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Background The corticosteroid choice for a lumbar transforaminal epidural steroid injection (TFESI) remains controversial. Whether to utilize particulate or nonparticulate steroid preparations for these injections remains an unanswered question in the literature. Objective To determine if a particulate or nonparticulate steroid is more effective in the treatment of electromyography (EMG)-confirmed lumbosacral radiculopathy. Design Multicenter retrospective cohort study. Setting Two tertiary academic spine centers. Patients Consecutive patients, aged 18 years or older, with EMG-confirmed lumbosacral radiculopathy. Interventions TFESI with a particulate or nonparticulate steroid to treat radicular pain within 6 months of EMG. Main Outcome Measures The primary outcome was the proportion of patients with ≥50% pain reduction on the numerical rating scale after TFESI. Secondary outcomes included mean numerical rating scale score reduction and number of repeat TFESIs. Short-term ( Results Seventy-eight patients, with an age ± standard deviation of 56 ± 16 years and a mean symptom duration of 49 ± 71 months, were included. Forty-one patients (52%) received dexamethasone, 23 (30%) received triamcinolone, and 14 (18%) received betamethasone. There was no statistically significant difference in the proportion of patients who reported ≥50% pain reduction between the particulate and nonparticulate groups at short-term follow-up (35%; 95% confidence interval [CI], 21-51 versus 28%; 95% CI, 13-43) or at intermediate follow-up (40%; 95% CI, 21-59 versus 39%; 95% CI, 19-59). There was no difference in the mean number of injections administered between groups at intermediate follow-up ( P = .26). Conclusions This study demonstrates no significant differences in pain reduction or the number of repeat injections with particulate compared with nonparticulate transforaminal epidural steroid injection in patients with EMG-confirmed painful lumbosacral radiculopathy. These findings suggest a new population for whom nonparticulate steroid appears to be an appropriate first-line therapy, although confirmation with a randomized study is needed. Level of Evidence III

Serotonin (5-HT) decreases NHE2 and NHE3 activities under acute conditions in human intestinal epithelial cells. Here, we have investigated the effects of 5-HT on expression of the human NHE3 gene and the mechanisms underlying its transcriptional regulation in differentiated C2BBe1 cells. Treatment of the human intestinal epithelial cell line, C2BBe1, with 5-HT (20 microM) resulted in a significant decrease in NHE3 mRNA and protein expression. In transient transfection studies, 5-HT repressed the NHE3 promoter activity by approximately 55%. The repression of the NHE3 promoter activity in response to 5-HT was accompanied by reduced DNA-binding activity of transcription factors Sp1 and Sp3 to the NHE3 promoter without alteration in their nuclear levels. Pharmacological inhibitors of protein kinase C reversed the inhibitory effect of 5-HT on the promoter activity. Our data indicate that 5-HT suppresses the transcriptional activity of the NHE3 promoter and this effect may be mediated by PKCalpha and modulation of DNA-binding affinities of Sp1 and Sp3.

An 83-year-old man with multiple medical problems, including gout, pseudogout, and renal insufficiency, presented with more than a year of proximal weakness. He had an extensive previous medical workup, including a normal creatinine kinase. His weakness persisted despite endurance and strength training. Electrodiagnostic findings were consistent with a myopathy, although without abnormal spontaneous activity and a length-dependent neuropathy. On the basis of these findings, colchicine was discontinued. The patient experienced marked symptomatic improvement within a week. Myopathies with neuropathies may be found with the use of colchicine. This case was unusual because of the absence of abnormal spontaneous activity and increased creatinine kinase, as typically reported with colchicine myopathy. Level of Evidence V

Background and aims: Chylomicron retention disease (CRD) is caused by mutations in the SARA2 gene that encodes the SAR1B protein, involved in the vesicular coat protein complex II-dependent transport of proteins/lipoproteins from the endoplasmic reticulum to the Golgi apparatus. Given the large spectrum of CRD phenotypes, it appears important to search for SARA2 polymorphisms and probe functional cause-effects resulting from SAR1B knockdown. Methods: To examine the allelic frequencies of the SARA2 genetic variants, SNPs were assessed in the promoter (2kb, 3.5 and 6 kb regions upstream of the transcription start site), exon 4 and exon 8 in CRD and control subjects. In addition, SAR1B was suppressed in HepG2 and Caco-2/15 cell lines by specific siRNA, and lipid transport was determined. Results: No changes were noted in the polymorphisms in the promoter region (7 variants), exon 4 (2 variants) and exon 8 (1 variant), suggesting that they do not play an essential role in the several biochemical and clinical abnormalities characterizing CRD patients. On the other hand, SAR1B silencing resulted in multiple alterations in lipids, apolipoproteins (apo) and lipoproteins in Caco-2/15 and HepG2 cells. It reduced the output of triglycerides (TG) and TG-rich lipoproteins. Furthermore, SAR1B silencing limited the synthesis of apo B-48 and apo B-100 in Caco-2/15 cells and HepG2 cells, respectively. Conclusions: Our functional experiments show that the suppression of SAR1B has a negative impact on apo B synthesis and lipid/lipoprotein secretion. If previous studies have established only an association between SAR1B defects and lipid transport abnormalities, our findings constitute the first direct demonstration illustrating the SAR1B deficiency cause-effects in enterocytes and hepatocytes. Acknowledgment: This study was supported by the Canadian Institutes of Health Research and the J.A. DeSeve Research Chair in Nutrition