Anna Lucas

Calculated Low-Density Lipoprotein Cholesterol Should Not Be Used for Management of Lipoprotein Abnormalities in Patients With Diabetes Mellitus

OBJECTIVE To assess the validity of calculated low-density lipoprotein cholesterol by the Friedewald formula for management of lipoprotein abnormalities in patients with diabetes mellitus. RESEARCH DESIGN AND METHODS Calculated LDL cholesterol by the Friedewald formula was compared with measured LDL cholesterol after separation by ultracentrifugation in 61 patients with type I diabetes, 50 patients with type II diabetes, and 116 healthy control subjects. RESULTS Calculated LDL cholesterol coincided with measured LDL cholesterol, with < 10% error, in 54 (49%) patients with diabetes mellitus, and 85 (73%) control subjects. Calculated LDL cholesterol was overestimated, with an error of > or = 10% of measured LDL cholesterol in 39% of patients and 26% of control subjects, and underestimated in 13 and 1%, respectively. Despite a good correlation between calculated and measured LDL cholesterol, the intraclass correlation coefficients demonstrated a poor concordance between calculated and measured LDL cholesterol, both in patients and control subjects. When comparing the mean differences of calculated and measured LDL cholesterol for diabetic subjects versus control subjects, significantly greater differences in type II (but not type I) diabetic subjects were seen. CONCLUSIONS Calculation of LDL cholesterol by the Friedewald formula may be inaccurate for assessment of cardiovascular risk in patients with type II diabetes and may not be appropriate for management of lipoprotein abnormalities in those diabetic patients.

Suppressive therapy with levothyroxine for solitary thyroid nodules

objective To evaluate the effect of treatment with TSH suppressive dose of levothyroxine In patients with benig nthyroid nodules.

Postpartum thyroid dysfunction and postpartum depression: are they two linked disorders?

OBJECTIVE Postpartum has been considered as a period of risk for developing postpartum depression (PD) by some but not all authors, and this PD has been linked with postpartum thyroid dysfunction (PPTD). The major aim of this study was to evaluate the relation between the presence of PPTD and PD.

Assay-dependent results of immunoassayable spontaneous 24-hour growth hormone secretion in short children.

ABSTRACT. Forty‐eight children, referred for evaluation of short stature, underwent 24‐hour spontaneous growth hormone (GH) secretion studies. The GH level in pooled sera was assessed for each child, using up to 11 commercial immunoassays. In a group of 15 children, the mean GH values obtained by nine of the assays were compared with the mean value given by a polyclonal radioimmunoassay (RIA) from Sorin: four gave higher results (p < 0.0001), three gave comparable results and two gave lower results (p < 0.001). The assay yielding the highest results (Nichols: 5.9 ± 2.3 ng/ml, mean ± SD) gave values that were approximately triple those obtained by the assay yielding the lowest results (Hybritech: 1.8 ± 0.8 ng/ml; p < 0.0001); both of these are monoclonal immunoradiometric assays (IRMAs). The GH concentrations measured in 24‐hour pools from 32 children using a monoclonal IRMA from Biomerieux were similar to those obtained using a polyclonal RIA from Farmos (2.8 ± 1.1 ng/ml and 2.9 ± 1.4 ng/ml, respectively) but significantly lower than those measured by another polyclonal RIA from Sorin (3.5 ±1.5 ng/ml). Two polyclonal assays (Biomérieux and Sorin) were then used to measure the GH levels in all of the 30‐minute samples and in the day, night and 24‐hour pools from the secretion studies of 22 children. The ratio of the results of the two assays remained fairly constant for a given child (although the GH levels in different 30‐minute samples differed considerably). However, the ratios between different children showed quite wide variation (from 2.03 to 1.04). It was concluded that the GH assay must be taken into account when evaluating data from GH secretion studies, and the disparity in the GH level measured by two or more assays may differ from child to child.

Upregulation of lipocalin 2 in adipose tissues of severely obese women: positive relationship with proinflammatory cytokines.

Because the role of lipocalin 2 (LCN2) in morbid obesity is still not well defined, the aim of this study was to evaluate the circulating levels and the expression of LCN2 in visceral (VAT) and subcutaneous adipose tissue (SAT) in severely obese (SO) women. We also analyzed its relationship with inflammatory cytokines in the same subjects. The study comprised 90 white women, 39 of whom were lean controls (BMI ≤25 kg/m2) and 51 SO (BMI ≥40 kg/m2). Both circulating and adipose tissue levels of LCN2 were quantified by enzyme‐linked immunosorbent assays. LCN2 mRNA levels from VAT and SAT were assessed by real‐time reverse transcriptase‐PCR (n = 60). LCN2 serum levels were significantly higher in the SO women than in the lean controls (P = 0.042), and were found to be strongly correlated with tumor necrosis factor receptor I (TNFR1) circulating levels. In the SO cohort, LCN2 serum levels were also associated with higher BMI values, but not with the homeostasis model assessments of insulin resistance (HOMA2‐IR). LCN2 mRNA expression was markedly higher in SO women than in lean women in both VAT (P = 0.043) and SAT (P = 0.031). In SAT, LCN2 was negatively correlated with adiponectin and adiponectin receptor‐2 expression, and positively with interleukin‐6 (IL‐6) expression. A strong positive correlation was also found between LCN2 expression and the mean diameter of adipocytes in VAT. Our results revealed that the circulating level of LCN2 is associated with obesity and BMI. LCN2 mRNA is over‐expressed in adipose tissue from SO subjects. Finally, the expression of LCN2 is strongly related to an expression profile of proinflammatory cytokines but not to insulin resistance in nondiabetic SO women.

Plasma visfatin levels and gene expression in morbidly obese women with associated fatty liver disease.

OBJECTIVES The few studies on the physiopathological role of visfatin in morbid obesity and the related metabolic diseases have led us to examine visfatin levels and its liver gene expression in morbidly obese women with non-alcoholic fatty liver disease (NAFLD). DESIGN AND METHODS We examined the circulating levels of visfatin by ELISA in serum samples from 95 morbidly obese women (MO) (BMI>40 kg/m(2)) who underwent bariatric surgery and 38 normal weight control women (BMI<25 kg/m(2)). We analysed visfatin liver and adipose tissue mRNA expression by RT-PCR. We evaluated the circulating levels and gene expression of adiponectin, resistin, RBP4, TNFα, IL6 and CRP. RESULTS Serum visfatin was significantly higher in MO compared with controls, and also in MO with NAFLD was significantly higher than MO with normal liver. We found that NAFLD diabetic patients presented similar serum visfatin levels than non-diabetic. Serum visfatin correlated with IL6 (r=0.496; p<0.001) and CRP levels (r=0.241; p=0.049). Liver visfatin expression was significantly higher in MO compared to controls and was also significantly higher in MO with NAFLD than in MO with normal liver. Visfatin liver expression correlated positively with resistin (r=0.436, p=0.018) and TNFα expression (r=0.328, p=0.028). Visfatin expression in adipose tissues was similar among the MO groups analysed. CONCLUSION Serum visfatin and its liver expression are higher in MO women with NAFLD, irrespective of the presence of diabetes. Serum visfatin and its liver expression correlate positively with pro-inflammatory factors. These findings suggest that visfatin may be a molecule related with fat inflammation in morbid obesity and fatty liver disease.

Increased levels and adipose tissue expression of visfatin in morbidly obese women: the relationship with pro‐inflammatory cytokines

Objective  The controversial results on the physiopathological role of visfatin led us to examine both circulating visfatin levels and gene expression in visceral (VAT) and subcutaneous fat (SAT) in a homogeneous group of morbidly obese women.

Renal Function Changes in Microalbuminuric Normotensive Type II Diabetic Patients Treated With Angiotensin-Converting Enzyme Inhibitors

OBJECTIVE To determine the effects of captopril on microalbuminuria and renal function in normotensive type II diabetic patients. RESEARCH DESIGN AND METHODS A total of 26 patients were randomized in two homogeneous groups for clinical and analytical data in a 6-mo follow-up study. Group A received captopril (initial dose: 12.5 mg daily, increased according to tolerance); group B was untreated. RESULTS Microalbuminuria decreased only in the treated group at 6 mo (P = 0.044) and a significant (P = 0.027) mean percentage change on microalbuminuria excretion between the groups was observed. Filtration fraction decreased in group A (baseline: 0.23 ± 0.03; 6 mo: 0.22 ± 0.04) and increased in group B (baseline: 0.22 ± 0.04; 6 mo: 0.25 ± 0.04) with a significant mean percentage change between the groups at 6 mo (P = 0.032). The mean percentage change in microalbuminuria was significantly correlated with a mean percentage change in diastolic blood pressure throughout the trial. Neither metabolic control nor sodium or protein intake changed in either group during the trial. CONCLUSIONS These results suggest that captopril can help arrest microalbuminuria in normotensive type II diabetic patients, with a decrease in diastolic blood pressure and filtration fraction after a 6-mo treatment.

Comparative effects of captopril versus nifedipine on proteinuria and renal function of type 2 diabetic patients

Our study compared the effects of an angiotensin-converting enzyme inhibitor (captopril) versus a calcium antagonist (nifedipine) on proteinuria and renal function in patients with diabetic nephropathy. A randomized follow-up study was designed. Type 2 diabetic patients, with established diabetic nephropathy (proteinuria greater than 0.5 g/24 h), were treated with nifedipine (10 patients, group A) or captopril (10 patients, group B) for 6 months. Arterial blood pressure, metabolic parameters, proteinuria and renal function were measured and compared. Mean percentage differences for glomerular filtration rate, renal plasma flow and filtration fraction between the two groups were calculated. No significant differences were observed in serum glucose, glycosylated hemoglobin (hemoglobin A1c), Na+, K+ or albumin in either group or between groups. Blood pressure decreased significantly with both treatments and mean blood pressure was significantly lower in group A compared with group B at 6 months (Mann-Whitney U-test, P = 0.03). Proteinuria was similar in both groups at randomization, but after 3 and 6 months of treatment significant reductions were observed only in the group treated with captopril (P less than 0.01). A significant decrease in filtration fraction was observed in group B with an increase in group A (Mann-Whitney U-test, P = 0.03). Multiple regression analysis identified the therapeutic agent administered as an independent variable for decrease in proteinuria. It is concluded that antihypertensive treatment with captopril, but not with nifedipine, reduced proteinuria in patients with diabetic nephropathy, although a better mean blood pressure was obtained with nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of two replacement regimens in primary adrenal insufficiency patients. effect on clinical symptoms, health-related quality of life and biochemical parameters.

Objective: To evaluate clinical symptoms, health-related quality of life (HRQL) and biochemical parameters in patients with primary adrenal insufficiency under treatment with two different hydrocortisone regimens (20mg- 0mg-10mg/day and 10mg-5mg-5mg/day), each maintained for 3 months and compare results obtained with those in healthy controls. Design, Patients and Methods: Twelve patients with primary adrenal insufficiency were studied. Clinical symptoms and HRQL with the Nottingham Health Profile (NHP) were evaluated and Na, K and serum cortisol determined at 09:00 h, 12:30 h and 17:30 h and urinary free cortisol (UFC) throughout the day. Control group comprised 19 healthy subjects. Results: No differences in specific adrenal insufficiency symptoms were detected between the two regimens. HRQL was worse in energy dimension assessed by the NHP compared to the general population, regardless of 20mg-0mg-10mg/day or 10mg-5mg-5mg/day treatment (p=0.03 and p=0.013). The total NHP score was only adversely affected when patients were on the 10mg-5mg-5mg/day hydrocortisone replacement regimen (p=0.008). Serum cortisol concentrations were higher than controls at 09:00 h, and lower at 17:30 h with both regimens, whereas serum cortisol at 12:30 h and UFC were within the 5th-95th percentile normal range only with the 10mg-5mg-5mg/day regimen. Conclusions: Patients with primary adrenal insufficiency had worse HRQL in the NHP energy dimension compared with the general population, regardless of the hydrocortisone regimen although total score for HRQL was worse only with the 10mg-5mg-5mg/day regimen. Patients on the thrice-daily hydrocortisone regimen showed a more physiological cortisol profile, leading us to recommend initially treating patients with this dose and increasing it in the case of impaired HRQL.