Follow-up assessment of two cases of trichloroethylene hypersensitivity syndrome: A case report

Huang,Yong‑Shun; Huang,Han‑Lin; Wu,Qi‑Feng; Xia,Li‑Hua; Huang,Ming; Qiu,Xin-Xiang; Zhou,Shan‑Yu

doi:10.3892/etm.2016.3357

Follow-up assessment of two cases of trichloroethylene hypersensitivity syndrome: A case report

Authors:
- Yong‑Shun Huang
- Han‑Lin Huang
- Qi‑Feng Wu
- Li‑Hua Xia
- Ming Huang
- Xin-Xiang Qiu
- Shan‑Yu Zhou
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Affiliations: Department of Occupational Medicine, Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, Guangdong 510300, P.R. China
Published online on: May 18, 2016 https://doi.org/10.3892/etm.2016.3357
Pages: 895-900
Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to explore the stability, curability and sequelae of cases of Trichloroethylene (TCE) Hypersensitivity Syndrome (THS), and to investigate the causal allergens of THS. Two cases of THS were followed‑up in the current study; both cases were healing following glucocorticoid therapy and were discharged >10 weeks prior to follow‑up. A questionnaire investigation, health examination and patch test were performed. Allergens of TCE and its metabolites, including chloral hydrate, trichloroethanol (TCOH) and trichloroacetic acid, were applied in the patch test; 4 controls were included. The two subjects were experiencing itching, pigmentation and xerosis of the skin, and had abnormal results in the ophthalmology Schirmer I test and tear break‑up time. The body temperature, liver function, superficial lymph nodes, blood, urine routine and autoimmune antibodies of two subjects were shown to be normal, and no new rashes had appeared. All mass concentration of chloral hydrate and TCOH were positive; 5.0% trichloroacetic acid was weakly positive, 0.5% trichloroacetic acid and all mass concentration of TCE were negative. All patch tests were negative in the 4 control subjects. The results suggest that THS was stable following treatment with glucocorticoid therapy. Dry eye syndrome may continue as a sequelae of THS. The patch test demonstrated that the mechanism underlying THS is delayed‑type hypersensitivity induced by TCE. In addition, as the hypersensitivity state in a THS rehabilitee could be sustained over a long period of time, it suggests that the metabolites of TCE, not TCE itself, are responsible for THS. Therefore, patients with THS should avoid contact with TCE and its metabolites, and avoid using hypnotic and anticonvulsive drugs containing chloral hydra as the primary ingredient.

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