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Atlantoaxial instability in os odontoideum with myelopathy.

STUDY DESIGN: This study analyzed the correlation between the atlantoaxial instability (especially sagittal plane rotatory instability) and myelopathy. Thirty-four patients with os odontoideum were reviewed in clinical symptoms and radiographs. OBJECTIVES: The results were correlated to provide a rationale for the genesis of myelopathy. SUMMARY OF BACKGROUND DATA: Instability of the atlantoaxial joint has been evaluated with atlantodental interval, space available for the spinal cord, instability index, and others. These are excellent indices for anteroposterior instability. However, they are insufficient for the evaluation of the multidirectional instability in os odontoideum. METHODS: Thirty-four patients were analyzed in three parameters on the lateral radiographs: the minimum distance from the posterior border of the C2 body to the posterior arch of atlas, the difference of the atlanto-axial angle between the flexion and extension position (sagittal plane rotation angle), and the change of space available for the spinal cord from flexion to extension (Instability Index). RESULTS: The correlation between the sagittal plane rotation angle and the instability index was low (r = 0.561). In patients with more than 20 degrees of the sagittal plane rotation angle, myelopathy was shown at a high rate (86%). Myelopathy was also shown at a high rate (90%) in the patients with more than 40% of the instability index. CONCLUSIONS: It is important to check the sagittal plane rotation angle and the instability index to evaluate the instability in os odontoideum. If the patient has either a sagittal plane rotation angle of more than 20 degrees or an instability index of more than 40%, he or she is likely to have the cord signs.

Adolescent↗

Arthrogenic muscle inhibition in the leg muscles of subjects exhibiting functional ankle instability.

BACKGROUND: Functional ankle instability or a subjective report of ;;giving way'' at the ankle may be present in up to 40% of patients after a lateral ankle sprain. Damage to mechanoreceptors within the lateral ankle ligaments after injury is hypothesized to interrupt neurologic feedback mechanisms resulting in functional ankle instability. The altered input can lead to weakness of muscles surrounding a joint, or arthrogenic muscle inhibition. Arthrogenic muscle inhibition may be the underlying cause of functional ankle instability. Establishing the involvement of arthrogenic muscle inhibition in functional ankle instability is critical to understanding the underlying mechanisms or chronic ankle instability. The purpose of this investigation was to determine if arthrogenic muscle inhibition is present in the ankle joint musculature of patients exhibiting unilateral functional ankle instability. METHODS: Twenty-nine subjects, 15 with unilateral functional ankle instability and 14 healthy control subjects, consented to participate. Bilateral soleus, peroneal, and tibialis anterior H-reflex and M-wave recruitment curves were obtained. Maximal H-reflex and maximal M-wave values were identified and the H:M ratios were calculated for data analysis. Separate 1 x 2 ANOVA were done for both the functional ankle instability and control groups to evaluate differences between limbs on the H:M ratios. Bonferroni multiple comparison procedures were used for post hoc comparisons (p < or = 0.05). RESULTS: The soleus and peroneal H:M ratios for subjects with functional ankle instability were smaller in the injured limb when compared with the uninjured limb (p < 0.05). No limb difference was detected for the tibialis anterior H:M ratio in the functional ankle instability group (p = 0.904). No side-to-side differences were detected for the H:M ratios in patients reporting no history of ankle injury (p > 0.05). CONCLUSIONS: Depressed H:M ratios in the injured limb suggest that arthrogenic muscle inhibition is present in the ankle musculature of patients exhibiting functional ankle instability. Establishing and using therapeutic techniques to reverse arthrogenic muscle inhibition may reduce the incidence of functional ankle instability.

Adult↗

Functional outcome and risk of recurrent instability after primary traumatic anterior shoulder dislocation in young patients.

BACKGROUND: The prevalence and risk factors for recurrent instability and functional impairment following a primary glenohumeral dislocation remain poorly defined in younger patients. We performed a prospective cohort study to evaluate these outcomes. We also aimed to produce guidelines for the design of future clinical trials, assessing the efficacy of interventions designed to improve the outcome after a primary dislocation. METHODS: We performed a prospective cohort study of 252 patients ranging from fifteen to thirty-five years old who sustained an anterior glenohumeral dislocation and were treated with sling immobilization, followed by a physical therapy program. Patients received regular clinical follow-up to assess whether recurrent instability had developed. Functional assessments were made and were compared for two subgroups: those who had not had instability develop and those who had received operative stabilization to treat recurrent instability. RESULTS: On survival analysis, instability developed in 55.7% of the shoulders within the first two years after the primary dislocation and increased to 66.8% by the fifth year. The younger male patients were most at risk of instability, and 86.7% of all of the patients known to have recurrent instability had this complication develop within the first two years. A small but measurable degree of functional impairment was present at two years after the initial dislocation in most patients. Sample-size calculations revealed that a relatively small number of patients with a primary dislocation would be required in future clinical trials examining the effects of interventions designed to reduce the prevalence of recurrent instability and improve the functional outcome. CONCLUSIONS: Recurrent instability and deficits of shoulder function are common after primary nonoperative treatment of an anterior shoulder dislocation. There is substantial variation in the risk of instability, with younger males having the highest risk and females having a much lower risk. Future clinical trials to evaluate primary interventions should evaluate the prevalence of recurrent instability and functional deficits, with use of an assessment tool specifically for shoulder instability, during the first two years after the initial dislocation.

Adolescent↗

Palmar radiocarpal dislocation resulting in ulnar radiocarpal translocation and multidirectional instability.

Posttraumatic ulnar radiocarpal translation is a rare, often subtle, highly unstable, and potentially devastating manifestation of severe "proximal radiocarpal ligamentous instability. Radiocarpal dislocation should alert the treating physician to the risks of the spectrum of radiocarpal instabilities. Radiocarpal instability may initially be masked or unappreciated owing to presentation without radiocarpal dislocation, local pain and swelling, initially normal standard wrist radiographs, lack of recognition, or delay in the appearance of a static lesion. The specificity, sequence, and extent of extrinsic radiocarpal and ulnocarpal ligament traumatic disruptions are not fully understood, vary with injury severity, and may differ in instances of dorsal as opposed to palmar subluxation or dislocation. Multidirectional (global) wrist instability typically accompanies this ulnar radiocarpal instability in its most severe form and consequences may be dire. The carpus may be difficult to reduce or maintain owing to marked instability, compressive forces across the wrist, and soft tissue or bony fragment interposition. Additional local distal radioulnar joint or intercarpal injuries may further confound stability and require their own specific and simultaneous treatment. Radiocarpal reduction and repair of the radioscaphocapitate ligament and radiolunate ligaments may be sufficient treatment for acute isolated palmar radiocarpal instability. Temporary K-wire fixation may be added as a precaution to prevent palmar carpal subluxation during the time of ligament healing. Radiocarpal reduction, palmar and dorsal soft-tissue repair, and temporary K-wire fixation comprise one method of treatment for early recognized cases of post-traumatic ligamentous ulnar radiocarpal transposition. Halikis et al have recommended radiolunate arthrodesis. Rayhack et al have suggested that limited or complete wrist arthrodesis may be indicated for patients with delayed presentation or in acute cases with extreme instability. Wrist arthrodesis is one means of management for patients with severe radiocarpal instability confounded by distal radioulnar joint or intercarpal instability, as seen in our patient. Damaged ligaments may have a poor blood supply and often may not hold sutures or heal well. Bone anchor sutures or some type of ligament augmentation may help to restore joint stability in some patients. Loss of stability may occur later owing to ligamentous laxity or inadequate soft-tissue healing. Radiolunate, radiocarpal, or complete wrist arthrodesis may be necessary to relieve pain, restore wrist alignment and stability, and reestablish extremity function for patients with chronic radiocarpal instability. Wrist symptoms, age, general health, hand dominance, and occupation may be among the factors that influence the necessity for and timing of reconstruction. Rayhack et al have also postulated that negative ulnar variance may accommodate the occurrence of ulnar radiocarpal translocation and confound repair owing to lack of buttress at the ulnocarpal joint. They further speculated that a joint leveling procedure might improve the support for ligamentous repair or reconstruction in these cases. Permanent functional impairment must be anticipated in patients with ulnar radiocarpal instability. Impairment has typically been commensurate with the extent of the initial lesion, additional confounding local lesions, and length of follow-up.

Accidents, Traffic↗

Instability after shoulder arthroplasty: results of surgical treatment.

BACKGROUND: Currently, there is little available information regarding the surgical treatment of instability following shoulder arthroplasty. The purpose of the present study was to review the results of revision surgery performed for the treatment of instability after shoulder arthroplasty to better define the causes of instability and the risk factors for an unsatisfactory outcome. METHODS: Between 1985 and 1999, thirty-three shoulders (seven of which had had a hemiarthroplasty and twenty-six of which had had a total shoulder arthroplasty) were treated surgically at our institution for anterior instability (nineteen shoulders) or posterior instability (fourteen shoulders). The primary arthroplasty had been performed for the treatment of degenerative arthritis in sixteen shoulders, arthritis of dislocation in six, acute fracture in four, rheumatoid arthritis in three, and other conditions in four. RESULTS: The instability was attributed to abnormal capsular tension and/or rotator cuff dysfunction in twenty-one shoulders, component malpositioning in one shoulder, and a combination of both in eleven shoulders. One shoulder was treated with removal of the components. In the remaining thirty-two shoulders, each of the elements that was contributing to the instability was specifically addressed at the time of surgery. Revision surgery restored stability in nine of the thirty-two shoulders. Anterior instability was associated with a higher failure rate than posterior instability was (p = 0.04). Although eleven shoulders had additional surgery for the treatment of recurrent instability, only fourteen of the thirty-three shoulders were stable at the time of the final follow-up. According to the Neer rating system, there were four excellent, six satisfactory, and twenty-three unsatisfactory results. CONCLUSIONS: Soft-tissue imbalance is present in most cases of instability following shoulder arthroplasty, and component malpositioning plays an additional role in some cases. More than one-half of the shoulders in the present study remained unstable despite attempts at revision. Surgical treatment of instability following arthroplasty is associated with only a modest success rate.

Adult↗

Microsatellite instability in Japanese gastric cancer.

BACKGROUND: Recent studies have shown that microsatellites are unstable in various types of cancers, and such genetic instability at the microsatellite loci (microsatellite instability) has been considered to play an important role in the development of cancer. However, the clinicopathologic significance of microsatellite instability in gastric cancer has not been clarified. METHODS: To elucidate the role of genetic instability in the development of gastric cancer, the presence of microsatellite instability was examined in 25 cases of gastric cancer using fresh-frozen tumor-normal paired samples using a polymerase chain reaction (PCR)-based method. Microsatellite instability was defined as tumors that showed altered banding patterns at two or more microsatellite loci. RESULTS: The incidence of microsatellite instability in gastric cancer cases was 4 of 25 patients (16%) and 4 of 26 cancers (15%). A significantly high incidence of microsatellite instability was observed in both the elderly (P < 0.01) and in lymph node metastasis-negative patients (P < 0.05). All patients with gastric cancer showing microsatellite instability were negative for lymphatic or venous permeation. A statistically significant association of microsatellite instability with no lymphatic permeation was thus observed (P < 0.05). CONCLUSIONS: This study revealed infrequent lymph node metastasis and lymph vessel invasion in the patients with gastric cancer demonstrating microsatellite instability. Although the number of examined cases was small, these findings suggest that gastric cancer that shows microsatellite instability may thus behave in a less malignant manner.

Chromosome Banding↗

Microsatellite instability in colorectal cancer: improved assessment using fluorescent polymerase chain reaction.

BACKGROUND & AIMS: Microsatellite instability was first described in hereditary nonpolyposis colorectal cancers and sporadic colorectal cancers, in which it was associated with a good prognosis. The aim of this study was to assess the advantages of a novel fluorescent assay for detecting microsatellite instability. METHODS: Eleven fluorescently tagged microsatellites and an automated DNA sequencer were used to investigate 54 sporadic colorectal adenocarcinomas. RESULTS: This fluorescent assay combined accurate allele sizing with cross-sectional data display and allowed improved assessment of microsatellite instability. Twenty-two percent of cancers (12 of 54) showed microsatellite instability with at least one marker. For tumors showing microsatellite instability, results were obtained for a minimum of eight markers. Six tumors showed microsatellite instability at high frequency (at least 63% of markers affected), and 42% of the patients who had a tumor showing microsatellite instability had a synchronous and/or metachronous colorectal tumor (vs. 7% of patients whose tumor did not show microsatellite instability). Patients with a microsatellite instability-positive tumor had an improved prognosis (P = 0.03). CONCLUSIONS: The use of this fluorescent assay improved the assessment of microsatellite instability with the automated analysis and cross-sectional data display. The assay identified a subgroup of patients who showed microsatellite instability and who also showed clinical features that differed from the microsatellite instability-negative cases.

Adenocarcinoma↗

Microsatellite instability in a population of sporadic colorectal cancers: correlation between genetic and pathological profiles.

BACKGROUND: Tumours with high-frequency microsatellite instability exhibit unique genotype and phenotype features, whereas the difference between low-frequency microsatellite instability and apparently stable tumours is far from being clear. AIMS: To identify distinctive genetic and pathological characteristics of low-frequency microsatellite instability tumours. METHODS: Microsatellite instability status of 57 sporadic colorectal cancers and its correlation with genetic, pathological and clinical features was analysed. RESULTS: High frequency microsatellite instability and low-frequency microsatellite instability and apparently stable cancers were different in terms of tumour localisation (p=0.015), frequency of APC mutations (p=0.012), occurrence of Crohn's-like/lymphoid reaction (p=0.0353) and morphological evidence of origin from an adenoma (p=0.0338). Specifically, in low-frequency microsatellite instability cancers, APC mutations were very frequent (76.9%, 10/13) and a Crohn's-like/lymphoid reaction was common (38.5%, 5/13). High-frequency microsatellite instability tumours were preferentially located in the right colon and exhibited a higher frequency of loss of heterozygosity at the FHIT locus compared with low-frequency microsatellite instability and apparently stable cases (p=0.0243). Dukes' stage (p=0.0021), tumour localisation (p=0.0410) and pattern of cancer growth (p=0.0374), were the only factors affecting patient survival. However, a borderline improvement was noted in overall survival in high-frequency microsatellite instability and low-frequency microsatellite instability cancer patients (p=0.062). CONCLUSIONS: These results indicate that low-frequency microsatellite instability tumours have different genetics and histological features and suggest that they are a distinct group of colorectal cancers.

Adult↗

Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy for colon cancer.

BACKGROUND: Colon cancers with high-frequency microsatellite instability have clinical and pathological features that distinguish them from microsatellite-stable tumors. We investigated the usefulness of microsatellite-instability status as a predictor of the benefit of adjuvant chemotherapy with fluorouracil in stage II and stage III colon cancer. METHODS: Tumor specimens were collected from patients with colon cancer who were enrolled in randomized trials of fluorouracil-based adjuvant chemotherapy. Microsatellite instability was assessed with the use of mononucleotide and dinucleotide markers. RESULTS: Of 570 tissue specimens, 95 (16.7 percent) exhibited high-frequency microsatellite instability. Among 287 patients who did not receive adjuvant therapy, those with tumors displaying high-frequency microsatellite instability had a better five-year rate of overall survival than patients with tumors exhibiting microsatellite stability or low-frequency instability (hazard ratio for death, 0.31 [95 percent confidence interval, 0.14 to 0.72]; P=0.004). Among patients who received adjuvant chemotherapy, high-frequency microsatellite instability was not correlated with increased overall survival (hazard ratio for death, 1.07 [95 percent confidence interval, 0.62 to 1.86]; P=0.80). The benefit of treatment differed significantly according to the microsatellite-instability status (P=0.01). Adjuvant chemotherapy improved overall survival among patients with microsatellite-stable tumors or tumors exhibiting low-frequency microsatellite instability, according to a multivariate analysis adjusted for stage and grade (hazard ratio for death, 0.72 [95 percent confidence interval, 0.53 to 0.99]; P=0.04). By contrast, there was no benefit of adjuvant chemotherapy in the group with high-frequency microsatellite instability. CONCLUSIONS: Fluorouracil-based adjuvant chemotherapy benefited patients with stage II or stage III colon cancer with microsatellite-stable tumors or tumors exhibiting low-frequency microsatellite instability but not those with tumors exhibiting high-frequency microsatellite instability.

Analysis of Variance↗

Lymphocyte-rich gastric cancer: associations with Epstein-Barr virus, microsatellite instability, histology, and survival.

Lymphocyte-rich gastric carcinomas may have a better prognosis than cancers without a pronounced host inflammatory response. Two subsets of gastric cancer-Epstein-Barr virus-positive and microsatellite instability high-have been associated with a lymphocyte-rich phenotype. We assessed relationships between tumor-infiltrating lymphocytes, Epstein-Barr virus status, microsatellite instability status, and cancer-specific survival in 110 resected gastric cancers. Seven patients had Epstein-Barr virus-positive cancer, including 4 (3.7%) of 107 consecutive patients. Tumors from 17 patients (16%) were designated microsatellite instability high on the basis of negative immunohistochemical staining for MLH1; all tumors had intact expression of MSH2 and MSH6. Epstein-Barr virus-positive cancers had increased tumor-infiltrating lymphocytes compared with Epstein-Barr virus-negative cancers (median 450/10 HPF versus 21/10 HPF, P <.001). Microsatellite instability-high cancers also had increased tumor-infiltrating lymphocytes compared with non-microsatellite instability-high cancers (median 150/10 HPF versus 20/HPF, P <.001). Microsatellite instability-high cancers affected older patients and were more likely to be intestinal in the Lauren classification and expanding in the Ming classification. By univariate analysis, decreased risk of death from gastric cancer was significantly associated with low tumor stage, expanding growth pattern, increasing tumor-infiltrating lymphocyte count, and microsatellite instability-high status. High tumor-infiltrating lymphocyte count and microsatellite instability-high status retained statistical significance as favorable prognostic factors after adjustment for tumor stage in multivariate analysis. Tumor-infiltrating lymphocyte count retained statistical significance as a favorable prognostic factor after adjustment for microsatellite instability-high status; but microsatellite instability-high status did not remain a significant independent prognosticator after adjustment for tumor-infiltrating lymphocyte count. The association between microsatellite instability-high cancers and high tumor-infiltrating lymphocyte counts may account for the association of microsatellite instability-high gastric cancers with improved survival.

Adenocarcinoma↗

Genomic instability of microsatellite repeats and its association with the evolution of chronic myelogenous leukemia.

Tumorigenesis has been shown to proceed through a series of genetic alterations involving protooncogenes and tumor-suppressor genes. Investigation of genomic instability of microsatellites has indicated a new mechanism for human carcinogenesis in hereditary nonpolyposis colorectal cancer and sporadic cancer and this instability has been shown to be related to inherited predisposition to cancer. This study was conducted to determine whether such microsatellite instability is associated with the evolution of chronic myelogenous leukemia (CML) to the blast crisis. Nineteen CML patients clinically progressing from the chronic phase to accelerated phase or blast crisis and 20 other patients in the CML chronic phase were studied. By polymerase chain reaction assay, DNAs for genomic instability in five separate microsatellites in chromosome arms 5q (Mfd27), 17p (Mfd41), 18q (DCC), 3p (CI3-9), and 8p (LPL) were examined. Differences in unrelated microsatellites of chronic and blastic phase DNAs in 14 of 19 patients (73.7%) were demonstrated. Somatic instability in five microsatellites, Mfd27, Mfd41, DCC, CI3-9, and LPL, was detected in 2 of 19 (10.5%), 8 of 19 (42.1%), 11 of 19 (57.9%), 4 of 17 (23.5%), and 4 of 17 (23.5%) cases. In 10 of 19 cases (52.6%), genetic instability in at least two of five microsatellites was observed and was categorized as replication error (RER+) phenotype. CML evolution cases with myeloid, lymphoid, and mixed phenotypes and the blast crisis and accelerated phase showed somatic instability in a number of microsatellites. No alterations in leukemic cells at the chronic phase could be detected in any microsatellites. These data indicate instability of microsatellites (RER+) but not familial predisposition to possibly be a late genetic event in the evolution of CML to blast crisis. In the microsatellite of the DCC gene, complicated alterations in band patterns caused by instability as well as loss of heterozygosity (LOH) were observed in 13 of 19 cases (68.4%): instability in 9 cases, instability plus LOH in 2 cases, and only LOH in 2 cases. These highly frequent alterations in microsatellites, including instability and LOH, suggesting that secondary events due possibly to loss of fidelity in replication and repair machinery may be significantly associated with CML evolution.

Adult↗

Reports of joint instability in knee osteoarthritis: its prevalence and relationship to physical function.

OBJECTIVE: To report the prevalence and relationship of self-reported knee instability to physical function in a sample of subjects with knee osteoarthritis (OA), and to discuss the implications of these observations for rehabilitation. METHODS: Subjects were 105 individuals (80 females) with knee OA who rated their knee instability severity on a 6-point numeric scale in response to the query "To what degree does giving way, buckling, or shifting of the knee affect your level of daily activity?" A principal component analysis was used to combine The Western Ontario and McMaster Universities pain, stiffness, and physical function subscale scores, and the Timed Get Up and Go Test score into a principal component score for physical function (PCPF). Other variables that could affect the PCPF such as age, sex, years with knee OA, radiographic severity of knee OA, knee pain, knee motion, and quadriceps strength were also recorded. The prevalence of self-reported knee instability was determined by calculating the proportion of subjects who reported each severity level of knee instability. Hierarchical regression analysis was performed to determine if the level of self-reported knee instability could predict the PCPF, even after accounting for the effects of the other variables. RESULTS: Sixty-three percent of the subjects reported knee instability during activities of daily living, and 44% reported that instability affects their ability to function. The severity of self-reported knee instability was associated with the PCPF (eta2=0.40, P <0.001), and after controlling for all other independent variables, significantly increased the prediction of the PCPF (r2=0.56, r2 change=0.05; P <0.001). CONCLUSION: The results indicate that a substantial proportion of individuals with knee OA report episodes of knee instability during activities of daily living, and instability affects physical function beyond that which can be explained by contributions from other impairments such as knee pain, range of motion, and quadriceps strength. Knee instability is a problem that should be specifically addressed in rehabilitation programs and may require interventions beyond those that address pain, joint motion, and muscular strength, to maximize the effectiveness of rehabilitation for individuals with knee OA.

Activities of Daily Living↗

Dynamic MR imaging and stress testing in glenohumeral instability: comparison with normal shoulders and clinical/surgical findings.

Our objectives were to test the hypotheses that: 1) during shoulder motion, glenohumeral alignment differs between asymptomatic shoulders and those with symptomatic instability; 2) during magnetic resonance (MR)-monitored physical exam or stress testing, glenohumeral alignment differs between asymptomatic shoulders and those with instability; and 3) glenohumeral translation during MR stress testing correlates with findings of shoulder instability by clinical exam and exam under anesthesia (EUA). Using an open-configuration 0.5 T MR imaging (MRI) system, we studied symptomatic shoulders in 11 subjects and compared them to their contralateral asymptomatic shoulders. Each shoulder was studied during abduction/adduction and internal/external rotation to determine the humeral head position on the glenoid. An examiner also performed the MR stress test on each shoulder by applying manual force on the humeral head during imaging. All shoulders were assigned an instability grade from the MR stress test, and this grade was correlated with: 1) clinical exam grade assigned during preoperative assessment by an orthopedic surgeon and 2) intraoperative instability grade by EUA immediately preceding arthroscopy. With dynamic abduction and internal/external rotation, the humeral head remained centered on the glenoid in 9 of 11 shoulders, but in two subjects there were dramatic demonstrations of subluxation. With stress testing, a trend toward more joint laxity was demonstrated in symptomatic than in asymptomatic joints (P = 0.11). MR grading of instability correlated directly with clinical grading in six cases and underestimated the degree of instability relative to clinical exam in the other cases. MR instability grading systematically underestimated instability compared with EUA in 7 of the 10 cases that underwent surgical repair. We concluded that dynamic MR evaluation of glenohumeral alignment did not demonstrate abnormalities in symptomatic shoulders in 8 of 10 patients, whereas 2 patients showed dramatic findings of subluxation. Manual stress testing during dynamic MR examination showed a strong correlation with clinical instability grading. Dynamic shoulder MR examination during stress testing could, with further validation, become a useful adjunct to shoulder instability evaluations. J. Magn. Reson. Imaging 2001;13:748-756.

Adolescent↗

Arthroscopic management of traumatic anterior shoulder instability in collision athletes: analysis of 204 cases with a 4- to 9-year follow-up and results with the suture anchor technique.

PURPOSE: The purpose of this study was to determine the effectiveness of arthroscopy in the selection of surgical procedure and treatment of both acute and recurrent traumatic anterior shoulder instability in rugby players by use of pre-established selection criteria. We describe the injury mechanisms, analyze the pathologic lesions and treatment indications based on surgical findings, and assess the results in patients treated with the arthroscopic suture anchor technique. METHODS: From November 1996 to November 2001, 204 rugby players with acute or recurrent traumatic anterior instability underwent an initial arthroscopic examination. Criteria such as type of Bankart lesion, tissue quality, and presence of bony defects were evaluated and used to determine the method of stabilization: arthroscopy or open stabilization. Open surgery was indicated in patients with bone humeral deficiencies greater than one fourth of the articular humeral head, bone glenoid deficiencies greater than 25% of the glenoid extension, capsular laxity with poor tissue quality, and humeral avulsion of the glenohumeral ligament; all other patients underwent arthroscopic reconstruction via the bone suture anchor technique. RESULTS: The mean follow-up was 5.9 years (range, 3.9 to 8.9 years). We performed arthroscopic stabilization in 39 cases of acute instability; only 1 case (2.5%) required the mini-open technique for reinsertion of humeral avulsion of the glenohumeral ligament. Of 158 cases of recurrent instability, 121 underwent arthroscopic stabilization, and 37 (23.4%) required reconstruction with open surgery. The main cause was bony deficiency (treated with the Latarjet procedure). The results of the arthroscopic reconstructions were evaluated by use of the Rowe scale and analyzed according to stability and range of motion. Good or excellent results were found in 94.9% of cases in the acute instability group and in 91.8% in the recurrent instability group, the poor results were due to instability recurrence. In the acute instability group there were 2 cases of recurrence (5.1%) while playing rugby. In the recurrent instability group there were 10 recurrences (8.3%). CONCLUSIONS: Arthroscopic stabilization was possible in 97.5% of our patients with acute instability and 76.6% of patients with recurrent instability based on the selection criteria for this population. We were able to obtain excellent results in 90% of cases using the suture anchor technique in rugby players with our selection criteria. LEVEL OF EVIDENCE: Level IV, therapeutic case series.

Adolescent↗

An evaluation of two scoring systems to predict instability in fractures of the distal radius.

BACKGROUND: Various scoring scales have been introduced in the management of patients with multiple injuries and lower extremity injuries. Two scoring systems have been introduced to predict instability in distal radius fractures. The purpose of this investigation was to evaluate the accuracy of these two models in predicting instability. METHODS: A prospective study of 105 consecutive patients sustaining unilateral closed distal radius fractures was performed. Two scoring systems--the MacKenney formula and the Adolphson formula--were used to calculate the probability of fracture instability on the basis of initial presentation and injury films. The predicted probability of instability calculated from both models was then compared with actual results of instability on the basis of specific radiographic criteria at follow-up. RESULTS: Final follow-up information was available on 80 patients. There were 44 unstable fractures and 36 stable fractures at final follow-up. Using the MacKenney formula, of the 38 fractures predicted to have a low probability of instability (Pinstability < 30%), 18 (47.4%) were found to be unstable. Using the Adolphson formula, of the 28 fractures predicted to have a low probability of instability (Pstability > 70%), 14 (50%) were actually unstable. CONCLUSION: Both scoring systems were found to underestimate the degree of fracture instability and to have a negative predictive value between 47 and 50% in a prospective series of patients. In fractures predicted to have a low probability of instability in both models, we found a poor correlation between predicted instability and actual instability. Our results demonstrate the limitations of two scoring systems in predicting fracture stability and in making clinical decisions on the basis of their results.

Adult↗

Evaluation of Bethesda guidelines in relation to microsatellite instability.

PURPOSE: The Bethesda guidelines were developed for selection of patients whose tumors should be tested for high microsatellite instability. This study examined the validity of the different Bethesda criteria in relation to microsatellite instability status to simplify their use in clinical practice. METHODS: A total of 164 patients with colorectal or hereditary nonpolyposis colorectal cancer-associated cancers were registered on the basis of the Amsterdam criteria without age limitations (11 cases), multiple tumors (2 cases), the accumulation of colorectal cancer in the family (no first-degree relatives affected or the index patient's age up to 50 years; 45 cases), an early age at onset up to 50 years (13 cases), morphologic and histopathologic manifestations (right-sided colorectal cancer, mucinous undifferentiated histology; 1 case), and the Bethesda criteria (92 cases). The microsatellite instability status of tumors was determined using the International Collaborative Group on Hereditary Non-Polyposis Colorectal Cancer marker reference panel. RESULTS: When applying all Bethesda criteria, high microsatellite instability tumors were identified in our hereditary nonpolyposis colorectal cancer registry with a sensitivity of 87 percent. Twenty-nine percent (27/92) of the Bethesda-positive patients displayed high microsatellite instability compared with 6 percent of patients (4/72) not meeting these criteria (P < 0.001). Only Bethesda Criteria 1, 3, and 4 showed a significantly different distribution of the microsatellite instability status when compared with those of the remaining patients registered (P < or = 0.001). These three criteria detected high microsatellite instability tumors in 48 percent (10/21), 50 percent (18/36), and 31 percent (21/67) of patients, respectively. When applying these criteria only, a cumulative detection rate of 77 percent of all (24/31) high microsatellite instability cases was found, thereby identifying 89 percent of high microsatellite instability tumors among the Bethesda-positive patients. Patients matching Criteria 1, 3, and 4 frequently showed hMSH2 or hMLH1 germline mutations and tumor-specific loss of protein expression. CONCLUSION: In our hereditary nonpolyposis colorectal cancer registry the complete Bethesda criteria showed the highest sensitivity to identify patients with high microsatellite instability tumors. However, for general medical practice outside academic centers, three criteria are reasonably accurate for adequate high microsatellite instability tumor selection.

Adult↗

Microsatellite instability as a marker in predicting metachronous multiple colorectal carcinomas after surgery: a cohort-like study.

PURPOSE: In case-control studies, it was reported that microsatellite instability might be helpful in predicting the development of metachronous multiple colorectal cancers. The purpose of this cohort-like study was to determine whether microsatellite instability is a novel independent marker in predicting metachronous colorectal carcinomas after colorectal cancer surgery. METHODS: Three hundred twenty-eight colorectal carcinoma patients were surveyed by periodic colonoscopy for at least three years after surgery. Among these, DNA from paraffin-embedded sections was available for 272 cases. DNA of these cases was studied for six microsatellite markers (five dinucleotide repeats, one mononucleotide repeat). Microsatellite instability phenotype was defined as alterations in one or more loci. RESULTS: Median follow-up period was 74 months, and the median number of colonoscopies was 4.6. The percentage of microsatellite instability-positive cases was 26.4 percent (72/272). Seventeen metachronous colorectal carcinomas were detected during the follow-up period. Incidences of metachronous colorectal carcinomas in microsatellite instability-positive and microsatellite instability-negative cases were 15.3 and 3 percent, respectively (P < 0.001). The cumulative five-year incidence of metachronous colorectal carcinomas was significantly higher in microsatellite instability-positive cases than in microsatellite instability-negative cases (12.5 vs. 2.5 percent, P < 0.0001). Logistic regression analysis of the relationship between incidence of metachronous colorectal carcinomas and possible risk factors (namely, coexistence of adenoma at the time of surgery, family history of colorectal carcinoma, history of extracolonic malignancy, and microsatellite instability status) showed that microsatellite instability and coexistence of adenoma were significant independent risk factors for the occurrence of metachronous colorectal carcinomas, with values of P = 0.001 and 0.02, respectively. CONCLUSION: These data indicate that microsatellite instability can be regarded as a novel independent and important marker for predicting the development of metachronous colorectal carcinoma after surgery.

Carcinoma↗

Variable levels of chromosomal instability and mitotic spindle checkpoint defects in breast cancer.

Cytogenetic analyses have revealed that many aneuploid breast cancers have cell-to-cell variations of chromosome copy numbers, suggesting that these neoplasms have instability of chromosome numbers. To directly test for possible chromosomal instability in this disease, we used fluorescent in situ hybridization to monitor copy numbers of multiple chromosomes in cultures of replicating breast cancer-derived cell lines and nonmalignant breast epithelial cells. While most (7 of 9) breast cancer cell lines tested are highly unstable with regard to chromosome copy numbers, others (2 of 9 cell lines) have a moderate level of instability that is higher than the "background" level of normal mammary epithelial cells and MCF-10A cells, but significantly less than that seen in the highly unstable breast cancer cell lines. To evaluate the potential role of a defective mitotic spindle checkpoint as a cause of this chromosomal instability, we used flow cytometry to monitor the response of cells to nocodazole-induced mitotic spindle damage. All cell lines with high levels of chromosomal instability have defective mitotic spindle checkpoints, whereas the cell lines with moderate levels of chromosomal instability (and the stable normal mammary cells and MCF10A cells) arrest in G(2) when challenged with nocodazole. Notably, the extent of mitotic spindle checkpoint deficiency and chromosome numerical instability in these cells is unrelated to the presence or absence of p53 mutations. Our results provide direct evidence for chromosomal instability in breast cancer and show that this instability occurs at variable levels among cells from different cancers, perhaps reflecting different functional classes of chromosomal instability. High levels of chromosomal instability are likely related to defective mitotic checkpoints but not to p53 mutations.

Breast Neoplasms↗