Serum copper and zinc concentrations in patients with chronic hepatitis C

The aim of this study was to measure the alterations in serum trace elements, including zinc and copper in patients with chronic hepatitis C and to compare them with the results of healthy individuals. Seventeen patients with chronic hepatitis C and 17 healthy individuals were included in this study. Serum zinc and cooper concentrations were measured by using atomic absorption spectrophotometer of patients with chronic hepatitis C and the results were statistically compared with those of healthy individuals. Serum zinc concentrations were 105.6+/-22.8 microg/dl in patients with chronic hepatitis C and 94.41+/-19 microg/dl in healthy controls, respectively. Serum copper concentrations were 103.17+/-20.8 microg/dl in patients with chronic hepatitis C and 90.8+/-14.3 microg/dl in healthy subjects, respectively. Serum zinc and copper concentrations were not found statistically different in patients with chronic hepatitis C compared with those of healthy individuals (p>0.05). In conclusion, serum trace element concentrations did not show statistical alterations in patients with chronic hepatitis C compared to healthy subjects.     

Serum copper and zinc concentrations in patients with chronic hepatitis B

The aim of this study was to measure the alterations in serum trace elements, including zinc and copper in patients with chronic hepatitis and to compare with the results of healthy individuals. The serum zinc and copper concentrations were measured by using atomic absorption spectrophotometer in sera of patients with chronic hepatitis and statistically compared with those of healthy individuals. One hundred and five subjects, 71 patients with chronic hepatitis B (46 asymptomatic carriers, 25 chronic active hepatitis B) and 34 healthy individuals were included in this study. Sera of patients with chronic hepatitis and statistically compared with those of healthy individuals. Serum zinc concentrations were 104+/-24.98 microg/dl in asymptomatic carriers, 97+/-16.03 microg/dl in chronic active hepatitis and 108+/-21.07 in healthy controls, respectively. Serum copper concentrations were 88+/-17.8 microg/dl in asymptomatic carriers, 86+/-20.02 microg/dl in patients with chronic active hepatitis B and 88+/-13.59 microg/dl in healthy controls, respectively. Serum zinc and copper concentrations were not statistically different in patients with chronic hepatitis B compared with those of healthy individuals (p>0.05). Serum trace element concentrations did not show statistical alterations in patients with chronic hepatitis B compared with healthy subjects.     

Trace element status (Se, Zn, Cu) in heart failure.

OBJECTIVE: It has been speculated that trace elements may play a role in the pathogenesis of heart failure. In the present study, we aimed to assess serum concentrations of selenium (Se), zinc (Zn) and copper (Cu) in patients with heart failure (HF) and to compare idiopathic dilated cardiomyopathy (IDCM) and ischemic cardiomyopathy (ICM) patients with healthy controls. METHODS: This study population included 54 HF patients (26 IDCM patients and 28 ICM patients) and 30 healthy subjects. Serum levels of selenium, zinc, and copper were assessed by atomic absorption spectrophotometry method. RESULTS: Serum concentrations of Se and Zn in HF patients were significantly lower than in healthy controls (p=0.000 and p<0.01, respectively). However, serum Cu concentrations in these patients were significantly higher than in controls (p=0.000). There were no significant difference in the trace elements status between IDCM and ICM patients (p>0.05 for all parameters). Relationships of the serum trace element concentrations studied with echocardiographic and hemodynamic parameters were not statistically significant. CONCLUSION: Our study showed that heart failure is associated with lower Se and Zn concentrations, and higher Cu concentration, and serum Se, Zn and Cu element profiles were similar in IDCM and ICM.     

Trace elements as a component of oxidative stress in COPD

OBJECTIVE: The purpose of this study was to assess the serum concentrations of those trace elements that act as a component of oxidative stress in COPD patients. Clinically stable COPD outpatients (n = 26) and healthy controls (n = 24) were studied. METHODOLOGY: Serum concentrations of copper (Cu) and zinc (Zn) were determined using a Varian Spectra AA220 flame atomic absorption spectrophotometer. Serum concentration of iron (Fe) was measured by the ferene assay, using a commercially available kit (IL Test Iron) with the ILAb 900 autoanalyser. The lipid peroxidation product malondialdehyde (MDA) in serum samples was measured spectrophotometrically in terms of TBARS (thiobarbituric acid reactive substances). RESULTS: The serum MDA concentration in COPD patients was found to be similar to the control group (0.68 +/- 0.15 nmol/mL vs 0.62 +/- 0.13 nmol/mL, respectively; P= 0.163). The serum concentrations of the trace elements in both study groups were in the normal reference range. There was no difference in Fe concentration between COPD patients and the control group (0.81 +/- 0.38 micro g/mL vs 0.92 +/- 0.41 micro g/mL; P= 0.360). Copper concentrations were higher (1.06 +/- 0.26 microg/mL vs 0.92 +/- 0.19 microg/mL; P <0.040); while zinc was lower in the COPD group compared to the controls (0.83 +/- 0.25 microg/mL vs 1.03 +/- 0.23 microg/mL; P= 0.006). Serum Zn concentrations were lower in the severe COPD patients compared to mild-moderate COPD patients (P = 0.038). CONCLUSION: The results of this study indicate that there are alterations in serum concentrations of trace elements in COPD patients, suggesting that they may play a role in the pathophysiology of this disease by virtue of their role in oxidative stress. We recommend further studies on the role of trace elements in the pathophysiology of COPD, their association with markers of oxidant/antioxidant status and on the clinical significance of their deficiency.     

Thyroid function in adrenocortical insufficiency during withdrawal and re-administration of glucocorticoid substitution

The regulatory function of glucocorticoids on thyroid hormone concentrations was studied in patients with adrenocortical insufficiency (ACI, n = 8) and in healthy subjects (n = 6). In patients with ACI withdrawal of glucocorticoid substitution for 84 h led to an increase in serum concentrations of total triiodothyronine (TT3) from 110 +/- 20 to 133 +/- 22 ng/dl and a decrease of serum reverse-T3 (rT3) from 23 +/- 6 to 18 +/- 6 ng/dl, whereas subsequent administration of dexamethasone (0.5 mg po q.i.d. for 3 days) induced a fall in TT3 (129 +/- 22 to 88 +/- 16 ng/dl) and a rise in rT3 (17 +/- 5 to 37 +/- 11 ng/dl) concentrations. Serum levels of total thyroxine (TT4) were unchanged by either withdrawal or re-administration of glucocorticoids. Basal plasma thyrotrophin (TSH) concentrations were unchanged by glucocorticoid withdrawal and fell from 2.2 +/- 1.5 to 1.1 +/- 0.8 mU/l during subsequent dexamethasone therapy. In healthy subjects a decrease of TT3 (89 +/- 8 to 69 +/- 8 ng/dl) and an increase in rT3 (19 +/- 5 to 32 +/- 8 ng/dl) concentrations were seen after stimulation of endogenous cortisol production by prolonged infusion of ACTH1-24 (0.5 mg, t = 8 h on 2 consecutive days), whereas concentrations of TT4 remained unchanged. During subsequent administration of dexamethasone serum level of both. TT3 and rT3 returned to basal levels. Thus, changes in thyroid hormone concentrations are induced by alterations of substitution therapy in patients with ACI. In healthy subjects the application of 2 mg dexamethasone/day following prolonged maximal stimulation of endogenous cortisol by iv ACTH may represent a state of relative glucocorticoid deficiency, thus explaining the observed hormonal changes, which are inverse to those generally induced in healthy man by endogenous or exogenous glucocorticoids.     

The effect of L-thyroxine replacement therapy on lipid based cardiovascular risk in subclinical hypothyroidism

The aim of our study was to assess the changes in serum lipid profiles after replacement therapy with L-T4 in patients with subclinical hypothyroidism (SCH), and to see whether there is an improvement in dyslipidemia based cardiovascular risk. Thirty non-smoker pre-menopausal women with newly diagnosed SCH (TSH between 4 and 10 microIU/ml) were involved in our study; twenty-six euthyroid healthy subjects were used as control group. TSH, free T3 (FT3), free T4 (FT4), total cholesterol (TC), triglyceride (TG), HDL cholesterol (HDL-C) and LDL cholesterol (LDL-C) levels were measured before and after 6 months of L-T4 (50-100 microg/ day) therapy. TSH levels were targeted as < 2.0 microIU/ml. LDL-C was calculated using the Friedewald formula, while the cardiovascular risk was assessed with the TC/HDL-C ratio. Pre-treatment serum TC and LDL-C concentrations in SCH patients were significantly higher than those of euthyroid subjects (199.8 +/- 22.2 vs 181.5 +/- 24.6 mg/dl, p < 0.01; 146.3 +/- 26.1 vs 124.8 +/- 12 mg/dl, p < 0.001, respectively). TC, LDL-C levels and the TC/HDL-C ratio were reduced significantly after 6-month replacement therapy (-21.1 +/- 34.4 mg/dl or -10.5%, p < 0.01; -21.5 +/- 30.3 mg/dl or -14.7%, p < 0.001, respectively; and TC/HDL-C from 4.8 +/- 0.6 to 4.1 +/- 0.5 mg/dl, p < 0.01), while body mass index (BMI) values did not change. In conclusion, even mild elevations of TSH are associated with changes in lipid profile significant enough to raise the cardiovascular risk ratio, and these changes are corrected once the patients have been rendered euthyroid.     

Serum insulin-like growth factor type 1, insulin-like growth factor-binding protein-1, and insulin-like growth factor-binding protein-3 concentrations in patients with thyroid dysfunction.

Thyroid hormones play a role in the regulation of insulin-like growth factor type 1 (IGF-1) and insulin-like growth factor-binding protein-3 (IGFBP-3) expression, and both IGF-1 and IGFBPs have been shown to be related to the function and growth of the thyroid. Our aim was to evaluate serum concentrations of IGF-1, IGFBP-1, and IGFBP-3 in patients with thyroid dysfunction before and after normalization of thyroid function. The study was performed in 86 patients with thyroid dysfunction (43 hyperthyroid and 43 hypothyroid patients) and 17 euthyroid subjects. Serum growth hormone (GH), insulin, IGF-1, IGFBP-1, and IGFBP-3 were measured in all patients before and after normalizing serum thyroid hormone concentrations. Hyperthyroid patients showed IGF-1 (198.8 +/- 17.0 microg/L) and IGFBP-3 levels (4.2 +/- 0.2 mg/L) similar to those found in the control group (217.9 +/- 20.3 microg/L and 4.2 +/- 0.3 mg/L, respectively). After therapy these levels significantly decreased to 156.6 + 11.1 microg/L (p < 0.01) and 3.3 +/- 0.1 mg/L (p < 0.001), respectively. IGFBP-1 concentrations were clearly higher than those found in controls (22.7+/- 2.6 vs. 5.7 +/- 1.5 microg/L, p < 0.001) and exhibited a significant reduction after therapy for thyroid hyperfunction (11.0 +/- 1.7 microg/L, p < 0.001). Patients with hypothyroidism showed serum concentrations of IGF-1 (161.5 +/- 13.1 microg/L, p < 0.05) and IGFBP-3 (3.2 +/- 0.3 microg/L, p < 0.05) significantly lower than those found in healthy volunteers. However, replacement therapy with levothyroxine did not induce any significant modification of these concentrations (152.6 +/- 10.6 microg/L and 3.2 +/- 0.2 mg/L, respectively). Similarly, patients with thyroid hypofunction exhibited raised levels of IGFBP-1 (15.5 +/- 0.9 microg/L, p < 0.05 vs. control group) that were significantly decreased after therapy (8.8 +/- 1.4 microg/L, p < 0.01). The results of the present study show that thyroid status affects GH/IGF axis. Hypothyroidism is associated with significant reductions of IGF-1 and IGFBP-3, and IGFBP-1 is elevated in both hypothyroidism and hyperthyroidism.     

Investigation of the hypothalamo-pituitary-adrenal axis and changes in the size of adrenal glands in acute brucellosis

The aim of the study was to investigate the hypothalamo-pituitary-adrenal (HPA) axis by ACTH stimulation test and the changes in adrenal size in acute brucellosis before and after therapy in a prospective study. Sixteen patients with acute brucellosis and 15 healthy subjects were included in the study during the last two years. Cortisol levels were assessed before, 30 and 60 minutes after ACTH (250 microg i.v.) injection and the size of the adrenals was measured in both groups. Mean basal cortisol levels in the patients before the therapy and after the therapy were 22.1 +/- 6.9 microg/dL and 11.3 +/- 6.0 microg/dL, respectively. The difference was statistically significant (p<0.001). There was also statistically significant difference for basal cortisol levels between the healthy subjects (12.2 +/- 4.6 microg/dL) and the patients before the therapy (p<0.001). Peak cortisol responses to ACTH were higher before the therapy in the patients with acute brucellosis (39.3 +/- 10.7 microg/dL) than in the healthy subjects (30.4 +/- 4.8 microg/dL, p = 0.014). However, there was no significant difference for peak cortisol levels in the patients before and after the therapy (32.7 +/- 8.0 microg/dL). Mean basal cortisol levels and peak cortisol responses to ACTH between the patients after the therapy and the healthy controls were similar. Both the maximum width of the adrenal glands and the width of the adrenal limbs were significantly greater before the therapy compared to healthy subjects and post-treatment period. We concluded that the HPA axis is activated and the adrenal glands are enlarged in acute brucellosis, which is reduced after appropriate therapy.     

Hepatocyte growth factor (HGF) in patients with acute brucellosis

In this prospective study, we investigated the serum levels of hepatocyte growth factor (HGF) and C-reactive protein (CRP) before and after the treatment of patients with acute brucellosis. The study comprised 58 patients with acute brucellosis and 30 healthy volunteers. Pre-treatment serum HGF levels of 58 patients with acute brucellosis (1548.6 +/- 220.1) were significantly higher than levels of the control group (401.4 +/- 69.7) (p < 0.001). Serum levels of HGF and CRP significantly decreased at the end of the treatment period (p < 0.001). Post treatment, levels did not differ from those of the control group (p > 0.05). Serum HGF levels of patients with acute brucellosis correlated to CRP and ALT levels (r: 0.922, 0.752; p < 0.001, respectively). Our findings suggest that serum HGF levels may be used as a supplementary marker to evaluate the effectiveness of the treatment in patients with acute brucellosis.     

Serum concentrations of adiponectin and resistin in hyperthyroid Graves' disease patients

This study was undertaken to determine whether serum adiponectin and resistin levels are influenced by hyperthyroidism and autoimmune factors and to find out whether their levels are dependent on the presence of ophthalmopathy. We measured serum concentrations of adiponectin and resistin in 76 patients (63 women, 13 men) with Graves' disease (GD) and compared them with levels of the control group which consisted of 30 healthy subjects. Patients were separated into two groups according to the presence or the absence of thyroid-associated ophthalmopathy (TAO). TAO (-) group consisted of 26 subjects without eye signs of GD and TAO (+) group included 50 subjects with ophthalmopathy. The latter group was further divided into 2 subgroups: with active TAO [26 patients, clinical activity score (CAS)> or =4] and with inactive TAO (24 patients, CAS<4). Groups did not differ in age, sex, body mass index (kg/m2) and smoking habits. Compared with euthyroid subjects, hyperthyroid GD patients had elevated mean serum adiponectin concentrations (19.96+/-4.97 microg/ml vs 15.01+/-3.99 microg/ml, p<0.001). However we did not observe any disparity between the TAO (-) and TAO (+) groups (20.60+/-5.06 microg/ml vs 19.63+/-4.94 microg/ml, p=ns). Comparing patients with a CAS> or =4 and patients with a CAS<4, we found similar mean serum concentrations of adiponectin (20.04+/-5.01 microg/ml vs 18.74+/-4.83 microg/ml, p=ns). Serum levels of resistin did not differ between the hyperthyroid patients and control subjects (13.11+/-4.26 ng/ml vs 12.82+/-4.75 ng/ml, p=ns). Serum resistin levels did not differ between TAO (+) and TAO (-) groups nor in patients with active and inactive TAO. Serum adiponectin correlated significantly with free T4 (FT4), free T3 (FT3), and TSH-R antibodies (TRAb) in GD patients (r=0.40, 0.41, and 0.37, respectively; p<0.001 for each). Serum resistin levels were not correlated with thyroid hormones and thyroid antibodies. The variables that in simple linear regression analyses were found to be correlated with serum adiponectin were then used in multiple regression analysis. In a model including adiponectin as dependent variable and FT4, FT3 and TRAb levels as independent variables, FT3 and TRAb remained as parameters independently related to adiponectin level (R2=0.35, p<0.001). CONCLUSIONS: Elevated serum adiponectin levels in GD patients are related to the degree of hyperthyroidism and autoimmune process. The presence and activity of ophthalmopathy is not a modifier of serum adiponectin and resistin.     

Serum concentrations of interleukin 6, osteocalcin, intact parathyroid hormone, and markers of bone resorption in patients with rheumatoid arthritis.

OBJECTIVE: To analyze serum concentrations of interleukin 6 (IL-6), osteocalcin, intact parathyroid hormone (PTH), and type 1 collagen carboxyterminal telopeptide (ICTP) as well as the urinary concentrations of crosslinked N-telopeptides of type 1 collagen (NTx) and deoxypyridinoline (Dpd) in patients with rheumatoid arthritis (RA) to investigate their role in the etiology of the osteopenia in this disease. METHODS: Using ELISA and radioimmunoassay methods, we estimated serum concentrations of IL-6, osteocalcin, ICTP, intact PTH, and spot urine concentrations of NTx and Dpd in 25 female patients with active RA, 25 female patients with suppressed disease, and 25 age matched healthy female controls. RESULTS: Patients with active RA had significantly higher (p < 0.001) concentrations of IL-6 (94.0+/-12.1 pg/ml) compared to patients with suppressed disease (13.2+/-0.8 pg/ml) and healthy controls (12.3+/-0.8 pg/ml). Serum osteocalcin was significantly lower (p < 0.001) in patients with active RA (1.9+/-0.2 ng/ml) compared to patients with suppressed disease (2.7+/-0.2 ng/ml) and the controls (2.9+/-0.2 ng/ml). Similarly, serum intact PTH was significantly lower (p < 0.001) in patients with active disease (29.9+/-1.5 ng/ml) compared to patients with suppressed RA (38.0+/-1.6 ng/ml) and controls (49.8+/-2.4 ng/ml). Serum ICTP was also significantly higher (p < 0.01) in patients with active RA (9.5+/-0.3 microg/l) versus patients with suppressed disease (4.1+/-0.2 microg/l) and controls (3.4+/-0.2 microg/l). In patients with active disease, spot urine concentrations of NTx (123.1+/-5.1 nmol bone collagen equivalent/mmol creatinine) and Dpd (15.1+/-0.7 nmol/mmol creatinine) were significantly higher (p < 0.001) than in patients with suppressed disease (58.4+/-2.5 nmol bone collagen equivalent/mmol creatinine and 10.1+/-0.5 nmol/mmol creatinine, respectively) and healthy controls (53.4+/-2.1 nmol bone collagen equivalent/mmol creatinine and 9.7+/-0.5 nmol/mmol creatinine, respectively). There were no significant correlations between serum IL-6 and serum ICTP (r = 0.2357, p = 0.257) or urinary NTx (r = 0.1436, p = 0.494) or between serum intact PTH and ICTP (r = 0.0206, p = 0.922) in patients with active RA. CONCLUSION: There are no significant correlations between bone resorption markers and serum IL-6 and intact PTH in patients with RA.     

Relation of serum total sialic acid concentrations with diabetic complications and cardiovascular risk factors in Kuwaiti Type 2 diabetic patients

Serum total sialic acid is a marker of the acute phase response. Elevated levels have also been associated with cardiovascular disease in the general Caucasian population and especially in Type 2 diabetic subjects. The purpose of this study was to estimate serum total sialic acid concentrations among Kuwaiti Type 2 diabetic subjects and to investigate its association with macro and microvascular diabetes-related complications in that population. Serum total sialic acid levels were estimated by an enzymatic spectro-photometric assay in two groups of subjects: (i) 358 Kuwaiti Type 2 diabetics (156 men and 202 women) referred for their annual evaluation to the specialised diabetic clinic at the main university teaching hospital in Kuwait, and (ii) 47 healthy age and sex matched non-diabetic Kuwaiti control population (13 men and 34 women). Serum sialic acid levels were significantly higher (P<0.001) among the diabetic patients (mean+/-S.D.) (81.2+/-13.2 mg/dl) compared to the non-diabetic controls (66.9+/-11.0 mg/dl). Kuwaiti diabetic women had significantly higher concentrations compared to diabetic men (85.2+/-12.1 vs. 75.9+/-13.0 mg/dl, P<0.001). Among the controls there was no significant gender difference in sialic acid levels of women, (68.3+/-11.6 mg/dl) versus men (63.2+/-8.2 mg/dl). The gender difference in the diabetic patients was unrelated to the degree of obesity. Significant correlations were found between serum total sialic acid concentrations and such cardiovascular risk factors as plasma levels of apolipoprotein B, low density lipoprotein cholesterol, triglycerides and uric acid in the diabetic subjects. Furthermore, there was a significant elevation in serum total sialic acid concentrations with increasing urinary albumin excretion, P<0.001, but not with retinopathy or neuropathy.     

Modifications of thymulin titers in patients affected with prolonged low or high zinc circulating levels are independent of patients' age

Thymulin (FTS) is a thymic hormone, the bioactivity of which depends on zinc (Zn) incorporation in its molecule (FTS bioactive form: Zn-FTS). Many hormones (T3, GH, PRL, Gn-RH 6-endorphin) and Zn are able to increase thymus trophism and Zn-FTS circulating levels, even in old animals, suggesting that age dependent thymic involution is a reversible phenomenon. FTS circulating levels and thymus trophism are age-dependent. In fact, the decrease of Zn-FTS starts from the age of 10-20 years and proceeds progressively. In 19 uremic patients on hemodialysis (mean age +/- SD: 44.7+/-11.7, range 29-60 years) and 58 patients with prolactinoma (mean age 31+/-7; range 18-58) we found low Zn-FTS levels (expressed as scalar dilution in form of 1/log(2)): 1.5+/-0.5 and 2.1+/-0.7, respectively, vs normal age and sex matched controls: 2.9+/-0.4 and 3.6+/-0.3, respectively; p<0.01. On the contrary, in 41 acromegalic patients (mean age 43+/-12; range 20-63 years) Zn-FTS levels were elevated (4.5+/-0.7 vs controls: 2.8+/-0.3, p<0.01). In all these patients, age-related differences of Zn-FTS circulating levels were lost and Zn-FTS titers were homogeneously low or high according to Zn levels. In fact, in uremic patients and in patients with prolactinoma, Zn levels were low (79+/-26 microg/dl and 82+/-23 microg/dl, respectively, vs control levels: 114+/-12 microg/dl, p<0.01), while They were high in acromegalic patients (141+/-44 microg/dl vs control levels: 112+/-11 microg/dl, p<0.01). After ZnSO(4) administration (400 mg per os/day) for six months. Zn levels increased over the normal range, both in patients with uremia and in patients with prolactinoma (136+/-15 microg/dl and 138+/-18 microg/dl, respectively; p<0.01). Also Zn-FTS levels increased homogeneously independently of age (5.2+/-0.7 and 5.3+/-0.8, respectively); p<0.01, both vs basal and control values; PRL circulating levels did not change. In 20 patients affected with prolactinoma and in 10 acromegalic patients, Zn and Zn-FTS decreased to the normal range, 6, or 12 months after surgical or pharmacological normalization of high PRL and GH circulating levels. In these patients, age-related titers of Zn-FTS were found, such as in controls. In conclusion: (i) Reduced Zn-FTS levels in patients affected with uremia or prolactinoma and the increased Zn-FTS titers present in acromegalic patients are related to low and high Zn circulating levels, respectively, underlining the importance of Zn in regulating thymulin secretion. (ii) When spontaneous (or induced) hyper- or hypo-zincemia occurs, age-related differences of Zn-FTS titers are lost, suggesting that Zn may overcome the effect of age on thymic function.     

Effect of di-N-propylacetic acid (valproic acid) on the TSH response to TRH--a presumptive role for gamma aminobutyric acid

The effect of di-n-propylacetic acid (valproic acid), an inhibitor of gamma aminobutyric acid (GABA) transaminase, was studied with reference to its effect on the serum concentration of thyroid hormones, baseline serum TSH concentration and TRH stimulated TSH release, in seven normal controls and six patients with primary hypothyroidism. All volunteers took 250 mg of valproic acid administered orally, four times daily for 3 days. Baseline serum T4 and TSH concentrations were unaffected by valproic acid administration (p less than 0.05) while serum T3 concentrations fell in all volunteers (p less than 0.001). Serum T3 concentration (mean +/- SD) fell from 116.3 +/- 18 ng/dl to 101.7 +/- 15 ng/dl in the control group and from 94.2 +/- 47.9 ng/dl to 81.5 +/- 43.2 ng/dl in the hypothyroid group. Valproic acid produced a decline in stimulated serum TSH concentrations (delta TSH--maximum increment above baseline) in all controls and patients studied (p less than 0.01). delta TSH (mean +/- SD) declined from 16.1 +/- 4.7 microunits/ml to 10.5 +/- 5.8 microunits/ml in the control subjects and from 43.1 +/- 25.4 microunits/ml to 29.7 +/- 18 microunits/ml in the hypothyroid patients. Based on the data presented, it is postulated that GABA plays an inhibitory role either by acting directly on the pituitary gland inhibiting TSH release, or by inducing the secretion of a hypothalamic TSH-inhibitory factor. The data do not exclude a direct pharmacological effect of valproic acid on pituitary TSH release. Decrease in serum T3 following valproic acid may be due to peripheral mechanisms.     

肝硬化患者血清微量元素研究

作者检测了15名肝硬化患者血清中17种微量元素和3种常量元素含量,并抽取42名健康人辅以对照。除血清Se由F-78脉冲极谱仪分析外,Fe、Cu、Mn、Zn、Co、Mo、Cr、Sn、V、Si、Ni、Al、Cd、Pb、Sr、Ti、Mg、Ca、P等19种元素采用ICAP-9000型等离子体直读光谱仪测定。结果表明,肝硬化患者血清Zn、Se低于对照组,但血清Cu、Cr、Sn、Si、Ni、Al、Pb、Mg等较高。进一步分析发现,肝硬化患者普遍低Se,血清Se平均值约占正常组1/3。低Se率和低Zn率高于健康人群。作者尝试探讨肝硬化血清微量元素变化的可能机制。     

BAL and serum IgG levels in healthy asymptomatic HIV-infected patients

OBJECTIVES: To determine if the increased susceptibility to bacterial infection in asymptomatic HIV-infected patients is associated with decreased total IgG or IgG2 levels in lung epithelial lining fluid. BACKGROUND: A decrease in lung IgG levels or subtypes has been proposed as contributing to the increased risk of bacterial lung infections in HIV-infected patients. Previous studies measuring lung lavage IgG concentrations have been inconsistent. METHODS: Twenty-three HIV patients and 25 control subjects underwent BAL. Both patient groups were of similar age, and had similar pulmonary function studies and body mass index. Smokers were equally represented in both groups, and the majority of subjects in both groups were male. Total IgG and IgG2 levels in lavage fluid were assayed in both cohorts and compared using a two-tailed Student's t test. RESULTS: The lung lining fluid IgG level in HIV-infected patients was 0.19 +/- 0.13 microg/microg of protein (mean +/- SD) vs 0.11 +/- 0.09 microg/microg of protein in control subjects (p < 0.05). The IgG(2) level in HIV patients was 0.034 +/- 0.038 microg/microg of protein and 0.014 +/- 0.01 microg/microg of protein in control subjects (p = 0.054). Lavage IgG levels reflected serum IgG values (correlation coefficient, 0.56; p < 0.001) but did not correlate with lung immunoglobulin-producing cells. CONCLUSIONS: The increased susceptibility to bacterial pneumonia in asymptomatic HIV-infected individuals is neither explained by depressed total IgG levels nor a deficiency in IgG(2) levels in the lungs. The strong correlation between serum and lavage IgG levels suggests that lavage IgG derives from serum.     

Exercise alters serum pneumoprotein concentrations

To determine the effect of exercise on serum levels of Clara cell protein (CC16) and surfactant-associated protein A (SP-A), serum was collected from 14 healthy subjects 1 h after maximal and sub-maximal exercise. Healthy volunteers participated on separate occasions in a control (no exercise) session, simulated firefighting tasks for 30 min (n=14), and intermittent treadmill exercise at near maximal heart rates for 60 min (n=10). Serum samples and induced sputum samples were collected 1 h post exercise. Induced sputum fluid was analyzed for tumor necrosis factor alpha (TNF-alpha), an inflammatory mediator produced by pulmonary macrophages. Serum CC16 levels increased significantly with both firefighting tasks (15+/-13 microg/L vs. 9+/-4 microg/L, P=0.047) and treadmill exercise (15+/-8 microg/L vs. 9+/-4 microg/L, P<0.01). Serum SP-A concentrations did not change compared to control with either firefighting tasks (247+/-106 microg/L vs. 247+/-96 microg/L, P=0.84) or treadmill exercise (251+/-89 microg/L vs. 285+/-87 microg/L, P=0.44). TNF-alpha concentrations in sputum supernatant showed no significant difference from controls. These results show an increase in serum CC16 after exercise. This must be considered when utilizing serum CC16 to determine the presence of lung injury in settings that combine exercise and toxic exposures.     

Elevated thyroxine levels due to increased thyroxine-binding globulin in acute hepatitis

Two patients are presented who had unexpected increases in serum thyroxine concentration due to acquired thyroxine-binding globulin excess associated with asymptomatic hepatitis. Serum hormone concentrations were also analyzed retrospectively in 10 outpatients with viral hepatitis. Acute hepatitis is associated with an increase in serum thyroxine and thyroxine-binding globulin concentrations and a corresponding decrease in the triiodothyronine resin uptake. In five patients, serum thyroxine concentration (mean +/- SD) was elevated at 21.08 +/- 5.86 micrograms/dl during illness, and decreased to 10.18 +/- 2.96 micrograms/dl during full recovery (p less than 0.05); serum thyroxine-binding globulin concentration was elevated at 2.14 +/- 0.36 mg/dl during illness, and decreased to 1.18 +/- 0.16 mg/dl during recovery (p less than 0.01). Interpretation of thyroid function test results can be difficult in patients with hepatitis. When serum thyroxine is elevated, careful attention to a decrease in the triiodothyronine resin uptake is essential to avoid the incorrect diagnosis of hyperthyroidism. Occasionally, this change in the triiodothyronine resin uptake may be the first evidence of occult hepatic inflammation.     

Thyroid function in patients undergoing maintenance hemodialysis: unexplained low serum thyroxine concentration.

Thyroid function was studied in 55 patients undergoing maintenance hemodialysis who were all judged to be clinically euthyroid. The dialysis patients, in comparison to normal control subjects, had significantly lower mean values for serum T4 (4.0 +/- 1.4 [SD] microgram/dl versus 7.9 +/- 1.5 microgram/dl, p less than 0.001), T3 (118 +/- 31 ng/dl versus 147 +/- 28 ng/dl, p less than 0.001), free T4 measured by equilibrium dialysis (1.22 +/- 0.38 ng/dl versus 2.15 +/- 0.67 ng/dl, p less than 0.001), free T3, free T4 index, and free T3 index. Serum TBG, measured by radioimmunoassay, was similar to that of the controls and serum TSH, 2.2 +/- 1.3 micromicron/ml, was also similar to that of control values, 2.0 +/- 1.1 micromicron/ml. The serum PBI did not change during the dialysis procedure, but serum inorganic iodine fell slightly from 2.1 +/- 1.1 microgram/dl before dialysis to 1.2 +/- 0.6 microgram/dl after dialysis (p less than 0.05). The marked reduction in serum total T4 and free T4 concentrations and the moderate reduction in serum total T3 and free T3 levels in apparently euthyroid patients undergoing hemodialysis has not been explained. The normal serum TSH levels in the face of these low concentrations of thyroid hormone suggests an abnormality in the control of TSH secretion in these patients.     

Identification of mildly oxidized low-density lipoprotein (electronegative LDL) and its auto-antibodies IgG in children and adolescents hypercholesterolemic offsprings

BACKGROUND: Oxidative modification of low-density lipoproteins (LDL) is an essential step in atherogenesis, generating minimally oxidized LDL, also called electronegative LDL [LDL(-)], which has chemotactic, cytotoxic and immunogenic properties. METHODS AND RESULTS: Serum LDL(-) and anti-LDL(-) auto-antibodies (IgG) were evaluated in 28 children and adolescents with familial hypercholesterolemia (FH) antecedents, with or without early coronary artery disease in first-degree relatives (eCAD), hypercholesterolemic (hc) or normocholesterolemic (nc) versus a control group of normocholesterolemic children without pathologic antecedents (C). ELISA method was used for detection of LDL(-) and anti-LDL(-) IgG. LDL(-) serum levels did not differ among the four groups (FH-eCAD-hc 41.4 +/- 24.9 microg/dl; FH-hc 38.3 +/- 11.2 microg/dl; FH-nc 47.3 +/- 17.0 microg/dl and C 44.2 +/- 28.8 microg/dl, p = 0.659). However, IgG anti-LDL(-) auto-antibodies were significantly higher in the control group in comparison to the FH groups with or without eCAD, independent of hypercholesterolemia or normocholesterolemia (FH-eCAD-hc 0.825 +/- 0.289 microg/dl; FH-hc 0.667 +/- 0.307 microg/dl; FH-nc 0.763 +/- 0.204 microg/dl and C 1.105 +/- 0.233 microg/dl, p = 0.006). When the auto-antibodies of groups with FH, with or without eCAD and with or without hypercholesterolemia were compared, no differences were found (p = 0.509). CONCLUSION: These results showed that FH and/or eCAD children and adolescents have lower titers of auto-antibodies anti-LDL(-) than children from normal families, independent of serum LDL-cholesterol or serum LDL(-).