Subclinical toxicity

A. Specific levels. Urinary thallium is normally less than 0.8 mcg/L. Concentrations greater than 20 mcg/L are evidence of excessive exposure and may be associated with subclinical toxicity during workplace exposures. Blood thallium levels are not considered reliable measures of exposure, except after large exposures. Hair levels are of limited value, mainly in documenting past exposure or in forensic cases. 

Effect. Potential biomarkers of the subclinical effects of hydrogen sulfide are decreases in the activities of the heme synthesis enzymes, ALA-S and Haem-S (Jappinen and Tenhunen 1990). These effects have nothing to do with the mechanism of toxicity, however. Neurological indices are also used as biomarkers of effect for hydrogen sulfide (Gaitonde et al. 1987 Kilbum 1993 Stine et al. 1976 Tvedt et al. 1991b). 

Youssef, S.A.H., Effect of subclinical lead toxicity on the immune response of chickens to Newcastle s disease virus vaccine, Res. Vet. Sci. 60, 13, 1996. 

Hathaway J A Subclinical effects of trinitrotoluene A review of epidemiology studies. In Richert DE (ed) Toxicity of Nitroaromatic Compounds, pp 255-274. New York, Hemisphere Publishing, 1985... 

Subclinical hyperthyroidism is defined as a suppressed TSH level (below the normal range) in conjunction with normal thyroid hormone levels. Cardiac toxicity (eg, atrial fibrillation), especially in older persons, is of greatest concern. The consensus of thyroid experts concluded that hyperthyroidism treatment is appropriate in those with TSH less than 0.1 mlU/L, while close monitoring of the TSH level is appropriate for those with less TSH suppression. 

Philadelphia School Children Subclinical Exposures in High and Low Risk Groups, EPA-NIEHS Conference on Low Level Lead Toxicity, Raleigh, North Carolina, October 1-2, 1973. 

Subclinical effects are often observed when molybdenum levels in soil exceed 3 pg/g an excess of molybdenum in forage is toxic to livestock. Deficiency diseases have been observed in livestock when soil molybdenum levels are below 0.5 pg/g. 

Toxicities included an infusion reaction consisting of fever, chills, pain, asthenia, nausea, and vomiting. This syndrome was typically observed after the initial infusion, was self-limited, and frequently did not recur with subsequent infusions. The most serious toxicity was cardiac dysfunction, defined as clinical findings of congestive heart failure and/or subclinical declines in cardiac ejection fraction, which was seen in 5% of patients. Cardiotoxicity was unanticipated, as it had not been detected in previous studies. The mechanism for this effect is unclear, but is likely related to trastuzumab s antiproferative effect on HER2-mediated homeostasis and response to injury. 

Given the potential hepatotoxicity of NSAIDs, some have suggested that raised transaminase levels are an early indicator of reversible liver toxicity during prolonged NSAID courses, and therefore should be monitored reasonably closely [31]. However, it should be noted that minor subclinical abnormalities in LFTs rarely represent acute liver injury [32, 33]. 

CISPLATIN TOPOTECAN t risk of bone marrow suppression, especially when topotecan is administered in doses >0.75 mg/m2 on days 1-5 and cisplatin in doses >50 mg/m2 on day 1 before topotecan Attributed to cisplatin inducing subclinical renal toxicity, possibly causing 1 clearance of topotecan Administer cisplatin on day 5 after topotecan if dose of topotecan is >0.75 mg/m2 and cisplatin dose is >50 mg/m2 with the use of granulocyte colony-stimulating factors... 

Halothane is a volatile general anesthetic that was introduced into the practice of clinical anesthesia in 1956. Shortly after its introduction two forms of hepatic injury were noted to occur in patients who received halothane anesthesia. A subclinical increase in blood concentration of transaminase enzymes is observed in 20% of patients and has been attributed to lipid peroxidation caused by the free radical formed by reductive metabolism of halothane as shown in Figure 16.7 (39/ 40). The second form of toxicity is a potentially fatal hepatitis-like reaction that is characterized by severe hepatocellular necrosis and is thought to be initiated by the oxidative formation of trifluoroacetyl chloride (Figure 16.7). Fatal hepatic necrosis occurs in only 1 of 35/000 patients exposed to halothane/ but the risk of this adverse event is greater in females and is increased with repeat exposure/ obesity/ and advancing age (40). Because the onset of halothane hepatitis is delayed but is more frequent and occurs more rapidly following multiple exposures/ and because these patients usually are febrile and demonstrate eosinophilia/ this reaction is suspected... 

Cirrhotic cardiomyopathy This term is defined as a left ventricular functional disorder due to stress (e. g. hyperdynamic circulation) or as pharmacological stimulation. But also the possibility of (toxically induced ) subclin-ical myocardial damage is discussed, especially because elevated troponin 1 serum values are detectable in every third patient. (81, 142, 187) (Troponin is connected with propomyosin in the actin filaments at regular intervals and, as a relaxing protein , has an important function in muscle metabolism, also in the heart). 

---