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.

A 45-day-old patient was admitted with dyspnea, hepatomegaly, tachycardia, holosystolic murmur in the precordial region, and continuous murmur at the right hypochondrium. Four cutaneous angiomas were noted. Instrumental examinations revealed congestive heart failure and multiple focal lesions in the liver with typical features of hemangiomas. The therapy with subcutaneous interferon-alfa-2a (IFN-alpha) was administered for 12 months with progressive regression of cutaneous hemangiomas, liver lesions, and cardiological alterations. IFN-alpha therapy was effective without any significant adverse effects.

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.

SUMMARY.The aim of this study was to determine the most appropriate urine collection for detecting differences in the excretion rates of albumin, -y glutamyl trans peptidase (GGT) and N-acetyl-(j-D-glucosaminidase (NAGA) between normotensive subjects and hypertensive patients on treatment. Twenty treated hypertensive patients, mean (SEM, standard error of mean) age; 52·2 (6'2) years and 20 normotensive subjects, mean age 49· 2 (4'2) years, were studied in a consecutive sampling design. Urinary excretion rates of albumin, GGT and NAGA were determined in consecutive timed urine samples collected overnight and during 3-5 h the next morning. Mean (SEM) overnight excretion rates for albumin, GGT and NAGA for normotensive subjects were 11·05 (1'18) ltg/min, 17·00 (2'20)mU/min and 6·55 (0'39)mU/min, respectively, which were significantly lower than those of hypertensive subjects which were 20· 77 (2' 14) ltg/min, 21· 84 (1'65) mU/min and 10·92 (0'87) mU/min, respectively (P<0·05). The mean (SEM) percentage increases in urinary albumin, GGT and NAGA in morning urine collections of normotensive subjects of 15· 22 (3' 88)0/0, 34' 04 (6' 45)% and 11· 54 (3' 63)%, respectively were significantly lower than 107·03 (15'04)%,121'96 (16'71)% and 72· 75 (7' 50)% found in hypertensive patients (P< 0,05). These data suggest that were urinary albumin and tubular enzyme excretion to be used as correlates of hypertensive renal damage, ambulatory urine collections may be more sensitive than overnight collections.

No abstract