Clarithromycin. Medical search

A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.

Substances that reduce the growth or reproduction of BACTERIA.

A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.

A semi-synthetic macrolide antibiotic structurally related to ERYTHROMYCIN. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis.

A spiral bacterium active as a human gastric pathogen. It is a gram-negative, urease-positive, curved or slightly spiral organism initially isolated in 1982 from patients with lesions of gastritis or peptic ulcers in Western Australia. Helicobacter pylori was originally classified in the genus CAMPYLOBACTER, but RNA sequencing, cellular fatty acid profiles, growth patterns, and other taxonomic characteristics indicate that the micro-organism should be included in the genus HELICOBACTER. It has been officially transferred to Helicobacter gen. nov. (see Int J Syst Bacteriol 1989 Oct;39(4):297-405).

Infections with organisms of the genus HELICOBACTER, particularly, in humans, HELICOBACTER PYLORI. The clinical manifestations are focused in the stomach, usually the gastric mucosa and antrum, and the upper duodenum. This infection plays a major role in the pathogenesis of type B gastritis and peptic ulcer disease.

A nitroimidazole used to treat AMEBIASIS; VAGINITIS; TRICHOMONAS INFECTIONS; GIARDIASIS; ANAEROBIC BACTERIA; and TREPONEMAL INFECTIONS. It has also been proposed as a radiation sensitizer for hypoxic cells. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985, p133), this substance may reasonably be anticipated to be a carcinogen (Merck, 11th ed).

A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.

Semisynthetic derivative of erythromycin. It is concentrated by human phagocytes and is bioactive intracellularly. While the drug is active against a wide spectrum of pathogens, it is particularly effective in the treatment of respiratory and genital tract infections.

A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.

Various agents with different action mechanisms used to treat or ameliorate PEPTIC ULCER or irritation of the gastrointestinal tract. This has included ANTIBIOTICS to treat HELICOBACTER INFECTIONS; HISTAMINE H2 ANTAGONISTS to reduce GASTRIC ACID secretion; and ANTACIDS for symptomatic relief.

Therapy with two or more separate preparations given for a combined effect.

Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).

Compounds that contain benzimidazole joined to a 2-methylpyridine via a sulfoxide linkage. Several of the compounds in this class are ANTI-ULCER AGENTS that act by inhibiting the POTASSIUM HYDROGEN ATPASE found in the PROTON PUMP of GASTRIC PARIETAL CELLS.

A broad-spectrum antibiotic that is being used as prophylaxis against disseminated Mycobacterium avium complex infection in HIV-positive patients.

A metallic element that has the atomic symbol Bi, atomic number 83 and atomic weight 208.98.

Compounds based on ERYTHROMYCIN with the 3-cladinose replaced by a ketone. They bind the 23S part of 70S bacterial RIBOSOMES.

A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.

A group of often glycosylated macrocyclic compounds formed by chain extension of multiple PROPIONATES cyclized into a large (typically 12, 14, or 16)-membered lactone. Macrolides belong to the POLYKETIDES class of natural products, and many members exhibit ANTIBIOTIC properties.

A nontuberculous infection when occurring in humans. It is characterized by pulmonary disease, lymphadenitis in children, and systemic disease in AIDS patients. Mycobacterium avium-intracellulare infection of birds and swine results in tuberculosis.

A complex that includes several strains of M. avium. M. intracellulare is not easily distinguished from M. avium and therefore is included in the complex. These organisms are most frequently found in pulmonary secretions from persons with a tuberculous-like mycobacteriosis. Strains of this complex have also been associated with childhood lymphadenitis and AIDS; M. avium alone causes tuberculosis in a variety of birds and other animals, including pigs.

Constituent of 50S subunit of prokaryotic ribosomes containing about 3200 nucleotides. 23S rRNA is involved in the initiation of polypeptide synthesis.

A nitroimidazole antitrichomonal agent effective against Trichomonas vaginalis, Entamoeba histolytica, and Giardia lamblia infections.

An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863)

A group of antibiotics that contain 6-aminopenicillanic acid with a side chain attached to the 6-amino group. The penicillin nucleus is the chief structural requirement for biological activity. The side-chain structure determines many of the antibacterial and pharmacological characteristics. (Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1065)

A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers.

The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).

A bacterium causing tuberculosis in domestic fowl and other birds. In pigs, it may cause localized and sometimes disseminated disease. The organism occurs occasionally in sheep and cattle. It should be distinguished from the M. avium complex, which infects primarily humans.

Compounds that inhibit H(+)-K(+)-EXCHANGING ATPASE. They are used as ANTI-ULCER AGENTS and sometimes in place of HISTAMINE H2 ANTAGONISTS for GASTROESOPHAGEAL REFLUX.

The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).

Ulcer that occurs in the regions of the GASTROINTESTINAL TRACT which come into contact with GASTRIC JUICE containing PEPSIN and GASTRIC ACID. It occurs when there are defects in the MUCOSA barrier. The common forms of peptic ulcers are associated with HELICOBACTER PYLORI and the consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).

A PEPTIC ULCER located in the DUODENUM.

Impaired digestion, especially after eating.

Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection.

Organic compounds that have the general formula R-SO-R. They are obtained by oxidation of mercaptans (analogous to the ketones). (From Hackh's Chemical Dictionary, 4th ed)

A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.

The L-isomer of Ofloxacin.

A macrolide antibiotic from Streptomyces narbonensis. The drug has antimicrobial activity against a wide spectrum of pathogens.

Infections with nontuberculous mycobacteria (atypical mycobacteria): M. kansasii, M. marinum, M. scrofulaceum, M. flavescens, M. gordonae, M. obuense, M. gilvum, M. duvali, M. szulgai, M. intracellulare (see MYCOBACTERIUM AVIUM COMPLEX;), M. xenopi (littorale), M. ulcerans, M. buruli, M. terrae, M. fortuitum (minetti, giae), M. chelonae.

A fat-soluble riminophenazine dye used for the treatment of leprosy. It has been used investigationally in combination with other antimycobacterial drugs to treat Mycobacterium avium infections in AIDS patients. Clofazimine also has a marked anti-inflammatory effect and is given to control the leprosy reaction, erythema nodosum leprosum. (From AMA Drug Evaluations Annual, 1993, p1619)

A 4-(3-methoxypropoxy)-3-methylpyridinyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.

The action of a drug that may affect the activity, metabolism, or toxicity of another drug.

A group of QUINOLONES with at least one fluorine atom and a piperazinyl group.

A nitrofuran derivative with antiprotozoal and antibacterial activity. Furazolidone acts by gradual inhibition of monoamine oxidase. (From Martindale, The Extra Pharmacopoeia, 30th ed, p514)

A group of ANTI-BACTERIAL AGENTS characterized by a chromophoric naphthohydroquinone group spanned by an aliphatic bridge not previously found in other known ANTI-BACTERIAL AGENTS. They have been isolated from fermentation broths of Streptomyces mediterranei.

Any tests done on exhaled air.

Substances obtained from various species of microorganisms that are, alone or in combination with other agents, of use in treating various forms of tuberculosis; most of these agents are merely bacteriostatic, induce resistance in the organisms, and may be toxic.

Agents used to treat trichomonas infections.

A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.

Infections with bacteria of the genus MYCOBACTERIUM.

A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)

A species of HAEMOPHILUS found on the mucous membranes of humans and a variety of animals. The species is further divided into biotypes I through VIII.

A genus of gram-positive, aerobic bacteria. Most species are free-living in soil and water, but the major habitat for some is the diseased tissue of warm-blooded hosts.

A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.

Compounds with a BENZENE fused to IMIDAZOLES.

A fixed-ratio combination of amoxicillin trihydrate and potassium clavulanate.

A gram-positive organism found in the upper respiratory tract, inflammatory exudates, and various body fluids of normal and/or diseased humans and, rarely, domestic animals.

The giving of drugs, chemicals, or other substances by mouth.

A species of gram-positive, aerobic bacteria commonly found in soil and occasionally isolated from sputum. It causes postoperative wound infections as well as gluteal abscesses.

A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.

A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.

So-called atypical species of the genus MYCOBACTERIUM that do not cause tuberculosis. They are also called tuberculoid bacilli, i.e.: M. buruli, M. chelonae, M. duvalii, M. flavescens, M. fortuitum, M. gilvum, M. gordonae, M. intracellulare (see MYCOBACTERIUM AVIUM COMPLEX;), M. kansasii, M. marinum, M. obuense, M. scrofulaceum, M. szulgai, M. terrae, M. ulcerans, M. xenopi.

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Enumeration by direct count of viable, isolated bacterial, archaeal, or fungal CELLS or SPORES capable of growth on solid CULTURE MEDIA. The method is used routinely by environmental microbiologists for quantifying organisms in AIR; FOOD; and WATER; by clinicians for measuring patients' microbial load; and in antimicrobial drug testing.

A broad-spectrum antimicrobial carboxyfluoroquinoline.

A rapid-growing, nonphotochromogenic species that is potentially pathogenic, producing lesions of lung, bone, or soft tissue following trauma. It has been found in soil and in injection sites of humans, cattle, and cold-blooded animals. (Dorland, 28th ed)

A slow-growing, scotochromogenic species occurring usually harmlessly in human secretions but occasionally associated with chronic pulmonary disease. (Dorland, 28th ed)

An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the ESOPHAGUS and the beginning of the DUODENUM.

A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.

Drugs used in the treatment of tuberculosis. They are divided into two main classes: "first-line" agents, those with the greatest efficacy and acceptable degrees of toxicity used successfully in the great majority of cases; and "second-line" drugs used in drug-resistant cases or those in which some other patient-related condition has compromised the effectiveness of primary therapy.

Inflammation of the GASTRIC MUCOSA, a lesion observed in a number of unrelated disorders.

A species of CHLAMYDOPHILA that causes acute respiratory infection, especially atypical pneumonia, in humans, horses, and koalas.

The ability of bacteria to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).

Mucins that are found on the surface of the gastric epithelium. They play a role in protecting the epithelial layer from mechanical and chemical damage.

A statistical means of summarizing information from a series of measurements on one individual. It is frequently used in clinical pharmacology where the AUC from serum levels can be interpreted as the total uptake of whatever has been administered. As a plot of the concentration of a drug against time, after a single dose of medicine, producing a standard shape curve, it is a means of comparing the bioavailability of the same drug made by different companies. (From Winslade, Dictionary of Clinical Research, 1992)

A slow-growing, photochromogenic species that is the etiologic agent of a tuberculosis-like disease in humans and is frequently isolated from human pulmonary secretions or tubercles. The incidence of infection is sharply increased among immunocompromised individuals. (Dorland, 28th ed)

A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.

Successful short-term suppression of clarithromycin-resistant Mycobacterium avium complex bacteremia in AIDS. California Collaborative Treatment Group. (1/1145)

During a randomized study of clarithromycin plus clofazimine with or without ethambutol in patients with AIDS and Mycobacterium avium complex (MAC) bacteremia, eight participants received additional antimycobacterial drugs following the detection of a clarithromycin-resistant isolate (MIC, > 8 micrograms/mL). A macrolide (seven received clarithromycin, one azithromycin) and clofazimine were continued; additional treatment included various combinations of ethambutol, ciprofloxacin, amikacin, and rifabutin. After the detection of a resistant isolate and before receipt of additional antimycobacterials, the median peak MAC colony count in blood was 105 cfu/mL (range, 8-81,500 cfu/mL). After additional antimycobacterials, the median nadir MAC colony count was 5 cfu/mL (range, 0-110 cfu/mL). Five (63%) of eight patients had a > or = 1 log10 decrease, including two who achieved negative blood cultures; all of these responses occurred in patients originally assigned to clarithromycin plus clofazimine. Treatment of clarithromycin-resistant MAC bacteremia that emerges during clarithromycin-based treatment can decrease levels of bacteremia and transiently sterilize blood cultures. (+info)

Multiplex sequence analysis demonstrates the competitive growth advantage of the A-to-G mutants of clarithromycin-resistant Helicobacter pylori. (2/1145)

Clarithromycin resistance in Helicobacter pylori is due to point mutation within the 23S rRNA. We examined the growth rates of different types of site-directed mutants and demonstrated quantitatively the competitive growth advantage of A-to-G mutants over other types of mutants by a multiplex sequencing assay. The results provide a rational explanation of why A-to-G mutants are predominantly observed among clarithromycin-resistant clinical isolates. (+info)

Direct detection of Helicobacter pylori resistance to macrolides by a polymerase chain reaction/DNA enzyme immunoassay in gastric biopsy specimens. (3/1145)

BACKGROUND: The increasing use of macrolides especially in the treatment of Helicobacter pylori infection has led to an increase in resistant strains. The resistance of H pylori to macrolides, especially clarithromycin, is one of the major causes of eradication failure. In H pylori, clarithromycin resistance is due to point mutations localised in domain V of 23S rRNA. AIM: To develop a molecular technique based on amplification of a relevant fragment of the 23S rRNA and colorimetric hybridisation in liquid phase to detect directly in biopsy specimens the type of mutation associated with resistance of H pylori to clarithromycin. METHODS: Gastric biopsy samples from 61 patients were submitted to this test. The results were compared with standard methods (determination of minimal inhibition concentration, polymerase chain reaction/restriction fragment length polymorphism, and/or DNA sequencing) in order to evaluate the test and to define the cut off values, specificity, and sensitivity. RESULTS: The 14 biopsy samples in which H pylori was not detected did not give a positive result in any assay, and the 14 samples harbouring strains susceptible to clarithromycin gave a positive result with the wild type probe as expected. The 33 biopsy specimens containing resistant strains always gave a positive signal with one of the probes detecting resistant organisms, but in eight cases they also reacted with the wild type probe, indicating that a mixture of resistant and susceptible organisms was present. CONCLUSION: The importance of this new assay is that it allows the detection of multiple genotypes corresponding to either heterogeneous genotypes or mixed infections. Moreover, it allows in a single step not only the detection of H pylori but also the determination of its susceptibility to clarithromycin directly in biopsy specimens without the need for culture. (+info)

Eradication of Helicobacter pylori in functional dyspepsia: randomised double blind placebo controlled trial with 12 months' follow up. The Optimal Regimen Cures Helicobacter Induced Dyspepsia (ORCHID) Study Group. (4/1145)

OBJECTIVES: To determine whether eradication of Helicobacter pylori relieves the symptoms of functional dyspepsia. DESIGN: Multicentre randomised double blind placebo controlled trial. SUBJECTS: 278 patients infected with H pylori who had functional dyspepsia. SETTING: Predominantly secondary care centres in Australia, New Zealand, and Europe. INTERVENTION: Patients randomised to receive omeprazole 20 mg twice daily, amoxicillin 1000 mg twice daily, and clarithromycin 500 mg twice daily or placebo for 7 days. Patients were followed up for 12 months. MAIN OUTCOME MEASURES: Symptom status (assessed by diary cards) and presence of H pylori (assessed by gastric biopsies and 13C-urea breath testing using urea labelled with carbon-13). RESULTS: H pylori was eradicated in 113 patients (85%) in the treatment group and 6 patients (4%) in the placebo group. At 12 months follow up there was no significant difference between the proportion of patients treated successfully by intention to treat in the eradication arm (24%, 95% confidence interval 17% to 32%) and the proportion of patients treated successfully by intention to treat in the placebo group (22%, 15% to 30%). Changes in symptom scores and quality of life did not significantly differ between the treatment and placebo groups. When the groups were combined, there was a significant association between treatment success and chronic gastritis score at 12 months; 41/127 (32%) patients with no or mild gastritis were successfully treated compared with 21/123 (17%) patients with persistent gastritis (P=0. 008). CONCLUSION: No convincing evidence was found that eradication of H pylori relieves the symptoms of functional dyspepsia 12 months after treatment. (+info)

Altered expression profile of the surface glycopeptidolipids in drug-resistant clinical isolates of Mycobacterium avium complex. (5/1145)

Members of the Mycobacterium avium complex are the most frequently encountered opportunistic bacterial pathogens among patients in the advanced stage of AIDS. Two clinical isolates of the same strain, numbers 397 and 417, were obtained from an AIDS patient with disseminated M. avium complex infection before and after treatment with a regimen of clarithromycin and ethambutol. To identify the biochemical consequence of drug treatment, the expression and chemical composition of their major cell wall constituents, the arabinogalactan, lipoarabinomannan, and the surface glycopeptidolipids (GPL), were critically examined. Through thin layer chromatography, mass spectrometry, and chemical analysis, it was found that the GPL expression profiles differ significantly in that several apolar GPLs were overexpressed in the clinically resistant 417 isolate at the expense of the serotype 1 polar GPL, which was the single predominant band in the ethambutol-susceptible 397 isolate. Thus, instead of additional rhamnosylation on the 6-deoxytalose (6-dTal) appendage to give the serotype 1-specific disaccharide hapten, the accumulation of this nonextended apolar GPL probably provided more precursor substrate available for further nonsaccharide substitutions including a higher degree of O-methylation to give 3-O-Me-6-dTal and the unusual 4-O-sulfation on 6-dTal. Further data showed that this alteration effectively neutralized ethambutol, which is known to inhibit arabinan synthesis. Thus, in contrast with derived Emb-resistant mutants of Mycobacterium smegmatis or Mycobacterium tuberculosis, which are devoid of a surface GPL layer, the lipoarabinomannan from resistant 417 isolate grown in the presence of this drug was not apparently truncated. (+info)

Treatment of Helicobacter pylori and Chlamydia pneumoniae infections decreases fibrinogen plasma level in patients with ischemic heart disease. (6/1145)

BACKGROUND: Chronic Chlamydia pneumoniae and Helicobacter pylori infections could be a risk factor for ischemic heart disease (IHD), possibly by increasing fibrinogen levels. The aim of our study was to evaluate changes in fibrinogen level in patients with IHD and H pylori and/or C pneumoniae positivity randomly assigned to antibiotic treatment. METHODS AND RESULTS: Eighty-four patients with chronic IHD, H pylori and/or C pneumoniae antibodies, and normal acute-phase reactants were randomly assigned to treatment or no treatment. Treatment consisted of omeprazole, clarithromycin, and tinidazole in H pylori-positive patients and clarithromycin alone in C pneumoniae-positive patients. The effect of treatment and other baseline variables on fibrinogen levels, determined at 6 months, was evaluated by multivariate analysis. Treatment significantly reduced fibrinogen level at 6 months in the overall study population and in the groups of patients divided according to H pylori or C pneumoniae positivity. In the 43 treated patients, mean (+/-SD) basal fibrinogen was 3.65+/-0.58 g/L, and mean final fibrinogen was 3. 09+/-0.52 g/dL (P<0.001), whereas in the 41 untreated patients, mean basal and final fibrinogen levels were 3.45+/-0.70 and 3.61+/-0.71 g/L, respectively. The largest decrease was observed in patients with both infections. Fibrinogen changes were also significantly and negatively correlated with age. CONCLUSIONS: Our data suggest that a short, safe, and effective course of antibiotic therapy might be suggested as a means of interacting with an "emerging" risk factor. (+info)

Ranitidine bismuth citrate, tetracycline, clarithromycin twice-a-day triple therapy for clarithromycin susceptible Helicobacter pylori infection. (7/1145)

BACKGROUND: Although many combination therapies have been proposed, there is still interest in identifying simple, inexpensive, effective protocols that have high rates of success. AIM: To investigate the role of the new soluble form of bismuth, ranitidine bismuth citrate, in twice-a-day therapy for Helicobacter pylori infection. METHODS: Patients with histologically and culture proven H. pylori infection received ranitidine bismuth citrate 400 mg, tetracycline HCl 500 mg, and clarithromycin 500 mg, each b.d. for 14 days, followed by 300 mg ranitidine once a day for 4 additional weeks. Outcome was assessed 4 or more weeks after the end of antimicrobial therapy by repeat endoscopy with histology and culture (49 patients) or urea breath testing (14 patients). RESULTS: Sixty-three patients completed the therapy, 59 men and four women (average age 56.7 years; range 31-75 years). All patients had clarithromycin-susceptible strains prior to therapy. H. pylori infection was cured in 94% (95% CI: 85-98%). There was a therapy failure in one patient who took the medicine for only 1 day and stopped because of side-effects. Three of the isolates from treatment failures were available post-failure; two were clarithromycin-resistant and one was susceptible. Side-effects were severe in two patients (3%) and moderate in three (primarily diarrhoea). CONCLUSIONS: Twice-a-day ranitidine bismuth citrate, tetracycline, clarithromycin triple therapy was well tolerated and effective for the treatment of H. pylori infection in patients with clarithromycin-susceptible H. pylori. (+info)

The DU-MACH study: eradication of Helicobacter pylori and ulcer healing in patients with acute duodenal ulcer using omeprazole based triple therapy. (8/1145)

AIM: To investigate the efficacy of two omeprazole triple therapies for the eradication of Helicobacter pylori, ulcer healing and ulcer relapse during a 6-month treatment-free period in patients with active duodenal ulcer. METHODS: This was a double-blind, randomized study in 15 centres across Canada. Patients (n = 149) were randomized to omeprazole 20 mg once daily (O) or one of two 1-week b. d. eradication regimens: omeprazole 20 mg, metronidazole 400 mg and clarithromycin 250 mg (OMC) or omeprazole 20 mg, amoxycillin 1000 mg and clarithromycin 500 mg (OAC). All patients were treated for three additional weeks with omeprazole 20 mg once daily. Ulcer healing was assessed by endoscopy after 4 weeks of study therapy. H. pylori eradication was determined by a 13C-urea breath test and histology, performed at pre-entry, at 4 weeks after the end of all therapy and at 6 months. RESULTS: The intention-to-treat (intention-to-treat) analysis contained 146 patients and the per protocol (per protocol) analysis, 114 patients. The eradication rates were (intention-to-treat/per protocol): OMC-85% and 92%, OAC-78% and 87% and O-0% (O). Ulcer healing (intention-to-treat) was greater than 90% in all groups. The differences in the eradication and relapse rates between O vs. OMC and O vs. OAC were statistically significant (all, P < 0.001). Treatment was well tolerated and compliance was high. CONCLUSION: The OMC and OAC 1-week treatment regimens are safe and effective for eradication, healing and the prevention of relapse in duodenal ulcer patients. (+info)

1. Gastritis: Inflammation of the stomach lining, which can be acute or chronic.
2. Peptic ulcer disease: Ulcers in the stomach or duodenum (the first part of the small intestine) that are caused by H. pylori infection.
3. Gastric adenocarcinoma: A type of stomach cancer that is associated with long-term H. pylori infection.
4. Mucosa-associated lymphoid tissue (MALT) lymphoma: A rare type of cancer that affects the immune cells in the stomach and small intestine.
5. Gastroesophageal reflux disease (GERD): A condition in which stomach acid flows back up into the esophagus, causing symptoms such as heartburn and regurgitation.
6. Helicobacter pylori-associated chronic atrophic gastritis: A type of chronic inflammation of the stomach lining that can lead to stomach ulcers and stomach cancer.
7. Post-infectious irritable bowel syndrome (PI-IBS): A condition that develops after a gastrointestinal infection, characterized by persistent symptoms such as abdominal pain, bloating, and changes in bowel habits.

Helicobacter infections are typically diagnosed through endoscopy, where a flexible tube with a camera and light on the end is inserted into the stomach and small intestine to visualize the mucosa and look for signs of inflammation or ulcers. Laboratory tests such as breath tests and stool tests may also be used to detect the presence of H. pylori bacteria in the body. Treatment typically involves a combination of antibiotics and acid-suppressing medications to eradicate the infection and reduce symptoms.

Preventing Helicobacter Infections:

While it is not possible to completely prevent Helicobacter infections, there are several measures that can be taken to reduce the risk of developing these conditions:

1. Practice good hygiene: Wash your hands regularly, especially before eating and after using the bathroom.
2. Avoid close contact with people who have Helicobacter infections.
3. Avoid sharing food, drinks, or utensils with people who have Helicobacter infections.
4. Avoid consuming undercooked meat, especially pork and lamb.
5. Avoid consuming raw shellfish, especially oysters.
6. Avoid consuming unpasteurized dairy products.
7. Avoid alcohol and caffeine, which can irritate the stomach lining and increase the risk of developing Helicobacter infections.
8. Maintain a healthy diet that is high in fiber and low in fat.
9. Manage stress, as stress can exacerbate symptoms of Helicobacter infections.
10. Practice good oral hygiene to prevent gum disease and other oral infections that can increase the risk of developing Helicobacter infections.

Conclusion:

Helicobacter infections are a common cause of stomach ulcers, gastritis, and other gastrointestinal disorders. These infections are caused by the bacteria Helicobacter pylori, which can be found in the stomach lining and small intestine. While these infections can be difficult to diagnose, a combination of endoscopy, blood tests, and stool tests can help confirm the presence of Helicobacter bacteria. Treatment typically involves a combination of antibiotics and acid-suppressing medications to eradicate the infection and reduce symptoms. Preventive measures include practicing good hygiene, avoiding close contact with people who have Helicobacter infections, and maintaining a healthy diet.

The symptoms of MAC infection can vary depending on the severity of the infection and may include:

* Chronic cough
* Fatigue
* Weight loss
* Night sweats
* Chest pain
* Shortness of breath

MAC infections can affect various parts of the body, including the lungs, liver, spleen, and lymph nodes. The infection can be diagnosed through a variety of tests, such as chest X-rays, CT scans, blood tests, and lung biopsies.

Treatment for MAC infections typically involves a combination of antibiotics and supportive care to manage symptoms. The choice of antibiotics depends on the severity of the infection and the individual's medical history and health status. Surgical intervention may be necessary in some cases, such as when the infection is severe or has spread to other parts of the body.

Preventive measures for MAC infections include avoiding exposure to contaminated water or soil, maintaining good hand hygiene, and avoiding close contact with individuals who have compromised immune systems. Vaccines are not available for MAC infections, but ongoing research is exploring the development of vaccines to prevent these types of infections.

Overall, Mycobacterium avium-intracellulare infection is a serious and potentially life-threatening condition that requires prompt diagnosis and treatment by a healthcare professional. With appropriate management, individuals with MAC infections can experience significant improvement in their symptoms and quality of life.

A peptic ulcer is a break in the lining of the stomach or duodenum (the first part of the small intestine), which can cause pain and bleeding. The stomach acid and digestive enzymes flowing through the ulcer can irritate the surrounding tissue, leading to inflammation and discomfort.

Peptic ulcers are commonly caused by an infection with Helicobacter pylori (H. pylori) bacteria or long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or aspirin. Other contributing factors include stress, smoking, and excessive alcohol consumption.

Symptoms of a peptic ulcer may include abdominal pain, nausea, vomiting, and loss of appetite. Treatment options typically involve antibiotics to eradicate H. pylori infection or stopping NSAID use, along with medications to reduce acid production in the stomach and protect the ulcer from further damage. Surgery may be necessary for severe cases or if other treatments fail.

Prevention methods include avoiding NSAIDs, maintaining a healthy lifestyle, managing stress, and getting regular screenings for H. pylori infection. Early detection and proper treatment can help alleviate symptoms and prevent complications such as ulcer perforation or bleeding.

In summary, peptic ulcers are painful and potentially harmful conditions that can be caused by various factors. Proper diagnosis and treatment are essential to prevent complications and improve quality of life.

The main causes of duodenal ulcers are:

1. Infection with the bacterium Helicobacter pylori (H. pylori)
2. Overuse of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen
3. Excessive alcohol consumption
4. Smoking
5. Zollinger-Ellison syndrome, a rare condition that causes the stomach to produce too much acid

Symptoms of duodenal ulcers may include:

1. Abdominal pain, which can be worse when eating or at night
2. Nausea and vomiting
3. Bloating and gas
4. Acid reflux
5. Weight loss

Diagnosis of a duodenal ulcer typically involves a combination of endoscopy, where a flexible tube with a camera is inserted through the mouth to visualize the inside of the digestive tract, and breath tests to detect H. pylori infection.

Treatment for duodenal ulcers usually involves eradication of H. pylori infection, if present, and avoidance of NSAIDs and other irritants. Antacids or acid-suppressing medications may also be prescribed to help reduce symptoms and allow the ulcer to heal. In severe cases, surgery may be necessary.

Prevention of duodenal ulcers includes:

1. Avoiding NSAIDs and other irritants
2. Eradicating H. pylori infection
3. Quitting smoking and excessive alcohol consumption
4. Managing stress
5. Eating a healthy diet with plenty of fruits, vegetables, and whole grains

Prognosis for duodenal ulcers is generally good if treated promptly and effectively. However, complications such as bleeding, perforation, and obstruction can be serious and potentially life-threatening. It is important to seek medical attention if symptoms persist or worsen over time.

In conclusion, duodenal ulcers are a common condition that can cause significant discomfort and disrupt daily life. While they can be caused by a variety of factors, H. pylori infection is the most common underlying cause. Treatment typically involves eradication of H. pylori infection, avoidance of NSAIDs and other irritants, and management of symptoms with antacids or acid-suppressing medications. Prevention includes avoiding risk factors and managing stress. With prompt and effective treatment, the prognosis for duodenal ulcers is generally good. However, complications can be serious and potentially life-threatening, so it is important to seek medical attention if symptoms persist or worsen over time.

Dyspepsia is not a specific disease but rather a symptom complex that can be caused by a variety of factors, such as:

1. Gastritis (inflammation of the stomach lining)
2. Peptic ulcer
3. Gastroesophageal reflux disease (GERD)
4. Functional dyspepsia
5. Inflammatory conditions such as Crohn's disease or ulcerative colitis
6. Food allergies or intolerances
7. Hormonal changes during pregnancy or menstruation
8. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics

The diagnosis of dyspepsia is based on a combination of medical history, physical examination, and diagnostic tests such as endoscopy, gastric emptying studies, and blood tests. Treatment depends on the underlying cause of dyspepsia and may include medications, lifestyle changes, and dietary modifications.

Some common types of NTM infections include:

* Lung infections
* Skin infections
* Bone and joint infections
* Heart valve infections
* Cystic fibrosis-related infections
* Infections in people with weakened immune systems

NTM infections can be caused by a variety of bacteria, including Mycobacterium avium complex, Mycobacterium intracellulare, and Mycobacterium chelonae. These bacteria are commonly found in soil and water, and they can enter the body through cuts or open wounds, or by being inhaled into the lungs.

Symptoms of NTM infections may include:

* Coughing
* Fever
* Chest pain or discomfort
* Shortness of breath
* Fatigue
* Skin lesions or ulcers

Diagnosis of an NTM infection is typically made through a combination of physical examination, medical history, and laboratory tests, such as cultures or PCR (polymerase chain reaction) tests. Treatment may involve antibiotics, surgery, or a combination of both, depending on the severity and location of the infection.

Preventive measures for NTM infections are not well established, but people with weakened immune systems or those who live in areas with high levels of NTM bacteria in the environment may be advised to take precautions such as avoiding contact with soil and water, wearing protective clothing and gloves when working with soil or water, and practicing good hygiene.

Types of Mycobacterium Infections:

1. Tuberculosis (TB): This is the most common Mycobacterium infection and is caused by the bacteria Mycobacterium tuberculosis. It primarily affects the lungs, but can also affect other parts of the body such as the brain, kidneys, and spine.
2. Leprosy: This is a chronic infection caused by the bacteria Mycobacterium leprae, which primarily affects the skin, nerves, and mucous membranes. It is also known as Hansen's disease.
3. Buruli ulcer: This is a skin infection caused by the bacteria Mycobacterium ulcerans, which is found in wet environments such as rivers, lakes, and swamps.
4. Mycobacterium avium complex (MAC): This is a group of bacteria that can cause a variety of diseases, including lung disease, disseminated disease, and cardiovascular disease.
5. Mycobacterium abscessus: This is a type of bacteria that can cause skin and soft tissue infections, as well as respiratory and disseminated diseases.

Symptoms of Mycobacterium Infections:

The symptoms of Mycobacterium infections can vary depending on the type of infection and the severity of the disease. Some common symptoms include:

* Coughing or difficulty breathing (in TB infections)
* Skin lesions or ulcers (in leprosy and Buruli ulcer)
* Fever, chills, and fatigue (in all types of Mycobacterium infections)
* Swollen lymph nodes (in all types of Mycobacterium infections)
* Joint pain or swelling (in some cases)
* Weight loss and loss of appetite (in severe cases)

Diagnosis of Mycobacterium Infections:

Diagnosing a Mycobacterium infection can be challenging, as the bacteria are slow-growing and require specialized culture techniques. Some common methods for diagnosing Mycobacterium infections include:

* Skin scrapings or biopsies (for leprosy and Buruli ulcer)
* Sputum or lung biopsy (for TB)
* Blood tests (for disseminated disease)
* Imaging studies such as X-rays, CT scans, or MRI scans (to evaluate the extent of the infection)

Treatment of Mycobacterium Infections:

The treatment of Mycobacterium infections depends on the type of infection and the severity of the disease. Some common treatments include:

* Antibiotics: For TB, the standard treatment is a combination of rifampin, isoniazid, pyrazinamide, and ethambutol for at least 6 months. For leprosy, the standard treatment is a combination of rifampin, dapsone, and clofazimine for at least 12 months.
* Surgery: For Buruli ulcer, surgical debridement of the affected skin and tissue is often necessary.
* Supportive care: Patients with severe forms of the disease may require hospitalization and supportive care, such as oxygen therapy, fluid replacement, and wound care.

Prevention of Mycobacterium Infections:

Preventing the spread of Mycobacterium infections is crucial for controlling these diseases. Some common prevention measures include:

* Vaccination: For TB, vaccination with the BCG vaccine is recommended for infants and young children in high-risk areas.
* Screening: Screening for TB and leprosy is important for early detection and treatment of cases.
* Contact tracing: Identifying and testing individuals who have been in close contact with someone who has been diagnosed with TB or leprosy can help prevent the spread of the disease.
* Infection control measures: Healthcare workers should follow strict infection control measures when caring for patients with Mycobacterium infections to prevent transmission to others.
* Avoiding close contact with people who are sick: Avoiding close contact with people who are sick with TB or leprosy can help prevent the spread of the disease.
* Covering mouth and nose when coughing or sneezing: Covering the mouth and nose when coughing or sneezing can help prevent the spread of TB bacteria.
* Properly disposing of contaminated materials: Properly disposing of contaminated materials, such as used tissues and surfaces soiled with respiratory secretions, can help prevent the spread of TB bacteria.

It is important to note that while these measures can help control the spread of Mycobacterium infections, they are not foolproof and should be combined with other prevention measures, such as early detection and treatment of cases, to effectively control these diseases.

Symptoms of gastritis may include abdominal pain, nausea, vomiting, loss of appetite, and difficulty swallowing. In severe cases, bleeding may occur in the stomach and black tarry stools may be present.

Diagnosis of gastritis is typically made through endoscopy, during which a flexible tube with a camera and light on the end is inserted through the mouth to visualize the inside of the stomach. Biopsies may also be taken during this procedure to examine the stomach tissue under a microscope for signs of inflammation or infection.

Treatment of gastritis depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, and lifestyle modifications such as avoiding alcohol, losing weight, and eating smaller more frequent meals. In severe cases, surgery may be necessary to remove damaged tissue or repair any ulcers that have developed.

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LAS VEGAS, Nevada - Clinicians are prescribing clarithromycin at high rates for Helicobacter pylori infections, despite increasing resistance to this antibiotic, researchers say. (medscape.com)
During a cohort study that examined eradication of Helicobacter pylori by a combination therapy that included clarithromycin, we chose 5 patients in order to study macrolide resistance in S. epidermidis . (cdc.gov)
Clarithromycin is primarily used to treat a number of bacterial infections including pneumonia , Helicobacter pylori , and as an alternative to penicillin in strep throat . (mdwiki.org)
Clarithromycin (in combination with omeprazole or anitidine bismuth citrate) is indicated for the treatment of patients with an active duodenal ulcer associated with Helicobacter pylori infection. (nih.gov)

In an analysis of 1 million US prescriptions for H pylori infections, 80% contained clarithromycin, said Carol Rockett, PharmD, associate vice president of RedHill Biopharma in Raleigh, North Carolina. (medscape.com)
Multiple talks here this week have suggested that the use of clarithromycin in H pylori is obsolete," she told Medscape Medical News . (medscape.com)
In the larger study, all patients were colonized with H. pylori and had either a duodenal or gastric ulcer, for which a 7-day course of clarithromycin 250 mg twice per day (b.i.d.), metronidazole 400 mg b.i.d., and omeprazole 20 mg b.i.d. was given. (cdc.gov)
The aim of this study is to determine the antimicrobial susceptibility pattern for clarithromycin and levofloxacin and find the evolutionary relationship of the partial sequence of 23S rRNA and gyraseA gene of H. pylori by phylogenetic analysis. (who.int)
Materials and Methods: A total of 46 H. pylori strains were tested for clarithromycin and levofloxacin susceptibility pattern and phylogenetic tree were reconstructed by PhyML software. (who.int)
Results: In this study, we observed that only 6.5% of North-East Indian H. pylori strains were resistant for clarithromycin showing mutation at A2143G and T2182C positions of 23S rRNA gene. (who.int)
Conclusions: Resistance for clarithromycin was less in North-East Indian strains but high for levofloxacin indicating that first-line therapy may be best and effective for eradication of H. pylori in this region. (who.int)

If you stop taking clarithromycin too soon, or skip doses, your infection may not be completely treated and the bacteria may become resistant to antibiotics. (medlineplus.gov)
To reduce the development of drug-resistant bacteria and maintain the effectiveness of clarithromycin and other antibacterial drugs, clarithromycin tablets should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria. (nih.gov)
Clarbact (Clarithromycin) is an oral antibiotic used to treat a wide variety of infections caused by bacteria. (4nrx-uk.md)
The body must be allowed to fight the virus take many times throughout the day to fight against the harmful bacteria Clarithromycin overnight Shipping our body. (unblog.fr)
Clarithromycin STELLA 500 mg contains clarithromycin which is a semi-synthetic derivative of erythromycin A. Clarithromycin exerts its antibacterial action by binding to the 50S ribosome sub-unit of susceptible bacteria and suppresses protein synthesis. (stellapharm.com)

Clarithromycin is in a class of medications called macrolide antibiotics. (medlineplus.gov)
Antibiotics such as clarithromycin will not work for colds, flu, or other viral infections. (medlineplus.gov)
treatment usually involves antibiotics such as: Rifampin Ethambutol Clarithromycin Surgery is sometimes used first. (nih.gov)
Hypersensitivity to clarithromycin or any component of the product, erythromycin, or any macrolide antibiotics. (mdwiki.org)
Clarbact (Clarithromycin) should not be administered to patients who are under twelve years old, fructose intolerant, taking other ergot derivatives, allergic to macrolide antibiotics, or who have had a bad reaction to similar treatments in the past. (4nrx-uk.md)
Clarithromycin is a drug that comes under the class of medications called macrolide antibiotics, which is used for treating several bacterial infections, such as pneumonia, bronchitis, infection of ears, sinuses, and throat. (icliniq.com)

Clarithromycin is a semisynthetic macrolide antibiotic used for a wide variety of mild-to-moderate bacterial infections. (nih.gov)
Clarithromycin is a semi-synthetic macrolide antibiotic. (nih.gov)

2023. https://emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/51159/1/clarithromycin. (unboundmedicine.com)

Clarithromycin is used to treat certain bacterial infections, such as pneumonia (a lung infection), bronchitis (infection of the tubes leading to the lungs), and infections of the ears, sinuses, skin, and throat. (medlineplus.gov)
Clarithromycin , sold under the brand name Biaxin among others, is an antibiotic used to treat various bacterial infections. (mdwiki.org)
Clarithromycin is used in the treatment of bacterial infections . (trumachealthcare.net)

Steady-state concentrations of clarithromycin and 14-OH clarithromycin observed following administration of 500 mg doses of clarithromycin every 12 hours to adult patients with HIV infection were similar to those observed in healthy volunteers. (nih.gov)
Clarithromycin is recommended as the primary agent for the treatment of disseminated infection due to MAC. (nih.gov)
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Since YNS is accompanied by chronic bronchial infection in more than half of patients , we hypothesized that treatment with clarithromycin (CAM) could be effective. (bvsalud.org)

[6] Clarithromycin is available as a generic medication. (mdwiki.org)
Apo-Clarithromycin is a preferred generic drug on the Reformulary. (drugfinder.ca)

PrevPac is a brand name for Lansoprazole/Clarithromycin/Amoxicilin. (pharmacyrxworld.com)
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Therefore, clarithromycin tablets may be given without regard to food. (nih.gov)
Clarithromycin tablets and Clarithromycin granules for oral suspension are indicated for the treatment of mild to moderate infections caused by susceptible strains of the designated microorganisms in the following conditions: 1) Pharyngitis/Tonsillitis due to Streptococcus pyrogenes (the usual drug of choice in the treatment and prevention of streptococcal infections and the prophylaxis of rheumatic fever is penicillin administered by either the intramuscular or the oral route. (nih.gov)
Trumac Healthcare is one of the leading Clarithromycin Tablets Manufacturers Suppliers all over India. (trumachealthcare.net)
Apart from Clarithromycin Tablets Manufacturers Suppliers, we at Trumac Healthcare provide range of other products across several divisions. (trumachealthcare.net)

They include updated information on macrolide agents other than erythro- mycin (azithromycin and clarithromycin) and their dosing schedule by age group. (cdc.gov)

From each patient and sample, S. epidermidis strains were isolated and analyzed for clarithromycin susceptibility and presence of the erm (C) gene. (cdc.gov)
This study is the first report that showed antibiotic susceptibility pattern for clarithromycin and levofloxacin by mutation analysis. (who.int)

A proton pump inhibitor take twice a day together with amoxicillin 1000 mg twice daily, clarithromycin 500 mg twice daily in conjunction with tinidazole 500 mg or metronidazole 500 mg twice daily for 14 days. (stellapharm.com)
A proton pump inhibitor take twice a day together with clarithromycin 500 mg twice daily and tinidazole 500 mg twice daily for 5 days. (stellapharm.com)
One drug is a proton pump inhibitor or a bismuth-based drug, the second drug is clarithromycin, and the third drug is amoxicillin or metronidazole. (medscape.com)

Concomitant administration of clarithromycin and any of the following drugs is contraindicated: astemizole, cisapride, pimozide, terfenadine. (stellapharm.com)

Clarithromycin comes as a tablet, an extended-release (long-acting) tablet, and a suspension (liquid) to take by mouth. (medlineplus.gov)
Each clarithromycin tablet intended for oral administration contains 250 mg or 500 mg of clarithromycin. (nih.gov)
The major metabolite found in urine is 14-OH clarithromycin, which accounts for an additional 10% to 15% of the dose with either a 250 mg or a 500 mg tablet administered every 12 hours. (nih.gov)

Pharmacokinetics and tolerability of extended-release clarithromycin. (nih.gov)
The nonlinearity of clarithromycin pharmacokinetics is slight at the recommended doses of 250 mg and 500 mg administered every 8 to 12 hours. (nih.gov)

Ketek), any other medications, or any of the ingredients in clarithromycin preparations. (medlineplus.gov)
Your doctor will probably tell you not to take clarithromycin if you are taking one or more of these medications. (medlineplus.gov)
ᐈ Search for cheaper Medications containing Clarithromycin? (rxeli.com)

No studies of Clarithromycin for MAC prophylaxis have been performed in pediatric populations and the doses recommended for prophylaxis are derived from Mycobacterium Avium Complex (MAC) treatment studies in children. (nih.gov)

Take clarithromycin until you finish the prescription, even if you feel better. (medlineplus.gov)
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Clarithromycin STELLA 500 mg is administered orally and may be given without regard to meals. (stellapharm.com)

Healthy Pregnancy Practices yassedd1528.unblog.fr a doctor suspects meningitis, they may cause Clarithromycin overnight Shipping sunburn, or skin rash, redness, itching, appropriate steps should be taken, Clarithromycin Overnight Shipping . (unblog.fr)

Clarithromycin Oral Suspension 125mg/5mL is an antibiotic and this product contains the medication in an easy to use suspension to give to your pet by mouth. (equinemedcare.com)
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Of the 31 patients, 27 received a regimen including clarithromycin. (medscape.com)
With clarithromycin, you can see that the efficacy is reduced in those patients who are rapid metabolizers," Rockett said. (medscape.com)
There is education needed to get the data out there that clarithromycin-based therapies may not be the right choice for patients," he said. (medscape.com)
In this phase III trial, 286 patients with MM ineligible for ASCT received Rd with or without clarithromycin until disease progression or unacceptable toxicity. (nature.com)
The addition of clarithromycin to Rd in untreated transplant ineligible MM patients does not improve PFS despite increasing the ≥CR rate due to the higher number of toxic deaths in the C-Rd arm. (nature.com)
Clarbact (Clarithromycin) may not be safe or suitable for all patients. (4nrx-uk.md)
Patients also need to have their weight checked every common UTI that has not Clarithromycin overnight Shipping or become severe. (unblog.fr)
Effectiveness of clarithromycin in patients with yellow nail syndrome. (bvsalud.org)

Clarithromycin is a white to off-white crystalline powder. (nih.gov)

Two study protocols were used to evaluate the reproductive, developmental, and general toxicity of 3'-azido-3'deoxythymidine (AZT) and clarithromycin in Swiss (CD-1 ® ) mice treated by oral gavage. (nih.gov)

Food does not affect the onset of formation of the antimicrobially active metabolite, 14-OH clarithromycin or its peak plasma concentration but does slightly decrease the extent of metabolite formation, indicated by an 11% decrease in area under the plasma concentration-time curve (AUC). (nih.gov)
With a 250 mg every 12 hours dosing, the principal metabolite, 14-OH clarithromycin, attains a peak steady-state concentration of about 0.6 mcg/mL and has an elimination half-life of 5 to 6 hours. (nih.gov)
The reactive metabolite is 14-OH Clarithromycin. (nih.gov)

pyogenes infections, Clarithromycin overnight Shipping as necrotising fasciitis, may be added antimicrobial for most cases of non In the U. Special thank goes to the staff of the hospital treated can cause a condition known as sepsis. (unblog.fr)

In comparison, after an oral dose of 250 mg (125 mg/5 mL) suspension every 12 hours, approximately 40% is excreted in urine as clarithromycin. (nih.gov)

You should begin to feel better during the first few days of treatment with clarithromycin. (medlineplus.gov)
We show that a 1-week course of clarithromycin selects for macrolide-resistant S. epidermidis that may persist up to 4 years after treatment. (cdc.gov)
Clarbact (Clarithromycin) should always be administered strictly according to your doctor`s instructions to get the safest and most effective results from treatment. (4nrx-uk.md)
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however, data establishing the efficacy of Clarithromycin in the subsequent prevention of rheumatic fever are not available at present. (nih.gov)

tell your doctor if you have or have ever had jaundice (yellowing of the skin or eyes) or other liver problems while taking clarithromycin. (medlineplus.gov)
Clarithromycin has been linked to rare instances of acute liver injury that can be severe and even fatal. (nih.gov)
Clarithromycin should not be used by people with a history of cholestatic jaundice and/or liver dysfunction associated with prior clarithromycin use. (mdwiki.org)

Clarithromycin therapy is recommended to continue for life if clinical and mycobacterial improvements are observed. (nih.gov)

Steady-state peak plasma clarithromycin concentrations were attained within 3 days and were approximately 1 to 2 mcg/mL with a 250 mg dose administered every 12 hours and 3 to 4 mcg/mL with a 500 mg dose administered every 8 to 12 hours. (nih.gov)
With a 500 mg every 8 to 12 hours dosing, the peak steady-state concentration of 14-OH clarithromycin is slightly higher (up to 1 mcg/mL), and its elimination half-life is about 7 to 9 hours. (nih.gov)

However, three of the six alternatives include clarithromycin. (medscape.com)

For a single 500 mg dose of clarithromycin, food slightly delays the onset of clarithromycin absorption, increasing the peak time from approximately 2 to 2.5 hours. (nih.gov)
Food also increases the clarithromycin peak plasma concentration by about 24%, but does not affect the extent of clarithromycin bioavailability. (nih.gov)

Breast milk If your earache is due to an contains a Clarithromycin overnight Shipping blend of synergistic ingredients designed to AOM) are among the most common illnesses in babies. (unblog.fr)

There is a subset who will do well with it, but I think where we're at now, with the frequency of macrolide prescriptions for other conditions, that clarithromycin is going to be a difficult therapy for a lot of people. (medscape.com)
We examined how a common therapy that includes clarithromycin affects normally colonizing Staphylococcus epidermidis . (cdc.gov)
In this study, we have assessed how a commonly used therapy that includes clarithromycin affects the normal microbiota of S. epidermidis . (cdc.gov)

Clarithromycin should be used in combination with other anti- mycobacterial drugs that have shown in vitro activity against MAC, including ethambutol, clofazimine, and rifampin. (nih.gov)

Anatomy1

Organisms12

Diseases8

Chemicals and Drugs44

Analytical, Diagnostic and Therapeutic Techniques and Equipment8

Phenomena and Processes6

Health Care3

Geographicals1

Successful short-term suppression of clarithromycin-resistant Mycobacterium avium complex bacteremia in AIDS. California Collaborative Treatment Group. (1/1145)

Multiplex sequence analysis demonstrates the competitive growth advantage of the A-to-G mutants of clarithromycin-resistant Helicobacter pylori. (2/1145)

Direct detection of Helicobacter pylori resistance to macrolides by a polymerase chain reaction/DNA enzyme immunoassay in gastric biopsy specimens. (3/1145)

Eradication of Helicobacter pylori in functional dyspepsia: randomised double blind placebo controlled trial with 12 months' follow up. The Optimal Regimen Cures Helicobacter Induced Dyspepsia (ORCHID) Study Group. (4/1145)

Altered expression profile of the surface glycopeptidolipids in drug-resistant clinical isolates of Mycobacterium avium complex. (5/1145)

Treatment of Helicobacter pylori and Chlamydia pneumoniae infections decreases fibrinogen plasma level in patients with ischemic heart disease. (6/1145)

Ranitidine bismuth citrate, tetracycline, clarithromycin twice-a-day triple therapy for clarithromycin susceptible Helicobacter pylori infection. (7/1145)

The DU-MACH study: eradication of Helicobacter pylori and ulcer healing in patients with acute duodenal ulcer using omeprazole based triple therapy. (8/1145)

Clarithromycin

Anti-Bacterial Agents

Amoxicillin

Azithromycin

Helicobacter pylori

Helicobacter Infections

Metronidazole

Erythromycin

Roxithromycin

Omeprazole

Anti-Ulcer Agents

Drug Therapy, Combination

Microbial Sensitivity Tests

2-Pyridinylmethylsulfinylbenzimidazoles

Rifabutin

Bismuth

Ketolides

Lansoprazole

Macrolides

Mycobacterium avium-intracellulare Infection

Mycobacterium avium Complex

RNA, Ribosomal, 23S

Tinidazole

Ethambutol

Penicillins

Ranitidine

Drug Resistance, Bacterial

Mycobacterium avium

Proton Pump Inhibitors

Drug Resistance, Microbial

Peptic Ulcer

Duodenal Ulcer

Dyspepsia

Anti-Infective Agents

Sulfoxides

Ofloxacin

Levofloxacin

Josamycin

Mycobacterium Infections, Nontuberculous

Clofazimine

Rabeprazole

Drug Interactions

Fluoroquinolones

Furazolidone

Rifamycins

Breath Tests

Antibiotics, Antitubercular

Antitrichomonal Agents

Tetracycline

Mycobacterium Infections

Rifampin

Haemophilus influenzae

Mycobacterium

Amikacin

Benzimidazoles

Amoxicillin-Potassium Clavulanate Combination

Streptococcus pneumoniae

Administration, Oral

Mycobacterium chelonae

Bulgaria

Minocycline

Double-Blind Method

Nontuberculous Mycobacteria

Treatment Outcome

Colony Count, Microbial

Ciprofloxacin

Mycobacterium fortuitum

Mycobacterium xenopi

Aza Compounds

Stomach

Quinolones

Antitubercular Agents

Gastritis

Chlamydophila pneumoniae

Drug Resistance, Multiple, Bacterial

Gastric Mucins

Area Under Curve

Mycobacterium kansasii

Point Mutation

Successful short-term suppression of clarithromycin-resistant Mycobacterium avium complex bacteremia in AIDS. California Collaborative Treatment Group. (1/1145)