Relations of serum aldosterone and microalbuminuria to left ventricular hypertrophy in patients with essential hypertension

Left ventricular hypertrophy [LVH] is an independent risk factor for cardiovascular morbidity and mortality in hypertensive patients. The identification of risk factors for the initiation of LVH in patients with hypertension [HTN] is important including microalbuminunuria [MAU] and hyperaldosteronism. Evaluation of the relationship of MAU and plasma aldosterone to blood pressure [BP] and LVH in patients with essential HTN. Thirty male patients with essential HTN and 15 healthy subjects as a control group were subjected to thorough clinical examination, transthoracic echocardiography, lipid profile, serum potassium, and serum aldosterone estimation. MAU was evaluated with dipstick Micral-II Test of fasting midstream morning urine on two successive days. Left ventricular mass index [LVMI] was calculated and values >134gm/m[2] were considered as LVH. Patients with LVMI >134 gm/m[2] had higher serum aldosterone, BMI, Interventricular septal thickness [IVST], Posterior wall thickness [PWT] and Relative wall thickness [RWT]. Serum aldosterone was significantly higher among the test hypertensive group and was positively correlated correlated with LVMI, RWT, PWT, IVST, LVM and negatively correlated with LV diastolic dimensions. MAU was positively correlated with systolic BP, Pulse pressure, BMI and LVMI and a strong relationship between MAU and serum aldosterone was detected. Aldosterone is an important contributor to the development of LVH and hypertensive nephropathy and strong relation between microalbuminuria and aldosterone is detected. The Value of selective aldosterone blockers in preventing target organ damage [TOD] awaits further investigation

Deterioration of glucose tolerance in non-diabetic non-IGT elderly population: potential role of Beta cell dysfunction and insulin insensitivity

Aim: As the human community develops, the group of aged individuals constitutes a larger percent of the total population. This particular group of people is characterized by increased incidence of macrovascular complications that are similar to those described in the metabolic syndrome or type 2 diabetes. Moreover, it is well known that the incidence as well as the prevalence of type 2 diabetes and impaired glucose tolerance is more common in old age people. The mechanism of age-related glucose intolerance is not yet completely clear. Subjects and A clinicobiochemical study was carried out comprising 20 apparently healthy non-diabetic nonobese old individuals [mean age 65 +/- 4.8 years] and 20 type 2 diabetic patients compared to 10 healthy young subjects. The senile group had no family history of diabetes. Cases with renal, hepatic, gastrointestinal, or endocrine abnormalities were excluded from the study. Intravenous glucose tolerance test [ivGTT] was done with sampling at 0, 5, 10, 15, 30, 45, and 60 min after glucose load and the following estimations were undertaken: glucose decay constant [kG], glucose and insulin areas under the curve, insulnogenic index, first phase insulin response, insulin resistance index and fractional insulin clearance. The senile and diabetic groups, when compared to the controls, had a ronsignificantly different fasting plasma glucose, but it was higher in diabetic patients. Fasting serum insulin was significantly higher in the studied groups than in the healthy control group. The senile group showed a significant reduction in glucose tolerance [KG 1.36 +/- 0.3%/min], decreased insulin sensitivity index [5.19 +/- 1.4 10-4 min-1 /[micro U/ml] and a marked reduction of first phase insulin response [2.45 +/- 0.78 micro U/ml per mg/dl], when compared with the control group. However, the degree of glucose intolerance and insulin insensitivity of the senile group was still significantly lower than that of type 2 diabetic patients. This study revealed that the insulin resistance seems to be a characteristic feature of the normal aging process and senility could be considered as an inevitable risk factor for glucose intolerance and metabolic syndrome with its accompanying health hazards. Conclusions: Insulin secretion, insulin clearance and interaction between insulin and target tissues are defective in elderly subjects. These functions are intermediate between healthy controls and NIDDM patients and may predispose the elderly population to the risk of impaired glucose tolerance or diabetes mellitus with its attendant macrovascular and microvascular complications

Vascular endotheliaf growtli factor [VEGF]: an association with diabetic microvascular complications

The mediators of diabetic microvascular complications remain largely unknown. As diabetic stinopathy is associated with ischaemic changes followed by neovascularization, a role has been proposed for vascular endothelial growth factor [VEGF] its pathogenesis. Subjects and Serum EGF levels were studied in 55 diabetic patients at ferent stages of their disease and microvascular mplications. It was first noted that ciculating VEGF levels were significantly higher in betic patients [421 +/- 309 pg/ml, mean +/- SD] npared to controls [188 +/- 145 pg/ml], P < 0.05. ther analysis showed VEGF levels to be highest in] etic patients with proliferate retinopathy 1 +/- 376 pg/ml]. The level in those with and without background retinopathy was comparable to that of controls [379 +/- 250 pg/ml]. A significant rise in serum VEGF was also detected in patients with significant proteinuria [662 +/- 276 pg/ml]. The level in those with icroalbuminuria was comparable to that of controls [375 +/- 273 pg/ml]. A positive, albeit weak, correlation was noted between serum VEGF and urinary albumin excretion [r= 0.27, P < 0.05]. This study confirms raised circulating level of VEGF in diabetic patients with advanced microvascular disease [proliferate retinopathy and established nephropathy]

Erythropoietic response to androgen replacement therapy Erythropoietic and role of IL-6 in aging male rats

Changes in iron status and bone marrow Junctions are frequently observed in the elderly. These phenomena are often associated with chronic diseases and/or neoplcfsmas. In a minority of elderly subjects; it is not possible to identify the causes of anemia. This study was carried out to clarify the functional capacity of the erthropoietic tissues of the aged rats, to investigate the role of IL-6 in erthropoietic activity, and to evaluate the short-term testosterone therapy. Thirty healthy male Sprague-Dawley rats were divided according to their age into group I [16-week-old; n = 6], group II [48-week-old; n=12], group III [72-week-old; n=I2]. Six rats enrolled in each elderly group [groups II and III] received s.c. testosterone propionate; 2 mg/100 g body weight every other day for 10 days [Groups lIb and Illb]. The remaining rats not received testesterone were named groups [Ila and IlIa]. One day after the last injection, bone marrow aspirates were performed to evaluate the erthropoietic activity and iron stores in the erythroid precursors. In addition, a peripheral haemogram and determination of serum levels of iron, TIBC, IL-6, and free testosterone were done. Significant age-linked changes were observed in the form of decreased serum levels of free testosterone, IL-6, TIBC, RBCs count, and Hb levels as well as an increase in serum iron level in groups Ila and IIla. Bone marrow hypocellularity with a decrease in the amount of iron storage were especially remarkable in Group IlIa. Moreover improvement in the function of erythropoietic tissues in Group lib indicated by erythroid hyperplasia and an increase in the amounts of iron storage. However, reduced serum IL-6 was not affected by testosterone therapy. These data reveal that senile anemias are of hypoproliferaitue character. Testosterone and IL-6 may be, at least in part, the important factors in determining an age-associated decrease in erythropoiesis