Introduction: Osteoporosis is seen in some 12-50 % patients with liver cirrhosis. Detrimental effects of alcohol are exerted directly on the bone cells and indirectly on hormones. Vitamin D is involved in osteoblast differentiation, bone matrix synthesis and bone mineralization, as well as in its decomposition. Vitamin D deficiency has been reported in about 2/3 patients with liver cirrhosis. Objective: Determination of vitamin D status, bone metabolic activity and bone mass in patients with alcoholic liver cirrhosis (ALC). Methods: Thirty male patients with ALC were investigated in the period October 2011-March 2012. Total vitamin D, parathormone, osteocalcin and CrossLaps were determined by the ECLIA method (electrochemiluminiscence immunoassay) using Elecsys 2010 analyzer. Bone mineral density was measured by means of dual-energy x-ray absorptiometry (DXA) using the Lunar Prodigy. Result analysis was performed using descriptive statistics and hypothesis testing, as well as nonparametric one-way analysis of variance, Kruskal-Wallis test, Mann-Whitney U-test, Pearson correlation coeffi cient. Results: Defi ciency in vitamin D (< 50 nmol/l) was noted in 66.66 % patients, with highest prevalence in Child-Pugh C class patients (chi-square = 5.878, p < 0.05). Osteocalcin levels were below the lower limit of normal in 86.7 % patients. CrossLaps was increased in only 20 % patients, but a signifi cant increase was noted in Child-Pugh C class patients. Osteoporosis was diagnosed in 20 % of patients, with no correlation with disease severity and vitamin D status. Conclusions: Vitamin D defi ciency is present in patients with ALC. Decrease in bone formation and bone mass is most probably multicausal (Tab. 2, Fig. 1, Ref. 30).
Screening for autoimmune thyroid diseases should be recommended in everyday clinical practice, in patients with primary organ-specific or organ non-specific autoimmune disease. Otherwise, in patients with primary thyroid autoimmune disease, there is no good reason of seeking for all other autoimmune diseases, although these patients have a greater risk of developing other autoimmune disease. Economic aspects of medicine require further analyzing of these data, from cost/benefit point of view to justified either mandatory screening or medical practitioner judgment.
Iodine, as a trace element, is a necessary and limiting substrate for thyroid gland hormone synthesis. It is an essential element that enables the thyroid gland to produce thyroid hormones thyroxine (T4) and triiodothyronine (T3). Synthesis of Thyroid Hormones and Iodine Metabolism. Three iodine molecules are added to make triiodothyronine, and four for thyroxine - the two key hormones produced by the thyroid gland. Iodine deficiency The proper daily amount of iodine is required for optimal thyroid function. Iodine deficiency can cause hypothyroidism, developmental brain disorders and goiter. Iodine deficiency is the single most common cause of preventable mental retardation and brain damage in the world. It also decreases child survival, causes goiters, and impairs growth and development. Iodine deficiency disorders in pregnant women cause miscarriages, stillbirths, and other complications. Children with iodine deficiency disorders can grow up stunted, apathetic, mentally retarded, and incapable of normal movements, speech or hearing. Excessive Iodine Intake. Excessive iodine intake, which can trigger a utoimmune thyroid disease and dysfunction. is on the other side. Iodine use in Case of Nuclear Catastrophe. In addition to other severe consuquences of radioactivity, high amount of radioactive iodine causes significant increase in incidence of thyroid gland carcinoma after some of the nuclear catastrophes (Hiroshima, Nagasaki, Chernobyl, Fukushima). The incidence of thyroid carcinoma was increased mostly in children. This paper was aimed at clarifying some of the possibilities of prevention according to the recommendations given by the World Health Organization.
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