Diagnostic Imaging Use for the Initial Evaluation of Low Back Pain by Primary Care Providers in the United States: 2011-2016

ObjectiveHigh-value care guidelines from multiple medical societies recommend against imaging for the initial evaluation of low back pain in the absence of red flag symptoms. We aimed to determine the current temporal and geographic landscape of imaging ordering patterns for this indication among US primary care providers.MethodsUsing a national commercial insurance claims database, we identified patients between 18 and 64 years old who presented to a primary care provider for an initial evaluation of low back pain between 2011 and 2016. Patients were identified via International Classification of Diseases codes, and the use of diagnostic imaging was identified by Current Procedural Terminology codes. Geographic regions were based on the location of patient residence.ResultsOverall, 627,118 encounters met inclusion criteria. Imaging acquisitions increased over time, from 14% of encounters in 2011 to 16% in 2016 (P < .01). Radiographs represented 96% of ordered imaging, CT 2%, and MRI 3%. The likelihood of having any imaging for low back pain varied significantly by US census region and by US state (P < .01). The greatest use of imaging was in the Midwest (13.9%) and the South (18.5%), and lowest in the Northeast and West (6.2% and 13.6%).DiscussionImaging utilization for the initial evaluation of low back pain by primary care providers has increased on a national level from 2011 to 2016, largely represented by radiographs. Significant regional variation also exists. Encouragingly, the use of advanced imaging has remained at a low level in the primary care setting (<1.0%).     

Pulmonary lesions in female Harlan Sprague-Dawley rats following two-year oral treatment with dioxin-like compounds

Dioxin and dioxin-related compounds have been associated with high incidences of pulmonary dysfunctions and/or cancers in humans. To evaluate the relative potencies of effects of these compounds, the National Toxicology Program completed a series of two-year bioassays which were conducted using female Harlan Sprague-Dawley rats. The rats were treated orally for up to 2 years with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3,3',4,4',5-pentachlorobiphenyl (PCB126), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), and a ternary mixture of TCDD, PCB126 and PeCDF. In addition to treatment-related effects reported in other organs, a variety of pulmonary lesions were observed that were related to exposure. Pulmonary CYP1A1-associated 7-ethoxyresorufin-O-deethylase (EROD) activity was increased in all dosed groups. The most common non-neoplastic lesions, which occurred in all studies, were bronchiolar metaplasia and squamous metaplasia of the alveolar epithelium. Cystic keratinizing epithelioma was the most commonly observed neoplasm which occurred in all studies. A low incidence of squamous cell carcinoma was associated only with PCB126 treatment. Potential mechanisms leading to altered differentiation and/or proliferation of bronchiolar and alveolar epithelia may be through CYP1A1 induction or disruption of retinoid metabolism.     

Advancing high-resolution manometry: evaluating the use of multiple rapid swallows versus apple viscous swallows in clinical practice

Esophagus - High-Resolution Manometry (HRM) with provocative maneuvers, such as Multiple Rapid Swallows (MRS) and Apple Viscous Swallows (AVS), is commonly utilized to diagnose esophageal...     

Studies on the frequency and pathogenesis of liver involvement in rheumatoid arthritis.

A systematic prospective survey of 100 outpatients with rheumatoid arthritis revealed that 45 had biochemical evidence of liver disease. In most cases this was due to increases in total serum alkaline phosphatase (ALP) and/or gammaglutamyl transpeptidase (GGT). Examination of serum ALP isoenzyme profiles in 50 of the patients showed that the liver isoenzyme was the sole or major component in 44 patients, including many with normal total ALP levels. 18% had raised serum liver ALP together with raised GGT, suggestive of an underlying hepatobiliary lesion. No correlation could be detected between raised serum levels of liver enzymes and the age or sex of the patient, duration or severity of arthritis, and drug or alcohol history. However, there was a significant correlation between raised serum ALP and lacrimal or salivary gland dysfunction. It is suggested that immunological mechanisms may be involved in the development of hepatic abnormalities in rheumatoid arthritis.     

Ethanol metabolism in the generation of new antigenic determinants on liver cells.

Antibodies directed against ethanol altered liver cell components have been detected in the serum of nearly 50% of patients with alcoholic liver disease although the pathogenetic mechanisms are unclear. The importance of ethanol metabolism in the generation of new antigenic determinants on liver cells was investigated by in vivo inhibition of alcohol or acetaldehyde dehydrogenase and an induced cytotoxicity assay. There was a significant reduction in cytotoxicity to hepatocytes isolated from rabbits treated with ethanol 1 g/kg when the metabolism of ethanol to acetaldehyde by alcohol dehydrogenase was inhibited. In contrast when the oxidation of acetaldehyde was inhibited by disulfiram cytotoxicity was significantly enhanced. These results show that ethanol metabolism is integral to the expression of the ethanol related determinant and suggest that an impaired ability to metabolism acetaldehyde could lead to the development of immunological reactions to alcohol altered liver membrane antigens.     

Spectrum of manifestations of Mycobacterium tuberculosis infection in primates infected with SIV

To characterize the manifestations of coinfection with M. tuberculosis and SIV infection, we studied 12 SIV-infected rhesus monkeys, six of which were infected intrabronchially with a low dose of Mycobacterium tuberculosis H37Rv. In the six coinfected animals, M. tuberculosis antigen-stimulated lung and blood cells produced high concentrations of IFN-gamma but not IL-4 8-16 weeks after infection. Of the three coinfected animals with high levels of plasma viremia, two developed disseminated tuberculosis and the other died of bacterial peritonitis. Of three coinfected animals with moderate levels of plasma viremia, two had no clinical or radiographic evidence of tuberculosis or progressive SIV infection for 6 months after infection. At neuropsy, pulmonary granulomata were observed and acid-fast organisms or M. tuberculosis were present. These clinical, immunologic and pathologic findings are consistent with those in humans with latent tuberculosis infection (LTBI), and suggest that a model of LTBI in SIV-infected primates can be developed. Such a model will permit delineation of the immunologic and microbial factors that characterize LTBI in HIV-infected persons.     

Changes in hepatitis B virus DNA polymerase in relation to the outcome of acute hepatitis type B.

Serum levels of hepatitis B virus specific DNA polymerase and hepatitis B e antigen were studied serially in 34 patients with hepatitis B virus infection--20 who had the acute illness and recovered, seven who died with fulminant disease, three who died as a result of subacute hepatic necrosis, and four who went on to develop chronic active hepatitis. DNA polymerase activity was present in 16 (80%) and HBeAg in 13 (65%) of the uncomplicated cases at presentation and in all of those patients from whom the initial sample was obtained before the peak in aminotransferase. Both markers disappeared after 30 days from the onset but DNAP remained persistently positive during a follow-up period of four to 10 months in the four patients who progressed to chronic hepatitis. These results indicate that DNAP and HBeAg are transiently present in all cases of acute hepatitis B. Only their persistence after the acute episode could represent a useful prognostic marker of chronically. In this respect, DNAP was more reliable in our patients than HBeAg. In uncomplicated acute hepatitis, the peak in DNAP levels, which defines the time of maximum virus replication in the liver, preceded the peak in aminotransferase levels. Among the 10 patients who developed massive liver damage after hepatitis B infection, DNAP was detected in five of the seven with fluminant hepatitis, with enzyme levels that were comparable with those observed in uncomplicated acute hepatitis and presentation, but not in the cases of subacute hepatic necrosis. These findings are consistent with the hypothesis that in hepatitis B infection, liver damage, whatever the severity, is not directly related to the degree of virus replication.     

Lymphocyte cytotoxicity to autologous hepatocytes in HBsAg positive chronic liver disease.

Lymphocytes from 39 patients with HBsAg positive chronic liver disease were incubated with their own hepatocytes to investigate mechanisms of lymphocyte-mediated liver damage. Cytotoxicity was significantly increased in 46% overall, and in 73% of those with chronic active hepatitis. Unlike HBsAg negative chronic active hepatitis where only non-T cells were cytotoxic, HBsAg positive patients had both cytotoxic T and non-T cells. A purified liver membrane complex (LSP) and aggregated IgG both blocked non-T cytotoxicity without affecting T cell cytotoxicity; this suggests that the former is probably an antibody-dependent cell-mediated reaction against normal membrane components. This was confirmed in preliminary studies which demonstrated that preincubation of hepatocytes with the F(ab)2' fragment of an anti-human IgG reduced non-T lymphocyte cytotoxicity. T-cell cytotoxicity was restricted to HBeAg-positive patients, suggesting a relationship between T-cell cytotoxicity and viral replication. Purified HBsAg, however, blocked cytotoxicity in only three of 11 cases. Non-T lymphocytes reacting with normal membrane components may contribute to liver damage in both 'autoimmune' and virus-associated chronic liver disease, whereas cytotoxic T-cells, probably reacting with viral determinants, are exclusive to those with viral replication.     

Neisseria gonorrhoeae Strain with Reduced Susceptibilities to Extended-Spectrum Cephalosporins

The spread of Neisseria gonorrhoeae strains with reduced susceptibility to extended-spectrum cephalosporins is an increasing public health threat. Using Etest and multiantigen sequence typing, we detected sequence type 1407, which is associated with reduced susceptibilities to extended-spectrum cephalosporins, in 4 major populated regions in California, USA, in 2012.