National guidelines for the judicious use of glycopeptides in Belgium.

OBJECTIVE: The 'HICPAC guidelines', published in the USA in 1995 stressed the crucial role of restrictive usage of glycopeptides in the strategy to limit the emergence and spread of resistant enterococci. Because controversy still remains in Belgium on the necessity and feasability of restricting glycopeptide usage, the infectious diseases advisory board (IDAB) developed a consensus statement on the judicious use of glycopeptides in Belgium. METHODS: The literature on the indications for glycopeptide treatment was reviewed, categorized and discussed by a working party of the IDAB.Consequently, the IDAB reached consensus on the warranted indications for glycopeptide use in Belgium. RESULTS: The opinion of the IDAB-members is reported in a consensus statement specifying the indications for treatment and for prophylaxis with glycopeptide antimicrobials, as well as the situations where glycopeptides should not be used, taking into account the specific epidemiology of bacterial resistance, the availability of antibiotics and the common prescribing practices in Belgium. CONCLUSIONS: The IDAB concludes that restrictive usage of glycopeptides must also be a priority in Belgium. Guidelines on the judicious use of these antibiotics adapted to the national situations must contribute to this objective.

Atrial natriuretic peptide during water deprivation or hemorrhage in rats. Relationship with arginine vasopressin and osmolarity.

The concentrations of atrial natriuretic peptide (ANP) in atria, hypothalami and plasma were investigated in relation to the variations of the plasma endogenous immunoreactive arginine vasopressin (Ir-AVP) during water deprivation or hemorrhage in normal conscious Wistar rats. Furthermore, the in vitro and in vivo effect of extracellular hyperosmolarity on ANP release from right atrium and hypothalamus was examined. Water deprivation elevated circulating immunoreactive ANP (Ir-ANP: pg/ml) to 153 +/- 7 (24 h); 174 +/- 1 (48 h) from the control level (109.6 +/- 7.8). This increase in Ir-ANP concentration which correlated with atrial (r = -0.93) or hypothalamic (r = -0.87) Ir-ANP content decrease, was associated with significantly enhanced levels of plasma Ir-AVP, plasma sodium, osmolarity and hematocrit. An acute volume depletion by hemorrhage significantly reduced plasma Ir-ANP (67 +/- 8.4 pg/ml) from the sham operated level (140 +/- 18 pg/ml). Plasma Ir-AVP was elevated dramatically (207.4 +/- 53.4 pg/ml) compared with the sham operated level (8.8 +/- 2.6 pg/ml). These results, indicating the lack of correlation between plasma Ir-ANP and Ir-AVP in vivo, suggest that the ANP secretion, which is regulated mainly by plasma volume, may be modulated by a change in plasma osmolarity. Extracellular hyperosmolarity stimulated the ANP release from superfused sliced normal rat atria and hypothalami.

Opposite effects of delta and mu opioid receptor agonists on the in vitro release of substance P-like material from the rat spinal cord.

Superfusion of slices from the dorsal half of the lumbar enlargement of rat spinal cord with Krebs-Henseleit medium supplemented with 30 microM bacitracin allowed the collection of substance P-like immunoreactive material (SPLI), which was released at a rate of approximately 10 pg/4 min. Tissue depolarization by an excess of K+ (30-60 mM) or veratridine (50 microM) induced a marked increase in SPLI outflow, provided that Ca2+ was present in the superfusing fluid. K+- or veratridine-induced SPLI overflow could be modulated in opposite directions by mu and delta opioid receptor agonists. Thus, the two preferential mu agonists Tyr-D-Ala-Gly-MePhe-Gly-ol (DAGO; 10 microM) and Tyr-D-Ala-Gly-MePhe-Met(O)5-OH (FK-33824; 0.1 microM) enhanced SPLI overflow from depolarized tissues, whereas the selective delta agonists Tyr-D-Thr-Gly-Phe-Leu-Thr (deltakephalin; 3 microM) and [2-D-penicillamine, 5-D-penicillamine]enkephalin (50 microM) reduced it. The effect of DAGO was antagonized by a low concentration (1 microM) of naloxone but not by the selective delta antagonist ICI-154129 (50 microM). In contrast, the latter drug prevented the inhibitory influence of delta agonists on K+-induced SPLI release. Complementary experiments with morphine (10 microM) and [2-D-alanine, 5-D-leucine]enkephalinamide (3 microM), in combination with 1 microM naloxone or 50 microM ICI-154129 for the selective blockade of mu or delta receptors, respectively, confirmed that the stimulation of mu receptors increased, whereas the stimulation of delta receptors reduced, SPLI overflow. The results suggest that, at the spinal level, and antinociceptive action of delta but not mu agonists might involve a presynaptic inhibition of substance P-containing primary afferent fibers.

Double-blind, placebo-controlled study of oxacillin combined with rifampin in the treatment of staphylococcal infections.

A total of 101 patients with proven Staphylococcus aureus infection were included in a double-blind, placebo-controlled study; this study compared oxacillin (12 g/day, intravenously) or vancomycin (2 g/day, intravenously) plus rifampin (1,200 mg/day, orally) with oxacillin or vancomycin plus placebo. We evaluated 65 patients. Of the patients tested, 33 received oxacillin plus rifampin (13 bacteremias), and 32 received oxacillin plus placebo (16 bacteremias). Clinical cure was achieved in 61% of the patients treated with oxacillin plus rifampin and in 56% of the patients treated with oxacillin plus placebo. Improvement was noted in 27 and 25%, respectively, and failure occurred in 9 and 18%, respectively. These differences were not statistically significant. Bacteriological failure occurred in 3 and 28%, respectively (P less than 0.05). None of the failures within the rifampin-treated group was associated with the emergence of a rifampin-resistant mutant. The rates of superinfection were similar in both groups. The geometric means of the serum bactericidal activity after 1, 6, and 11 h were, respectively, 22, 17, and 9 after treatment with oxacillin plus rifampin and 25, 3.4, and 2.3 after treatment with oxacillin plus placebo. It was suggested that the addition of rifampin to oxacillin or vancomycin might only be beneficial to severely ill patients.

Ticarcillin-clavulanic acid therapy in severe infections.

Twenty patients with severe infections were treated with a fixed combination of ticarcillin + clavulanic acid. Nineteen of them had severe underlying diseases. Fifteen were bacteraemic; four of these were in shock. Eleven were infected with microorganisms resistant in vitro to ticarcillin. Eleven were clinically cured, 6 improved and 3 failed to respond, the latter being infected with ticarcillin-resistant microorganisms (2 E. coli, 1 P. mirabilis). Six patients experienced side-effects, which were usually mild and reversible, consisting mainly of moderate elevation of serum transaminases. In one patient ticarcillin-clavulanic acid was stopped due to worsening of a pre-existing drug hepatitis.

[Enzymatic character and subcellular localization of the transformation reaction of 18 hydroxycorticosterone to aldosterone]. / Caractère enzymatique et localisaiton subcellulaire de la réaction de transformation de la 18 hydroxycorticostérone en aldostérone.

The authors study in vitro the conversion of 18 hydroxycorticosterone into aldosterone in duck adrenal subcellular fractions. The enzymatic nature of this conversion is studied by classical enzymologic tests. All results are in favor of an enzymatic conversion and this enzyme is strictly located in the mitochondrial fraction. Results concerning this localisation are expressed as specific activity and relative specific activity. Preliminary results on further experimental data point out that this conversion depends on the energetic state of mitochondria. Complete electron transfer blokage inhibits this transformation whereas respiratory chain blokage with a NADPH generating system and ATP supplementation does not seem to produce any inhibition. Oligomycine and guanidine stimulation suggest that ATP or its precursors may be involved in this reaction.