Although inflammatory or degenerative changes in salivary glands have been demonstrated in genetic animal models of diabetes mellitus and in experimental diabetes, no information is available in diabetics on the possible leakage in saliva of cytosolic enzymes as markers of salivary cell injury. Aspartate (GOT) and alanine (GPT) aminotransferases and lactate dehydrogenase (LDH) were determined in saliva samples collected by the Salivette method from well-controlled insulin-dependent (IDDM n = 11) and non-insulin-dependent (NIDDM n = 18) diabetic patients and from age-cross-matched healthy subjects (n = 33). In IDDM salivary concentrations of GOT (112.55 +/- 23.94 UI/L) and LDH (1120.27 +/- 168.31 UI/L) were similar to those found in the NIDDM (90.94 +/- 19.64, and 1255.43 +/- 221.40 UI/L respectively), but higher (p < 0.05) than those observed in normal subjects (33.09 +/- 3.71, and 423.58 +/- 39.94, UI/L respectively). GPT was higher in NIDDM than IDDM, which in turn was higher than in normal subjects (42.78 +/- 14.72, 16.45 +/- 3.74 and 6.85 +/- 1.52 UI/L respectively). Salivary and serum values of GOT, GPT and LDH were not correlated. Determination of cytosolic enzymes in saliva may be useful for monitoring the diabetic involvement of salivary glands.
In essential hypertension, the severity of cardiovascular damage is only weakly related to clinic blood pressure (BP), whereas a better relationship seems to exist with BP recorded during stressful situations. The present study compared BP levels measured during laboratory stress testing and 24-h ambulatory monitoring with regard to their relationship with cardiac end-organ involvement. BP recorded during a mental and a physical challenge and during 24-h ambulatory monitoring was related to Doppler echocardiography characteristics of left ventricular structure and filling in 63 untreated essential hypertensives and in 32 healthy subjects. In the hypertensive group, only a weak relationship was observed between left ventricular mass and clinic BP; the strength of this association was not improved by BP measured during mental task and cycle ergometry, and was slightly but not significantly higher for BP recorded during ambulatory monitoring. In multivariate analysis, left ventricular mass was independently predicted by stroke index and 24-h systolic BP. Among the different pressure measures, 24-h, daytime, and nighttime BPs bore the only significant relation to relative wall thickness. In the normotensive group, no significant relationship was observed between left ventricular mass and different measures of BP. Doppler indexes of left ventricular diastolic filling did not significantly relate to any BP measurement in the hypertensive group, and generally bore a significant inverse relationship to various BP recordings in the normotensive group. To summarize, stress testing BP does not help in identifying hypertensive patients with increased left ventricular mass.
SYNOPSIS A method for the differential determination of plasma antithrombins, antithrombin III and U macroglobulin, is described. The method is based on the selective inactivation of plasma (x2 macroglobulin by treatment with 01 M methylamine for 10 minutes at 37°C and on the observation that antithrombin III and a2 macroglobulin inhibited in defibrinated plasma low concentrations of thrombin without mutual interference and according to pseudo-first order reaction. In healthy subjects antithrombin III was shown to account for about 70% of the total antithrombin activity. But in patients with liver cirrhosis, where low levels of total antithrombin activity were observed, the relative contribution of antithrombin III was found to be noticeably lower.
The aim of this study was to investigate possible abnormalities in salivary electrolytes in hypertensives treated with ace-inhibitors (ACE-I) or calcium antagonists (Ca-ANT) at low or normal sodium intake. Hypertensives treated with ACE-I (n.14) or Ca-ANT (n.22) and 13 normotensives were studied during normal or restricted Na intake. Na, K, Ca, Mg and Cl were determined in saliva samples collected by using a standardized adsorption procedure (SALIVETTE). Na intake was evaluated by determination of the 24-hr urinary Na excretion. Similar concentrations of Na, K, Ca, and Cl were found in normotensives and in hypertensives treated with ACEI or Ca-ANT both at low or normal Na diet. Magnesium in saliva appeared reduced in ACEI-treated hypertensives (0.28 +/- 0.06 mmol/l) in comparison to the similar values of normotensives (0.53 +/- 0.05) and Ca-ANT treated hypertensives (0.54 +/- 0.07). In normotensives and in treated hypertensives lowering of Na intake did not change the salivary content of Ca, Mg and Cl but produced in saliva a reduction of Na associated to a rise in K. Salivary Na/K ratio was significantly correlated with 24 hr urinary Na excretion in normotensives (r = 0.77; p < 0.05) and in hypertensives treated with ACE-I (r = 0.74; p < 0.05) or Ca-ANT (r = 0.62; p < 0.05). The low salivary magnesium in ACE-I-HT may have a role in the occasional ACEI-dependent dysgeusia. Salivary Na/K ratio may be used as a rough index of Na intake in treated hypertensives.
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