Citations

Abstract Objectives Symptomatic myopathy in sarcoidosis patients is not always due to sarcoid myopathy (ScM). We investigated the clinical and pathological spectrum including myxovirus resistance protein A (MxA) expression among sarcoidosis patients. Methods We reviewed the Mayo Clinic database (May 1980–December 2020) to identify sarcoidosis patients with myopathic symptoms and pathological evidence of myopathy. Results Among 5885 sarcoidosis patients, 21 had symptomatic myopathy. Eight carried a diagnosis of sarcoidosis 5.5 years (median) prior to myopathy onset. Eleven patients had ScM. The remaining had non-sarcoid myopathies (five IBM, one immune-mediated necrotizing myopathy, one non-specific myositis, two non-specific myopathy and one steroid myopathy). Estimated frequency of IBM is 85 per 100 000 sarcoidosis patients. The following features were associated with non-sarcoid myopathies (P < 0.05): (i) predominant finger flexor and quadriceps weakness, (ii) modified Rankin scale (mRS) >2 at time of diagnosis, (iii) creatine kinase >500 U/l, and (iv) absence of intramuscular granulomas. Sarcoplasmic MxA expression was observed in scattered myofibres in three patients, two of whom were tested for DM-specific autoantibodies and were negative. Immunosuppressive therapy led to improvement in mRS ≥1 in 5/10 ScM, none of the five IBM, and 3/3 remaining patients with non-sarcoid myopathies. Discussion Symptomatic myopathy occurred in 0.36% of sarcoidosis. IBM was the second most common cause of myopathies after ScM. Frequency of IBM in sarcoidosis is higher than in the general population. Recognition of features suggestive of alternative aetiologies can guide proper treatment. Our findings of abnormal MxA expression warrant a larger study.

AbstractIntroduction/AimsComplex repetitive discharges (CRDs) are spontaneous electromyography (EMG) waveforms often associated with chronic neurogenic or myopathic diseases, but incidentally identified CRDs have also been described. In this study we describe the distribution and possible significance of incidentally seen CRDs in otherwise normal electrodiagnostic studies.MethodsA retrospective chart review was performed of all patients with CRDs incidentally documented on otherwise normal electrodiagnostic studies at Mayo Clinic from January 2013 through December 2020. Each patient's clinical symptoms, referral reason, electrodiagnostic report, and imaging studies were analyzed using descriptive statistics.ResultsNinety‐four patients (86 females; mean age, 62 years; range, 20 to 86 years) and 107 CRDs were studied. The most common neuromuscular reasons for electrodiagnostic referrals included radiculopathy, peripheral neuropathy, and myopathy. Mean symptom duration was 43 months (range, 1 to 312 months). Eighty‐five patients had a CRD identified in one muscle (range, in all patients, one to five muscles). CRDs were identified most frequently in tensor fasciae latae (n = 21), biceps brachii (n = 16), and gluteus maximus (n = 9). Of the 58 patients in whom imaging was available, 46 (79%) had abnormalities that corresponded to the myotome in which the CRDs were visualized, most commonly L5 (n = 19) and C6 (n = 12). Of these 46 patients, 28 (61%) were referred for radicular or limb pain.DiscussionCRDs can be incidentally noted on otherwise normal electrodiagnostic studies, most commonly in L5 and C6 myotomes. The mechanism of CRDs in the absence of electrodiagnostic features of axon loss or remodeling is unknown.

Abstract The Obesity Paradox describes the counterintuitive finding that although obesity contributes to the development of chronic conditions such as chronic kidney disease and cardiovascular disease, obesity seems to improve mortality in patients with these diseases. This paradox has also been sited in the critical care literature in regard to acute kidney injury, obesity and mortality. This study's objective is to examine the impact of obesity and post-surgical acute kidney injury on hospital length of stay and 2-year mortality after orthopedic surgery. We reviewed the electronic medical records of all adult elective orthopedic surgery patients over 2 years in a large academic hospital. The 1783 patients who met inclusion criteria were divided into obese (body mass index, BMI ≥ 30, n = 1123) and non-obese groups (BMI <30, n = 660). Demographics, medications, comorbidities, and perioperative variables were included in multivariable logistic regression analyses with acute kidney injury, length of hospital stay, and two-year mortality as primary outcomes. Outcomes were analyzed for the entire group, the obese cohort and the non-obese cohort. Acute kidney injury developed in 5% of the post-surgical orthopedic patients. Obesity increased the likelihood of developing acute kidney injury post orthopedic surgery (odds ratio [OR] = 1.82; 95% Confidence interval [CI] 1.05–3.15, P = .034). Acute kidney injury increased length of stay by 1.3 days and increased the odds of two-year mortality (OR = 2.08; 95% CI 1.03–4.22, P = .041). However, obese patients had a decreased likelihood of two-year mortality (OR = 0.53; 95% CI 0.33–0.84, P = .009). In adult orthopedic surgery patients, obesity increased the risk of acute kidney injury. Patients who developed an acute kidney injury had longer hospital stays and higher two-year mortality. Paradoxically, obesity decreased two-year mortality.