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OBJECTIVES: An experimental gingivitis model was used to analyse the influence of alcohol in mouthwashes containing 0.15% triclosan and zinc chloride on the formation of supragingival plaque, the development of gingivitis and the appearance of adverse events. MATERIAL AND METHODS: Using a double-blind crossover design, 30 subjects underwent two consecutive experimental phases with two 0.15% triclosan and zinc chloride mouthwashes, differentiated mainly by their excipient (hydroalcoholic or aqueous). In each phase, the subjects discontinued all oral hygiene measures and were treated solely with the randomly assigned experimental mouthwash for 21 days. Each experimental phase was preceded by a 14-day washout period in which, after receiving a complete oral prophylaxis, the subjects were instructed to perform thorough oral hygiene procedures. Gingivitis and plaque levels were assessed at the start and end of both the experimental phases. RESULTS: The evolution of the gingivitis and plaque indices showed no statistically significant differences between both treatments. The mean gingival index increased from 0.30 to 0.38 with the non-alcoholic mouthwash and from 0.32 to 0.42 with the hydroalcoholic mouthwash. The respective changes in plaque index were from 0.88 to 1.93 and from 0.94 to 1.92. The hydroalcoholic mouthwash produced a larger number of fresh symptoms (p=0.033), oral itching being the most reported. CONCLUSIONS: Alcohol does not influence the effectiveness of a 0.15% triclosan and zinc chloride mouthwash against gingivitis development and supragingival plaque formation. The absence of alcohol significantly decreases the incidence of adverse events produced by the mouthwash.

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OBJECTIVE: To clarify the functional state of the somatotropinergic system in patients with Alzheimer's disease (AD) and in patients with vascular dementia (VD) in relation with somatostatin cerebrospinal levels. DESIGN We studied the GH response to GHRH in controls and in AD and VD patients and correlated their responses with somatostatin cerebrospinal levels. PATIENTS: Twelve control subjects and 56 patients, 28 with AD and 28 with VD, were studied. A GHRH test was performed in every case. One hundred mcg of GHRH was administered as a intravenous bolus and blood samples were drawn at -15, 0, 30, 60, 90 and 120 minutes. Cerebrospinal fluid was obtained after lumbar puncture. Measurements of GH and somatostatin were determined by specific radioimmunoassay. RESULTS: The GH response to GHRH exhibited no difference between AD and VD patients (12.2 +/- 2 mcg/l vs 9.9 +/- 1.8). There were 17 AD patients and 16 VD patients with exaggerated GH response to GHRH. There was no difference between cerebrospinal levels of somatostatin (30 +/- 2.1 pg/mL in AD patients vs 42 +/- 2.4 in VD patients), and there was no correlation among GH response to GHRH and cerebrospinal levels. CONCLUSION: In our study we observed no difference between the AD and VD patients in GH response to GHRH and no difference in somatostatin cerebrospinal levels in these patients.

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Somatostatin-like immunoreactivity levels (SLI) in cerebrospinal fluid (CSF) were determined in twenty-three patients with untreated parkinsonian syndrome (15 with Idiopathic Parkinson's disease (IPD) and 8 with other forms of parkinsonism) at the moment of clinical diagnosis (mean duration of disease 1.1 +/- 0.2 years), and in 26 subjects without neurological symptoms. None of the IPD patients had a diagnosis of dementia at the moment of inclusion in the study. CSF-SLI content was found to be significantly higher in patients with parkinsonian syndrome (107.9 +/- 9.8 pg/ml) than in control subjects (73.5 +/- 8.4 pg/ml). The increase was also significant when controls were compared with IPD patients. In addition, a positive correlation between SLI and homovanillic acid was found in CSF of all patients. A test of learning memory was used to evaluate the mental state of patients and a significant increase in CSF-somatostatin levels was observed in patients with Idiopathic Parkinson's disease and severe affectation of memory. These results indicate that in the early steps of untreated parkinsonian syndrome, somatostatin concentration in cerebrospinal fluid may increase, probably due to the neurodegenerative depletion of somatostatin from striatal or cortical neurons.

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We studied the growth hormone (GH) response to GH-releasing hormone (GHRH) and the thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) in four groups of patients with dementia and examined whether GH and TSH secretion is altered in patients with Alzheimer's disease. The four groups included those with Alzheimer's disease (n = 28), parkinsonism with dementia (n = 10), progressive supranuclear palsy with dementia (n = 10), and dementia of vascular origin (n = 28). The results showed no differences among the four groups in GH response to GHRH (12.2 +/- 2, 10.7 +/- 2, 8.9 +/- 1.1, and 9.9 +/- 1.9 micrograms/ml, respectively); there was no correlation between GH response to GHRH and sex, stage of the disease, or cerebral atrophy. The proportion of patients with exaggerated, normal, or lower GH response was similar in the four groups in terms of TSH response to TRH (9.2 +/- 0.9, 11.1 +/- 1, 11.1 +/- 1, and 10.3 +/- 1 mU/ml, respectively), nor was there a correlation between TSH response to TRH and sex, stage of the disease, cerebral atrophy, or GH response to GHRH. The proportion of those with exaggerated, normal, or lower TSH response was similar in the four groups. Cerebrospinal somatostatin levels were similar in Alzheimer's disease and vascular dementia patients. These findings indicate that neither GH response to GHRH nor TSH response to TRH provides a useful diagnostic adjunct in Alzheimer's disease patients.

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OBJECTIVE: To measure salivary testosterone in women with systemic lupus erythematosus (SLE). METHODS: We investigated concentrations of salivary testosterone in 13 women with active SLE and 47 women with inactive SLE, and in 72 healthy female controls. RESULTS: We found a significant decrease in salivary testosterone concentrations in glucocorticoid-treated SLE patients (mean +/- SD 0.06 +/- 0.04 nmoles/liter) but no differences in concentrations in untreated patients (0.09 +/- 0.03 nmoles/liter), compared with the healthy controls (0.11 +/- 0.04 nmoles/liter). CONCLUSION: Glucocorticoid treatment appears to cause a decrease in the salivary testosterone level. Measurement of salivary testosterone is a simple way of monitoring androgen metabolism in patients with SLE.

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The biological variation of several relative lipid quantities, calculated as the ratios between the concentrations of various serum lipids and apolipoproteins, has been estimated over a one-year period. The medians of the within-subject biological coefficient of variation, separated by sex when significant differences exist, were 15.4% for [apolipoprotein A-I]/[apolipoprotein B], 6.8% for [high-density lipoprotein (HDL)-cholesterol]/[cholesterol], 10.5% and 17.6% (women and men, respectively) for [HDL2-cholesterol]/[HDL-cholesterol], 13.6% for [HDL2-cholesterol]/[HDL3-cholesterol], 10.6% for [low-density lipoprotein (LDL)-cholesterol]/[apolipoprotein B], 10.6% and 8.7% (women and men, respectively) for [LDL-cholesterol]/[cholesterol], and 6.3% for [LDL-cholesterol]/[HDL-cholesterol]. From these data, we have calculated the critical difference for significant change detection, the index of individuality, and the goal for the between-day imprecision. Concerning within-subject biological variation, the best ratios for the detection of risk of coronary heart disease and the monitoring of intervention are [LDL-cholesterol]/[HDL-cholesterol] and [HDL-cholesterol]/[cholesterol]. The index of individuality obtained in this study indicates that the use of population-based reference values is inadequate for interpreting the ratios studied.

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New homogeneous enzyme immunoassays for the determination of thyroxine and thyroxine uptake have been developed. The CEDIA assays are based on the cloned enzyme donor immunoassay technology, which involves fragments of beta-galactosidase prepared by genetic engineering. The assays have been adapted for Boehringer Mannheim/Hitachi analysers. The CEDIA T4/T Uptake assays were evaluated in eleven clinical chemistry laboratories on various Boehringer Mannheim/Hitachi analysis systems, using a 2-point calibration. The analytical range of the T4 test was 10 to 258 nmol/l thyroxine. The T uptake test had a measuring range between 20-50%. Depending on the concentration of the analyte (samples from hypo-, eu- or hyperthyroid patients), mean coefficients of variation ranged from 1.8 to 4.8% within-run and from 4.1 to 6.5% between-run for the T4 assay. Even better coefficients of variation were obtained for the T uptake assay (1.4 to 2.3% within-run, 2.8 to 3.3% between run). The relative inaccuracy of the CEDIA assays with respect to values assigned by other tests was satisfactory in various control sera. The T4 assay was compared with one radioimmunoassay, one enzyme immunoassay and one fluorescence polarisation immunoassay. Slopes ranging from 0.9 to 1.1 and intercepts ranging from -10 to +10 nmol/l thyroxine were obtained with two exceptions. The results of the T uptake test correlated reasonably with those of other thyroxine-binding methods. No interference was observed with icteric and lipaemic sera. Haemoglobin up to 4 g/l had no significant influence. Results of the CEDIA T Uptake test are mainly used for calculation of the free thyroxine index, in which the thyroxine value is corrected for variations of thyroxine-binding protein concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

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