INFLU-ZINC THROAT TABLETS (Each tablet contains Vitamin C/ Echinacea/ Zinc/ Willow/ Selenium 180mg/50mg/12,5mg/1,2mg/50mcg)

Indications

• Vitamin C deficiency
• Scurvy
• Adjunct therapy in iron overload conditions

Dosage

Children: Child 1 month–3 years: 125–250 mg daily in 1–2 divided doses; Child 4–11 years: 250–500 mg daily in 1–2 divided doses; Child 12–17 years: 0.5–1 g daily in 1–2 divided doses.

Adults: 500 mg daily, taken in 1-2 divided doses, depending on the clinical condition and dietary needs.

Mechanism of action

Ascorbic acid functions primarily as a reducing agent, facilitating enzymatic reactions in the body, including the hydroxylation of proline and lysine in collagen synthesis. It also plays a role in the absorption of iron from the gastrointestinal tract and enhances the immune response.

Pharmacodynamics

Ascorbic acid is crucial for the maintenance of connective tissue and is involved in the metabolism of several amino acids. Its antioxidant properties help to mitigate oxidative stress and may play a role in reducing the risk of chronic diseases.

Pharmacokinetics

Ascorbic acid is absorbed in the intestines and is widely distributed throughout the body. The renal clearance of ascorbic acid is dose-dependent, with higher doses leading to increased excretion. The half-life varies but is generally around 15 to 30 minutes in healthy individuals, with tissue saturation levels influencing its retention.

Contra-indications

• Hypercalcaemia
• Hyperoxaluria
• Patients with cardiac dysfunction

Adverse effects

• Abdominal pain
• Headache
• Nausea
• Vomiting
• Diarrhoea
• Constipation
• Weight loss
• Polyuria
• Sweating
• Thirst
• Vertigo

Interactions

• Increases risk of cardiovascular adverse effects with iron chelators
• Increases risk of cardiovascular adverse effects with deferiprone
• Increases risk of cardiovascular adverse effects with desferrioxamine

Precautions

• Use with caution in patients with iron overload
• Monitor for symptoms of overdose

Pregnancy

High doses teratogenic in animals but therapeutic doses unlikely to be harmful.

Storage

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

Formulations

• Ascorbic acid 50 mg tablets
• Ascorbic acid 100 mg tablets
• Ascorbic acid 200 mg tablets
• Ascorbic acid 250 mg tablets
• Ascorbic acid 500 mg capsules

Indications

• Selenium deficiency
• Supportive therapy in conditions requiring antioxidant support
• Potential adjunct in cancer prevention strategies

Dosage

Children: Refer to BNF for Children for specific dosing information.

Adults: Initially 100–500 micrograms daily, adjusted according to response and serum levels.

Mechanism of action

Selenium is metabolized to selenophosphate and selenocysteine, which are essential for the synthesis of selenoproteins. This process involves the incorporation of selenium into proteins through a specialized tRNA that recognizes the RNA sequence UGA, which is facilitated by SECIS structures and SBP-2 proteins. Key selenoproteins, like glutathione peroxidases, help protect cells from oxidative damage, thus playing a significant role in reducing the risk of diseases such as atherosclerosis and certain cancers.

Pharmacodynamics

Selenium is incorporated into various selenoproteins that perform essential functions, including antioxidant activity, redox balance, and regulation of thyroid hormones. Its role in antioxidant defense mechanisms is particularly important for protecting cells against reactive oxygen species (ROS). Selenium supplementation has been linked to improved immune function and potential cancer prevention.

Pharmacokinetics

Selenium is absorbed through the gastrointestinal tract, and its bioavailability can vary based on the source and form of selenium. Once absorbed, it is distributed to various tissues, where it is incorporated into selenoproteins. Selenium is primarily excreted through urine, and its half-life can depend on dietary intake and individual metabolism. Selenium status can be assessed through blood levels of selenoproteins and selenium itself.

Adverse effects

• Nausea
• Anaemia
• Aplastic anaemia
• Skin reactions
• Gastrointestinal disorders

Precautions

• Selenium supplementation should not be given unless there is good evidence of deficiency.
• Use caution in patients with a history of hypersensitivity to selenium or its compounds.

Pregnancy

Limited information is available regarding selenium supplementation during pregnancy. Consult specialist sources for guidance.

Breast-feeding

Limited information is available; the effect of selenium on copper levels in milk is conflicting, and its impact on the infant is unknown.

Storage

After opening, store in a refrigerator (2–8°C).

Formulations

• Tablets (e.g., L-Selenomethionine 200 micrograms, SelenoPrecise 100 micrograms)
• Capsules (e.g., Trientine dihydrochloride 250 mg)
• Injection solutions (e.g., Sodium selenite 50 micrograms per 1 ml)

Indications

• Prevention of the common cold
• Treatment of upper respiratory tract infections
• Support for immune system function

Dosage

Children: Refer to specific product guidelines as doses can vary depending on the formulation and concentration of echinacea.

Adults: Refer to specific product guidelines as doses can vary depending on the formulation and concentration of echinacea.

Mechanism of action

Echinacea is thought to stimulate the immune system by increasing the activity of macrophages and other immune cells. It may enhance the production of cytokines, which are critical for coordinating the immune response. The active components, including alkylamides, glycoproteins, and polysaccharides, may also exhibit anti-inflammatory effects.

Pharmacodynamics

Echinacea shows immunomodulatory effects, enhancing phagocytosis, promoting the release of interferons, and increasing the number of white blood cells. It may also exhibit antioxidant properties, reducing oxidative stress in immune cells. These effects contribute to its potential in reducing the duration and severity of cold symptoms.

Pharmacokinetics

The pharmacokinetics of echinacea are not well-defined due to its complex mixture of active compounds. However, it is known to be rapidly absorbed after oral administration, with peak plasma concentrations occurring within 1 to 2 hours. The elimination half-life is variable, and the bioavailability of its active components can be influenced by factors such as preparation method and individual metabolism.

Contra-indications

• Hypersensitivity to echinacea or any of its components
• Autoimmune diseases (e.g., multiple sclerosis, lupus)
• Severe allergies, particularly to plants in the Asteraceae family

Adverse effects

• Allergic reactions including rash, itching, and swelling
• Gastrointestinal upset such as nausea and diarrhea
• Dizziness
• Headache

Interactions

• May interact with immunosuppressants, potentially reducing their effectiveness
• Possible interaction with anticoagulants, increasing the risk of bleeding
• May affect the metabolism of certain medications by influencing cytochrome P450 enzymes

Precautions

• Use with caution in individuals with allergies, especially to plants
• Caution in patients with asthma, as it may exacerbate symptoms
• Consult healthcare professional before use in patients with liver disorders

Pregnancy

Safety during pregnancy has not been established; use with caution and consult a healthcare professional.

Breast-feeding

Limited data available; consult a healthcare professional before use while breastfeeding.

Storage

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

Formulations

• Oral capsules
• Liquid extracts
• Teas

Indications

• Headaches
• Muscle pain
• Osteoarthritis
• Rheumatic pain
• Fever

Dosage

Children: Refer to specific product guidelines or consult a healthcare professional for appropriate dosing in children.

Adults: Dosage varies based on the preparation and concentration of willow bark extract. It is advisable to refer to specific product guidelines or consult a healthcare professional.

Mechanism of action

The primary mechanism of action of willow bark is attributed to salicin and its derivative salicylic acid, which inhibit the enzyme cyclooxygenase (COX). This inhibition leads to decreased synthesis of prostaglandins, which are mediators of pain and inflammation. The anti-inflammatory effects are also associated with the modulation of inflammatory cytokines.

Pharmacodynamics

Willow bark exhibits analgesic, anti-inflammatory, and antipyretic effects. The onset of pain relief may occur within one to two hours after administration, with effects lasting for several hours. The efficacy of willow bark may vary depending on the preparation and dosage used. It is generally considered to have a lower gastrointestinal risk compared to synthetic NSAIDs.

Pharmacokinetics

Salicin is absorbed in the gastrointestinal tract and is metabolized to salicylic acid in the liver. The peak plasma concentration of salicylic acid occurs approximately 1-2 hours after ingestion. The elimination half-life of salicylic acid varies based on dosage and individual metabolism, typically ranging from 2 to 3 hours. Salicylic acid is primarily excreted by the kidneys.

Contra-indications

• Hypersensitivity to salicylates
• Active peptic ulcer disease
• Severe renal impairment
• Bleeding disorders

Adverse effects

• Gastrointestinal irritation
• Nausea
• Vomiting
• Tinnitus
• Allergic reactions
• Headache
• Rash

Interactions

• Increased risk of bleeding with anticoagulants such as warfarin
• Potential interaction with other non-steroidal anti-inflammatory drugs (NSAIDs)
• May reduce the effectiveness of antihypertensive medications

Precautions

• Use with caution in patients with asthma
• Monitor for signs of gastrointestinal bleeding
• Use with caution in elderly patients due to increased risk of adverse effects

Pregnancy

Not recommended during pregnancy due to potential risks to the fetus, particularly in the third trimester.

Breast-feeding

Use with caution as salicylates can pass into breast milk and may affect the nursing infant.

Storage

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

Formulations

• Willow bark extract (various concentrations)
• Capsules
• Tablets
• Tinctures

Mechanism of action

Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA. This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality. The most important selenoproteins seem to be the glutathione peroxidases and thioredoxin reductases which are part of the body's defenses againts reactive oxygen species (ROS). The importance of selenium in these anti-oxidant proteins has been implicated in the reduction of atherosclerosis by preventing the oxidation of low density lipoprotein. Selenium supplementation is also being investigated in the prevention of cancer and has been suggested to be beneficial to immune function. Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach. /Selenium/ Selenium status can also influence thyroid hormone function via the deiodinase enzymes. Selenium is a critical component of the deiodinase enzymes, including iodothyronine 5'-deiodinases, which convert the prohormone thyroxine (T4) to the active circulating form, triiodothyronine (T3). Selenium is also a component of GPX, the main enzyme responsible for protecting thyroid cells against oxidative damage. GPX is involved in the detoxification of hydrogen peroxide, which is produced in the thyroid during the conversion of T4 to T3. /Selenium/ Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low in the organism. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenium may have a role in hepatic heme metabolism that is related to GPX or lipid peroxidation. Selenocysteine is specifically found in some proteins (e.g., glutathione peroxidase); selenomethionine appears to randomly substitute for methionine in protein synthesis. This appears to be an additional mechanism for intermediate- or chronic-duration toxicity. Skin, hair, and nail damage are significant indicators of chronic selenium overexposure. The mechanism causing these integumentary effects is unclear, but could be related to the high selenium concentrations in these tissues as a consequence of the substitution of selenium for sulfur in certain amino acids, including the disulfide bridges that pr

Pharmacodynamics

Selenium is incorporated into many different selenoproteins which serve various functions throughout the body.