Hepatic fat content is a determinant of postprandial triglyceride levels in type 2 diabetes mellitus patients with normal fasting triglyceride

Postprandial hypertriglyceridemia is common in type 2 diabetes mellitus (T2D). Significant numbers of T2D patients who have normal fasting triglyceride (TG) have postprandial hypertriglyceridemia. The role of regional adipose tissue and adiponectin on postprandial TG responses in this group of T2D patients is unclear. This study aimed to examine the contribution of regional adipose tissue and adiponectin to the variation of postprandial TG responses in T2D patients who have normal fasting TG levels. Thirty-one Thai T2D patients who had fasting TG<1.7 mmol/L were studied. All were treated with diet control or sulphonylurea and/or metformin. None was treated with lipid-lowering agents. Mixed-meal test was performed after overnight fast. Plasma glucose, insulin, and TG were measured before and 1, 2, 3, and 4 hours after the test. Adiponectin was measured in fasting state. Visceral as well as superficial and deep subcutaneous abdominal adipose tissues were determined by magnetic resonance imaging, and hepatic fat content (HFC) was determined by magnetic resonance spectroscopy. Univariate and multivariate regression analyses of postprandial TG and regional adipose tissue and metabolic parameters were performed. The TG levels before and 1, 2, 3, and 4 hours after the mixed meal were 1.32+/-0.40 (SD), 1.40+/-0.41, 1.59+/-0.40, 1.77+/-0.57, and 1.80+/-0.66 mmol/L, respectively (P<.0001). The area under the curve (AUC) of postprandial TG was positively and significantly correlated with fasting TG (r=0.84, P<.0001) and log.HFC (r=0.456, P=.033) and was inclined to be correlated with log.deep subcutaneous adipose tissue (r=0.38, P=.05) and sex (r=0.326, P=.073). The AUC of postprandial TG was not correlated with age, body mass index, waist circumference, log.superficial subcutaneous adipose tissue, log.visceral adipose tissue, hemoglobin A1c, fasting glucose, AUC.glucose, log.fasting insulin, log.AUC.insulin, log.homeostasis model assessment%B, log.homeostasis model assessment of insulin resistance, and adiponectin. Only fasting TG (beta=.815, P<.0001) and log.HFC (beta=.249, P=.035) predicted AUC of postprandial TG in regression model (adjusted R2=0.84, P<.0001). In conclusion, in T2D patients with normal fasting TG, the increase of postprandial TG levels is directly determined by fasting TG level and the amount of hepatic fat.     

Risk of Calcium Oxalate Nephrolithiasis after Calcium or Combined Calcium and Calcitriol Supplementation in Postmenopausal Women

Although calcium supplementation can cause hypercalciuria, the risk of nephrolithiasis has been shown to decrease rather than increase among subjects who had a higher calcium intake. Hypercalciuria is also a well-established side effect of calcitriol administration. However, the risk of nephrolithiasis is not well defined. The present study was undertaken to prospectively determine the effect of calcium with or without calcitriol on physicochemical risk factors associated with calcium oxalate nephrolithiasis in Thai postmenopausal women with osteoporosis. Subjects consisted of 53 Thai women more than 10 years postmenopausal who were randomly allocated to receive 750 mg of calcium carbonate supplement alone (n= 28) or 750 mg of calcium carbonate plus 0.5 mg calcitriol (n= 25) daily. Mean ± SEM for age was 65.3 ± 1.1 years, body weight 53.5 ± 1.3 kg. Urine samples for biochemical assays were collected at baseline and 3 months after treatment. Supersaturation for calcium oxalate stone formation was assessed from the 24 h urine constituents by the Tiselius’s index, AP(CaOx). Three months of calcium supplement alone resulted in a modest, but not significant, increase in urinary calcium (baseline, 2.90 ± 0.43 mmol/day; after treatment 3.58 ± 0.54 mmol/day) with no change in urinary oxalate, citrate or magnesium. In contrast, calcium together with calcitriol caused a significant increase in urinary calcium (baseline, 2.87 ± 0.41 mmol/day; after treatment, 4.08 ± 0.57 mmol/day; p<0.05). No significant change in other urine constituents after treatment with calcium and calcitriol was detected. Therefore, AP(CaOx) did not significantly increase either after calcium alone (baseline, 1.17 ± 0.39; after treatment, 1.36 ± 0.28) or after calcium plus calcitriol (baseline, 1.09 ± 0.17; after treatment, 1.09 ± 0.19). However, after treatments, 12 subjects (23%) – 6 receiving calcium supplement alone and 6 receiving calcium plus calcitriol supplement – had high AP(CaOx) values (greater than the upper limit of 95% CI for AP(CaOx) derived from non-stone-forming Thai women). The post-treatment/baseline ratio was 3.21 ± 0.74 for urinary calcium, 1.01 ± 0.19 for urinary oxalate, and 2.23 ± 0.42 (median 1.15) for AP(CaOx). The post-treatment/baseline ratio of calcium, but not for urinary oxalate, had a significant correlation with the post-treatment/baseline ratio of AP(CaOx). Our findings suggest that the alteration in the risk of calcium oxalate nephrolithiasis based on urinary composition is related to the alteration in urinary calcium. The risk of calcium oxalate nephrolithiasis does not increase significantly after calcium or combined calcium and calcitriol supplement in the majority of postmenopausal women with osteoporosis. Received: 10 March 1999 / Accepted: 16 November 1999     

Oestrogen-receptor-alpha gene polymorphism affects response in bone mineral density to oestrogen in post-menopausal women

OBJECTIVE: An oestrogen-receptor-alpha (ERalpha) gene polymorphism has been variably reported to be related to bone mass. To investigate whether this ERalpha gene polymorphism is associated with a functional difference, we assessed the response in bone mineral density (BMD) to oestrogen therapy in post-menopausal women in relation to ERalpha gene polymorphism. PATIENTS AND MEASUREMENTS: Subjects consisted of 124 Thai post-menopausal women. Sixty-three of the women were less than 6 years post-menopausal and 61 were more than 10 years post-menopausal with vertebral or femoral osteoporosis as defined by BMD T-score less than - 2.5. Subjects were randomly allocated to receive 0.3 mg (n = 67) or 0.625 mg (n = 57) of conjugated equine oestrogen (CEE). All subjects also took 5 mg medroxyprogesterone acetate. Vertebral and femoral neck BMD were measured at baseline and 1 year after treatment. Data were expressed as mean +/- SEM. Capital P represents the absence of the restriction site while lower-case p indicates the presence of the restriction site. RESULTS: For subjects on 0.625 mg CEE, BMD at L2-4 increased significantly after 1 year in those with pp (n = 20) Pp (n = 29) and PP genotypes (n = 8) (P < 0.001). However, in subjects on 0.3 mg CEE, BMD at L2-4 increased significantly after 1 year in subjects with Pp (n = 34, + 7.6 +/- 1.5%, P < 0.001) and PP genotypes (n = 13, + 6. 9 +/- 1.0%, P < 0.001), but not in those with pp genotype (n = 20, + 2.3 +/- 2.1%, P = NS). After adjusting for age and years since menopause, the change in vertebral BMD was still lower in those without the P allele compared to those with the P allele (P < 0.05). Femoral BMD did not significantly change regardless of dose of CEE and genotype. CONCLUSIONS: We conclude that ERalpha gene polymorphism affects skeletal response to oestrogen in post-menopausal women. The effect of ERalpha gene polymorphism appears to be site-specific and does not relate to biochemical markers of bone turnover. Determination of ERalpha genotype may help identify post-menopausal women who will have more skeletal benefit from oestrogen therapy.     

Spontaneous echo contrast on transthoracic echocardiography and left atrial thrombus in rheumatic mitral valve disease patients: A clinicopathologic study

The association of spontaneous echo contrast and thrombus in the left atrium in patients with mitral valve disease is controversial. This study was undertaken to determine whether there is an independent association between spontaneous echo contrast on transthoracic echocardiography (TTE) and intraoperative evidence of left atrial thrombus and to evaluate the clinical implications of spontaneous echo contrast in patients with symptomatic rheumatic mitral valve disease. A total of 255 patients who underwent surgery for rheumatic mitral valve disases were preoperatively evaluated by transthoracic two-dimensional and Doppler echocardiography. Spontaneous echo contrast in the left atrium was carefully sought. The left atrium was carefully searched for evidence of thrombus intraoperatively. The association of spontaneous echo contrast and left atrial thrombus was determined by univariate and multivariate analysis. Of the patients studied, 77 (30%) had left atrial thrombus. Left atrial thrombus was found in 47 and 21 % of patients with and without spontaneous echo contrast, respectively (p < 0.001). Spontaneous echo contrast and atrial fibrillation were found to be the only two independent predictors of left atrial thrombus (odds ratio = 2.16; 95% confidence interval 1.15-4.04 p < 0.05, and odds ratio = 6.98; 95% confidence interval 3.45-14.16, p < 0.001, respectively). It was concluded that there is an independent association between spontaneous echo con trast on TTE and left auial thrombus in patients with mitral valve disease requiring surgical correction. These patients are at high risk for left atrial thrombus and should, therefore, be con sidered for long-term anticoagulation.     

Panel 2.5: mass-casualty management and hospital care

This is a summary of the presentations and discussion of Panel 2.5, Mass-Casualty Management and Hospital Care of the Conference, Health Aspects of the Tsunami Disaster in Asia, convened by the World Health Organization in Phuket, Thailand, 04-06 May 2005. The topics discussed included issues related to mass-casualty management and hospital care as pertain to the responses to the damage created by the Tsunami. It is presented in the following major sections: (1) key questions; (2) recommendations; and (3) conclusions. Subsections of the conclusion section include: (1) lessons learned; (2) what was done well?; and (3) what could have been done better?.     

Drug eruptions in Bangkok: a 1-year study at Ramathibodi Hospital

Background As new drugs are introduced onto the market, it is important to determine those that can cause cutaneous reactions and with what frequency. In addition, drugs that have been used for a long period of time may cause new types of eruption that have not been observed previously. The purpose of this study was to evaluate the types of drug eruption and the causative agents in a hospital-based population for a period of 1 year. Methods All in- and outpatients consulting for drug eruptions at the Dermatology Clinic, Ramathibodi Hospital from June 1995 to May 1996 were included in the study. The history and physical examination were performed by one of the authors. In suspected cases, a skin biopsy was carried out to confirm the diagnosis. Rechallenge tests with suspected drugs were performed with informed consent. Results One hundred and thirty-two patients were enrolled in the study. The most common types of drug eruption were maculopapular eruption, fixed drug eruption, and urticaria. Antimicrobial agents were found to be the most common causative drugs, followed by antipyretic/anti-inflammatory agents and drugs acting on the central nervous system. Conclusions Although the most common type of drug eruption and the most common causative agents were not different from those found in previous studies, the new generation of antibiotics and antifungal agents were found to be a frequent cause of drug eruptions. New types of drug eruption, such as generalized exanthematous pustulosis and acral erythema, were observed in this study.     

Serum testosterone and its relation to bone mineral density and body composition in normal males

OBJECTIVE Bone mineral density (BMD) declines with age in both men and women, predisposing the elderly to osteoporosis and fractures. Although there are extensive data about post-menopausal osteoporosis, there is relatively little information concerning the decrease in BMD with age in normal men, particularly the contribution of declining gonadal function with age to BMD. In the present study, we investigated the effect of age on the pituitary-gonadal axis in normal males and its relation to BMD and body composition. SUBJECTS Ninety healthy Thai males in the Bangkok Metropolitan area without a history of smoking or significant alcohol consumption were studied. MEASUREMENTS Serum testosterone (T), free testosterone (FT), LH and FSH were measured by radioimmunoassay in fasting blood samples obtained In the morning between 0600 and 1000h. BMD at anteroposterior L2-L4, lateral L2-L4, femoral neck, femoral trochanter and Ward's triangle were determined by dual-energy X-ray absorptiometry. RESULTS There were significant declines with age in BMD at lateral L2-L4 (r= 0.37, P < 0.001), femoral neck (r=?0.49, P<0.0001), Ward's triangle (r=?0.54, P < 0.0001) but not at anteroposterior L2-L4 or femoral trochanter. Serum FT (r=?0.56, P < 0.0001) but not T (r=?0.19, P= 0.07) decreased with age. Serum LH (r= 0.27, P <0.001) and FSH (r= 0.4, P <0.0001) increased with age suggesting a defect in gonadal androgen synthesis or possibly a secretion of bioinactive LH. Serum FT concentrations were significantly correlated to lateral L2-L4 (r= 0.27, P<0.05), femoral neck (r= 0.48, P < 0.0001) and Ward's triangle (r= 0.50, P < 0.0001) BMD. After controlling for age, declining FT with age was still associated with a decrease In BMD in femoral neck (P < 0.05) and Ward's triangle (P < 0.05) but not in lateral L2-L4. The proportion of body fat increased with age (r= 0.3, P < 0.01). Decreased serum T, but not FT, was associated with increased body fat after age was taken into account (P < 0.0001). CONCLUSIONS There is a decline in serum free testosterone together with increases In LH and FSH with age In healthy males. The decrease in serum free testosterone Is partially associated with the age-related decline in bone mineral density added to the effect of age at the femoral neck and Ward's triangle. Testosterone but not free testosterone Is associated with age-related increase in body fat.     

Hepatic insulin and glucagon receptors in pregnancy: their role in the enhanced catabolism during fasting

The response to dietary deprivation in late pregnancy, as compared to the non-pregnant condition, is more rapid and profound in terms of mobilization of fuels frm peripheral tissues as well as hepatic ketogenesis and gluconeogenesis ("accelerated starvation"). We examined the potential role of hepatic insulin and glucagon receptors in mediating these changes by comparing 48-h fasted 18-day pregnant and age-matched nongravid rats. Molar ratios for insulin:glucagon in peripheral and portal blood were significantly higher in the pregnant rats. Insulin binding to purified liver plasma membrane receptors, when appropriately corrected for differences in insulin degradation by the membrane system, was marginally diminished in the pregnant animals. Glucagon binding and adenylate cyclase activation by glucagon was indistinguishable in the two groups of animals. On the basis of portal vein hormone concentrations and the values for receptor binding, liver insulinization relative to glucagonization appears to be unchanged or slightly increased in the fasted pregnant rat compared to the fasted nongravid rat. Thus, it seems unlikely that much of the "accelerated starvation" response in late pregnancy can be ascribed to diminished insulin and/or increased glucagon availability at the hepatocellular level. Instead, it is hypothesized that postreceptor events play the major role in sustaining the intrahepatic realignments of established fasting in late pregnancy.