Obesity-related changes in the composition of the body interfere with the proper functioning of the thyrotropic axis, leading to its disturbances and changes in the structure of the thyroid gland. Distinguishing what is related to obesity and what constitutes pathological changes is crucial for the proper treatment of patients. In this paper authors present a case of a patient with a diet-induced obesity, whose only abnormalities in thyroid assessment included an elevated level of thyroid stimulating hormone (TSH) and hypoechoic thyroid gland on ultrasound. Based on this clinical situation, we reviewed literature in order to establish rules regarding management of thyroid disorders in obese individuals. The most common obesity-related thyroid abnormality is an isolated increase of TSH, without clinical symptoms of hypothyroidism, defined as hyperthyrotropinaemia. In obese adults, autoimmune thyroid disease is found equally often as in the normal-weight population. Thyroid enlargement, increased risk of nodules, and decreased echogenicity, not related to autoimmunity, is frequent among obese individuals. Weight loss leads to the normalisation of TSH levels and thyroid echogenicity. Excessive weight can influence both the TSH level and ultrasound image of the thyroid gland; however, these findings can be reversed by weight reduction. Therefore, in asymptomatic obese patients elevated TSH should not be treated with thyroid hormone replacement.
Background: Dual antiplatelet therapy (DAPT) is recommended after elective percutaneous coronary intervention (PCI) in PFT (36.5 ± 47 PRU) arms as compared to the control arm (176 ± 67.8 PRU), p = 0.01 and p = 0.03, respectively. PMI appeared in 17 (37%) (Cardiol J 2017; 24, 3: 284-292)
Aggregometry and genotyping are methods of platelet function testing, which can be beneficial for high-risk patients undergoing invasive cardiac procedures. An optimal level of platelet reactivity (PR) should be maintained. There are discrepancies between individuals and their response to clopidogrel, accounting for the incidence of poor responders from 5% to 44%. This phenomenon predisposes the patients to increased risk of ischaemic events and thereby overall poorer clinical outcome. Prasugrel and tricagrelor are newer without genetic correlation to their action, however associated with increased bleeding risk. Aggregometry methods assess platelet reactivity at the exact moment of blood sampling. They reflect "phenotype" of the patient and vary after drug administration or dose change. The most popular tests are Light Transmission Aggregometry, Vasodilator-Stimulated Protein, VerifyNow, Multiple Electrode Aggregometry and Thrombelastography. There is proven genetic correlation between some cytochrome enzymes on clopidogrel response. The most widely tested is gene CYP2C19, which produces the enzyme transforming clopidogrel into an active metabolite. The CYP2C19*2 allele carriers have higher PR which can result in more thrombotic events. The manuscript shows the most recent evidence behind platelet function testing. Aggregometry is shown to be beneficial in 5 trials and 1 meta-analysis, while one paper was of different opinion. Ten studies show a positive clinical effect of genotyping on patients' outcome, while one does not support it. The best method of identifying high-risk individuals could be both methods and personalisation of antiplatelet therapy may decrease adverse ischaemic outcomes (Adv Clin Exp Med 2015, 24, 4, 687-693).
Src family kinases are one of the most important signal transmitters in platelets. Some receptors have well documented interactions with SFKs, while other have not been examined in humans or data about its association originated from single studies. Further studies are necessary to confirm the findings and reduce falsepositive associations.
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