Functional Somatic Syndromes Are Associated With Varied Postoperative Outcomes and Increased Opioid Use After Spine Surgery: A Systematic Review.

STUDY DESIGN: Systematic Review. OBJECTIVE: To perform a systematic review assessing the relationship between functional somatic syndromes (FSSs) and clinical outcomes after spine surgery. METHODS: A systematic review of online databases (PubMed and Web of Science) through December 2021 was conducted via PRISMA guidelines to identify all studies investigating the impact of at least one FSS (fibromyalgia, irritable bowel syndrome (IBS), chronic headaches/migraines, interstitial cystitis, chronic fatigue syndrome, multiple chemical sensitivity) on outcomes after spine surgery. Outcomes of interest included patient reported outcome measures (PROMs), postoperative opioid use, cost of care, complications, and readmission rates. RESULTS: A total of 207 records were identified. Seven studies (n = 40,011 patients) met inclusion criteria with a mean MINORS score of 16.6 out of 24. Four studies (n = 21,086) reported postoperative opioid use; fibromyalgia was a strong risk factor for long-term opioid use after surgery whereas the association with chronic migraines remains unclear. Two studies (n = 233) reported postoperative patient reported outcome measures (PROMs) with mixed results suggesting a possible association between fibromyalgia and less favorable PROMs. One study (n = 18,692) reported higher postoperative complications in patients with fibromyalgia. CONCLUSION: Patients with fibromyalgia and possibly migraines are at higher risk for prolonged postoperative opioid use and less favorable PROMs after spine surgery. There is limited research on the relationship between other Functional somatic syndromes (FSSs) and outcomes following spine surgery. Growing evidence suggests the variation in outcomes after spine procedures may be attributed to non-identifiable organic patient factors such as FSSs.

Bilateral Chronic Quadriceps Tendon Ruptures Treated with Hamstring Autograft Reconstruction: A Case Report.

CASE: A 30-year-old semiprofessional football player presented with chronic bilateral quadriceps tendon ruptures. Both quadriceps tendon ruptures were unsuitable for isolated primary repair because of tendon retraction and immobility. A novel reconstruction technique using semitendinosus and gracilis tendon autografts was performed to restore both lower extremities' disrupted extensor mechanisms. At the final follow-up, the patient regained excellent motion of both knees and returned to high-intensity activity. CONCLUSION: Chronic quadriceps tendon ruptures present challenges related to tendon quality and mobilization. Reconstruction with hamstring autograft using a Pulvertaft weave through the retracted quadriceps tendon in a high-demand athletic patient represents a novel approach for treating this injury.

Etiology of limb girdle muscular dystrophy 1D/1E determined by laser capture microdissection proteomics.

Limb girdle muscular dystrophy 1D/1E (OMIM nomenclature LGMD1D, Human Gene Nomenclature Committee LGMD1E), a skeletal and cardiac myopathy, has previously been linked to chromosome 6q23. We used laser capture microdissection to isolate cytoplasmic inclusions from skeletal muscle from a patient with LGMD1D/1E, performed mass spectrometry-based proteomics on these minute inclusions, and identified through bioinformatics desmin as their major constituent. Sequencing in this patient and family members identified the genetic basis of the previously reported 6q23 linked LGMD1D/1E to be due to an intron splice donor site mutation (IVS3+3A>G) of the desmin gene located on chromosome 2q35.

Transcriptional profiling of the transition from normal intestinal epithelia to adenomas and carcinomas in the APCMin/+ mouse.

Mutations in the adenomatous polyposis coli (APC) gene that result in excessive beta-catenin-induced cell signaling are implicated in the risk of colon cancer. Although the mechanism of APC-mediated tumorigenesis is known, the pathways that translate beta-catenin signaling into tumor growth in vivo are undefined. To address this, gene expression profiles of normal intestinal epithelial cells were compared with those from adenomas and carcinomas from APC(Min/+) mice, a model of APC-related colorectal cancer. The gene expression profiles of adenomas and carcinomas were very similar, which is consistent with the theory that carcinomas progress from adenomas in this model system. Tumors had altered transcript abundance for members of several pathways that influence cell growth and proliferation including growth factors/receptors, molecules involved in apoptosis, and protein processing and catabolism enzymes. Comparison of gene expression between adenomas and carcinomas revealed nine differentially expressed transcripts. These included members of three growth-regulating pathways, and the results are consistent with the increased growth potential of carcinomas. SRY-box containing gene 17 (Sox 17), a negative regulator of beta-catenin signaling, and calbindin-D9K, a factor that enhances calcium transport, were more highly expressed in adenomas than carcinomas (approximately 4-fold and 15- to 22-fold, respectively). Transcript abundance for insulin-like growth factor binding protein 5, which mediates insulin-like growth factor function, was 2.6-fold greater in carcinomas. Because the changes in gene expression observed in this study are directly associated with a deficiency in APC, the data provide new insights into how loss of this important tumor suppressor translates into benign and malignant tumor growth.