China
Africa
Explore chapters and articles related to this topic
Pharmacological and Toxicological Aspects Associated with H1 Receptor Antagonists
Published in Sam Kacew, Drug Toxicity and Metabolism in Pediatrics, 1990
Although the antihistaminics share a similar mechanism of action, structural differences exist between these agents. The drugs to be discussed and the chemical classification are provided in Table 1. The drugs shown in Table 1 are currently available and have been reported to produce adverse effects in children. Other antihistaminic drugs also produce toxicity, but have been removed from the druggists’ shelves. Examples of these latter drugs include methapyrilene, pyranisamine, and prophenpyridamine.6 This list of antihistaminics is far from the total number of drugs available; however, the agents described include those for which data are available on the affects in children.
Toxicogenomics in Toxicologic Pathology
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Arun R. Pandiri, David E. Malarkey, Mark J. Hoenerhoff
Mechanistic toxicogenomics in the liver has facilitated the investigation of mechanisms of toxicity of various hepatotoxins, including carbon tetrachloride (Holden et al. 2000), arsenic (Lu et al. 2001), acetaminophen (Heinloth et al. 2004; Reilly et al. 2001), methapyriline (Hamadeh et al. 2002b), furan (Hamadeh et al. 2004), methotrexate, and phenytoin (Huang et al. 2004), enzyme inducers (Hamadeh et al. 2002a; Waring et al. 2001b; Bulera et al. 2001; Burczynski et al. 2000), TCDD and dioxin-like compounds (Boverhof et al. 2006; Kopec et al. 2008), benzene (Heijne et al. 2005), bromobenzene (Heijne et al. 2003, 2004), aromatic hydrocarbons, indomethacin, carbamazepine (Waring et al. 2001a,b), and oxidant stress/electrophilic reactive compounds (McMillian et al. 2004), among others. Furthermore, many investigators have shown a correlation between gene expression changes and histopathologic endpoints specific for a mechanism of action for a particular hepatotoxin. For example, in order to gain insight into the mechanisms of toxicity of methapyrilene (MP), Hamadeh et al. (2002) evaluated global gene expression in livers from rats exposed to MP for 1, 3, and 7 days, and phenotypically anchored gene expression to resulting histopathologic lesions (Hamadeh et al. 2002b). Exposure of rats to MP resulted in hepatocellular necrosis, bile duct hyperplasia, periportal inflammatory cell infiltration, and microvesicular steatosis in treated animals. Results of hierarchical clustering revealed that samples clustered, based upon the severity of histopathologic lesions and changes in gene expression, reflected alterations in genes associated with hepatocellular necrosis, biliary hyperplasia, altered fatty acid metabolism, and inflammation, increasing in severity with increasing dose. By phenotypically linking pathology endpoints with gene expression, the authors were able to associate the morphologic changes resulting from hepatotoxicity to specific changes in gene expression, and identify low dose effects that were undetectable by histopathology.
The clinical relationship between histamine-1 receptor antagonists and risk of cancer: a systematic review and meta-analysis
Published in Expert Review of Anticancer Therapy, 2023
Elham Bakhtiari, Nasrin Moazzen, Amir Amirabadi, Hamid Ahanchian
The risk of cancer was investigated in all case-control studies [10,13,16–18]. The risk of breast cancer was investigated in two studies [16,18]. Kelly et al. [16] studied the risk of breast cancer according to use of antihistamines in 11,628 women. Relative risk was estimated for regular use of antihistamines (>4 days per week for equal to or more than 4 weeks beginning equal to or more than 1 year before admission). Antihistamines studied included chlorpheniramine, doxylamine, triprolidine, brompheniramine, terfenadine, hydroxyzine, diphenhydramine, pyrllamlne, phenyttoxamine, cyproheptadlne, dexbrompheniramine, methapyrilene, astemizole, clemastine, dimethindene, antazoline, promethazlne, pyrrobutamlne, carblnoxamine, pheniramine, dimennydrtnate, tripelennamine, thenyldiamlne, loratadine, trimethobenzamide, pyribenzamine, trimeprazine, and other ones. The cancer risk was calculated according to type and duration of antihistamines. Duration were including less than 1 year, 1–4 years, 5–9 years, and equal to or more than 10 years. The risk of cancer was not associated with the type of antihistamines. In duration of more than 10 years, the risk of cancer was 0.5 (0.95% CI = (0.3–0.8)).
MiR-122 and other microRNAs as potential circulating biomarkers of drug-induced liver injury
Published in Expert Review of Molecular Diagnostics, 2018
Lawrence S. Howell, Lucy Ireland, B. Kevin Park, Christopher E. Goldring
Yamaura et al. induced hepatocellular necrosis in the perivenous and periportal regions by dosing rats with APAP and methapyrilene, respectively. They noted large upregulations of miRNA in the serum of rats between the two dosing groups, such as increases in miR-122, but also uniquely upregulated and downregulated miRNAs (APAP: 8 upregulated, 4 downregulated, methapyrilene: 6 upregulated, 5 downregulated), which may indicate a unique zonated biomarker [70]. They noted in a follow-up paper that the miRNAs that are upregulated in serum do not necessarily correlate to miRNA that are downregulated in liver tissue following DILI, indicating a potentially more complex method of miRNA release than a simple deposition of highly abundant miRNA into bio-fluids [60].