Disease relevance of Clindamycin hydrochloride

• Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals [1].
• Both treatment regimens--cefoxitin given alone and clindamycin and gentamicin given together--resulted in similar infection rates, drug toxicity, duration of hospitalization, and costs [2].
• A quantifiable neurologic assessment was used prospectively to evaluate the clinical outcome of patients with AIDS and toxoplasmic encephalitis who were treated with oral clindamycin (600 mg four times a day) and pyrimethamine (75 mg every day) for six weeks [3].
• BACKGROUND: Babesiosis is a tick-borne, malaria-like illness known to be enzootic in southern New England. A course of clindamycin and quinine is the standard treatment, but this regimen frequently causes adverse reactions and occasionally fails [4].
• Although treatment with clindamycin and quinine reduces the duration of parasitemia, infection may still persist and recrudesce and side effects are common [5].

Psychiatry related information on Clindamycin hydrochloride

• In order to obtain a meaningful data to help in decision making, a double blind, randomized study was performed to investigate whether cefazolin alone or a combination of gentamicin and clindamycin was more effective in prophylaxis [6].
• The results are discussed on the basis of inflammatory reaction elicited from the foreign body and the characteristics of clindamycin in connection with the host's defense mechanisms [7].

High impact information on Clindamycin hydrochloride

• CONCLUSIONS: For the treatment of babesiosis, a regimen of atovaquone and azithromycin is as effective as a regimen of clindamycin and quinine and is associated with fewer adverse reactions [4].
• The most common adverse effects with atovaquone and azithromycin were diarrhea and rash (each in 8 percent of the subjects); with clindamycin and quinine the most common adverse effects were tinnitus (39 percent), diarrhea (33 percent), and decreased hearing (28 percent) [4].
• Moreover, parasite death occurs with peculiar kinetics that are identical to those observed after exposure to clindamycin and macrolide antibiotics, which have been proposed to target protein synthesis in the apicoplast [8].
• Conversely, clindamycin (and functionally related compounds) immediately inhibits plastid replication upon drug application-the earliest effect so far described for these antibiotics [8].
• MAIN OUTCOME MEASURES: Trends in macrolide use (1993-1999) and resistance and factors associated with resistance, including examination of 2 subtypes, the M phenotype, associated with moderate minimum inhibitory concentrations (MICs), and the MLS(B) phenotype, associated with high MICs and clindamycin resistance [9].

Chemical compound and disease context of Clindamycin hydrochloride

• Pseudomembranous enterocolitis resulting from therapy with antibiotics such as clindamycin and lincomycin hydrochloride monohydrate does not always respond to drug and vigorous medical support [10].
• Treatment with antibiotics, including intravenous ciprofloxacin, rifampin, and clindamycin, and supportive therapy appears to have slowed the progression of inhalational anthrax and has resulted to date in survival [11].
• We conducted a double-blind, controlled trial of low-dose (150 mg/d) oral clindamycin hydrochloride vs placebo to prevent recurrent staphylococcal skin infections [12].
• The commonest antibiotic used was clindamycin, and chronic osteomyelitis did not develop in patients treated with this antibiotic, whereas all 9 patients who had chronic sequelae necessitating sequestrectomy had received cloxacillin either alone or in combination with another antibiotic [13].
• Therapy with clindamycin plus tobramycin produced an adequate short-term clinical response in 16 of 19 patients, although patients with severe salpingitis at laparoscopy responded slowly [14].

Biological context of Clindamycin hydrochloride

• Potentiation of opsonization and phagocytosis of Streptococcus pyogenes following growth in the presence of clindamycin [15].
• INTERPRETATION: Treatment of asymptomatic abnormal vaginal flora and bacterial vaginosis with oral clindamycin early in the second trimester significantly reduces the rate of late miscarriage and spontaneous preterm birth in a general obstetric population [16].
• Therefore, the pharmacokinetics and serum bactericidal activities of ciprofloxacin in combination with clindamycin or metronidazole were investigated using a randomized crossover study design in 10 healthy volunteers [17].
• Comparison of the tiamulin binding site with other PTC targeting drugs, like chloramphenicol, clindamycin and streptogramins, may facilitate the design of modified or hybridized drugs that extend the applicability of this class of antibiotics [18].
• Prothrombin time (PT) prolongation occurred more frequently in patients given moxalactam (19 of 47 patients) than in patients given the combination of tobramycin and clindamycin (9 of 47 patients) (p less than 0.05) [19].

Anatomical context of Clindamycin hydrochloride

• Ribosomes encoded by these genes are predicted to be sensitive to the lincosamide/macrolide class of antibiotics, and may serve as the functional target for azithromycin, clindamycin, and other protein synthesis inhibitors in Toxoplasma and related parasites [20].
• These studies indicate that clindamycin colitis in rabbits is caused by overgrowth of a clostridial species, which releases a heat-labile toxic protein of mol wt of 45,000 capable of necrosing colonic epithelial cells [21].
• The findings that clindamycin markedly inhibits intestinal water transport and induces net secretion in the ileum may explain the reversible watery diarrhea that many patients experience when treated with clindamycin [22].
• We demonstrated the presence of a toxic substance(s) in the feces of hamsters developing clindamycin-induced enterocolitis [23].
• Cell-free, sterile filtrates of cecal contents of rabbits with clindamycin colitis contained a toxin that was lethal for mice and cytotoxic for HeLa-cell monolayers [21].

Associations of Clindamycin hydrochloride with other chemical compounds

• At the same time there was a significant increase in the percentage of isolates resistant to erythromycin, clindamycin, ciprofloxacin, gentamicin, trimethoprim, and rifampicin (p < 0.001 for each)-resistance characteristics often seen in MRSA [24].
• FINDINGS: TCAs of gentamicin and clindamycin with TVA-Bier were significantly higher compared with intravenous or intra-arterial injection [25].
• The mechanism by which clindamycin causes these transport defects is unknown but did not involve the cyclic AMP or cyclic GMP systems, increased mucosal permeability, or alterations of mucosal morphology [22].
• The weak bases chloroquine, ammonium chloride, methylamine, and clindamycin all raised the intralysosomal pH and inhibited neutrophil oxidative metabolism at concentrations ranging from 0.1 to 100 mmol/L [26].
• The biochemical mechanism of lincosaminide inactivation was elucidated by determination of the structure of inactivated lincomycin and clindamycin by physicochemical techniques, including UV absorption spectrophotometry, 31P and 1H nuclear magnetic resonance, and periodate oxidation [27].

Gene context of Clindamycin hydrochloride

• We examined the suppressive effect of clindamycin (CLDM) on CAZ-induced release of endotoxin by cultured E. coli and the subsequent production of inflammatory cytokines (tumor necrosis factor alpha [TNF-alpha] and interleukin-1 beta [IL-1 beta]) [28].
• Proton pump inhibitor treatment of clindamycin-treated mice elevated the gastric pH and facilitated the establishment of colonization of the large intestine by vancomycin-resistant Enterococcus spp [29].
• Here it is shown that the Escherichia coli msbB mutant, which elaborates defective, penta-acylated lipid A, is practically as resistant to a representative set of hydrophobic solutes (rifampin, fusidic acid, erythromycin, clindamycin, and azithromycin) as the parent-type control strain [30].
• Thus, it is concluded that CYP3A4 appears to account for the largest proportion of the observed P450 catalytic clindamycin S-oxidase activity in vitro, and this activity may be extrapolated to the in vivo condition [31].
• Of the P450 enzymes examined, only the activity of CYP3A4 was inhibited (approximately 26%) by coincubation with clindamycin (100 microM) [31].

Analytical, diagnostic and therapeutic context of Clindamycin hydrochloride

• METHODS: Case-control studies were performed at three of the four hospitals to assess the relation of the use of clindamycin to C. difficile-associated diarrhea [1].
• The pathophysiology of antibiotic-associated colitis was studied in rabbits with severe ileocolitis induced by oral administration of clindamycin [21].
• Perfusion with clindamycin altered intestinal water and electrolyte transport in a dose-related manner [22].
• These effects were not seen with intraperitoneal injection of clindamycin or endotoxin, only small amounts of which were present in the filtrate [23].
• Passive immunization against clostridial toxins was protective against clindamycin-associated colitis in this model [32].

References