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Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Zbigniew W. Wojcinski, Lydia Andrews-Jones, Daher Ibrahim Aibo, Rie Kikkawa, Robert Dunstan
Hair, scales, feathers, nails, claws, and horns are all derived from skin and thus have a similar response to toxic agents as epidermis. Hair follicles may respond to a toxicant with loss (hypotrichosis, alopecia), proliferation (hypertrichosis), alterations in the hair cycle, or a color change. Depilatory agents, such as eflornithine HCl (VaniqaTM), have been developed as treatments for excessive hair (Hickman et al. 2001). In toxic alopecia, the effect on the hair follicle will depend on the stage of hair growth. There are four phases to the hair cycle: anagen (active growth), catagen (regression), telogen (resting), and exogen (hair loss). Anagen is the actively growing phase of the hair cycle, and therefore subject to chemical toxicity that effects rapidly growing cells or inhibits mitotic activity of proliferating cells in the hair bulb. The effect on hair with this type of toxicity is manifested within days or weeks and may occur with colchicine (antigout agent) or chemotherapeutic agents (e.g., doxorubicin) (Figure 21.5a). The telogen phase toxicity occurs by different mechanisms and may appear over a period of several months. For example, chronic exposure to the heavy metal thallium (previously used in rodenticides) causes alopecia, ulceration, and hyperkeratosis and parakeratosis of skin and hair epithelia through a mechanism of inhibition of cysteine incorporation into keratin and interference with energy production in hair bulb cells, resulting in premature telogen and consequent hair shedding (Cavanagh and Gregson 1978). Other toxicants that cause alopecia from chronic exposure by a similar mechanism include copper, mercury, cadmium, and arsenic (Pierard 1979; Haschek et al. 2010). The list of toxic chemicals that may cause alopecia is quite extensive, including retinoids, interferons, lithium, heparin, coumarins, β-adrenergic blockers, androgens, progesterone-estrogen combination, cytotoxic drugs (e.g., acyclovir), bromocriptine, selenium, mimosine, iodine, propanolol, triparanol, phenylglycidyl ether, and dixyrazine (Moore et al. 1983; Haschek et al. 2010). Administration of a progesterone-estrogen combination (i.e., quingestanol acetate and quinesterol) to female Wistar rats caused hair loss, which did not recover during the 30-week observation period after cessation of treatment (Lumb et al. 1985). A suppurative to pyogranulomatous infundibular folliculitis has been described in rats after oral administration of canertinib, an irreversible inhibitor of the EGF receptor (Brown et al. 2008). Methoxychlor and its metabolites (mono-OH methoxychlor and bis-OH methoxychlor) inhibit growth and induce atresia of antral follicles in rodents and baboons (Gupta et al. 2007).
Antipsychotics as a method of suicide: population based follow-up study of suicide in Northern Finland
Published in Nordic Journal of Psychiatry, 2021
Arja Mainio, Liisa Kuusisto, Helinä Hakko, Pirkko Riipinen
Every pharmacological drug was collected from death certificates. The antipsychotics were then classified into first- and second-generation groups, using the Anatomical Therapeutic Chemical (ATC) classification system (WHO database) [17]. First-generation antipsychotics included: chlorpromazine, chlorprothixene, dixyrazine, haloperidol, levomepromazine, perphenazine, promazine and thioridazine. Second-generation antipsychotics included: clozapine, melperone, olanzapine, quetiapine, risperidone and sulpiride.