ANOMEX SUPPOSITORY

Indications

• Adrenocortical insufficiency
• Inflammatory bowel disease
• Severe acute asthma
• Acute hypersensitivity reactions
• Congenital adrenal hyperplasia
• Replacement therapy in adrenal insufficiency

Dosage

Children: For children aged 1-5 months: Initially 25 mg 3 times a day, adjusted according to response. For children aged 6 months-5 years: Initially 50 mg 3 times a day, adjusted according to response. For children aged 6-11 years: Initially 100 mg 3 times a day, adjusted

Adults: 100-500 mg 3-4 times a day or when required. For replacement in adrenocortical insufficiency, 20-30 mg once daily, adjusted according to response.

Mechanism of action

Hydrocortisone binds to the glucocorticoid receptor, leading to decreased vasodilation and permeability of capillaries, inhibition of leukocyte migration to inflammation sites, and changes in gene expression that promote anti-inflammatory pathways. It inhibits phospholipase A2, NF-kappa B, and other inflammatory transcription factors, stabilizing leukocyte lysosomal membranes and reducing the release of destructive enzymes. High doses can raise sodium levels and decrease potassium levels through mineralocorticoid receptor activity.

Pharmacodynamics

Hydrocortisone's pharmacodynamic profile includes the inhibition of various inflammatory mediators and the promotion of anti-inflammatory cytokines. Its effects are dose-dependent, with lower doses providing anti-inflammatory benefits, while higher doses exhibit immunosuppressive effects. It has a wide therapeutic index and moderate duration of action.

Pharmacokinetics

Hydrocortisone is metabolized primarily in the liver, with its effects lasting for several hours to days. The onset of action varies with the route of administration, being more rapid when given intravenously. Its half-life is influenced by factors such as dose and administration route, and it is excreted through urine as metabolites.

Contra-indications

• Systemic fungal infections
• Hypersensitivity to hydrocortisone or any excipients

Adverse effects

• Increased risk of infections
• Hyperglycemia
• Hypertension
• Fluid retention and edema
• Gastrointestinal disturbances
• Mood changes
• Osteoporosis
• Peptic ulcer disease
• Cushing's syndrome with long-term use

Interactions

• Mitotane: Moderate decrease in hydrocortisone exposure
• Rifampicin: Moderate decrease in hydrocortisone exposure
• Cobicistat: Unknown effect, potential increase in hydrocortisone exposure
• Idelalisib: Unknown effect, potential increase in hydrocortisone exposure
• Clarithromycin: Unknown effect, potential increase in hydrocortisone exposure

Precautions

• Use with caution in patients with diabetes
• Monitor for signs of infection during therapy
• Consider dose adjustment in patients with hepatic impairment
• Gradual withdrawal is recommended to avoid adrenal insufficiency after prolonged therapy

Pregnancy

Hydrocortisone is categorized as category C. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Hydrocortisone 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

• Injectable form (sodium succinate)
• Modified-release tablets
• Immediate-release tablets

Indications

• Localized pain relief
• Dermatological conditions requiring anesthesia
• Minor surgical procedures
• Skin irritation relief

Dosage

Children: Paediatric dosing should be determined based on the child's weight and age, and specific guidelines should be consulted for appropriate dosing recommendations.

Adults: For adult patients, the dosage depends on the specific formulation and intended use, and should be guided by clinical judgment. Refer to product-specific guidelines for detailed dosing information.

Mechanism of action

Lidocaine, the active component, exerts its effects by inhibiting voltage-gated sodium channels, which decreases neuronal excitability and conduction of impulses in sensory nerves. This results in a reversible loss of sensation in the targeted area. Zinc acetate contributes to the formulation by acting as an astringent, promoting tissue repair and reducing inflammation.

Pharmacodynamics

The pharmacodynamics of acetatelidocainezinc are primarily attributed to lidocaine's rapid onset of action and its ability to provide localized anesthesia. The depth and duration of anesthesia depend on the concentration of lidocaine and the duration of application. Zinc acetate enhances the therapeutic effects by providing additional benefits such as reduced irritation and inflammation at the site of application.

Pharmacokinetics

Lidocaine is rapidly absorbed through the skin and mucous membranes, reaching peak plasma concentrations quickly after topical application. It is metabolized primarily in the liver via cytochrome P450 enzymes, particularly CYP3A4 and CYP1A2, and its elimination half-life varies based on the route of administration and individual patient factors. Zinc acetate is minimally absorbed systemically and primarily acts locally at the site of application.

Contra-indications

• Hypersensitivity to lidocaine or any component of the formulation
• Severe heart block
• Caution in patients with a history of seizures
• Pregnancy category C

Adverse effects

• Local irritation or burning at the application site
• Allergic reactions including rash or urticaria
• Systemic absorption may lead to CNS effects such as dizziness, tinnitus, or seizures
• Cardiovascular effects including hypotension or arrhythmias

Interactions

• May interact with other local anesthetics, increasing the risk of systemic toxicity
• Caution when used with antiarrhythmic drugs, as they may enhance toxicity
• Concurrent use with other CNS depressants may increase the risk of CNS effects

Precautions

• Use with caution in patients with hepatic impairment due to altered metabolism
• Monitor for signs of systemic absorption and toxicity, especially in children and elderly patients
• Assess for pre-existing cardiac conditions before administration

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Lidocaine is excreted in breast milk. Caution should be exercised when administered to a nursing mother.

Storage

Store at room temperature, away from light and moisture. Do not freeze.

Formulations

• Topical cream
• Gel
• Solution for injection

Indications

• Wound healing
• Skin ulcers
• Burns
• Dermatitis
• Psoriasis
• Chronic skin conditions

Dosage

Children: Refer to specific product guidelines or clinical protocols for dosing information.

Adults: Refer to specific product guidelines or clinical protocols for dosing information.

Mechanism of action

Oxideallantoin exerts its effects through several biological pathways. It promotes cell proliferation and migration, which are crucial for wound healing. The compound also exhibits antioxidant properties, which help in reducing oxidative stress in damaged tissues. Additionally, oxideallantoin is believed to stimulate the synthesis of collagen and other extracellular matrix components, enhancing the repair and regeneration of skin.

Pharmacodynamics

The pharmacodynamics of oxideallantoin involve its interaction with skin cells, leading to increased cell turnover and enhanced healing processes. Its ability to reduce inflammation and promote angiogenesis (the formation of new blood vessels) also contributes to its therapeutic effects in skin repair. Additionally, oxideallantoin's moisturizing properties help to improve skin hydration, further supporting skin health.

Pharmacokinetics

The pharmacokinetics of oxideallantoin include absorption, distribution, metabolism, and excretion characteristics that are typical for topical agents. When applied to the skin, oxideallantoin is readily absorbed into the epidermal layers. It is not extensively metabolized and is primarily excreted unchanged. The onset of action is typically rapid, with effects observed shortly after application.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Headache
• Allergic reactions

Precautions

• Use with caution in patients with known allergies to similar compounds
• Monitor for signs of an allergic reaction during initial doses

Pregnancy

There is limited data on the safety of oxideallantoin in pregnancy. Use only if the benefits outweigh the risks.

Breast-feeding

It is not known whether oxideallantoin is excreted in human 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

• Topical ointment
• Cream
• Gel

Mechanism of action

The short-term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels. Following topical application, corticosteroids produce anti-inflammatory, antipruritic, and vasoconstrictor actions. The activity of the drugs is thought to result at least in part from binding with a steroid receptor. Corticosteroids decrease inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes; inhibiting macrophage accumulation in inflamed areas; reducing leukocyte adhesion to capillary endothelium; reducing capillary wall permeability and edema formation; decreasing complement components; antagonizing histamine activity and release of kinin from substrates; reducing fibroblast proliferation, collagen deposition, and subsequent scar tissue formation; and possibly by other mechanisms as yet unknown. Corticosteroids, especially the fluorinated corticosteroids, have antimitotic activity on cutaneous fibroblasts and the epidermis. /Corticosteroids/ Reactive oxygen species (ROS) generation by polymorphonuclear leukocytes (PMNL) and mononuclear cells (MNC) is inhibited following the intravenous administration of hydrocortisone. This is associated with a parallel decrease in intranuclear NFkappaB, known to modulate inflammatory responses including ROS generation. Plasma levels of interleukin-10 (IL-10), an anti-inflammatory and immunosuppressive cytokine produced by TH2 cells, are also increased after hydrocortisone administration. In this study, we have investigated the effect of hydrocortisone on p47(phox) subunit, a key component of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in MNC and the pharmacodynamics of this effect with ROS generation and plasma IL-10 levels /were investigated/. p47(phox) subunit protein levels in MNC showed a progressive decrease after hydrocortisone administration. It reached a nadir at 4 hours and increased thereafter to a baseline level at 24 hours. ROS generation also decreased, reached a nadir between 2 and 4 hours, and returned to a baseline level at 24 hours. IL-10 concentrations increased, peaked at 4 hours, and reverted to the baseline levels at 24 hours. In conclusion, p47(phox) subunit suppression may contribute to the inhibition of ROS generation in MNC after hydrocortisone administration. This suppression occurs in parallel with the suppression of NFkappaB and an increase in IL-10 plasma levels. Therefore, it would appear that the decrease in intranuclear NFkappaB and an increase in IL-10 may cause the inhibitory modulation on p47(phox) subunit and ROS generation by MNC following hydrocortisone and other glucocorticoids.

Pharmacodynamics

Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index and a moderate duration of action. Patients should stop taking the medication if irritation or sensitization occurs.