"Results of a prospective study of acute liver failure at 17 tertiary care centres in the United States". Ann. Intern. Med. 137 (12).947–54. doi:10.7326/0003-4819-1371220021217000007. PMID 12484709. S2CID 11390513. Pirmohamed M, Breckenridge AM, Kitteringham NR, Park BK (1998). "Adverse drug reactions". BMJ. 316 (7140):12958. doi:10.1136/bmj.316.7140.1295. PMC 1113033. PMID 9554902. Manov I, Motanis H, Frumin I, Iancu TC (2006). "Hepatotoxicity of anti-inflammatory and analgesic drugs: ultrastructural aspects". Acta Pharmacol. Sin. 27 (3): 259–72. doi:10.1111/j.1745-7254.2006.00278.x. PMID 16490160. S2CID 26874901. Alpers DH, Sabesin SM (1982). Schiff L; Schiff ER (eds.). Diseases of the liver. Philadelphia: JB Lippincott. pp. 813–45
Chalasani, Naga P.; Hayashi, Paul H.; Bonkovsky, Herbert L.; Navarro, Victor J.; Lee, William M.; Fontana, Robert J.; Practice Parameters Committee of the American College of Gastroenterology (2014). "ACG Clinical Guideline: The Diagnosis and Management of Idiosyncratic Drug-Induced Liver Injury". The American Journal of Gastroenterology. 109 (7):950966. doi:10.1038/ajg.2014.131. PMID 24935270. S2CID 2417493
Patel T, Roberts LR, Jones BA, Gores GJ (1998). "Dysregulation of apoptosis as a mechanism of liver disease: an overview". Semin. Liver Dis. 18 (2): 105–14. doi:10.1055/s-2007-1007147. PMID 9606808
Mumoli N, Cei M, Cosimi A (2006). "Drug-related hepatotoxicity". N. Engl. J. Med. 354 (20):21913,author,reply21913. doi:10.1056/NEJMc060733. PMID 16710915
Bénichou C (1990). "Criteria of drug-induced liver disorders. Report of an international consensus meeting". J. Hepatol. 11 (2): 272–6. doi:10.1016/0168-8278(90)90124-A. PMID 2254635
Blazka ME, Wilmer JL, Holladay SD, Wilson RE, Luster MI. (1995) Role of pro‑inflammatory cytokines in acetaminophen hepatotoxicity. Toxicol Appl Pharmacol 1995;133:43‑52
Yadav V, Rai R, Yadav A, Pahuja M, Solanki S, et al. (2012) Evaluation of antibacterial activity of Callicarpa macrophylla Vahl.
However, a low basal metabolic rate was known to be non-specific, also present in malnutrition. The first laboratory test to be helpful in assessing thyroid status was the serum protein-bound iodine, which came into use around the 1950s. In 1971, the thyroid stimulating hormone (TSH) radioimmunoassay was developed, which was the most specific marker for assessing thyroid status in patients. Many people who were being treated based on basal metabolic rate, minimizing hypothyroid symptoms, or based on serum protein-bound iodine, were found to have excessive thyroid hormone. The following year, in 1972, a T3 radioimmunoassay was developed, and in 1974, a T4 radioimmunoassay was developed. Other animals
In veterinary practice, dogs are the species most commonly affected by hypothyroidism. The majority of cases occur as a result of primary hypothyroidism, of which two types are recognized: lymphocytic thyroiditis, which is probably immune-driven and leads to destruction and fibrosis of the thyroid gland, and idiopathic atrophy, which leads to the gradual replacement of the gland by fatty tissue. There is often lethargy, cold intolerance, exercise intolerance, and weight gain. Furthermore, skin changes and fertility problems are seen in dogs with hypothyroidism, as well as a number of other symptoms. The signs of myxedema can be seen in dogs, with prominence of skin folds on the forehead, and cases of myxedema coma are encountered. The diagnosis can be confirmed by blood test, as the clinical impression alone may lead to overdiagnosis. Lymphocytic thyroiditis is associated with detectable antibodies against thyroglobulin, although they typically become undetectable in advanced disease.