Citations

Background There are sparse data available regarding outcome of meniscal repair performed at the time of ACL reconstruction in the pediatric and adolescent population. Purpose To review the results of meniscal repair performed at the time of ACL reconstruction in pediatric and adolescent patients. Study Design Case series; Level of evidence, 4. Methods The records of all patients age 18 years or younger who underwent meniscal repair at the time of ACL reconstruction between 1990 and 2005 were reviewed. Ninety-nine patients (56 female, 43 male) with an average age of 16 years (range, 13-18) were included. Average injury to surgery interval was 107 days (range, 2-1109). Clinical outcomes were assessed at a mean of 8 years postoperatively (range, 2-19). A multivariate model was used to compare this cohort with a previously published cohort of patients with isolated meniscal tears. Results The clinical success rate of meniscal repair was 84% for simple tears, 59% for displaced bucket-handle tears, and 57% for complex tears (74% overall). Twenty-six menisci (26% overall) failed repair and 25 patients underwent repeat arthroscopic surgery (19 partial meniscectomies, 6 re-repairs). The average Tegner and International Knee Documentation Committee scores were 6.2 (range, 2-10) and 90.3 (range, 52-100), respectively. Risk factors for failure included complex and bucket-handle tear (P = .01), medial meniscal tears (P = .03), and skeletal immaturity (P = .01). Compared with isolated meniscal repairs in a similar pediatric and adolescent population, complex tears repaired in combination with ACL reconstruction did significantly better (57% vs 13%; P = .004). Conclusion Clinically successful repair of meniscal tears treated at the time of ACL reconstruction in patients 18 years or younger depends on tear type, with complex and bucket-handle tears being negative prognostic factors. Complex tears have a higher rate of clinical success when repaired at the time of ACL reconstruction versus when repaired in isolation.

Oligopeptide derivatives of metenkephalin were found to stimulate growth-hormone (GH) release directly by pituitary somatotrope cells in vitro in 1977. Members of this class of peptides and nonpeptidyl mimetics are referred to as GH secretagogues (GHSs). A specific guanosine triphosphatate-binding protein-associated heptahelical transmembrane receptor for GHS was cloned in 1996. An endogenous ligand for the GHS receptor, acylghrelin, was identified in 1999. Expression of ghrelin and homonymous receptor occurs in the brain, pituitary gland, stomach, endothelium/vascular smooth muscle, pancreas, placenta, intestine, heart, bone, and other tissues. Principal actions of this peptidergic system include stimulation of GH release via combined hypothalamopituitary mechanisms, orexigenesis (appetitive enhancement), insulinostasis (inhibition of insulin secretion), cardiovascular effects (decreased mean arterial pressure and vasodilation), stimulation of gastric motility and acid secretion, adipogenesis with repression of fat oxidation, and antiapoptosis (antagonism of endothelial, neuronal, and cardiomyocyte death). The array of known and proposed interactions of ghrelin with key metabolic signals makes ghrelin and its receptor prime targets for drug development.

Stiff skin syndrome, an autosomal dominant congenital form of scleroderma, is caused by mutations in the domain of fibrillin-1 that mediates integrin binding.