New in the general journals: A chart review suggests rethinking recommendations about monitoring osteoporosis treatments. Also: Stroke as a presenting symptom for fungus-infected spinal injections, and more ...
Last week's articles on rheumatology topics in the major non-rheumatology journals.
“Due” for a Scan: Examining the Utility of Monitoring DensitometryJAMA Intern Med. Published online July 22, 2013
Many professional guidelines recommend dual-energy x-ray absorptiometry (DXA) scans every one or two years while a patient is receiving treatment for low bone mineral density (BMD). However, monitoring DXA rarely leads to treatment changes. In a chart review of 549 patients, with a median of one scan every 2.4 years, most scans (84%) resulted in no treatment changes, even when DXA showed a significant decrease in BMD. Routine use of DXA for average-risk women receiving treatment should be “reconsidered.”
Vascular Complications of Fungal Meningitis Attributed to Injections of Contaminated Methylprednisolone AcetateJAMA Neurol. published online, July 22, 2013
Patients with fungal meningitis caused by epidural spinal injections of contaminated methylprednisolone for low back pain may present with acute ischemic stroke. These cases are a “diagnostic dilemma,” because they also have one or more traditional factors for stroke. They should be given early antifungal treatment without waiting for a definitive diagnosis. This report describes three patients, mean age 75 years. Two died.
Stiff Person Syndrome
Neuronal Surface and Glutamic Acid Decarboxylase Autoantibodies in Nonparaneoplastic Stiff Person Syndrome JAMA Neurol. published online, July 22, 2013
Autoantibodies in stiff person syndrome (SPS) bind to a neuronal surface target in the hippocampus and brainstem. Patients with SPS have high titers of autoantibodies to glutamic acid decarboxylase (GAD, which is required for synthesis of γ-aminobutyric acid (GABA), and impaired GABAergic neurons are implicated in SPS. However, when autoantibodies from SPS patients were incubated with GABAergic neurons, the autoantibodies co-localized not only to GAD but also to neuronal surface proteins. In mice, these human autoantibodies bound to the hippocampus and brainstem.