalloproteinase-3 (MMP-3)], pain-related molecules (CGRP, calcitonin gene-related peptide; NGF, nerve growth factor; SP, substance P), and PI3K/Akt signaling pathway-related proteins. RESULTS: Briefly speaking, TSG-6 and IL-1ß expression levels were significantly increased in CDD patient tissues; and IL-1ß treatment could significantly increase TSG-6 expression in HNPCs. Further research revealed that, in addition to greatly promoting sGAGs synthesis, TSG-6 over-expression also inhibited TNF-α, IL-8, and IL-6 expression and ECM degradation in IL-1ß-induced HNPCs. (The collagen II and aggrecan expression was up-regulated and MMP-3 expression was down-regulated.) Furthermore, over-expression of TSG-6 could decrease the levels of CGRP, NGF, and SP protein expression and activate the PI3K/Akt signaling pathway in IL-1ß-treated HNPCs. CONCLUSION: TSG-6 inhibits inflammatory responses, ECM degradation, and expression of pain-related molecules in IL-1ß-induced HNPCs by activating the PI3K/Akt signaling pathway.