BackgroundRecently, some studies suggested that clinical diagnosis of fibromyalgia is inaccurate and does not reflect current definitions. However, this hypothesis has not been tested. We examined whether fibromyalgia was accurately diagnosed in the community.MethodsWe surveyed 3276 primary care patients to determine current fibromyalgia status by criteria (CritFM). We also determined whether the patients had a physician's diagnosis of fibromyalgia (MDFM) and the level of symptom severity as measured by the polysymptomatic distress scale (PSD).ResultsThe prevalence of MDFM and CritFM was 6.1% (95% confidence interval [CI] 5.3%, 6.9%) and 5.5% (95% CI 4.8%, 6.3%), respectively. However, only 32.2% with MDFM met 2016 criteria (CritFM), and only 35.4% with CritFM also had MDFM. The kappa statistic for diagnostic agreement was 0.296 (minimal agreement). The mean PSD score was 12.4 and 18.4 in MDFM and CritFM, respectively. The odds ratio for being a woman compared with being a man was 3.2 for MDFM versus 1.9 for CritFM, P = 0.023. Of the patients with MDFM, 68.3% received specific fibromyalgia pharmacotherapy.ConclusionsThere is little agreement between MDFM and CritFM. Only one‐third of MDFM satisfy fibromyalgia criteria, and only one‐third of patients who meet the criteria have a clinical diagnosis of fibromyalgia. Physician diagnosis is biased and more likely in women. Fibromyalgia treatment is common in MDFM (70.7%). Overall, MDFM appears subjective and unrelated to fibromyalgia criteria. There appears to be no common definition of fibromyalgia in the community.

Background: Hepatocytes metabolize the vast majority of ingested ethanol. This metabolic activity results in hepatic toxicity and impairs the ability of hepatocytes to replicate. Previous work by our group has shown that ethanol metabolism results in a G2/M cell cycle arrest. The intent of these studies was to discern the roles of acetaldehyde and reactive oxygen, two of the major by-products of ethanol metabolism, in the G2/M cell cycle arrest. Methods: To investigate the role of ethanol metabolites in the cell cycle arrest, VA-13 and VL-17A cells were used. These are recombinant Hep G2 cells that express alcohol dehydrogenase or alcohol dehydrogenase and cytochrome P450 2E1, respectively. Cells were cultured with or without ethanol, lacking or containing the antioxidants N-acetylcysteine (NAC) or trolox, for three days. Cellular accumulation was monitored by the DNA content of the cultures. The accumulation of the cyclin-dependent kinase, Cdc2 in the inactive phosphorylated form (p-Cdc2) and the cyclin-dependent kinase inhibitor p21 were determined by immunoblot analysis. Results: Cultures maintained in the presence of ethanol demonstrated a G2/M cell cycle arrest that was associated with a reduction in DNA content and increased levels of p-Cdc2 and p21, compared with cells cultured in its absence. Inclusion of antioxidants in the ethanol containing media was unable to rescue the cells from the cell cycle arrest or these ethanol metabolism-mediated effects. Additionally, culturing the cells in the presence of acetaldehyde alone resulted in increased levels of p-Cdc2 and p21. Conclusions: Acetaldehyde produced during ethanol oxidation has a major role in the ethanol metabolism-mediated G2/M cell cycle arrest, and the concurrent accumulation of p21 and p-Cdc2. Although reactive oxygen species are thought to have a significant role in ethanol-induced hepatocellular damage, they may have a less important role in the inability of hepatocytes to replace dead or damaged cells.

Nivolumab is a programmed cell death receptor (PD-1) inhibitor therapy for aggressive cancers; however, it poses a risk of immune-related adverse side effects. We present a 73-year-old male with renal cell carcinoma who developed myasthenia gravis (MG) after being treated with nivolumab, proven by acetylcholine receptor antibodies. Our patient presented with symptoms of fatigue and upper and lower extremity weakness, eventually resulting in respiratory failure as a result of MG. Nivolumab is an emerging therapy for advanced cancers but poses severe immune-related adverse events. Clinicians using PD-1 inhibitors should have a high index of suspicion of autoimmune diseases so that early discontinuation and treatment can be established to limit long-term morbidity and mortality.

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Chronic ankylosing spondylitis can lead to several rare long-term complications including cauda equina syndrome and inflammatory discitis especially without treatment. These complications are uncommon, but there is evidence that they can be treated with anti-tumor necrosis factor (TNF) inhibitors.We present a case of a 52-year-old male with a 30-year history of undiagnosed ankylosing spondylitis with cauda equina syndrome on initial outpatient presentation with a negative lumbosacral magnetic resonance imaging (MRI). He was admitted later that month and was found to have thoracic discitis from MRI requiring emergent decompressive laminectomy. The neurosurgeon collected a culture of the surgical site which showed rare Gram-positive cocci on Gram stain. Infectious disease was consulted, and he was started on empiric vancomycin. The culture from the surgical site did not grow any organisms. Interventional radiology (IR) aspirated the T7-T8 disk area one week later. The initial Gram stain showed rare Gram-negative rods this time, and cefepime was added to the patient's antibiotic regimen. The culture from the disk aspiration again grew no organisms. Rheumatology was then consulted and hypothesized that the patient's discitis could be secondary to inflammation from long-standing ankylosing spondylitis. The hospitalist, infectious disease specialist, and rheumatologist reviewed the case and recommended a six-week course of vancomycin and cefepime despite the negative cultures as an infectious etiology could not be excluded. He did show some clinical improvement after surgery and was started on adalimumab following completion of empiric antibiotics.This case highlights the difficulty in distinguishing between an infectious and inflammatory etiology for discitis in the setting of long-standing ankylosing spondylitis. The initiation of biological therapy without completely excluding the possibility of infection could lead to devastating consequences. It will likely be necessary to empirically treat for infection with these cases for the foreseeable future until there are more definitive tests to diagnose or exclude infectious discitis.