LOOBID TABLETS

Indications

• Bacterial infections
• Complicated urinary-tract infections
• Lower respiratory-tract infections
• Skin infections
• Gonorrhoea
• Pelvic inflammatory disease
• Prostatitis
• Acute pyelonephritis

Dosage

Children: Refer to the BNF for Children for specific dosing guidance.

Adults: 200–400 mg daily for 3 days for uncomplicated urinary-tract infections; for severe or complicated infections, the dose may be increased to 400 mg twice daily for 7–10 days. In cases of renal impairment, the dose should be adjusted based on creatinine clearance.

Mechanism of action

Ofloxacin acts by inhibiting bacterial DNA gyrase and topoisomerase IV, enzymes crucial for DNA replication and transcription. This inhibition prevents normal cell division, leading to cell death. Ofloxacin has a significantly higher affinity for bacterial DNA gyrase compared to mammalian enzymes, making it effective against infectious pathogens.

Pharmacodynamics

As a quinolone antibiotic, ofloxacin demonstrates bactericidal activity, meaning it kills bacteria rather than merely inhibiting their growth. Its mechanism is primarily through the disruption of DNA supercoiling, a vital process for bacterial cell division and viability. The drug's broad-spectrum activity allows it to target a wide variety of bacterial pathogens, enhancing its utility in clinical settings.

Pharmacokinetics

Ofloxacin is well-absorbed after oral administration, with a bioavailability of approximately 98%. It is primarily metabolized in the liver and excreted through the kidneys, necessitating caution in patients with hepatic or renal impairment. The elimination half-life is about 4 to 7 hours, which supports twice-daily dosing for effective therapeutic levels.

Contra-indications

• Hypersensitivity to ofloxacin or other quinolones
• History of tendon disorders related to fluoroquinolone use
• Severe hepatic impairment
• History of QT interval prolongation
• Concurrent use of drugs that prolong the QT interval

Adverse effects

• Nausea
• Diarrhea
• Headache
• Dizziness
• Tendonitis and tendon rupture
• QT interval prolongation
• Photosensitivity
• Rash
• Anaphylaxis

Interactions

• Antacids containing magnesium or aluminum (may reduce absorption)
• Cationic drugs (e.g., iron salts, sucralfate)
• Warfarin (may enhance anticoagulant effect)
• Drugs that prolong the QT interval (e.g., class IA and III antiarrhythmics)

Precautions

• Use with caution in patients with a history of seizures or CNS disorders
• Monitor for signs of tendon damage
• Assess renal function prior to dosing, especially in elderly patients
• Caution in patients with a history of myasthenia gravis

Pregnancy

Manufacturer advises use only if the benefit outweighs the risk, as systemic quinolones have been associated with risks during pregnancy.

Breast-feeding

Ofloxacin is excreted in breast milk; caution is advised when administering to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Protect from light.

Formulations

• 200 mg tablets
• 400 mg tablets
• Injectable solution (200 mg in 100 mL)
• Eye drops (0.3% solution)

Indications

• Bladder cancer
• Tuberculosis vaccination

Dosage

Children: Refer to the BNF for Children for appropriate dosing based on indication.

Adults: Refer to specific guidelines based on indication. For bladder cancer, a common regimen is instillation once a week for six weeks.

Mechanism of action

BCG works by stimulating the immune system, particularly through the activation of T-cells and macrophages. It enhances the immune response against tumor cells and Mycobacterium tuberculosis, promoting the release of cytokines and other immune mediators that contribute to the destruction of cancerous cells and pathogens.

Pharmacodynamics

The pharmacodynamics of BCG involve the induction of a robust immune response characterized by the activation of both innate and adaptive immunity. This includes the proliferation of T-lymphocytes and the production of cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukins, leading to increased immune surveillance and anti-tumor activity. The effectiveness of BCG is influenced by factors such as the host's immune status and the presence of any concurrent infections.

Pharmacokinetics

BCG is administered locally, and its pharmacokinetics are determined by the route of administration. After intravesical administration, BCG remains in the bladder and exerts its effects locally, with minimal systemic absorption. The half-life and clearance of BCG can vary based on the patient's immune response and presence of any concurrent conditions.

Interactions

• normal immunoglobulin + bacillus calmette-gurin vaccine: Unknown (decreases efficacy)

Pregnancy

Bacillus Calmette-Guérin (BCG) vaccine can be administered during pregnancy if the potential benefit outweighs the potential risk.

Breast-feeding

BCG vaccine may be administered during breastfeeding; however, caution is advised.

Storage

Store at 2-8 degrees Celsius. Do not freeze.

Formulations

• Bacillus Calmette-Guérin vaccine

Indications

• Metabolic acidosis
• Lactic acidosis
• Support in shock or severe dehydration
• Exercise physiology research

Dosage

Children: Refer to clinical guidelines for specific dosing recommendations based on the clinical condition being treated.

Adults: Refer to clinical guidelines for specific dosing recommendations based on the clinical condition being treated.

Mechanism of action

Lactic acid primarily functions by contributing to the acid-base balance in the body. It can serve as a substrate for gluconeogenesis in the liver and is utilized in the Cori cycle, where it is converted back to glucose. Furthermore, lactic acid can act as a signaling molecule in various physiological processes, influencing metabolism and cellular responses during hypoxic conditions.

Pharmacodynamics

Lactic acid dissociates into lactate and hydrogen ions in solution, which can lead to a decrease in pH (acidosis) when produced in excess. Its accumulation in the body is indicative of anaerobic metabolism, often observed during intense exercise or in conditions of oxygen deprivation. The body can buffer the effects of lactic acid through bicarbonate and other mechanisms, maintaining homeostasis.

Pharmacokinetics

Lactic acid is rapidly absorbed and distributed throughout the body. It is metabolized primarily in the liver, where it can be converted to glucose or further metabolized to carbon dioxide and water. The elimination half-life of lactate varies depending on the metabolic state of the individual and the presence of underlying conditions. Renal function also plays a role in the clearance of lactate from the body.

Adverse effects

• Nausea
• Vomiting
• Abdominal pain
• Diarrhea
• Hypersensitivity reactions

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of metabolic acidosis
• Caution in patients with liver disease

Pregnancy

Lactic acid is generally regarded as safe, but clinical use should be evaluated on a case-by-case basis during pregnancy.

Breast-feeding

Considered safe for use during breastfeeding, but consult healthcare provider for individual cases.

Storage

Store at room temperature, away from direct sunlight and moisture.

Formulations

• Lactic acid injection
• Lactic acid oral solution

Indications

• Heart failure
• Hypertension
• Mitochondrial disorders
• Neurodegenerative diseases
• Statin-associated myopathy

Dosage

Children: Refer to specific dosing guidelines in clinical literature or pharmacological references.

Adults: Refer to specific dosing guidelines in clinical literature or pharmacological references.

Mechanism of action

Coenzyme Q10 acts as an electron carrier in the mitochondrial electron transport chain, facilitating ATP synthesis. It also exhibits antioxidant properties by scavenging free radicals and regenerating other antioxidants, thus protecting cellular components from oxidative damage. Its involvement in maintaining mitochondrial membrane potential is critical for energy production.

Pharmacodynamics

Coenzyme Q10 enhances energy production in cells, particularly in tissues with high energy demands, such as the heart and skeletal muscles. Its antioxidant action helps reduce oxidative stress, which is implicated in various pathological conditions, including cardiovascular diseases and aging. Clinical studies suggest that it may improve cardiac function and exercise tolerance in patients with heart failure and may have a positive effect on blood pressure.

Pharmacokinetics

Coenzyme Q10 is absorbed in the gastrointestinal tract, with bioavailability influenced by its formulation (solubility and presence of fats). Peak plasma concentrations are typically reached within 6 to 8 hours post-ingestion. It is metabolized in the liver and has a half-life of around 33 hours. Coenzyme Q10 is excreted primarily in the bile and urine. Its absorption can be enhanced when taken with meals that contain fat.

Pregnancy

Consult healthcare provider for risks versus benefits.

Breast-feeding

Consult healthcare provider for risks versus benefits.

Storage

Store in a cool, dry place away from light.

Indications

• Bacterial vaginosis
• Amoebiasis
• Giardiasis
• Trichomoniasis
• Infections caused by anaerobic bacteria

Dosage

Children: Dosing in children is determined based on weight and the specific indication. Refer to the BNF for Children for appropriate dosing guidelines.

Adults: The usual adult dose is 1.5 g orally once daily for 5 days for bacterial vaginosis or 1 g orally once daily for 3 days for amoebiasis. Refer to the BNF for specific indications and adjustments.

Mechanism of action

Ornidazole exerts its antimicrobial effects through the reduction of its nitro group by anaerobic bacteria and protozoa, resulting in the formation of reactive intermediates that interact with microbial DNA. This leads to the disruption of DNA synthesis and ultimately causes cell death. The drug's activity is primarily directed towards anaerobic organisms, including certain protozoa.

Pharmacodynamics

Ornidazole demonstrates a concentration-dependent bactericidal effect against susceptible organisms. Its activity is influenced by the reduction potential of the nitro group, which is crucial for its antimicrobial action. Ornidazole has a broad spectrum of activity, particularly against anaerobes and protozoa, and has been shown to be effective in both in vitro and in vivo models of infection.

Pharmacokinetics

Ornidazole is rapidly and completely absorbed following oral administration, achieving peak plasma concentrations within 1 to 3 hours. It is widely distributed throughout the body, including the central nervous system. The drug is metabolized mainly in the liver, with a half-life of approximately 8 to 10 hours. Excretion occurs primarily through the urine, with a small fraction eliminated unchanged.

Contra-indications

• Hypersensitivity to ornidazole or any of its components
• History of neurological disorders, particularly seizures

Adverse effects

• Nausea
• Vomiting
• Headache
• Dizziness
• Dry mouth
• Metallic taste
• Peripheral neuropathy

Interactions

• Alcohol: Concurrent use may lead to disulfiram-like reactions including flushing, tachycardia, and vomiting
• Anticoagulants: May enhance the effects of warfarin and other anticoagulants
• Other neurotoxic agents: Increased risk of neurological side effects

Precautions

• Use with caution in patients with a history of seizures
• Monitor liver function in patients with hepatic impairment
• Discontinue if neurological symptoms occur

Pregnancy

Ornidazole is not recommended during pregnancy unless the benefit outweighs the risk, particularly in the first trimester.

Breast-feeding

Ornidazole is excreted in breast milk, caution is advised when administering to nursing mothers.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Tablets: 500 mg
• Infusion: 100 mg/100 mL

Dosage

Children: Refer to specific drug guidelines as dosing varies based on the medication interacting with pores.

Adults: Refer to specific drug guidelines as dosing varies based on the medication interacting with pores.

Mechanism of action

Pores in cellular membranes allow for selective permeability based on size, charge, and polarity, enabling specific molecules to pass through. For example, ion channels are a type of pore that allows ions to flow across membranes, influencing cellular excitability and signaling. Drugs that target these pores can modulate their opening and closing, thereby altering cellular activity.

Pharmacodynamics

The pharmacodynamics of drugs that interact with pores typically involves the modulation of ion flow or the transport of solutes across cell membranes. This can lead to changes in cellular excitability, neurotransmission, and muscle contraction, depending on the specific type of pore targeted. The effects can be rapid, occurring within seconds, or gradual, depending on the drug and its pharmacological action.

Pharmacokinetics

The pharmacokinetics of substances passing through pores involves absorption, distribution, metabolism, and excretion (ADME). The size and chemical properties of the molecule determine how efficiently it can traverse a pore. Small polar molecules may diffuse more readily, while larger or charged molecules may require specific transport mechanisms. The rate of absorption through pores can influence a drug's onset of action and overall therapeutic effect.

Pregnancy

Data on the use of pores during pregnancy is limited. Caution is advised.

Breast-feeding

Information regarding the safety of pores during breastfeeding is not well established.

Storage

Store in a cool, dry place away from direct sunlight.

Mechanism of action

Ofloxacin acts on DNA gyrase and toposiomerase IV, enzymes which, like human topoisomerase, prevents the excessive supercoiling of DNA during replication or transcription. By inhibiting their function, the drug thereby inhibits normal cell division. Quinolone(s) (QNs) is widely used in infection therapy due to its good antimicrobial characteristics. However, QNs-induced arthropathy of immature animals has led to restrictions on the therapeutic use of these antimicrobial agents. The exact mechanism(s) of QNs-induced chondrotoxicity remain unknown. In the present study, .../the authors/ investigated the possible mechanism of ofloxacin (one typical QNs)-induced injuries of chondrocytes. Juvenile rabbit joint chondrocytes cultured in alginate microspheres were incubated with ofloxacin at concentrations of 0, 2, 5, 10, 20, and 40 microg/mL for up to 96 hr. Concentration of 10 microg/mL ofloxacin induced apoptosis of chondrocyte with visible apoptotic signs, including degradation of poly(ADP-ribose) polymerase, caspase-3 activation, and DNA ladder formation. Furthermore, extracellular signal-regulated kinase 1/2 (phospho-ERK1/2) and growth factor receptor-bound protein 2 (Grb2) were significantly reduced, and similar changes were also observed in the beta(1)-integrin receptor as assessed by immunoblotting. However, the mRNA level of beta(1)-integrin obtained from reverse transcription-polymerase chain reaction remained unchanged. Results of beta(1)-integrin immunoprecipitation have also shown that beta(1)-integrin did not interact with activated intracellular signaling proteins. In addition, ofloxacin did not induce apoptosis and decrease beta(1)-integrin expression in chondrocytes supplemented with Mg(2+), and the ofloxacin-induced apoptosis was caspase-8-dependent, inhibition of which did not affect the expression mode of phospho-ERK1/2 and beta(1)-integrin. Our results demonstrate that ofloxacin affects beta(1)-integrin receptor functions and the ERK mitogen-activated protein kinase signaling pathway, causing caspase-8-dependent apoptosis after exposure of 48 hr. Quinolones are widely used in infection therapy due to their good antimicrobial characteristics. However, there potential joint chondrotoxicity on immature animals has stood in the way of the therapeutic application of these agents, the exact mechanism of which is still unclear. This study was undertaken to investigate the role of oxidative damage in ofloxacin (one typical quinolones)-induced arthropathy. Chondrocytes from juvenile rabbit joints were incubated with ofloxacin at concentrations of 0, 5, 10, 20, 40 and 80 ug/mL, respectively. The extent of oxidative damage was assessed by measuring the reactive oxygen species level, activities of antioxidant enzymes, and oxidative damage to some macromolecules. It was observed that ofloxacin induced a concentration-dependent increase in intracellular reactive oxygen species production, which may be an early mediator of ofloxacin cytotoxicity. Similarly, ofloxacin resulted in a significant lipid peroxidation, revealed by a concentration-dependent increase in the level of thiobarbituric acid reactive substances. At the same time, ofloxacin induced DNA damage in a concentration-dependent manner for 24 hr measured by comet assay, which may be a cause for overproduction of reactive oxygen species. Furthermore, antioxidant enzyme activities, such as glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD), were rapidly decreased after treatment with ofloxacin. In addition, SOD decline and reactive oxygen species production were strongly inhibited, and the loss in cell viability was partly abated by additional glutathione (GSH), N-acetylcysteine (NAC) and dithiothreitol (DTT). In conclusion, these results clearly demonstrated that ofloxacin could induce oxidative stress, lipid peroxidation and DNA oxidative damage to chondrocytes. Ofloxacin is a quinolone antimicrobial agent. The mechanism of action of ofloxacin and o

Pharmacodynamics

Ofloxacin is a quinolone/fluoroquinolone antibiotic. Ofloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Ofloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria.