Errate: Effectiveness of Hydro-Dissection of the Piriformis Muscle Plus Low-Dose Local Anesthetic Injection for Piriformis Syndrome: A Report of 2 Cases.

The authors have discovered an error in their figures and have provided replacement figures which have been corrected. Specifically, the positions of "Lateral" and "Medial" were reversed, and the positions of "Ischium" and "Sacrum" were reversed. Additionally, the solid lines at the boundaries of each muscle and bone have been removed, and only the nerves have been marked with dotted lines, which is a common notation in ultrasound images. The authors would also like to add the following Acknowledgment: The authors are grateful to Tadashi Kobayashi and Yoshihiko Shiraishi for advising us on the accurate anatomy of ultrasound images. Reference: Mihiro Kaga, Takeshi Ueda. Effectiveness of Hydro-Dissection of the Piriformis Muscle Plus Low-Dose Local Anesthetic Injection for Piriformis Syndrome: A Report of 2 Cases. Am J Case Rep, 2022; 23: e935346. DOI: 10.12659/AJCR.935346.

Effectiveness of Hydro-Dissection of the Piriformis Muscle Plus Low-Dose Local Anesthetic Injection for Piriformis Syndrome: A Report of 2 Cases.

BACKGROUND Piriformis syndrome causes severe buttock and low back pain and numbness of the lower limbs, leading to difficulty in walking. The lack of unified diagnostic criteria for piriformis syndrome until 2018 made it difficult to diagnose; therefore, it is often underestimated, and some patients do not receive appropriate treatment. Treatment methods include local anesthetic injection, steroid injection, and local botulinum toxin injection. However, the most effective drug for the treatment of severe piriformis syndrome has not been established. This report aimed to propose a new and more effective treatment for piriformis syndrome with a minimal risk of adverse effects. CASE REPORT We performed ultrasound-guided hydro-dissection of the superficial and deep surfaces of the piriformis muscle under local anesthesia (a mixture of 18 mL of saline and 2 mL of 1% lidocaine) in 2 flexion, adduction, and internal rotation test-positive patients with tenderness of the piriformis muscle. In both patients, symptoms improved quickly after injection. One required hospital treatment but gradually returned to previous activities of daily living (ADL) status 5 days after admission and was then discharged. The other patient received 2 injections weekly to improve ADL status with continued lifestyle guidance. CONCLUSIONS Hydro-dissection by ultrasound-guided injection of a very low concentration of local anesthetic is effective and has lower risk of adverse effects, thus making it more convenient for the treatment of piriformis syndrome than conventional treatments, such as local anesthetics, steroids, and botulinum toxin injection.

Ascorbate sensitizes human osteosarcoma cells to the cytostatic effects of cisplatin.

Osteosarcoma (OS) is the most common malignant bone tumor and a leading cause of cancer-related deaths in children and adolescents. Current standard treatments for OS are a combination of preoperative chemotherapy, surgical resection, and adjuvant chemotherapy. Cisplatin is used as the standard chemotherapeutic for OS treatment, but it induces various adverse effects, limiting its clinical application. Improving treatment efficacy without increasing the cisplatin dosage is desirable. In the present study, we assessed the combined effect of ascorbate on cisplatin treatment using cultured human OS cells. Co-treatment with ascorbate induced greater suppression of OS cell but not nonmalignant cell proliferation. The chemosensitizing effect of ascorbate on cisplatin treatment was tightly linked to ROS production. Altered cellular redox state due to increased ROS production modified glycolysis and mitochondrial function in OS cells. In addition, OS cell sphere formation was markedly decreased, suggesting that ascorbate increased the treatment efficacy of cisplatin against stem-like cells in the cancer cell population. We also found that enhanced MYC signaling, ribosomal biogenesis, glycolysis, and mitochondrial respiration are key signatures in OS cells with cisplatin resistance. Furthermore, cisplatin resistance was reversed by ascorbate. Taken together, our findings provide a rationale for combining cisplatin with ascorbate in therapeutic strategies against OS.

Sunitinib Versus Sorafenib as Initial Targeted Therapy for mCC-RCC With Favorable/Intermediate Risk: Multicenter Randomized Trial CROSS-J-RCC.

PURPOSE: The present study compared the efficacy of sunitinib and sorafenib as first-line treatment of metastatic clear cell renal cell carcinoma (mCC-RCC) with favorable or intermediate Memorial Sloan Kettering Cancer Center (MSKCC) risk. PATIENTS AND METHODS: Treatment-naive patients with mCC-RCC were randomized to receive open-label sunitinib followed by sorafenib (SU/SO) or sorafenib followed by sunitinib (SO/SU). The primary endpoint was first-line progression-free survival (PFS). The secondary endpoints were total PFS and overall survival (OS). RESULTS: Of the 124 patients enrolled at 39 institutions from February 2010 to July 2012, 120 were evaluated. The median first-line PFS duration was 8.7 and 7.0 months in the SU/SO and SO/SU groups, respectively (hazard ratio [HR], 0.67; 95% confidence interval [CI], 0.42-1.08). The total PFS and OS were not significantly different between the SU/SO and SO/SU groups (27.8 and 22.6 months; HR, 0.73; 95% CI, 0.428-1.246; and 38.4 and 30.9 months; HR, 0.934; 95% CI, 0.588-1.485, respectively). The subgroup analysis revealed that the total PFS with SU/SO was superior to the total PFS with SO/SU in the patients with favorable MSKCC risk and those with < 5 metastatic sites). SO/SU was superior to SU/SO for patients without previous nephrectomy. CONCLUSIONS: No statistically significant differences were found in first-line PFS, total PFS, or OS between the 2 treatment arms (ClinicalTrials.gov identifier, NCT01481870).

Therapeutic outcomes of neoadjuvant and concurrent androgen-deprivation therapy and intensity-modulated radiation therapy with gold marker implantation for intermediate-risk and high-risk prostate cancer.

OBJECTIVES: To investigate the therapeutic outcomes of neoadjuvant and concurrent androgen-deprivation therapy and intensity-modulated radiation therapy with gold marker implantation for intermediate- and high-risk prostate cancer. METHODS: This was a retrospective study of 325 patients with intermediate- or high-risk prostate cancer according to the National Comprehensive Cancer Network guidelines who underwent androgen-deprivation therapy and intensity-modulated radiation therapy (76 Gy) after gold marker implantation between 2001 and 2010. RESULTS: The 5-year distant metastasis-free survival rate was significantly lower for very high-risk patients than for intermediate- and high-risk patients (82.6% vs 99.4% and 96.5%, respectively; P < 0.01). The 5-year biochemical relapse-free survival rates significantly declined with increasing prostate cancer risk (P < 0.01), and were 95.9%, 87.2%, and 73.1% for the intermediate-risk, high-risk and very high-risk patients, respectively. Acute genitourinary and gastrointestinal toxicity grade ≥3 were not observed in any of the patients. Late grade 3 genitourinary toxicity occurred in 0.3% of patients. CONCLUSION: Combination androgen-deprivation therapy and 76-Gy intensity-modulated radiation therapy with gold marker implantation offers good therapeutic outcomes with few serious complications in patients with intermediate- and high-risk prostate cancer.

Efficacy and safety of axitinib versus sorafenib in metastatic renal cell carcinoma: subgroup analysis of Japanese patients from the global randomized Phase 3 AXIS trial.

OBJECTIVE: Axitinib is a potent and selective second-generation inhibitor of vascular endothelial growth factor receptors 1, 2 and 3. The efficacy and safety of axitinib in Japanese patients with metastatic renal cell carcinoma were evaluated. METHODS: A subgroup analysis was conducted in Japanese patients enrolled in the randomized Phase III trial of axitinib versus sorafenib after failure of one prior systemic therapy for metastatic renal cell carcinoma. RESULTS: Twenty-five (of 361) and 29 (of 362) patients randomized to the axitinib and sorafenib arms, respectively, were Japanese and included in this analysis. Median progression-free survival in Japanese patients was 12.1 months (95% confidence interval 8.6 to not estimable) for axitinib and 4.9 months (95% confidence interval 2.8-6.6) for sorafenib (hazard ratio 0.390; 95% confidence interval 0.130-1.173; stratified one-sided P = 0.0401). The objective response rate was 52.0% for axitinib and 3.4% for sorafenib (P = 0.0001). The common all-causality adverse events (all grades) in Japanese patients were dysphonia (68%), hypertension (64%), hand-foot syndrome (64%) and diarrhea (56%) for axitinib, and hand-foot syndrome (86%), hypertension (62%) and diarrhea (52%) for sorafenib. The safety profiles of axitinib and sorafenib in Japanese patients were generally similar to those observed in the overall population, with the exceptions of higher incidences of hypertension, dysphonia, hand-foot syndrome, hypothyroidism and stomatitis. CONCLUSIONS: Axitinib is efficacious and well tolerated in Japanese patients with previously treated metastatic renal cell carcinoma, consistent with the results in the overall population, providing a new targeted therapy for these Japanese patients.

Treatment outcomes of sorafenib for first line or cytokinerefractory advanced renal cell carcinoma in Japanese patients.

The objective of the present study was to document the treatment efficacy and safety of sorafenib in Japanese patients with advanced renal cell carcinoma (RCC). A retrospective analysis of 50 consecutive patients with metastatic RCC between January 2005 and December 2009 was carried out. Patients received sorafenib after failed cytokine therapy or first-line sorafenib treatment. All received 400 mg of sorafenib orally twice daily. Five of 14 patients with bone metastases were also given bisphosphonates. Tumor response was evaluated every 1-2 months according to the Response Evaluation Criteria in Solid Tumors. Adverse events (AE) were evaluated at each visit during and after treatment, and were recorded according to the National Cancer Institute's Common Terminology Criteria for Adverse Events version 3.0. Dose modification of sorafenib was permitted if grade 3 or 4 AE occurred. Treatment continued until disease progression or treatment intolerance occurred. Partial response, and stable disease as best objective responses were observed in 11 (22%) and 23 (46%) patients, respectively. Median progression-free survival was 7.3 months and median overall survival was 11.9 months. All patients experienced AE and one or more grade 3/4 AE occurred in 43 of 50 (86%) patients. Although it requires close monitoring, sorafenib treatment seemed to be effective in the present study population.

[Effect of oral lactosucrose supplementation on human enteric oxalate-degrading bacteria].

A variety of oxalate-degrading bacteria including Oxalobacter formigenes and some species of Bifidobacterium are known to colonize the human intestinal tract. Oral lactosucrose supplementation promotes the growth of Bifidobacterium in the human intestine. Therefore, we investigated the effect of oral lactosucrose supplementation on enteric oxalate-degrading bacteria in twelve healthy men (age ranging from 25 to 39 years). Lactosucrose was orally administered 10 g daily for 2 weeks without restriction of dietary intake. The total number of oxalate-degrading bacteria in feces and the 24-hour urinary excretion of oxalate were examined before and after lactosucrose supplementation. The total number of oxalate degrading-bacteria was significantly increased by lactosucrose supplementation (9.20 +/- 0.44 versus 9.77 +/- 0.46, p<0.05), although there was no significant change in the urinary oxalate excretion. The oxalate degrading-bacteria isolated from feces was biochemically identified as Bifidobacterium adolescentis. In conclusion, oral supplementation of 10 g lactosucrose daily for 2 weeks was effective in multiplying oxalate-degrading bacteria, but not in reducing urinary oxalate excretion under free non-restricted dietary intake. In addition, it was suggested that various species of Bifidobacterium were related to degradation of oxalate in the human intestine.

Association of absence of intestinal oxalate degrading bacteria with urinary calcium oxalate stone formation.

AIM: Urinary concentration of oxalate is considered an important factor in the formation of renal stones. Dietary oxalate is a major contributor to urinary oxalate excretion in most individuals. Furthermore, oxalate degrading bacteria have been isolated from human feces. We investigated the significance of oxalate degrading bacteria for urinary oxalate excretion and urinary stone formation. METHODS: Twenty-two known calcium oxalate stone-forming patients (stone formers) and 34 healthy volunteers (non-stone formers) were included in the study. Stool specimens were inoculated into pepton yeast glucose (PYG) medium supplemented with oxalate under anaerobic condition at 37 C for one week. After the incubation period, each colony was checked for the loss of oxalate from the culture medium. A 24-h urine sample was collected in 43 individuals and analyzed for oxalate excretion. RESULTS: Twenty-eight of 34 (82%) healthy volunteers and 10 of 22 (45%) calcium oxalate stone formers were colonized with oxalate degrading bacteria. Calcium oxalate stone formers were more frequently free of oxalate degrading bacteria (P < 0.01). Urinary excretion of oxalate in those with oxalate degrading bacteria was significantly less than in those without oxalate degrading bacteria (P < 0.05). Hyperoxaluria (> 40 mg/day) was found in four of 27 individuals (15%) with oxalate degrading bacteria compared to seven of 16 (44%) without oxalate degrading bacteria (P < 0.05), suggesting an association between the absence of oxalate degrading bacteria and the presence of hyperoxaluria. CONCLUSION: The absence of oxalate degrading bacteria in the gut could promote the absorption of oxalate, thereby increasing the level of urinary oxalate excretion. The absence of oxalate degrading bacteria from the gut appears to be a risk factor for the presence of absorptive hyperoxaluria and an increased likelihood of urolithiasis.