Kidney
Urinary excretion of glutathione-S-transferase alpha (Bruning, Sundberg et al. 1999), α1-microglobulin (Bolt, Lammert et al. 2004), β2-microglobulin (Nagaya, Ishikawa et al. 1989) and N-acetyl-β-D-glucosaminidase (Brogren, Christensen et al. 1986; Selden, Hultberg et al. 1993) are used to indicate kidney damage, but neither marker is specific to TCE-induced damage; a number of short-chain halogenated hydrocarbons can produce similar effects (Agency for Toxic Substances and Disease Registry 1997).
Liver
Biochemical abnormalities are uncommon after acute TCE exposures. Rarely have elevations of serum hepatic transaminases (serum glutamic-oxaloacetic transaminase (SGOT) or aspartate aminotransferase (AST), serum glutamic-pyruvic transaminase (SGPT) or alanine aminotransferase (ALT)), bilirubin, and creatinine resulted from acute TCE exposure; (Rasmussen, Brogren et al. 1993; Agency for Toxic Substances and Disease Registry 1997) nevertheless, liver and kidney function and serum creatinine tests should be performed to establish baselines.
Heart
Electrocardiogram and continuous cardiac monitoring should be considered for heavily exposed persons.
Gastrointestinal
Ingestion of large amounts of TCE, which can cause profuse diarrhea, can produce an electrolyte imbalance.
Nervous System
Because the trigeminal, optic, and facial nerves can be impaired by exposure to dichloroacetylene, changes in the visual fields and trigeminal nerve potentials can be noted (Szlatenyi and Wang 1996).
Immune System
Two studies that may be of value are Kahn and Letz (1989) and American College of Physicians (1989).
If it had been indicated, laboratory evaluation of immunologic host-defense defects would consist of three phases.
The preliminary screening is a complete blood count with differential smear and quantitative immunoglobulin levels. These tests, together with history and physical examination, will identify more than 95% of patients with primary immunodeficiencies.
The second testing phase consists of readily available studies including B-cell function (such as antibodies and response to immunization), T-cell function (skin tests and contact sensitization), and complement levels.
The first two phases combined will detect most immunodeficiencies amenable to conventional treatment with gamma globulin or plasma.
The third phase (in-depth investigation) consists of testing induction of B-lymphocyte differentiation in vitro, stimulated by pokeweed mitogen and histological and immunofluorescent examination of biopsy specimens; T-cell surface markers; assays of T-cell helper or killer cell functions; and functional assays using appropriate target cells. It is inappropriate to perform the latter tests on environmentally exposed patients except for epidemiologic research.
If the patient's concerns include an increased risk of autoimmune illnesses, general evaluation for autoimmune diseases might include
- C-reactive protein (CRP)
- evaluation of the antinuclear antibody (ANA)
- the erythrocyte sedimentation rate (ESR)
If a specific autoimmune disease is suspected, appropriate serologic markers should be assessed, where available. |
