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==Laboratory Findings==
==Laboratory Findings==


*There are no diagnostic laboratory findings associated with [disease name].
OR
*An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
*An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
*[Test] is usually normal among patients with [disease name].
*[Test] is usually normal among patients with [disease name].
Line 34: Line 32:


*Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
*Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
LABORATORY FINDINGS — Laboratory findings useful in the assessment of giant cell arteritis (GCA) include routine hematological testing, selected serum chemistry tests, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).
Hematology — A normochromic anemia is often present prior to therapy and improves promptly after the institution of glucocorticoids. The anemia is occasionally profound [82]. Many patients also have a reactive thrombocytosis [83,84]. The leukocyte count is usually normal, even in the setting of widespread systemic inflammation.
Serum albumin — The serum albumin level is often moderately decreased at diagnosis but responds quickly to the institution of glucocorticoids.
Hepatic enzymes — Elevated serum concentrations of hepatic enzymes, especially the alkaline phosphatase, occur in 25 to 35 percent of patients. The elevations are typically modest and revert to normal with glucocorticoid therapy.
ESR and C-reactive protein — A characteristic laboratory abnormality in many patients with GCA is a high ESR, which can reach 100 mm/hour [37,84]. The CRP is nearly always commensurately elevated, though prospective head-to-head studies on the use of the ESR and CRP for the diagnosis and management of GCA are lacking. Among patients with a paraproteinemia or some other cause of a spuriously elevated or depressed ESR, the CRP level is more reliable. (See "Acute phase reactants", section on 'Clinical use'.)
Less striking elevations of the ESR [37], however, can be seen even before glucocorticoid therapy has begun. In a population-based study of 167 patients from Olmsted County, 18 (11 percent) had an ESR less than 50 mm/hour and 9 (5 percent) less than 40 mm/hour before treatment was initiated. The patients with an ESR less than 40 mm/hour were less likely to experience systemic symptoms such as malaise, fever, or weight loss; nevertheless, their clinical manifestations, including risk of visual loss, were indistinguishable from those in patients with a higher ESR [85]. In another series of 173 biopsy-proven cases, 12 patients (5.8 percent) had ESR values less than 46 mm/hour [86].
An additional retrospective study from Olmsted County found normal values for both the ESR and CRP in 4 percent of 177 patients with biopsy-proven GCA at the time of diagnosis [87].
Neither the ESR nor the CRP is a specific biomarker for GCA. Abnormalities in the ESR and CRP can help calibrate the diagnostic probability of GCA, but normal values do not absolve the clinician of the responsibility to pursue the diagnosis in an appropriate clinical setting, nor do marked elevations certify that a diagnosis of GCA is correct. (See "Diagnosis of giant cell arteritis".)
Interleukin-6 — Elevated serum interleukin (IL)-6 concentrations appear to be related closely to clinical disease activity in GCA [88] and may better correlate with clinical relapse than the ESR [89]. However, IL-6 assays are not routinely available, and their clinical utility remains unproven.


==References==
==References==

Revision as of 16:42, 5 April 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2]

Overview

An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].

OR

Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

OR

[Test] is usually normal for patients with [disease name].

OR

Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

OR

There are no diagnostic laboratory findings associated with [disease name].

Laboratory Findings

  • An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
  • [Test] is usually normal among patients with [disease name].
  • Laboratory findings consistent with the diagnosis of [disease name] include:
    • [Abnormal test 1]
    • [Abnormal test 2]
    • [Abnormal test 3]
  • Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

LABORATORY FINDINGS — Laboratory findings useful in the assessment of giant cell arteritis (GCA) include routine hematological testing, selected serum chemistry tests, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).

Hematology — A normochromic anemia is often present prior to therapy and improves promptly after the institution of glucocorticoids. The anemia is occasionally profound [82]. Many patients also have a reactive thrombocytosis [83,84]. The leukocyte count is usually normal, even in the setting of widespread systemic inflammation.

Serum albumin — The serum albumin level is often moderately decreased at diagnosis but responds quickly to the institution of glucocorticoids.

Hepatic enzymes — Elevated serum concentrations of hepatic enzymes, especially the alkaline phosphatase, occur in 25 to 35 percent of patients. The elevations are typically modest and revert to normal with glucocorticoid therapy.

ESR and C-reactive protein — A characteristic laboratory abnormality in many patients with GCA is a high ESR, which can reach 100 mm/hour [37,84]. The CRP is nearly always commensurately elevated, though prospective head-to-head studies on the use of the ESR and CRP for the diagnosis and management of GCA are lacking. Among patients with a paraproteinemia or some other cause of a spuriously elevated or depressed ESR, the CRP level is more reliable. (See "Acute phase reactants", section on 'Clinical use'.)

Less striking elevations of the ESR [37], however, can be seen even before glucocorticoid therapy has begun. In a population-based study of 167 patients from Olmsted County, 18 (11 percent) had an ESR less than 50 mm/hour and 9 (5 percent) less than 40 mm/hour before treatment was initiated. The patients with an ESR less than 40 mm/hour were less likely to experience systemic symptoms such as malaise, fever, or weight loss; nevertheless, their clinical manifestations, including risk of visual loss, were indistinguishable from those in patients with a higher ESR [85]. In another series of 173 biopsy-proven cases, 12 patients (5.8 percent) had ESR values less than 46 mm/hour [86].

An additional retrospective study from Olmsted County found normal values for both the ESR and CRP in 4 percent of 177 patients with biopsy-proven GCA at the time of diagnosis [87].

Neither the ESR nor the CRP is a specific biomarker for GCA. Abnormalities in the ESR and CRP can help calibrate the diagnostic probability of GCA, but normal values do not absolve the clinician of the responsibility to pursue the diagnosis in an appropriate clinical setting, nor do marked elevations certify that a diagnosis of GCA is correct. (See "Diagnosis of giant cell arteritis".)

Interleukin-6 — Elevated serum interleukin (IL)-6 concentrations appear to be related closely to clinical disease activity in GCA [88] and may better correlate with clinical relapse than the ESR [89]. However, IL-6 assays are not routinely available, and their clinical utility remains unproven.

References

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