Reducing Radiation Exposure in Lumbar Transforaminal Epidural Steroid Injections with Pulsed Fluoroscopy: A Randomized, Double-blind, Controlled Clinical Trial.

BACKGROUND: Fluoroscopy-guided lumbar transforaminal epidural steroid injections (L-TFESI) result in radiation exposure that carries risks to patients, physicians, and procedural staff. OBJECTIVE: We aim to evaluate the feasibility of using pulsed fluoroscopy to safely reduce radiation exposure during L-TFESI. STUDY DESIGN: This is a prospective, double-blind, randomized controlled trial. SETTING: This study took place in a single-center, academic, outpatient interventional pain management clinic. METHODS: Patients undergoing L-TFESI were randomly assigned to either continuous mode fluoroscopy (high-dose), pulsed fluoroscopy with 8 pulses per second (medium-dose), or pulsed fluoroscopy with one pulse per second (low-dose). Data on radiation doses and other clinical and demographic factors were also collected. RESULTS: In total, 231 cases were analyzed in the high-dose group (n = 81), medium-dose group (n = 72), and low-dose group (n = 78). Mean radiation effective dose (µSv) was 121 in the high-dose group, 57.9 in the medium-dose group, and 34.8 in the low-dose group (P < 0.001). The incidence of inadequate image quality in the pulsed groups was 6% (9/150). The body mass index (BMI, mean ± SD) was significantly higher in patients with inadequate image quality (37.3 ± 7.2) than with adequate quality (30.5 ± 7.2, P = 0.005). LIMITATIONS: Radiation doses were measured using the meter on C-arm fluoroscopes rather than by direct measurement. CONCLUSIONS: The use of pulsed fluoroscopy during L-TFESI resulted in radiation dose reduction of up to 72.1% without causing any significant adverse events. Pulsed fluoroscopy should be considered as an initial fluoroscopic setting for L-TFESI to reduce radiation exposure. KEY WORDS: Radiation, epidural, fluoroscopy, injection, exposure, pulse.

Bacterial expression, purification, and characterization of rat kidney-type mitochondrial glutaminase.

The human gene that encodes the kidney-type glutaminase (KGA) spans 84-kb, contains 19 exons, and encodes two alternatively spliced mRNAs. Various segments of the rat KGA cDNA were PCR amplified and cloned into a bacterial expression vector to determine whether the N- and C- terminal ends of the glutaminase protein were essential for activity. A recombinant glutaminase, lacking the coding sequence contained in exon 1, was found to be fully active. In contrast, proteins that lacked sequences from exons 1 and 2 and exons 1-3 were inactive. An additional construct that corresponded to the sequence encoded by exons 2-14 also retained full activity. Both of the fully active, truncated proteins were purified to apparent homogeneity using an incorporated N-terminal His(6)-tag and Ni(2+)-affinity chromatography. The K(M) values for glutamine of the native and recombinant forms of glutaminase were nearly identical. However, the two truncated forms of the glutaminase exhibit the characteristic phosphate activation profile only when dialyzed into a buffer lacking phosphate. Dialysis versus 10mM Tris-phosphate was sufficient to form an active tetramer. Thus, the deleted N-terminal sequence may contribute to the phosphate-dependent oligomerization and activation of the native glutaminase.