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CAP Home > CAP Reference Resources and Publications > cap_today/cap_today_index.html > CAP Today Archive 2001 > September 2001 Q & A
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  Q & A

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cap today

September 2001

Q.  Our clinic providers order only an HIV antibody test when patients are seen for exposure to a sexually transmitted disease. The test we order from our reference laboratory is an enzyme immunoassay procedure for HIV-1 antibodies with confirmation by Western blot if needed. This is also the only HIV order used when our employees experience needle-stick exposures. Only one test is done; no additional testing is performed at a later date.

What are the recommended guidelines for ensuring that exposure has not resulted in infection?

A.  A laboratory considering how to evaluate and test a health care worker potentially exposed to HIV should also involve individuals from the institution that employs the worker. The infection control, safety, and employee health departments and committee members should be involved in the decision-making process.

The Centers for Disease Control and Prevention published an excellent article detailing the Public Health Service guidelines for managing health care workers' exposure to HIV.1 These guidelines provide recommendations for appropriate postexposure management, including laboratory testing for HIV infection.

At our institution, HIV-antibody testing by enzyme immunoassay is performed on the exposure source and the exposed health care worker. Confirmation by Western blot testing of all anti-HIV results reported as reactive by EIA is recommended. If the source person is negative or unknown, our institution does followup HIV-antibody tests on the exposed health care worker at six and 12 weeks and six months. Some employers have decided to forgo further testing of such employees after a negative result.

Reference
1. Public Health Service guidelines for the management of health-care worker exposures to HIV and recommendations for postexposure prophylaxis. Centers for Disease Control and Prevention. MMWR. 1998;47(RR-7):1-33.

Thomas Merrick, MD
Department of Pathology
Presbyterian-St. Luke’s Medical Center Denver
Chair, CAP Safety Committee

Q.  We are planning to upgrade our glucose meters and have been evaluating different manufacturers' devices. Any information you can provide on the performance of these meters would be helpful.

A.  Please see the Web site of the Point-of-Care Testing Center for Teaching and Research, University of California at Davis (www.poctctr.ucdavis.edu), regarding the performance of handheld glucose devices. Visit the "Recent Projects" section to locate direct links to peer-reviewed research articles. The site also features a new “Education Modules” section containing online presentations about point-of-care testing.

Gerald S. Kost, MD, PhD
Director
Point-of-Care Testing Center for
Teaching and Research
University of California, Davis

Q.  Is C-reactive protein specific for inflammation associated with rheumatoid arthritis? If not, what other conditions result in elevated C-reactive protein?

A.  C-reactive protein originates in the liver. It is a so-called acute phase reactant, which is present in the blood at all times. In the absence of any specific major inflammatory stimulus, the levels are relatively low: usually less than 5 mg/L, and in many people below 1 mg/L. In a given individual, these low levels are moderately stable over time, presumably the result of the action of proinflammatory cytokines, such as interleukin-6. Since no genetic polymorphisms have been identified that affect CRP levels, the variation among people is felt to represent differences in low-level subclinical inflammation (microinflammation) associated with the presence of or progression of conditions such as atherosclerosis, the multiple metabolic syndrome (insulin resistance syndrome), and other chronic disease processes. This position has been borne out by the many studies demonstrating that CRP is an independent cardiovascular disease risk factor.

There is little specificity of CRP for any single condition. In an individual, CRP levels can be quite dynamic, and sharp rises follow any major inflammatory stimulation, such as infection, arthritis, or physical trauma. CRP levels can achieve values over 1,000-fold higher than the baseline values in a given person. However, these dramatic rises are usually short-lived, and values quickly fall back to their baseline levels.

CRP traditionally was believed to augment the immune response, particularly cell-mediated responses. However, since CRP has been identified as a cardiovascular disease risk factor, renewed examination has revealed a broad range of functions.

Among other activities, CRP can activate the complement system, cause the expression of the major procoagulant tissue factor on the surface of monocytes, and cause endothelial cells to express cell adhesion molecules. While much remains to be discovered, this protein has recently shown many new faces.

Bibliography
1. Cermak J, Key N, Bach R, et al. C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor. Blood. 1993;82:513-520.
2. Lagrand WK, Visser CA, Hermens WT, et al. C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon? Circulation. 1999;
100:96-102.
3. Macy EM, Hayes TE, Tracy RP. Variability in the measurement of C-reactive protein in healthy subjects: implications for reference interval and epidemiological applications. Clin Chem. 1997;43:52-58.
4. Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation. 2000;102:2165-2168.
5. Pepys M, Baltz M. Acute phase proteins with special reference to C-reactive protein and related proteins and serum amyloid A protein. Adv Immunol. 1983;34:141-212.
6. Tracy RP. Inflammation markers and coronary heart disease. Curr Opin Lipidol. 1999;10:435-441.
7. Tracy RP, Macy E, Bovill E, et al. Lifetime smoking exposure affects the association of C-reactive protein with cardiovascular disease risk factors and subclinical disease in healthy elderly subjects. Arterioscler Thromb Vasc Biol. 1997;17:2167-2176.

Russell P. Tracy, PhD
Professor of pathology and biochemistry
Director, Laboratory for Clinical
Biochemistry Research
University of Vermont
Colchester

   
 

 

 

   
 
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