Elevated intraneural vascularization of the median nerve proximal to the arteriovenous fistula in hemodialysis patients suspected of carpal tunnel syndrome: A case series.

Patients with end-stage kidney disease may require creation of an arteriovenous fistula in order to receive hemodialysis treatment. The creation may result in several complications, including carpal tunnel syndrome. Early diagnosis and treatment are essential to relieve symptoms, prevent permanent nerve damage, and improve quality of life. However, the sensory and motor disturbances resembling carpal tunnel syndrome could be related to other etiologies than external compression of the median nerve underneath the transverse ligament. This case report presents eight patients with a radiocephalic arteriovenous fistula, who all had symptoms of carpal tunnel syndrome. Ultrasonographic examination showed a segmental intraneural hypervascularization of a large vessel inside the median nerve proximal to the wrist and arteriovenous fistula anastomosis with garland-like course as well as multiple flow velocities. The neurophysiological findings showed a significant decreased velocity in the ipsilateral forearm to the arteriovenous fistula.

Transcriptional regulation of CYP2B1 induction in primary rat hepatocyte cultures: repression by epidermal growth factor is mediated via a distal enhancer region.

Phenobarbital (PB) alters expression of numerous hepatic genes, including genes involved in xenobiotic metabolism. Phenobarbital-dependent induction of cytochrome P-450 2B1 (CYP2B1) is subject to regulation by cytokines [e.g., by epidermal growth factor (EGF)], hormones [e.g., by growth hormone (GH)], or the cellular redox status. To investigate mechanisms involved in regulation of CYP2B1 transcription, we performed promoter activation studies using primary rat hepatocyte cultures transiently transfected with individual CYP2B1 promoter-luciferase reporter gene constructs. The 2679-bp native 5'-flanking region of the CYP2B1 gene conferred reporter gene activation by PB and the potent PB-like inducer permethrin (PM). Furthermore, this region mediated EGF- and GH-dependent repression of gene activation by PB-like inducers. A wide promoter mapping strategy with constructs bearing internal CYP2B1 promoter deletions led to identification of a distal responsive CYP2B1 enhancer region at -2230 to -2170, encompassing the section equivalent to the 51-bp PB-responsive enhancer module situated in the distal mouse Cyp2b10-5'-flanking region. The distal CYP2B1 enhancer region conferred gene activation by PM, repression of PM-dependent activation by EGF, and enhancement of activation by the antioxidant N-acetylcysteine (NAC). Mutational analyses of the region at -2230 to -2170 suggested that the mechanisms of PB-dependent induction of CYP2B1 and the modulating effects by EGF or NAC are closely related.