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Hand (N Y). 2008 Jun;3(2):129-34. doi: 10.1007/s11552-007-9079-6. Epub 2007 Oct 3.

Serological tests for diagnosis and staging of hand-arm vibration syndrome (HAVS).

Author information

  • 1Department of Plastic Surgery, Medical College of Wisconsin, 8700 Watertown Plank Road, Milwaukee, WI, 53226, USA. dskao@hotmail.com

Abstract

The current gold standard for the diagnosis and staging of hand-arm vibration syndrome (HAVS) is the Stockholm workshop scale, which is subjective and relies on the patient's recalling ability and honesty. Therefore, great potentials exist for diagnostic and staging errors. The purpose of this study is to determine if objective serum tests, such as levels of soluble thrombomodulin (sTM) and soluble intercellular adhesion molecule-1 (sICAM-1), may be used in the diagnosis and staging of HAVS. Twenty two nonsmokers were divided into a control group (n = 11) and a vibration group (n = 11). The control group included subjects without history of frequent vibrating tool use. The vibration group included construction workers with average vibrating tool use of 12.2 years. All were classified according to the Stockholm workshop scale (SN, sensorineural symptoms; V, vascular symptoms. SN0, no numbness; SN1, intermittent numbness; SN2, reduced sensory perception; SN3, reduced tactile discrimination; V0, no vasospasmic attacks; V1, intermittent vasospasm involving distal phalanges; V2, intermittent vasospasm extending to middle phalanges; V3, intermittent vasospasm extending to proximal phalanges; V4, skin atrophy/necrosis). All control subjects were SN0 V0. Seven out of 11 vibration subjects were SN1 V1, and 4 out of 11 were SN1 V2. A 10-cm(3) sample of venous blood was collected from each subject. The sTM and sICAM-1 levels were determined by enzyme-linked immunosorbent assay. The mean plasma sTM levels were as follows: control group = 2.93 +/- 0.47 ng/ml, and vibration group = 3.61 +/- 0.24 ng/ml. The mean plasma sICAM-1 levels were as follows: control group = 218.8 +/- 54.1 ng/ml, and vibration group = 300.3 +/- 53.2 ng/ml. The sTM and sICAM-1 differences between control and vibration groups were statistically significant (p < 0.0002 and p < 0.001, respectively). When reference ranges provided by Hemostasis Reference Lab were used as cut-off values, all sTM and sICAM-1 levels were within range, except three vibration individuals (27%) who had sICAM-1 levels greater than the reference range. This was not statistically significant (p = 0.08). When subjects were compared based on the Stockholm workshop scale, mean plasma sTM levels were SN0 V0 group = 2.93 +/- 0.47 ng/ml, SN1 V1 group = 3.59 +/- 0.25 ng/ml, and SN1 V2 group = 3.65 +/- 0.27 ng/ml, and mean plasma sICAM-1 levels were SN0 V0 = 219 +/- 54.1 ng/ml, SN1 V1 = 275 +/- 33.5 ng/ml, and SN1 V2 = 345 +/- 54.6 ng/ml. The difference in sTM level among the three groups was statistically significant (p < 0.001). The difference in sICAM-1 level among the three groups was also statistically significant (p < 0.002). The sTM and sICAM-1 levels are statistically higher in subjects with HAVS, with levels proportional to the disease severity. However, large population studies are needed to determine the "real-life" standard reference ranges for sTM and sICAM-1.

PMID:
18780088
[PubMed]
PMCID:
PMC2529134
Free PMC Article

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