Fish arsenic may influence human blood arsenic,selenium, and T4:T3 ratio

The effects of an arsenic-rich fish diet and selenium (Se) supplementation on blood arsenic (As), Se, and thyroid hormones were studied in 32 women divided into four equal groups. Groups 1 and 4 received 400 μg Se-methionine daily, group 2 received 400 μg selenite daily, and group 3 received placebo tablets for 15 wk. In addition, groups 1–3 increased their fish intake, eating at least three fish dinners weekly. Mean blood Se concentrations (initially 1.68 ± 0.24 μmol/L) increased twofold in the Se-methionine groups (p < 0.0001) and by 32% in the selenite group (p < 0.01). Group means of blood As concentrations increased by 63% (p < 0.01), 50% (p < 0.01), 106% (p < 0.01), and 29% (p < 0.05) in the four groups, respectively. Analyzed As intake from duplicate portions of consumed fish correlated with final blood As concentrations (r=0.85, p < 0.001, n=32). In the group not receiving Se, there was a positive correlation between final blood As concentrations and plasma T4 : T3 ratio (r=0.80, p < 0.02, n=8). Initially, blood As concentrations correlated negatively with both T3 and T4 in plasma, but this correlation disappeared upon Se supplementation. The results demonstrate that increased intake of fish may influence blood As concentrations and that circulating thyroid hormones may be influenced by Se-As interactions.     

Selenium supplementation of children in a selenium-deficient area in China

Keshan disease is a cardiomyopathy restricted to the endemic areas of China and seen in residents having an extremely low selenium (Se) status. Prophylactic administration of sodium selenite has been shown to decrease significantly the incidence of acute and subacute cases. The aim of the study was to assess the relative bioavailability of selenite versus organic Se-yeast in a Se-deficient area in China with a randomized double-blind double-dummy design. Healthy children (n=30) between 14 and 16 yr of age were randomized into three equal groups receiving either 200 μg/d selenite Se or 200 μg/d Se-yeast or placebo for 12 wk. Blood was drawn at baseline, 4, 8, and 12 wk and 4 wk postsupplementation. The plasma Se concentration (mean ± SD) was 0.16±0.03 μmol/L at baseline. Selenite and Se-yeast supplementation increased plasma Se to plateau values, 1.0±0.2 and 1.3±0.2 μmol/L, respectively. In red cells, Se-yeast increased the selenium level sixfold and selenite threefold compared to placebo. The relative bioavailability of Se-yeast versus selenite measured as glutathione peroxidase (GSHPx) activity was similar in plasma, red blood cells, and platelets. GSHPx activity reached maximal levels in plasma and platelets of 300% and 200%, respectively, after 8 wk compared to the placebo group, but continued to increase in red cells for 16 wk. Our study showed that although both forms of Se were equally effective in raising GSHPx activity, Se-yeast provided a longer lasting body pool of Se. Se-yeast may be a better alternative to selenite in the prophylaxis of Keshan disease with respect to building up of body stores.     

Iloprost for the attenuation of ischaemia/reperfusion injury in a distant organ

The objective of this study was to investigate antioxidant and cytoprotective properties of iloprost in a distant organ after ischaemia reperfusion injury. Male Wistar rats were divided into two groups. After application of anesthaesia both hindlimbs were occluded. A 2-h reperfusion procedure was carried out after 60 min of ischemia. Study group (STU) rats (n=10) received 10 microg kg(-1) iloprost in 1 ml of saline from the tail vein 10 min before reperfusion. Control (CON) group rats (n=10) received an equal amount of saline. The rats were sacrificed by injection of a high dose of thiopentone sodium. Blood and tissue samples (right kidneys) were taken for analysis. Differences in malondialdehyde (MDA), myeloperoxidase (MPO), Na+-K+ ATPase and total antioxidant capacity (TAC) between the groups were analysed. MPO, MDA and TAC levels in the sera of CON and STU groups were 1.60+/-0.26 U l(-1), 11.42+/-5.23 nmol ml(-1), 8.30 x 10(-2)+/- 3.93 x 10(-2) nmol ml(-1) h(-1) and 1.07+/-0.11 U l(-1), 7.60+/-1.81 nmol ml(-1) and 0.15+/-3.23 x 10(-2) nmol ml(-1) h(-1) (p=0.0001, p=0.043 and p=0.0001 respectively). MPO, ATPase and MDA levels in kidneys for CON and STU groups were 1.24+/-0.58 U g(-1), 85.70+/-52.05 nmol mg(-1), 17.90+/-7.40 nmol ml(-1) and 0.78+/-0.31 U g(-1), 195.90+/-56.13 nmol mg(-1) and 10.10+/-0.99 nmol ml(-1) (p=0.046, p=0.0001 and p=0.009 respectively). When given prior to reperfusion, the positive effect of iloprost in the attenuation of distant organ reperfusion injury has been demonstrated.     

Trace Element Levels in Hashimoto Thyroiditis Patients with Subclinical Hypothyroidism

The present study was conducted to evaluate the serum copper, zinc, magnesium, and selenium levels in patients with subclinical hypothyroidism in the iodine-rich region of Ankara, Turkey. The effects of hormone replacement therapy on these elements were also studied in these patients. Basal levels of selenium and iron in patients were significantly lower than control group (67.7 +/- 10.4 vs. 83.7 +/- 17.3 microg/dl, p = 0.02; 55.7 +/- 38 vs 275.7 +/- 24, P = 0.03 microg/dl). Serum magnesium levels were significantly higher in patient group (2.16 +/- 0.31 vs 1.95 +/- 0.13 mg/dl, P < 0.0001). There was a correlation between selenium levels with hsCRP (r = -0.408, p = 0.007). HsCRP levels in patients with selenium levels <80 microg/l (n = 31) was significantly higher than hsCRP levels in patients with selenium levels >80 microg/l (n = 12; 1.99 +/- 1.0; 1.02 +/- 0.9, p = 0.014). None of these biochemical risk factors and trace elements have changed after euthyroidism in patients with SH when compared to pretreatment levels. Selenium deficiency may contribute to cardiovascular disease risk in these patients.     

Selenium and glycogen levels in diabetic patients

Selenium in serum and selenium and glycogen in erythrocytes were determined in diabetic patients divided into noninsulin-dependent (n=50) and insulin-dependent (n=31) groups according to the etiopathogenesis of their diabetes. Selenium was determined by the method of atomic absorption spectrometry. Serum level of selenium was statistically significantly different in patients with either noninsulin-dependent (59.23±12.2 μg/L) or insulin-dependent (58.23±16.7 μg/L) diabetes mellitus as compared with the control group of 62 subjects (64.2±11.5 μg/L; p<0.05). There was no statistically significant difference in the serum levels of selenium between the groups of patients with noninsulin-dependent and insulin-dependent diabetes mellitus. The levels of erythrocyte glycogen were 2.0580±1.326, 2.0380±1.735, and 2.0036±1.3537 μg/g Hb in the control group, noninsulin-dependent group, and insulin-dependent group, respectively, with no statistically significant between-group difference. The decreased levels of selenium in serum and erythrocytes of diabetic patients suggest the possible role of glutathione peroxidase activity.     

Selenium and immunocompetence in patients with head and neck cancer

This randomized double-blind placebo-controlled study aimed to determine whether oral intake of 200 μg/d of sodium selenite, a dose within the safe and adequate daily intake (50–200 μg/d) recommended by the U.S. Food and Nutrition Board, will abrogate depressed or enhance normal-level immune functions of patients receiving therapy for squamous cell carcinoma of the head and neck. Subjects were given one selenium/placebo tablet/d for 8 wk, beginning on the day of their first treatment for the disease (e.g., surgery, radiation, or surgery and radiation) and their immune functions were monitored. Supplementation with selenium (Se) during therapy resulted in a significantly enhanced cell-mediated immune responsiveness, as reflected in the ability of the patient’s lymphocytes to respond to stimulation with mitogen, to generate cytotoxic lymphocytes, and to destroy tumor cells. The enhanced responsiveness was evident during therapy and following conclusion of therapy. In contrast, patients in the placebo arm of the study showed a decline in immune responsiveness during therapy, which was followed, in some patients, by an enhancement, but the responses of the group remained significantly lower than baseline values. The data also show that at baseline, patients entered in the study had significantly lower plasma Se levels than healthy individuals, and patients in stage I or II of disease had significantly higher plasma selenium levels than patients in stage III or IV of disease.     

Treatment of subclinical hypothyroidism reduces atherogenic lipid levels in a placebo-controlled double-blind clinical trial.

Many studies have found clinical and metabolic alterations in subclinical hypothyroidism, however, there are disagreements about the benefits of levothyroxine therapy. The objective of the present study was to analyze the effects of 6 months of treatment on the lipid profile of patients with subclinical hypothyroidism. A randomized double blind, placebo-controlled clinical assay was conducted. Sixty patients were enrolled in stratified random allocation by TSH levels that generated similar groups in average: free thyroxine levels, lipid levels, age, clinical score, and sedentary. At 6 months, 18 patients in the levothyroxine and 20 in the placebo group were reevaluated and a fall in all atherogenic lipid variables was observed with treatment. The TC and LDL-c variations (-22.6+/-37.2 and -18.5+/-34.6 mg/dl, respectively) in the group that received LT4 were statistically different (p=0.023 and p=0.012) from those occurring in the placebo group (+7.3+/-37.1 and +14.7+/-40.6 mg/dl). Baseline characteristics associated with better improvement in the levels of TC and LDL-c were the presence of TPO-Ab, TSH levels >8.0 microUI/ml, Body Mass Index >or=25 kg/m2, and the presence of menopause. We concluded that treatment with dose-adjusted levothyroxine reduced atherogenic lipid levels in some patients. Further studies to determine the effects of LT4 replacement in specific subgroups of SH patients are still necessary, especially in patients with TSH <8.0 microUI/ml.     

Urinary selenium excretion in selenite-loaded sheep and subsequent Se dynamics in blood constituents

Renal selenium excretion in sheep was measured during intravenous infusion of sodium selenite, and the post-infusion dynamics of Se levels in whole blood, plasma and red blood cells (RBC) were investigated for the next 5 days. The plasma Se level increased almost twenty fold with the infusion of Na2SeO3 (from 0.39 +/- 0.02 to 7.83 +/- 0.33 micromol x L(-1), P < 0.001) compared with the baseline value. The selenium concentration in urine (0.07 +/- 0.02 vs. 18.53 +/- 2.56 micromol x L(-1), P < 0.001), the amount of Se excreted (0.14 +/- 0.07 vs. 21.40 +/- 2.31 nmol x min(-1), P < 0.001) and the renal clearance of Se (0.1 9 +/- 0.03 vs. 3.01 +/- 0.34 mL x min(-1), P < 0.001) were found to be highly significantly elevated during selenite loading. The clearance measurements showed no changes in the urinary flow rate or in the glomerular filtration rate. During and at the end of infusion the highest Se level was attained in plasma, followed by whole blood and RBC. The plasma Se level fell rapidly within 10 min after the end of infusion, but the concentration of Se in RBC was stable up to the fourth hour, when it started to decrease too. On day 5 the Se concentrations in plasma, RBC and whole blood were found to be only slightly but still significantly higher than before the selenite infusion. The large disproportion between the infusion rate of Se (8.76 microg x min(-1)) and its renal excretion rate (1.69 microg x min(-1)) found in clearance measurements suggests low glomerular filtration of infused selenium, which might primarily be caused by the binding of selenite metabolites to blood constituents. The presented results confirm the low bioavailability to ruminants of Se from sodium selenite.     

Monitoring of Changes in Selenium Concentration in Goat Milk During Short-Term Supplementation of Various Forms of Selenium

The goal of the experiment was to monitor the changes in the selenium concentration in goat milk during short-term oral supplementation of three different forms of selenium. The experiment involved 24 lactating goats of white shorthaired breed. Group C was the control; group S received selenium in the form of selenium-enriched yeast, group L in the form of lactate, and group B in the form of proteinate. Individual selenium preparations were administered individually orally in 250 μg Se dose per animal for 20 days. After the beginning of selenium supplementation, the selenium concentration in milk during the first 5 days grew gradually in group S. Between days 7 and 20 of Se supplementation, the mean Se concentrations in milk in groups were 12.53 ± 3.69 μg l⁻¹ (C), 25.90 ± 6.30 μg l⁻¹ (S), 13.14 ± 3.54 μg l⁻¹ (L), 11.70 ± 3.69 μg l⁻¹ (B). Differences between group S and other groups (C, B, L) were highly significant (p < 0.0001). Based on our results, selenium in the form of lactate and proteinate was excreted into the milk similarly, but selenium in the form of yeast, which contains high amount of selenomethionine, was excreted by milk in the highest amounts.     

Differential suppression of menstrual fluid prostaglandin F2a, prostaglandin E2, 6-keto prostaglandin F1a and thromboxane B2 by suprofen in women with primary dysmenorrhea

Eleven women with primary dysmenorrhea completed a randomized, double-blind, placebo-controlled, three-way cross-over study comparing 200 and 400mg suprofen. Menstrual fluid volume did not change. Mean+/-S.E.M. menstrual fluid PGF2a was significantly suppressed from 18.9+/-1.9 microg (placebo) to 10.9+/-1.7 and 9.3+/-2.1 microg with 200 and 400 mg suprofen, respectively (p=<0.005). PGE2 dropped from 7.8+/-0.9 to 4.6+/-0.8 and 4.6+/-1.1 microg (p=<0.05) and TxB2 from 17.5+/-4.3 to 7.5+/-2.9 and 3.6+/-1.3 microg (p=<0.01), respectively. 6-Keto PGF1a was significantly suppressed (2.7+/-0.4 to 1.9+/-0.5 microg, p=<0.025) with only 400 mg suprofen. Six subjects rated placebo poor and five fair to very good. In contrast, nine rated suprofen excellent to fair while two rated poor. Thus, suprofen was clinically effective but the differential suppression of prostanoids favors 200mg which spares 6-keto PGF1a.     

Mathematical modeling shows exenatide improved beta-cell function in patients with type 2 diabetes treated with metformin or metformin and a sulfonylurea.

The incretin mimetic exenatide improved glycemic control and reduced body weight in patients with type 2 diabetes inadequately controlled with metformin+/-a sulfonylurea. We assessed postprandial beta-cell function by mathematical modeling, independent of confounding effects from differing ambient glucose levels among treatments. Subjects were 63% males, 55+/-10 years, BMI 33+/-6 kg/m2, HbA1C 8.1+/-1.1% (+/- SD) randomized to 5 microg exenatide or placebo twice daily for 4 weeks. Subsequently, one arm remained at 5 microg twice daily, one arm escalated to 10 microg twice daily, and one treatment arm remained on placebo for 26 weeks. Subjects continued metformin+/-a sulfonylurea. A subset with meal tests at baseline and week 30 were analyzed (n=73). Outcome measures were the model-based beta-cell function parameters dose-response relating insulin secretion to glucose concentration, rate sensitivity, and potentiation. Exenatide reduced postprandial glucose excursions. Modeling predicted an upward shift of the beta-cell dose-response. Model-predicted insulin secretion rate at a reference glucose concentration increased 72% (10 microg), increased 40% (5 microg), or decreased 21% (placebo) at week 30 [ p=0.015 (10 microg); p=0.045 (5 microg); vs. placebo]. At week 30, the 2-hour post-meal to basal potentiation factor ratio was increased to 1.53+/-0.10 (10 microg; p=0.0142 vs. placebo) or 1.40+/-0.08 (5 microg; p=0.0402 vs. placebo) compared with 1.15+/-0.06 (placebo). Exenatide caused an upward shift of the beta-cell dose-response and enhanced potentiation of insulin secretion. This model suggests exenatide improved beta-cell function in patients with type 2 diabetes treated with metformin+/-a sulfonylurea.     

Endocrine, luteal and follicular responses after the use of the short-term protocol to synchronize ovulation in goats

The effect of the so-called Short-Term Protocol (5-day progesterone treatment+PGF(2)alpha) on ovarian activity and LH surge was studied in goats. The goats received 250IU eCG at the time of device withdrawal (eCG group; n=7), or 200microg of EB (estradiol benzoate) 24h after device withdrawal (EB group; n=8), or received neither eCG nor EB (control group; n=8). The Short-Term Protocol induced greater (4.1+/-1.1ng/ml) progesterone serum concentrations at 24h after start of the treatment, that declined to 0.2+/-0.1ng/ml at 12h after device withdrawal. In all of the groups, the maximum concentration of estradiol-17beta was reached at about 36h after device withdrawal. Maximum concentration was greater in the EB group (76.9+/-24.6pmol/l) than in the control group (41.8+/-9.0pmol/l; P<0.01), with the eCG group showing intermediate concentration (70.3+/-32.5pmol/l; P=NS). The LH peak occurred earlier in the eCG group (38.4+/-2.0h after device withdrawal) and in the EB group (41.0+/-4.1h), than in the control group (46.3+/-5.1h; P<0.05). Ovulation occurred earlier in the eCG group (5/7) and in the EB group (8/8) (58.8+/-2.7h and 63.0+/-5.6h, respectively), than in the control group (7/8) (70.2+/-8.3h; P<0.05). In summary, the Short-Term Protocol induced similar concentrations of progesterone among treated goats. In addition, eCG or EB resulted in a similar increase in estradiol-17beta and a similar LH surge, which induced ovulation in most females (86.7%) in a consistent interval (about 60h) after the end of progesterone exposure.     

Metabolism of l-Selenomethionine and Selenite by Probiotic Bacteria: In Vitro and In Vivo Studies

Since selenium supplements have been shown to undergo biotransformation in the gut, probiotic treatment in combination with selenium supplements may change selenium disposition. We investigated the metabolism of L-selenomethionine (SeMet) and selenite by probiotic bacteria in vitro and the disposition of selenium after probiotic treatment followed by oral dosing with SeMet and selenite in rats. When SeMet was incubated anaerobically with individual antibiotic-resistant probiotic strains (Streptococcus salivarius K12, Lactobacillus rhamnosus 67B, Lactobacillus acidophilus L10, and Bifidobacterium lactis LAFTI? B94) at 37°C for 24 h, 11-18% was metabolized with 44-80% of SeMet lost being converted to dimethyldiselenide (DMDSe) and dimethylselenide (DMSe). In similar incubations with selenite, metabolism was more extensive (26-100%) particularly by the lactobacilli with 0-4.8% of selenite lost being converted to DMSe and DMDSe accompanied by the formation of elemental selenium. Four groups of rats (n?=?5/group) received a single oral dose of either SeMet or selenite (2 mg selenium/kg) at the time of the last dose of a probiotic mixture or its vehicle (lyoprotectant mixture used to maintain cell viability) administered every 12 h for 3 days. Another three groups of rats (n?=?3/group) received a single oral dose of saline or SeMet or selenite at the same dose (untreated rats). Serum selenium concentrations over the subsequent 24 h were not significantly different between probiotic and vehicle treated rats but appeared to be more sustained (SeMet) or higher (selenite) than in the corresponding groups of untreated rats. Probiotic treated rats given SeMet also had selenium concentrations at 24 h that were significantly higher in liver and lower in kidney than untreated rats given SeMet. Thus, treatment with probiotics followed by SeMet significantly affects tissue levels of selenium.     

Effect of Selenium on the Interaction Between Daunorubicin and Cardiac Myosin

The interactions between selenium (sodium selenite), anthracycline antibiotics daunorubicin (DNR), and major contractile protein cardiac myosin (CM) were investigated. The results showed that the binding force between selenium and CM was 100 times stronger than that of DNR and CM. There was no marked influence on fluorescence intensity of DNR-CM at selenium concentrations of up to 20 μM. The co-administration of selenium (0.5-10.0 μg Se/ml) together with DNR resulted in a significant reduction in mice cardiotoxicity. However, selenium at the dose of 50.0 or 100.0 μg Se/ml afforded no obvious protection. The data indicate that selenium in the form of sodium selenite at appropriate dosage (<10.0 μg Se/ml) diminish the cardiac toxicity of DNR, potentially allowing the use of DNR at higher dosages in clinical cancer chemotherapy.     

The prostacyclin analogue beraprost sodium prevents development of arterial stiffness in elderly patients with cerebral infarction

Prostacyclin (PGI(2)) inhibits platelet aggregation, smooth muscle cell proliferation, and vasoconstriction. Arterial stiffness assessed by pulse wave velocity (PWV) predicts mortality in various cardiovascular diseases. To study the preventive effects of a prostacyclin analogue, beraprost sodium, on arterial PWV values in elderly patients with cerebral infarction. Forty-four patients with a history of cerebral infarction received beraprost sodium (120 microg/day p.o.) or no beraprost sodium (control) for 3 months. Arterial PWV and ankle brachial indices (ABI) were determined prior to starting the medication and after 3 months of medication. Initially, there were no differences in age, blood pressure, and body mass index. Further, PWV or ABI did not differ between the beraprost sodium group (n = 22) and the control group (n = 22). After 3 months, PWV in beraprost sodium group was significantly reduced (-123 +/- 282) when compared with the control group (147 +/- 274)(P = 0.006). ABI was not significantly different when comparing the two groups at 3 months. Long-term administration of beraprost sodium prevents the decline in arterial biomechanics in elderly patients with cerebral infarction.     

Chromogranin A, a member of neuroendocrine secretory proteins as a selective marker for laboratory diagnosis of pheochromocytoma

The function of chromogranin A (CGA) is reviewed, and the radioimmunometric determination of plasma CGA was evaluated as a marker of pheochromocytoma using a comparison of pheochromocytoma patients immediately before surgery (group P, n=25, 635+/-451 ng/ml) with other groups of patients, i.e. pheochromocytoma patients approximately 1 year after removal of tumor (group PP, n=13, 69+/-33 ng/ml), medullary thyroid carcinoma patients (group M, n= 22, 106+/-59 ng/ml), congenital adrenal hyperplasy patients (n=33, 65+/-40 ng/ml), and controls (n=31, 66+/-29 ng/ml). A CGA level above cut off value 130 ng/ml was found in 24 of 25 patients in group P, 1 (relapse) of 13 patients in group PP, and 4 of 22 patients in group M. In the group P we found a significant association between the size of the tumors removed and plasma CGA concentrations (p=0.0016), and also a significant (p=0.0016) relationship between plasma CGA concentrations and PASS score rating the malignity of pheochromocytoma. We can conclude that plasma CGA concentration as determined by radioimmunometric assay (which is simple without the necessity of special laboratory equipment) is an effective marker of pheochromocytoma with association to malignity and tumor mass.     

Selenium supplementation and blood rheological improvement in Japanese adults

In order to study the prevention effect of selenium in the development of cardiovascular disease, we investigated the effects of selenium supplementation on the blood rheological properties. Eleven healthy adults were administered with 200 microg of selenium in the form of selenium yeast per day for 1 wk. Before and after the supplementation, serum selenium concentration, glutathione peroxidase (GPx) activity, biochemical indices, and the blood fluidity of the subjects were measured. The blood fluidity was measured using a (microchannel array flow analyzer) by the passage time of 100 microL of heparinized whole blood through the microchannel array. The selenium supplementation significantly (p = 0.001) shortened the mean blood passage time from 44.0 +/- 5.7 to 37.5 +/- 2.8 s. Serum selenium concentration significantly (p = 0.008) increased from 109.8 +/- 10.2 to 124.5 +/- 16.7 microg/L. Meanwhile, the GPx activity did not increased significantly (p = 0.058). The mean GPx activity of the subjects before supplementation was 171.0 +/- 16.1 Deltammol NADPH/min/L and 180.9 +/- 17.8 Deltammol NADPH/min/L after supplementation. Factor analysis of the passage time and biochemical indices of the subjects showed that blood fluidity improvement was related to the metabolic modification of lipoproteins during the selenium supplementation. These results showed that selenium supplementation improved the blood fluidity, without increasing the GPx activity of the subjects.     

Determination of selenium in serum by FI-HG-AAS and calculation of dietary intake

A method was developed for the determination of selenium concentration in serum by flow injection-hydride generation-atomic absorption spectrometry (FI-HG-AAS) following microwave digestion of serum samples and reduction of selenate to selenite. The detection limit of the method was 0.3 μg Se/L and the characteristic concentration, corresponding to the 0.0044 absorbance signal, was 0.12 μg Se/L. The results from the analysis of two Seronorm standard reference materials showed good agreement with the certified values. The method was then used to analyze selenium in sera of Austrian and Slovenian people for the calculation of dietary intakes. The selenium concentrations in sera of mothers at delivery, their neonates, and the male and female adults were 71 ± 14, 42 ± 6, 75 ± 21, and 65 ± 16 μg/L for the Austrians and 62 ± 15, 34 ± 7, 70 ± 12, and 66 ± 15 μg/L for the Slovenians. The dietary intakes of selenium of the mothers and the male and the female adults were calculated as 52, 37, and 46 μg/d for the Austrians and 45, 38, and 32 μg/d for the Slovenians.     

Selenium status in psoriasis and its relationship with alcohol consumption

The aim of the study was to examine the influence of alcohol consumption on the severity of psoriasis and selenium (Se) concentration and Se-dependent gluathione peroxidase activity in plasma (pl-GSH-Px) and in erythrocytes (RBC-GSH-Px) in psoriatic patients. Thirty-five in-patients with psoriasis lasting <10 mo and 42 with psoriasis lasting >3 yr constituted groups 1 and 2, respectively. The severity of psoriasis was assessed using the PASI scoring system and the consumption of alcohol, using a structured questionnaire. The Se concentration was 47.11±11.61 μg/L in group 1 and 38.69±13.22 μg/L in group 2 (p<0.05), the pl-GSH-Px was 0.15±0.04 U/mL and 0.14±0.04 U/mL (p>0.05), and the RBC-GSH-Px was 13.97±4.27 U/g Hb and 13.16±3.85 U/g Hb (p>0.05), respectively. In excessive drinkers (<10% of patients, all males), the Se concentration was 32.84±10.88 μg/L, the pl-GSH-Px was 0.15±0.03 U/mL, and the RBC-GSH-Px was 11.64±3.32 U/g Hb. A low RBC-GSH-Px correlated to the consumption of high-grade alcoholic beverages (R=−0.45, p<0.05) and to the PASI value (R=−0.37, p<0.05) in group 2. Depressed Se concentration and Se-dependent GSH-Px can be related to the severity and a duration of psoriasis. The excessive consumption of alcohol is associated with severity of the disease and with low activity of GSH-Px in erythrocytes in patients with long-lasting psoriasis.     

Serum leptin and adiponectin concentrations in patients infected with human immunodeficiency virus type 1 (HIV-1) on antiretroviral therapy

The lipodystrophy syndrome with dyslipidaemia and insulin resistance is side-effect of combined antiretroviral therapy (CART). Aim of the study: to describe the influence of CART on leptin and adiponectin concentration in connection with lipids levels in HIV-infected patients on antiretroviral therapy. BMI, serum leptin, adiponectin, triglycerides, total cholesterol, HDL- and LDL-cholesterol concentrations were measured in 56 HIV(+) patients before and on CART; average of treatment duration 38.4 +/-13.2 months. Significant increase of BMI (p=0.0268) of (22.6 +/- 3.3 before and 23.5 +/- 3.4 kg/m2 on therapy, respectively) and all analyzed lipids were found. Mean adiponectin concentration in treated patients was significantly (7.256 +/- 3.551 microg/ml) lower than mean value before treatment (8.395 +/- 3.568 microg/ml; p=0.0011). Mean values of leptin concentrations did not differ significantly (before therapy 3.721 +/- 0.347 log10; on therapy 3.1737 +/- 0.353 log10). Significant positive correlation between BMI and leptin concentrations was found before, as well as during CART (r=0.5333; p<0.0001), but negative correlation between adiponectin and leptin concentrations (r=-0.2677; p=0.042). Leptin and adiponectin concentrations did not revealed significant correlation with lipids levels before therapy. The decrease of adiponectin concentration on CART correlated negatively with total (r=-0.2912; p=0.0310) and LDL-cholesterol (r=-0.310; p=0.0225). CART lasting longer than 2 years resulted in the decrease of adiponectin concentration, with lack of influence on leptin concentration in analyzed group. The increase of total cholesterol and LDL-cholesterol in correlation with the decrease of adiponectin concentration confirms that CART induces metabolic disturbances related to higher risk of atherosclerosis and its sequel.