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PubMedDate not supplied

Clindamycin in the treatment of obstetric and gynecologic infections: a review.

The spectrum of clindamycin's activity includes anaerobes and gram-positive aerobes other than enterococci. No inactivation or incompatibility of clindamycin phosphate has been shown in intravenous solutions usually used clinically. After oral administration, clindamycin is almost completely absorbed, with mean peak serum levels reached in 45 to 60 minutes. Clindamycin is widely distributed in many body fluids and tissues. Its normal half-life is two to three hours, and thus it can be given at six-hour intervals. Because of its excellent coverage against anaerobes, gram-positive cocci, and Chlamydia trachomatis, clindamycin is the preferred antimicrobial agent for serious infections of the female genital tract. Clindamycin plus tobramycin or an aminoglycoside is effective treatment for pelvic inflammatory disease, particularly when a tubo-ovarian abscess is present. In post-cesarean section endometritis, clindamycin plus gentamicin has been shown to be more effective than any other treatment. Clindamycin (alone or with an aminoglycoside) has been used successfully in posthysterectomy vaginal cuff infections and, with an aminoglycoside, in septic abortions. Clindamycin has been well tolerated in studies of animals and human subjects; its most significant side effects develop in the gastrointestinal system.

Abortion, Septic↗
PubMed1991

Comparison of cortical bone and serum concentrations of clindamycin achievable by direct local infusion and intravenous administration.

Tibial cortical bone and serum concentrations of clindamycin were compared using two drug delivery methods in dogs. An implantable drug pump, used to continuously infuse clindamycin directly into the cortical bone, was compared with clindamycin administered i.v. Dosage for the direct continuous infusion was 4 mg/kg/day, and 44 mg/kg/day for the i.v. bolus regimen. Serum concentrations of clindamycin were significantly higher during i.v. bolus administration when compared with those achieved during pump infusion (p less than 0.05). However, tibial cortical bone concentrations were significantly higher during pump infusion than were those achieved by i.v. bolus. When examining serum and bone clindamycin concentrations over 21 days of direct local infusion, there was no significant difference in concentrations between sampling days within each tissue (p greater than 0.05). Furthermore, there were significantly greater concentrations of clindamycin in the cortical bone than in the serum at each sampling period (p less than 0.05). Results indicate that delivery of clindamycin to canine bone by implantable drug pump achieve significantly higher bone concentrations than i.v. bolus administration of the drug at higher dosages. Direct infusion also can sustain high concentrations in cortical bone without increasing systemic concentrations of clindamycin.

Animals↗
PubMed1975

Microbial kinetics of drug action against gram-positive and gram-negative organisms. III: Effect of lincomycin and clindamycin combinations on Staphylococcus aureus and Escherichia coli.

The functional dependencies of apparent first-order generation rate constants kapp, of drug-affected cultures on drug concentrations indicate that lincomycin and clindamycin possess the same mechanism of action, which is bacteriostatic, against Staphylococcus aureus. Clindamycin also possesses another mechanism of action, which is bactericidal, at high concentration levels. However, clindamycin possesses only one of the two mechanisms of lincomycin action, which is bacteriostatic, against Escherichia coli. The relative potency of action of a clindamycin-lincomycin combination against Staph. aureus is variable, and the effective ratio ranges between 5:1 and 9:1; the effective ratio against E. coli is fixed at 6:1 over a wide concentration range. This difference is attributed to differences in bioavailability and/or binding characteristics of the drugs for bioreceptors, as a consequence of structural modifications in the drug molecules, and to differences in modes of action in the respective organisms. Mixtures containing equipotent fractions of clindamycin and lincomycin show "equivalence" or "indifference" of effects on Staph. aureus. The combined action of the mixtures can be quantitatively predicted from the separate dose-response curves of either component drug alone. Therefore, it is concluded that clindamycin and lincomycin may bind to the same receptor site that is engaged in microbial protein synthesis to inhibit the generation of Staph. aureus. However, combinations of clindamycin and lincomycin are less active than the a priori equipotent concentration of either drug alone in their action against E. coli, demonstrating unequivocally an antagonism of effects. Furthermore, the degree of antagonism is dependent on the order of addition of the drugs, which is attributed to the possibility that clindamycin and lincomycin bind differently on active and allosteric loci of the same receptor site functionally engaged in protein synthesis in E. coli. A rational approach to the quantification and prediction of combined antibiotic action must, therefore, be based not only on the kinetics and mechanisms of action as well as on the dose-response relationship over a wide concentration range for the separate antibiotics but also on the strain and species of the test organism.

Clindamycin↗
PubMed1989

Selection of constitutively resistant mutants of inducible clindamycin-resistant Bacteroides vulgatus.

The rate of spontaneous mutation to constitutive clindamycin resistance and the kinetics of selection of such mutants in preinduced and non-preinduced cells was evaluated in the Bacteroides vulgatus strain RYC18F6 (original MIC less than or equal to 0.25 micrograms/ml), which shows inducible resistance to clindamycin and erythromycin. Mutants demonstrating a high level of constitutive resistance to clindamycin (64 micrograms/ml) occurred at a frequency of 10(-7). Culture in broth containing either subinhibitory or inhibitory levels of clindamycin resulted in induction of clindamycin resistance. This permitted survival of a part of the population that seemed to facilitate the further growth of constitutively resistant mutants (up to a frequency of 10(-1)). At both low and high clindamycin concentrations mutants appeared to be selected over merely induced cells. Preincubation of cultures with erythromycin gave rise to an apparently higher level of induction. Under these circumstances, the selection of constitutively resistant mutants was less effective (10(-4). The use of erythromycin or clindamycin against populations of Bacteroides spp. exhibiting inducible resistance may contribute to selection of mutants showing constitutive clindamycin resistance.

Bacteroides↗
PubMed2005

Clindamycin-paclitaxel pharmacokinetic interaction in ovarian cancer patients.

INTRODUCTION: Plasma protein binding is an important factor for many drugs that can influence the tissue distribution and pharmacokinetics. alpha(1)-acid glycoprotein (AGP) is an acute-phase protein that can increase in plasma of patients with several pathological conditions including cancer. Studies performed in cultured cells indicate that paclitaxel cytotoxicity is reduced by adding AGP and the sensitivity to paclitaxel is restored by displacing its binding to AGP with clindamycin, resulting in an increased paclitaxel cell uptake. The purpose of this study was to evaluate whether clindamycin modifies paclitaxel pharmacokinetics also in cancer patients. PATIENTS AND METHODS: Sixteen patients with advanced ovarian cancer, previously treated with surgery and chemotherapy were enrolled in this study. A pharmacokinetic study of paclitaxel was performed in the first three cycles of the consolidation therapy (paclitaxel and carboplatin) in each patient. In these cycles paclitaxel was administered alone and with two different doses (600 and 1,200 mg) of concurrent clindamycin. The sequence of the three treatments was randomly assigned in each patient in order to avoid the same order of treatments. RESULTS: Paclitaxel pharmacokinetics were partly modified by the concurrent administration of clindamycin. C (max) and AUC(0-last) of paclitaxel were significantly higher when the drug was given alone than when it was coadministered with 1,200 mg clindamycin. Moreover, AGP concentrations seem to have a small but statistically significant influence on paclitaxel pharmacokinetic, since AUC(0-last) showed a positive significant correlation with AGP plasma concentration when paclitaxel was given alone. The linear relation was lost when paclitaxel was coadministered with 1,200 mg clindamycin. Toxicity was not influenced by the coadministration of clindamycin. CONCLUSION: The hypothesis that clindamycin could affect paclitaxel pharmacokinetics seems to be verified with this study. Nevertheless, changes induced by giving the combination of the two drugs are minimal and thus of questionable clinical relevance.

Aged↗
PubMed1988

Clindamycin-induced alteration of ganglionic function. II. Effect of nicotinic receptor-channel function.

The postsynaptic effects of clindamycin have been analyzed in bullfrog sympathetic ganglion B cells using single electrode current and voltage clamp recordings and two electrode voltage clamp measurements. Clindamycin added to the bathing solution in the concentration range, 2.5 x 10(-4) to 5 x 10(-4) M, inhibited fast ganglionic transmission. In addition, local application of clindamycin decreased depolarizations produced by direct application of acetylcholine and decreased the amplitude of miniature excitatory postsynaptic potentials (MEPSPs) evoked by tetanic stimulation of the preganglionic trunk. In contrast, clindamycin did not change the amplitude or time course of the slow EPSP elicited by preganglionic stimulation (30 Hz for 10 s) or muscarinic depolarizations produced by local acetylcholine application to preparations pretreated with 25-50 microM (+)-tubocurarine. In voltage-clamped ganglion cells, excitatory postsynaptic current (EPSC) amplitude initially was increased and then decreased with increasing concentrations of clindamycin (0.5 x 10(-5) to 2.5 x 10(-4) M). The EPSC time course in control cells was exponential. After exposure to clindamycin, the EPSC decay was composed of two exponential components. The time constant of the fast component decreased and the time constant of the slow component increased with increasing concentrations of clindamycin. The two time constants of EPSCs obtained in clindamycin were independent of membrane voltage between -50 and -100 mV. We concluded that the block of fast ganglionic transmission is primarily due to a postsynaptic site of action, at least part of which is due to a concentration-dependent, but voltage-independent blockade of open nicotinic receptor channel complexes.

Acetylcholine↗
PubMed1997

Clindamycin resistance in the Bacteroides fragilis group: association with hospital-acquired infections.

A retrospective study was conducted to assess the relationships between clindamycin resistance in members of the Bacteroides fragilis group, previous antimicrobial therapy, and the context for the development of infection, whether in the community or during hospitalization. Eighty-five clindamycin-resistant clinical strains (one isolate per patient) isolated from January 1988 to October 1994 were matched (one to one) with clindamycin-susceptible isolates recovered during the same period, and the charts of the patients from whom the isolates were recovered were reviewed retrospectively. Of the clindamycin-resistant strains, 65% were recovered from patients with hospital-acquired infections compared with 40% of the clindamycin-susceptible strains (odds ratio [OR], 2.75; 95% confidence interval [CI], 1.41-5.38; P = .002). Prior antimicrobial therapy for > or = 48 hours was also associated with clindamycin resistance (OR, 2.33; 95% CI, 1.16-4.70; P = .02). However, clindamycin resistance remained associated with hospital-acquired infections independent of prior antimicrobial therapy (Mantel-Haenszel weighted average OR, 2.22; 95% CI, 1.03-4.89; P = .04). Clinicians should consider the risks for clindamycin resistance when treating hospital-acquired infections caused by members of the B. fragilis group.

Adult↗
PubMed1983

Genetic analysis of clindamycin resistance in Bacteroides species.

The genetic basis of clindamycin and tetracycline resistance in species of Bacteroides was studied in 13 resistant clinical isolates; 10 isolates were resistant to high levels of clindamycin (greater than 160 micrograms/ml) and three were resistant to low levels of clindamycin (5-20 micrograms/ml). All of the isolates were resistant to tetracycline. None of the strains with low-level clindamycin resistance could transfer resistance to either antibiotic. Three isolates resistant to high levels of clindamycin transferred tetracycline resistance to a sensitive Bacteroides fragilis recipient, and one of these (strain 1126) also transferred high-level clindamycin resistance. None of the transfer-proficient strains of Bacteroides contained plasmid DNA. However, DNA homology was detected by hybridization between the clindamycin resistance plasmid pBF4 isolated in France and sequences in our high-level clindamycin-resistant strains from California. A common homologous 4.8 megadalton EcoR1 fragment was identified in the whole cell DNA of the transfer-proficient strain 1126 of B. fragilis and two other species of the B. fragilis group.

Bacteroides↗
PubMed1989

Comparative study of clindamycin, imipenem, oxacillin and vancomycin in the infected granuloma pouch model.

In a rat granuloma pouch model, Staphylococcus aureus infection was treated with clindamycin, oxacillin or vancomycin and Bacteroides fragilis infection with clindamycin or imipenem. The model simulates a subcutaneous abscess and has the advantage of permitting frequent sampling of exudate for bacterial counts and antibiotic levels in the same animal. In staphylococcal infection all drugs reduced the bacterial counts in the infected pouch by 1-1.7 log, with a significant effect lasting for 3 h after the last injection. A 1.06-1.4 log reduction lasted for 24 h with clindamycin and oxacillin, but there was only an 0.3 log reduction at 24 h with vancomycin. The ratio of the drug concentration in the infected pouch to the MIC was highest with clindamycin (2.3) compared to oxacillin (1.6) and vancomycin (0.8). With Bact. fragilis infection the bacterial counts dropped 1.5 log at 3 h after the last injection with clindamycin and imipenem. At 24 h the counts were reduced 1.0 log with clindamycin and 0.5 log with imipenem. The ratios of pouch fluid concentration to MIC was 7.6 and 4.08 for imipenem and clindamycin, respectively, at 3 h, and 1.0 and 2.3 for imipenem and clindamycin at 24 h.

Animals↗
PubMed1994

Mucosal concentration and excretion of clindamycin by the human stomach.

Each of 12 patients undergoing routine diagnostic upper gastrointestinal endoscopy received a single iv infusion of clindamycin phosphate 300 mg over 10 min. During the endoscopy, mucosal biopsies of the gastric antrum and fundus were obtained at varying times following the infusion. The clindamycin concentrations in the biopsies and in serum samples also taken after the infusion were determined. In addition, six healthy volunteers participated in a cross-over study on two different days. On both days, each subject received a single iv infusion of clindamycin phosphate 300 mg, immediately after which, gastric secretion was stimulated by iv pentagastrin (2 micrograms/kg/h) which was infused continuously over 150 min. On one of the study days, acid secretion by the stomach was inhibited by a slow iv infusion of ranitidine 50 mg. Clindamycin concentrations in gastric aspirates and serum samples collected after the infusion were determined. Concentrations of clindamycin in the fundal mucosa were significantly higher than the simultaneous serum concentrations (median ratio of tissue concentration to serum concentration, 2.0; P < 0.005) while concentrations in the antral mucosa were similar to those in serum (median ratio, 1.2; P = 0.65). Ranitidine significantly inhibited pentagastrin-stimulated acid secretion as demonstrated by a decrease in the volume of gastric aspirate when ranitidine was administered compared with when it was not administered (P < 0.01). Clindamycin concentrations in gastric juice were approximately one and one-half times higher than those in serum samples obtained simultaneously, both during stimulation of gastric acid secretion with pentagastrin and during inhibition of pentagastrin-stimulated acid secretion with ranitidine. Gastric juice concentrations of clindamycin were significantly higher following administration of ranitidine than after stimulation of gastric secretion by pentagastrin alone. Fundal mucosal and gastric juice concentrations of clindamycin exceeded the hypothetical maximum serum concentrations, indicating that accumulation in the stomach occurred against a concentration gradient.

Adult↗
PubMed2001

In vitro selection of resistance to clindamycin related to alterations in the attenuator of the erm(TR) gene of Streptococcus pyogenes UCN1 inducibly resistant to erythromycin.

A clinical isolate of Streptococcus pyogenes UCN1 intermediate to erythromycin (MIC 1 mg/L) and susceptible to clindamycin (MIC 0.03 mg/L) harboured an inducible erm(TR) gene encoding a ribosomal methylase. We have selected in vitro, in the presence of concentrations of clindamycin ranging from 0.12 to 1 mg/L, one-step mutants that are highly resistant to this antibiotic (MIC 64 mg/L) at a frequency of 10(-7). By contrast, in an erythromycin-susceptible strain of S. pyogenes UCN5, mutants could be selected only by a low concentration of clindamycin (0.12 mg/L) at a frequency of 10(-9). Clindamycin resistance in four of six S. pyogenes UCN1 mutants was associated with deletions of 163 and 6 bp, as well as a tandem duplication of 101 bp in the regulatory sequence of the erm(TR) gene. The role of these structural alterations in clindamycin resistance was demonstrated by cloning the erm(TR) gene from the wild-type and mutant strains in Escherichia coli DB10, a mutant susceptible to macrolides. Clindamycin resistance was expressed only when the erm(TR) gene was preceded by an altered attenuator. Mutations could lead to the formation of mRNA secondary structures accounting for the accessibility of the ribosome-binding site and the initiation codon of the ErmTR methylase to the ribosomes, and subsequently for the translation of the erm(TR) transcripts. The easy selection in one step of mutants resistant to high levels of clindamycin by concentrations of this antibiotic ranging from four to 40 times the MIC leads us to recommend caution in the use of clindamycin therapy in group A Streptococcus infections.

Anti-Bacterial Agents↗
PubMed1999

Community-acquired and clindamycin-susceptible methicillin-resistant Staphylococcus aureus in children.

BACKGROUND: Recognition of children with community-acquired (CA) infections caused by clindamycin-susceptible, methicillin-resistant Staphylococcus aureus (MRSA) prompted a retrospective study in two Chicago hospitals conducted from 1987 through 1997. METHODS: Laboratory records of MRSA isolates, antibiotic susceptibilities and information from patient medical records were reviewed. RESULTS: One hundred eleven MRSA isolates from 103 children were studied with 51 isolates CA and 77 susceptible to clindamycin. The CA infections were less frequently associated with prior surgery (P = 0.0039) or a foreign body (P = 0.0001), and clindamycin-susceptible MRSA infections were less frequently associated with a foreign body (P = 0.001) compared with nosocomially acquired or clindamycin-resistant MRSA infections. Clindamycin-susceptible MRSA sources were mostly skin, wound or abscess (69%). Soft tissue diagnoses predominated (70%), but 16% were serious invasive infections. Ninety percent of clindamycin-susceptible MRSA were susceptible to erythromycin and/or trimethoprim-sulfamethoxazole. Antibiotic undertreatment (45%) or overtreatment (17%) of children with the clindamycin-susceptible MRSA occurred, but clindamycin appeared to be effective when used. CONCLUSION: The impact of these organisms could be substantial if they become more frequent or widespread. S. aureus is a potential pathogen in large numbers of pediatric patients; microbiologic evaluation and both presumptive and definitive treatment of all these children may need to be changed.

Abscess↗
PubMed1982

Clindamycin versus nafcillin or methicillin in the treatment of Staphylococcus aureus osteomyelitis in children.

The treatment of osteomyelitis due to Staphylococcus aureus was evaluated by randomized trial in 12 children who received clindamycin and 13 children who received nafcillin or methicillin. In the nafcillin/methicillin group, the mean duration of intravenous (IV) therapy was 27 days (range 14 to 38 days) plus 3.7 weeks (range 0 to 8 weeks) of oral therapy with dicloxacillin. In the clindamycin group, the mean duration of IV therapy was 5.8 days (range three to ten days) plus 4.7 weeks (range three to nine weeks) of oral therapy with clindamycin. The geometric means (GMs) of peak serum bactericidal titers for IV therapy were 45 (range 16 to 256) and seven (2 to 256) for nafcillin/methicillin and clindamycin respectively. The GMs of peak serum inhibitory and bactericidal titers for oral therapy with clindamycin were 99 (range 16 to 512) and four (range 1 to 128) and were generally within one dilution of the IV titer. The outcome of therapy was excellent for ten children in the nafcillin/methicillin group and for 11 children in the clindamycin group. In the clindamycin group, the outcome did not correlate with achieving a peak bactericidal titer of greater than 1:8. Clindamycin administered IV until the patient is afebrile for three consecutive days and then orally for approximately four weeks is an alternative to nafcillin/methicillin in the therapy of S aureus osteomyelitis in children.

Administration, Oral↗
PubMed2004

Natural history of bacterial vaginosis and intermediate flora in pregnancy and effect of oral clindamycin.

OBJECTIVE: We sought to describe the natural history of abnormal vaginal flora in pregnancy and estimate the efficacy of oral clindamycin in eradicating it and preventing relapse. METHODS: This was a subanalysis of a randomized trial of oral clindamycin for abnormal vaginal flora in pregnancy. All 494 enrolled women were asked to provide a vaginal smear 2 weeks after treatment and every second participant to provide further smears at 20, 24, 28, 32, and 36 weeks of gestation. We used Nugent score of Gram-stained smears to assess the cure rate among the clindamycin group and the rate of spontaneous resolution among the placebo group. RESULTS: Posttreatment smears were available for 462 women (231 in each of the clindamycin and placebo arms). The prevalence of abnormal flora posttreatment was 10% (22 of 231) in the clindamycin group compared with 93% (214 of 231) in the placebo group (P <.001). Two hundred nineteen women obtained 4 weekly smears; slides for 84 women were lost, and results were available for 135 women (69 clindamycin, 66 placebo). In the clindamycin group, the prevalence of abnormal flora was 15% at 20 weeks of gestation and 17% at 36 weeks of gestation compared with 69% at 20 weeks of gestation and 43% at 36 weeks of gestation in the placebo group. CONCLUSION: Oral clindamycin eradicated abnormal flora in 90% of treated pregnant women and maintained a normal flora in two thirds of women throughout pregnancy. Almost one third of untreated women in our study had spontaneous resolution of abnormal flora by 20 weeks of gestation. Because previous research has shown that spontaneous resolution does not modify the risk of preterm birth, early screening is essential.

Administration, Oral↗
PubMed2005

Increasing clindamycin resistance among methicillin-resistant Staphylococcus aureus in 57 northeast United States military treatment facilities.

BACKGROUND: Increasing community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) has led many to use clindamycin for CA-MRSA disease, whereas others suggest caution because of inducible clindamycin resistance and rely on drugs such as trimethoprim-sulfamethoxazole (TMP-SMX). AIM: To analyze the change in antibiotic susceptibility pattern of S. aureus isolates from 2001 to 2004 in a closed health care system, a period during which clindamycin and TMP-SMX use increased 99 and 62%, respectively. METHODS: S. aureus cultures from 57 military hospitals and clinics from 2001-2002 and 2003-2004 were compared for body site and antibiotic sensitivity, particularly the potentially inducible clindamycin-susceptible erythromycin-resistant pattern. A portion was evaluated by a double disk diffusion test (D test). RESULTS: Numbers of S. aureus-positive cultures obtained from "wound" sites rose significantly in both pediatric (138 to 215, P < 0.001) and adult (715 to 972, P < 0.001) isolates, with a rise in MRSA in children (6 of 138 to 60 of 215, P < 0.001) and in adults (161 of 715 to 324 of 972, P < 0.001). Clindamycin resistance increased among pediatric S. aureus isolates (1 of 207 to 13 of 327, P < 0.05), whereas >96% remained TMP-SMX-susceptible. Five methicillin-susceptible S. aureus (MSSA), 2 MRSA of 41 pediatric and 36 MSSA, 43 MRSA of 437 adult S. aureus specimens were D test-positive. CONCLUSIONS: In late 2004, most S. aureus from our region are still beta-lactam-susceptible. Most of the MRSA are still susceptible to clindamycin and do not appear to have inducible resistance. We must closely monitor the rates of constitutive and inducible clindamycin resistance as well as consider treatment alternatives that may slow the rate of clindamycin resistance.

Adolescent↗
PubMed2005

Clindamycin skin testing has limited diagnostic potential.

We examined the role of clindamycin prick and intradermal skin testing in a tertiary care clinic population. Experience with diagnostic modalities such as prick and intradermal testing has been limited with clindamycin. A retrospective chart review was conducted for patients with immunologic reactions temporally associated with clindamycin who were referred to the Drug Safety Clinic (Toronto, Ontario). A total of 31 patients were identified who had undergone prick and intradermal skin testing. All 31 negative immediate prick and intradermal tests were followed by a 150 mg oral dose of clindamycin. 10/31 (32%) subjects had significant reactions to the oral clindamycin provocation. 2 patients reported delayed reactions at the clindamycin intradermal test sites. Our experience suggests that prick and intradermal skin testing is not adequate in identifying patients with previous allergic reactions associated with clindamycin. Oral provocation tests can be used in patients with histories of clindamycin adverse reactions; however, it should be offered on a risk-benefit basis.

Administration, Oral↗
PubMed1999

Prophylactic administration of clindamycin 2% vaginal cream to reduce the incidence of spontaneous preterm birth in women with an increased recurrence risk: a randomised placebo-controlled double-blind trial.

OBJECTIVE: To test the hypothesis that prophylactic administration of clindamycin 2% vaginal cream can reduce the incidence of preterm birth in a high risk population. DESIGN: A multi-centre, randomised, double-blind, placebo-controlled trial. SETTING: Twelve city hospitals in The Netherlands. PARTICIPANTS: One hundred and sixty-eight women with a singleton pregnancy and a history of a spontaneous preterm delivery in the preceding pregnancy. INTERVENTIONS: Clindamycin 2% vaginal cream, or placebo cream, administered daily for seven days at 26 and 32 weeks of gestation. MAIN OUTCOME MEASURES: Spontaneous preterm birth at < 37 weeks, admission for threatened preterm labour, neonatal infectious morbidity. RESULTS: In the intention-to-treat analysis no difference was found in overall preterm birth between clindamycin and placebo (23% vs 18%, respectively). In the subgroup who completed the trial and administered all medication, more women delivered before 34 weeks in the clindamycin group (1.4% in the placebo vs 9.0% in the clindamycin group; P < 0.05). The length of admissions for threatened preterm labour did not differ. More infectious neonatal morbidity was seen in the clindamycin group (5/83 vs 0/85; P < 0.05). CONCLUSION: Clindamycin 2% vaginal cream given prophylactically to women with a spontaneous preterm birth in the preceding pregnancy did not prevent preterm delivery or reduce the number of admissions for threatened preterm labour. The neonatal infectious morbidity in the group treated with clindamycin was significantly higher and a major concern.

Adult↗
PubMed1982

Membrane transport of clindamycin in alveolar macrophages.

The use of antibiotics which can penetrate phagocytic cells and kill intracellular organisms is desirable in the treatment of chronic facultative bacterial infections. Recently, we reported that several antibiotics were selectively concentrated by rabbit alveolar macrophages. Clindamycin accumulation was especially marked. In the present study we evaluated the plasma membrane transport (initial uptake) of clindamycin in alveolar macrophages. The transport of clindamycin is an active process, as documented by requirements for cellular viability, elevated environmental temperature, metabolic energy, and establishment of the 40- to 50-fold cellular/extracellular gradient. Energy for membrane transport of the drug depended at least in part upon mitochondrial oxidative respiration and cell membrane Na-K pump activity. Kinetic analysis of active clindamycin transport revealed it to be saturable, with a high binding affinity (Km = 1 mM) and a high velocity of uptake (Vmax = 15.8 nmol/45 s per 10(6) cells). Clindamycin uptake was not influenced by the presence of hexose or amino acids, but was inhibited by nucleosides (adenosine, puromycin). Decreased clindamycin transport in the presence of puromycin was typical of competitive inhibition (increased Km, unchanged Vmax). Conversely, competitive inhibition of adenosine transport by clindamycin was documented. Thus, clindamycin is transported into alveolar macrophages via the nucleoside system. The potential biological consequences of this unique antibiotic transport mechanism are of interest.

Absorption↗