Group Of Hypothyroid Patients Research Articles

CHARACTERISTICS OF CIRCADIAN BLOOD PRESSURE PROFILE IN PATIENTS WITH ACUTE CORONARY SYNDROME AND THEIR ASSOCIATION WITH THYROID FUNCTION

The paper presents the results of a study of circadian arterial blood pressure (ABP) profile in patients with Acute Coronary Syndrome (ACS) and their association with thyroid-stimulating hormone (TSH) levels.
 Aim. To conduct a comparative analysis of circadian BP monitoring (CBPM) indicators in patients with ACS and their association with the TSH level.
 Materials and Methods. The study includes 125 patients with ACS aged 36 to 81 (mean age - 60.98± 0.81 years old). The patients were divided into two groups according to thyroid function. Group one (I) included 51 individuals (40.8%) - hypothyroid patients (TSH level>4mIU/ml), mean age - 62.51±1.18 years old; Group II included 74 individuals (59.2%) - euthyroid patients (TSH level 0.4-4mIU/ml), mean age - 59.93±1.08 years old. The serum-free thyroxine (FT4) levels were within the normal range in both groups. In the general group, the proportion of individuals with unstable angina (UA) was 28.8%, and with myocardial infarction (MI) - 71.2%. In particular, in Group I, the proportion of individuals with UA was 23.53%, and with MI - 76.47%; in Group II, the proportion of individuals with UA was 32.43%, and with MI - 67.57%, p>0,05 between Groups I and II. The circadian BP monitoring was carried out using the Biomed ВАТ41-2 device after stabilization of the patient's condition (on the second day of hospital admission). The following indicators have been determined: systolic BP (SBP) - daytime, nighttime, and average daily (24 hours) (SBPd, SBPn, and SBPav); diastolic BP (DBPd, DBPn, and DBPav); pulse BP (PBPd, PBPn, and PBPav); time index (TI) for SBPd, SBPn, and SBPav (SBPd TI, SBPn TI, and SBPav TI) and DBP (DBPd TI, DBPn TI, and DBPav TI); variability of SBPd, SBPn, and SBPav (SBPd var, SBPn var, and SBPav var) and DBP (DBPd var, DBPn var, and DBPav var); average daily index for SBP (SBP AvDI) and DBP (DBP AvDI); average daily heart rate (HRav). To study thyroid function in patients enrolled, TSH and FT4 levels were determined by chemiluminescent immunoassay method on the ARCHITECT iSystem analyzer using reagent kits for the quantitative determination of TSH (ARCHITECT TSH) and FT4 (ARCHITECT Free T4).
 Results and Discussion. The comparison of the CBPM results in both groups of patients with ACS shows significantly higher mean nighttime (SBPn and DBPn) levels in Group I patients compared to Group II patients: SBPn - by 6.27% (125.44±2.98 mm Hg (I) versus 117.58±2.26 (II), p<0,05), DBPn - by 6.15% (73.65±1.91 mm Hg (I) versus 69.12±1.62 (II), p<0,05), in the absence of a significant between-group difference between the mean levels of respective daytime and average daily indicators. Mean DBPn TI value also turned out to be significantly higher in Group I patients compared to Group II patients - by 33.69% (42.47±4.60% (I) versus 28.16±3.60% (II), p<0.01). Significant difference was detected between mean SBP AvDI and DBP AvDI indicators in hypothyroid patients (I) versus respective indicators in euthyroid patients (II): SBP AvDI (I) 2.52±1.25% versus SBP AvDI (II) 5.99±0.98, p<0.05; and DBP AvDI (I) 4.69±1.38% versus DBP AvDI (II) 8.88±1.32, p<0.05.
 Conclusions. 1. Mean nighttime BP indicator (SBPn, DBPn, and DBPn TI) levels were significantly higher in the Group of hypothyroid patients with ACS, compared to euthyroid patients. In addition, the proportion of patients whose mean nighttime SBP and DBP levels exceeded the permissible values (SBPn<120, DBPn<70 mm Hg) was significantly higher in the Group of hypothyroid patients (I) compared to the Group of euthyroid patients (II). 2. Every third hypothyroid patient (I) (SBP AvDI: 37.25% and DBP AvDI: 31.37%) had a night-peaker circadian BP profile, characterized by nighttime BP increase instead of reduction, which suggests an extremely unfavorable prognosis. The findings may signal an additional adverse effect of thyroid dysfunction on arterial tone and, accordingly, BP regulation, which brings about a high risk of complications of ACS.

Prevalence of depression in group of hypothyroid patients and its relationship with the level of hypothyroidism.

Background and aims: To study the prevalence of depression among a sample of clinical and subclinical hypothyroid patients, in addition to the correlation between thyroid-stimulating hormone and depression severity. Study design: A cross-sectional study in Al Mouwasat University Hospital, Damascus, Syria. Materials and methods: A total of 114 patients diagnosed with hypothyroidism were evaluated by interview using the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria. Results and conclusion: The prevalence of depression among patients with hypothyroidism (either clinical or subclinical) was 31.57%. Higher depression rates were observed in clinical hypothyroidism patients compared with subclinical hypothyroidism patients. In addition, depression severity was also higher in the clinical hypothyroidism group. Increased rate and severity of depression with increased TSH levels. However, the rate and severity of depression are inversely proportional to the duration of the diagnosis of hypothyroidism.

THYROID DYSFUNCTION IN PATIENTS WITH CHRONIC KIDNEY DISEASE

It is known that patients with chronic kidney disease (CKD) often have hypothyroidism. In patients with CKD, iodine excretion in the urine is disrupted. The high content of iodine in the thyroid gland and tissues leads to a disruption in the synthesis and peripheral metabolism of thyroid hormones. In hypothyroidism, there is a disruption of sodium and water reabsorption in the proximal tubule, the volume of the filtrate increases, the volume of the tubular apparatus overloads, and the eGFR decreases.THЕAIM:to study the occurrence of hypothyroidism in patients with different stages of CKD, to evaluate the parameters of thyroid status and antithyroid antibodies in patients with CKD.PATIENTS AND METHODS.953 patients from I.P. Pavlov SPbSMU clinics (screening group) were examined. TSH, free T4, serum creatinine were defined and eGFR was calculated using the formula CKD-EPI in all patients. A group of patients with hypothyroidism accounted for 466 patients. Patients with a normal TSH of 0.4-2.5 mIU / L (comparison group) were selected from the screening group.RESULTS.eGFR in the screening group and in the group of hypothyroid patients correlated with age. Hypothyroidism was associated with female sex and older age. In the group of patients with advanced stage CKD (3B-5), the incidence of subclinical and manifest hypothyroidism was 3 times higher than in the group with normal GFR (GFR> 90 ml / min, p = 0.007). In the group of patients with hypothyroidism, the frequency of advanced stages of CKD (3B-5) was 2 times higher than in the comparison group (p = 0.02). In patients with CKD, a direct correlation was found between GFR and free T3 (r = 0.34, p = 0.02). Thyroid peroxidase antibodies were revealed in 64% of patients with CKD with hypothyroidism.CONCLUSION.Hypothyroidism is associated with chronic kidney disease. For patients with CKD, there is a syndrome of euthyroid pathology ("low T3" syndrome). Hypothyroidism in patients with CKD is not always the outcome of autoimmune thyroiditis.

Prevalence of diabetes mellitus and impaired fasting glucose among hypothyroid patients

Background: The association between autoimmune thyroid diseases and autoimmune diabetes is well established. However, the association between type 2 Diabetes and thyroid disease is unclear. Studies conducted on this topic worldwide have revealed varying results. The aims of this study were to assess the prevalence of diabetes and impaired fasting glucose in a group of hypothyroid patients in Sri Lanka and to assess the relationship between severity and etiology of hypothyroidism with diabetes and impaired fasting glucose. Method: This descriptive (prospective) study was conducted at the Endocrine clinic, Teaching Hospital, Ragama over a period of 12 months, where all the new and follow up patients with hypothyroidism (both overt and subclinical hypothyroid patients) attending the clinic during this study period were included until the sample size is achieved. Interviewer-administered questionnaire was used to obtain relevant data from the patient and from the clinic book. Fasting blood sugar was done for all patients. When FBS ≥ 100mg/dl, the test was repeated. For patients who had repeatedly elevated FBS ≥ 100mg/dl, Urine for micro albumin and serum creatinine were also checked. If the urine micro albumin was elevated, the test was repeated after 3 months. The presence of retinopathy was assessed by the ophthalmology team. Results: Majority of the study population consisted of females (91%). Mean age of the study population was 44.7 (SD – 12.1). 85.6% of the patients had overt hypothyroidism and 14.4% had subclinical hypothyroidism. The overall prevalence of diabetes mellitus among the study population was 15.6%. Prevalence of impaired fasting glucose was 31%. The prevalence of diabetes, impaired fasting glucose as well as dysglycaemia among patients with overt hypothyroidism and the subclinical hypothyroidism not significantly different (p-0.905, p-0.931, p-0.982). There was no significance difference between the etiology of hypothyroidism and in the prevalence of diabetes and impaired fasting glucose (p- 0.079, p- 0.182 respectively). None of the newly diagnosed patients with diabetes had microvascular complications. Conclusion: Overall prevalence of both overt and subclinical hypothyroidism was not associated with type 2 diabetes mellitus and the severity of hypothyroidism did not have an effect on the development of any form of hyperglycemia. There was no significant association between the etiology of hypothyroidism and in the prevalence of diabetes as well as impaired fasting glucose. Even though the age, the body mass index, the presence of hypertension and the family history were significantly associated with the development of diabetes mellitus, the gender and the sedentary lifestyle did not show a significant association with the development of diabetes in our study population.

Particularities of endothelial dysfunction in hypothyroid patients.

It is well known that hypothyroidism promotes the premature onset of subclinical atherosclerosis. This condition is defined by endothelial dysfunction (ED) and increased arterial stiffness (AS) and leads to augmentation of peripheral vascular resistance. To assess the presence and severity of ED and to follow its evolution under therapy in three groups of hypothyroid patients, we used three different noninvasive methods: carotidian intima-media thickness (IMT), flow mediated vasodilatation (FMD), and AS. The study group consisted of 56 young, hypothyroid women without associated cardiovascular pathology or risk factors for atherosclerosis. We selected our patients in order to have normal IMT (< 0.9 mm) and assessed the basal diameter of the brachial artery and the alterations of FMD and of AS parameters: pulse wave velocity (PWV) and augmentation index (AIx). We found, in all patients, a reduced basal diameter of brachial artery, pathological patterns of FMD, and increased values of PWV and AIx, compared to controls, in relation with the severity of thyroid dysfunction. We documented an improvement of ED after therapy with L-thyroxin. ED, documented in hypothyroid patients by means of three noninvasively methods, was strongly related to the severity of thyroid disease. We detected, in all three subgroups, significant alterations of FMD and AS, even in the absence of structural changes, documented by a normal IMT. ED improved consistently after restoring the euthyroid state.

Thyroid Hormones Influence Human Dendritic Cells' Phenotype, Function, and Subsets Distribution

Dendritic cells (DCs) are the most effective antigen-presenting cells and key regulators of immune response. The immunoregulatory properties of DCs strongly depend on the microenvironment in which DCs have been matured and activated. Thyroid hormones are an important part of this environment and regulate many vital processes including growth and cellular metabolism. The aim of the study was an analysis of the influence of thyroid hormones on blood DC subtypes ex vivo, including the surface expression of molecules involved in antigen presentation, costimulation, and maturation, as well as on functional properties of DCs in vitro. Blood samples for the quantitative and phenotypic analysis of peripheral blood plasmacytoid and myeloid DC subtypes were collected from thyroidectomized patients at two time points: (i) at the time of the so-called stimulation with endogenous thyrotropin-a group of hypothyroid patients after l-thyroxine (L-T(4)) withdrawal (pretreatment group)-and (ii) after 2 months of L-T(4) administration for thyrotropin suppression-a posttreatment group. The phenotype of DCs including HLA-DR, costimulatory molecules (CD40, CD80, and CD86), and maturation marker CD83 was assessed by flow cytometry. The influence of isolated peripheral blood DCs on autologous peripheral blood mononuclear cell proliferation and cytokine secretion (interferon alpha, interleukin-12) under triiodothyronine (T(3)) deficiency or T(3) excess was investigated in culture experiments. The percentage of peripheral blood plasmacytoid and myeloid DCs was higher after L-T(4) administration when compared with the pretreatment group. Moreover, the expression of CD86 on both DC subtypes was higher in the L-T(4) treated than in the hypothyroid patients. In the in vitro experiments, T(3) stimulation increased CD86 expression on cultured DCs. The phenotypic difference was paralleled by enhanced ability of T(3)-stimulated DCs to activate interleukin-12 secretion and proliferation of autologous peripheral blood mononuclear cells (PBMLs) in coculture experiments. In the present study, we provide for the first time an evidence that the thyrometabolic status has an influence on the phenotype and function of human peripheral blood DCs. This observation may be of potential importance for the understanding of the pathogenesis of immune and endocrine disorders.

Inhibition of thyrotropin-stimulated iodide uptake in FRTL-5 thyroid cells by crude immunoglobulin fractions from patients with goitrous and atrophic autoimmune thyroiditis.

We studied the effects of crude immunoglobulin (Ig) fractions of serum from patients with goitrous and atrophic autoimmune thyroiditis on TSH-, thyroid-stimulating immunoglobulin (TSI)-, forskolin-, and dibutyryl cAMP-stimulated 125I uptake by FRTL-5 thyroid cells. TSH-stimulated 125I uptake was inhibited by the Ig fractions from 15 patients with atrophic thyroiditis who had serum TSH binding inhibitor Igs (TBII), 10 (62.5%) of 16 TBII-negative patients with atrophic thyroiditis, 7 (43.8%) of 16 hypothyroid patients with goitrous thyroiditis who had no TBII activity, and only 2 (15.4%) of 13 euthyroid patients with goitrous thyroiditis who were negative for TBII. The mean inhibition of TSH-stimulated 125I uptake produced by the crude Igs from the former 3 groups of hypothyroid patients was statistically significant (P less than 0.001, P less than 0.001, and P less than 0.01, respectively) and correlated closely with the ability of the Ig fractions to inhibit TSI-stimulated 125I uptake (r = 0.882) and TSH-stimulated cAMP accumulation (r = 0.929). The inhibition of TSH- or TSI-stimulated 125I uptake by Ig samples containing TBII correlated significantly with the TBII activities. On the other hand, in the presence of Igs from TBII-negative hypothyroid patients, the inhibition of TSH-stimulated 125I uptake correlated significantly with that of forskolin-stimulated 125I uptake (r = 0.685). Although 6 (12.8%) of 47 Ig samples from hypothyroid patients inhibited dibutyryl cAMP-stimulated 125I uptake, the activities were marginal. These findings suggest that at least 2 types of antibodies are involved in the inhibition of TSH- or TSI-stimulated 125I uptake: 1 being a competitive inhibitor of TSH binding to its receptors, and another exerting influence on a step subsequent to TSH or TSI binding, presumably through adenylate cyclase inhibition.

Serum free thyroid hormones in different degrees of hypothyroidism and in euthyroid autoimmune thyroiditis.

Serum total and free T4 and T3, thyroxine-binding globulin (TBG) and TSH, basal and 20, 30 and 60 min after TRH (200 micrograms, iv), were evaluated in 125 hypothyroid patients (38 with severe, 23 with mild, and 64 with subclinical hypothyroidism), in 35 euthyroid subjects with autoimmune thyroiditis, and in 51 healthy controls. T4/TBG and T3/TBG ratios were also calculated. A significant decrease in all indices of thyroid function except for T3 occurred simultaneously with a significant increase in basal and TRH-stimulated TSH levels from healthy subjects to subclinical hypothyroids, from subclinical to mild and from mild to severe hypothyroids; euthyroid patients with autoimmune thyroiditis did not differ from healthy subjects. All severe hypothyroid patients had low T4 as well as free T4 (FT4), free T3 (FT3), T4/TBG and T3/TBG ratios, but among mild and subclinical hypothyroids direct determination of FT4 and FT3 proved to be a better index of thyroid function than determination of T4 and T3 even after correction for TBG levels. FT4 was the most commonly abnormal index (19 of 23 subjects with mild and 14 of 64 with subclinical disease). Regression analysis showed that FT4, T4/TBG ratio, T4, and FT3 had a significant inverse correlation with TSH in hypothyroid patients. Discriminant analysis showed that among the thyroid parameters, FT4 is the variable which discriminates best between control subjects and the 3 groups of hypothyroid patients. These data extend previous reports and in a large series of patients confirm the biological meaning and the clinical value of direct measurement of serum free thyroid hormones in hypothyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

PLASMA NORADRENALINE AND BLOOD PRESSURE IN HYPOTHYROID PATIENTS: EFFECT OF GRADUAL THYROXINE TREATMENT

High plasma noradrenaline (PNA) levels have been reported in hypothyroid patients and hypothyroidism has been associated with hypertension. To explore the relationship between PNA and blood pressure (BP) in hypothyroid patients, and the effects of gradual thyroxine replacement, a prospective study was performed comparing BP, heart rate (HR) and PNA in a normotensive and a hypertensive group of hypothyroid patients before and during gradual thyroxine substitution. Thyroxine treatment reduced the BP; the reduction in supine BP was greater in the hypertensive than in the normotensive group. HR increased similarly in both groups during treatment. PNA was elevated in the normotensive group before treatment and decreased gradually during thyroxine treatment. The hypertensive group had normal PNA levels. The present study indicates that normotensive, in contrast to hypertensive, hypothyroid patients have increased sympathetic nervous activity. Although the mechanism is unclear, thyroid replacement therapy can reverse hypertension in hypothyroid patients.

A retrospective study of audiological function in a group of congenital hypothyroid patients

A retrospective survey has been carried out on audiological function in 46 congenital hypothyroid cases; mental and physical development were also assessed, as well as the adequacy of substitutive therapy. Using traditional audiometry it was found that 50% of the congenital hypothyroid patients were hypocusic. Severe and profound hearing loss (5 cases) was found in the group of hypothyroid patients with dyshormonogenesis, whereas only one-third of patients with thyroid agenesis presented a mild or moderate hearing loss not related to the time of diagnosis and treatment. The hearing loss was twice as frequent in the patients with clinical hypothyroidism. Using electro-physiological techniques, the early or slow potentials were comparable between hypocusic or normocusic patients; however a longer latency of the slow vertex responses was observed in the hypothyroid group as compared to the normal population. The mean estimated I.Q. was about 2 standard deviations below the average; however 30% of subjects had normal or above normal intellectual level, this percentage rises to 55% if only patients below 16 years are considered. The height was significantly shorter only in the late treated patients (1 year). No correlations were found among audiological and psychological variables, nor between these variables and height. All patients were on desiccated thyroid, but therapy was inadequate in 26% of cases and subclinical hypothyroidism was found in 33% of cases.

Thyroid-induced mania in hypothyroid patients.

This retrospective study, based on 18 case reports, describes an organic affective syndrome, manic type, occurring shortly after the initiation of thyroid replacement in hypothyroid patients. The symptomatology and homogeneity of the syndrome offers insight into the relationship between thyroid activity and affective disturbance. The patients experiencing mania showed concurrent psychopathology at the time of replacement therapy, frequently had a past history of personal or familial psychiatric disorder and were given dosages in the high range of normal. The potential morbidity of the manic state was considerable. These findings suggest that a group of hypothyroid patients at risk can be identified. In such a group, lower initial dosages and gradual increases in dosage may be indicated.

The influence of triiodothyronine (T3) treatment on the resin uptake of 131I-triiodothyronine.

ABSTRACT The effects of T3 treatment on the resin uptake of 131I-T3 as well as on serum thyroxine, have been studied in a euthyroid normal control group, in a group of hypothyroid patients, and in a group of pregnant women. T3 therapy resulted in a decline in the resin uptake of 131I-T3 in the normal control group; this was considered due to a suppression of serum thyroxine (consequent to TSH suppression), with a consequent increase in the amount of unsaturated thyroxine binding globulin. In patients with hypothyroidism, however, the resin uptake of 131I-T3 actually increased as a result of T3 treatment. Since the serum thyroxine in this group could not decrease any further as a result of the T3 administration, the T3 was truly additive, saturating more TBG binding sites, thus increasing the resin uptake of 131I-T3. In the pregnant group, large doses of T3 also caused an increase in the resin uptake of 131I-T3. While the decline in serum thyroxine was only modest, it was still greater than the accompanying rise in serum T3, so that the net amount of circulating thyroid hormone was less in the post treatment phase. Thus, the rise in the resin uptake of 131I-T3 is not completely explicable in this group.