Trichoton At

Trichoton At Uses, Dosage, Side Effects, Food Interaction and all others data.

Acetylcysteine has a mucolytic activity through its free sulfhydryl group. It acts directly on the mucoproteins to open the disulfide bonds and thus lowers the viscosity of the mucous and facilitates its removal by the muco-cillary action and expectoration. Acetylcysteine improves the phagocytic capacity of the alveolar macrophages, thus protecting lungs from a variety of insults. Acetylcysteine is a precursor to glutathione, the most important intra & extra-cellular antioxidant (the safest & most convenient)

Acetylcysteine is indicated for mucolytic therapy and in the management of acetaminophen overdose. It has a short duration of action as it is given every 1-8 hours depending on route of administration, and has a wide therapeutic window. Patients should be counselled regarding diluting oral solutions in cola for taste masking, the risk of hypersensitivity, and the risk of upper gastrointestinal hemorrhage.

A water-soluble, enzyme co-factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk.

Biotin is a water-soluble B-complex vitamin which is composed of an ureido ring fused with a tetrahydrothiophene ring, which attaches a valeric acid substituent at one of its carbon atoms. Biotin is used in cell growth, the production of fatty acids, metabolism of fats, and amino acids. It plays a role in the Kreb cycle, which is the process in which energy is released from food. Biotin not only assists in various metabolic chemical conversions, but also helps with the transfer of carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often recommended for strengthening hair and nails. Consequenty, it is found in many cosmetic and health products for the hair and skin. Biotin deficiency is a rare nutritional disorder caused by a deficiency of biotin. Initial symptoms of biotin deficiency include: Dry skin, Seborrheic dermatitis, Fungal infections, rashes including erythematous periorofacial macular rash, fine and brittle hair, and hair loss or total alopecia. If left untreated, neurological symptoms can develop, including mild depression, which may progress to profound lassitude and, eventually, to somnolence; changes in mental status, generalized muscular pains (myalgias), hyperesthesias and paresthesias. The treatment for biotin deficiency is to simply start taking some biotin supplements. A lack of biotin in infants will lead to a condition called seborrheic dermatitis or "cradle cap". Biotin deficiencies are extremely rare in adults but if it does occur, it will lead to anemia, depression, hair loss, high blood sugar levels, muscle pain, nausea, loss of appetite and inflamed mucous membranes.

Copper is a transition metal and a trace element in the body. It is important to the function of many enzymes including cytochrome c oxidase, monoamine oxidase and superoxide dismutase . Copper is commonly used in contraceptive intrauterine devices (IUD) .

Copper is incorporated into many enzymes throughout the body as an essential part of their function . Copper ions are known to reduce fertility when released from copper-containing IUDs .

A metallic element of atomic number 30 and atomic weight 65.38. It is a necessary trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Zinc deficiency is associated with anemia, short stature, hypogonadism, impaired wound healing, and geophagia. It is identified by the symbol Zn .

A newer study suggests implies that an imbalance of zinc is associated with the neuronal damage associated with traumatic brain injury, stroke, and seizures .

Understanding the mechanisms that control brain zinc homeostasis is, therefore, imperative to the development of preventive and treatment regimens for these and other neurological disorders .

Trichoton At
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Trichoton At
Generic	Acetylcysteine + Biotin + Copper + L-selenium + Pantothenic Acid [vit B5] + Zinc
Type	Tablet
Therapeutic Class
Manufacturer	Med Manor Organics Pvt Ltd
Available Country	India
Last Updated:	September 19, 2023 at 7:00 am

Uses

Acetylcysteine is used for an adjunctive treatment for patients with abnormal, viscid or inspissated mucus secretions associated with conditions such as-

Acute and chronic bronchopulmonary disorders (e.g. pneumonia, bronchitis, emphysema, tracheobronchitis, chronic asthmatic bronchitis, tuberculosis, bronchiectasis, primary amyloidosis of the lung) Atelectasis caused by mucus obstruction Pulmonary complications of cystic fibrosis Pulmonary complications of thoracic and cardiovascular surgery Post-traumatic chest conditions.

It is effective in all respiratory airways disease causing formation of a dense secretion that cannot be or can only partially be expectorated such as acute and chronic bronchitis, laryngitis, sinusitis, tracheitis, infuenza & bronchial asthma. Acetylcysteine is also used for the treatment of Paracetamol overdose. Treatment option is optimal if given within 8 hours of Paracetamol ingestion.

Biotin is a B-complex vitamin found in many multivitamin products.

For nutritional supplementation, also for treating dietary shortage or imbalance.

Copper is a transition metal found in a variety of supplements and vitamins, including intravenous solutions for total parenteral nutrition (TPN).

For use in the supplementation of total parenteral nutrition and in contraception with intrauterine devices .

Zinc is an essential element commonly used for the treatment of patients with documented zinc deficiency.

Zinc can be used for the treatment and prevention of zinc deficiency/its consequences, including stunted growth and acute diarrhea in children, and slowed wound healing. It is also utilized for boosting the immune system, treating the common cold and recurrent ear infections, as well as preventing lower respiratory tract infections .

Trichoton At is also used to associated treatment for these conditions: Acetaminophen Overdose, Chronic Rhinitis, Corneal Diseases, Corneal ulceration, Crusting Rhinitis, Keratopathy, Rhinitis, Sinusitis, Vasomotor Rhinitis, Acute Rhinitis, Subacute Rhinitis, Airway secretion clearance therapyVitamin Deficiency, Nutritional supplementationEmergency Contraception, IUD, Trace Element Deficiency, Dietary supplementationCandidiasis, Common Cold, Diaper Dermatitis, Diaper Rash, Eye redness, Iron Deficiency (ID), Ocular Irritation, Skin Irritation, Sunburn, Wilson's Disease, Zinc Deficiency, Dietary and Nutritional Therapies, Dietary supplementation

How Trichoton At works

A number of possible mechanisms for the mucolytic activity of acetylcysteine have been proposed. Acetylcysteine's sulfhydryl groups may hydrolize disulfide bonds within mucin, breaking down the oligomers, and making the mucin less viscous. Acetylcysteine has also been shown to reduce mucin secretion in rat models. It is an antioxidant in its own right but is also deacetylated to cysteine, which participates in the synthesis of the antioxidant glutathione. The antioxidant activity may also alter intracellular redox reactions, decreasing phosphorylation of EGFR and MAPK, which decrease transcription of the gene MUC5AC which produces mucin.

In the case of acetaminophen overdoses, a portion of the drug is metabolized by CYP2E1 to form the potentially toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). The amount of NAPQI produced in an overdose saturates and depletes glutathione stores. The free NAPQI promiscuously binds to proteins in hepatocytes, leading to cellular necrosis. Acetylcysteine can directly conjugate NAPQI or provide cysteine for glutathione production and NAPQI conjugation.

Biotin is necessary for the proper functioning of enzymes that transport carboxyl units and fix carbon dioxide, and is required for various metabolic functions, including gluconeogenesis, lipogenesis, fatty acid biosynthesis, propionate metabolism, and catabolism of branched-chain amino acids.

Copper is absorbed from the gut via high affinity copper uptake protein and likely through low affinity copper uptake protein and natural resistance-associated macrophage protein-2 . It is believed that copper is reduced to the Cu1+ form prior to transport. Once inside the enterocyte, it is bound to copper transport protein ATOX1 which shuttles the ion to copper transporting ATPase-1 on the golgi membrane which take up copper into the golgi apparatus. Once copper has been secreted by enterocytes into the systemic circulation it remain largely bound by ceruloplasmin (65-90%), albumin (18%), and alpha 2-macroglobulin (12%).

Copper is an essential element in the body and is incorporated into many oxidase enzymes as a cofactor . It is also a component of zinc/copper super oxide dismutase, giving it an anti-oxidant role. Copper defiency occurs in Occipital Horn Syndrome and Menke's disease both of which are associated with impaired development of connective tissue due to the lack of copper to act as a cofactor in protein-lysine-6-oxidase. Menke's disease is also associated with progressive neurological impairment leading to death in infancy. The precise mechanisms of the effects of copper deficiency are vague due to the wide range of enzymes which use the ion as a cofactor.

Copper appears to reduce the viabilty and motility of spermatozoa . This reduces the likelihood of fertilization with a copper IUD, producing copper's contraceptive effect . The exact mechanism of copper's effect on sperm are unknown.

Zinc has three primary biological roles: catalytic, structural, and regulatory. The catalytic and structural role of zinc is well established, and there are various noteworthy reviews on these functions. For example, zinc is a structural constituent in numerous proteins, inclusive of growth factors, cytokines, receptors, enzymes, and transcription factors for different cellular signaling pathways. It is implicated in numerous cellular processes as a cofactor for approximately 3000 human proteins including enzymes, nuclear factors, and hormones .

Zinc promotes resistance to epithelial apoptosis through cell protection (cytoprotection) against reactive oxygen species and bacterial toxins, likely through the antioxidant activity of the cysteine-rich metallothioneins .

In HL-60 cells (promyelocytic leukemia cell line), zinc enhances the up-regulation of A20 mRNA, which, via TRAF pathway, decreases NF-kappaB activation, leading to decreased gene expression and generation of tumor necrosis factor-alpha (TNF-alpha), IL-1beta, and IL-8 .

There are several mechanisms of action of zinc on acute diarrhea. Various mechanisms are specific to the gastrointestinal system: zinc restores mucosal barrier integrity and enterocyte brush-border enzyme activity, it promotes the production of antibodies and circulating lymphocytes against intestinal pathogens, and has a direct effect on ion channels, acting as a potassium channel blocker of adenosine 3-5-cyclic monophosphate-mediated chlorine secretion. Cochrane researchers examined the evidence available up to 30 September 2016 .

Zinc deficiency in humans decreases the activity of serum thymulin (a hormone of the thymus), which is necessary for the maturation of T-helper cells. T-helper 1 (Th(1)) cytokines are decreased but T-helper 2 (Th(2)) cytokines are not affected by zinc deficiency in humans [A342417].

The change of Th(1) to Th(2) function leads to cell-mediated immune dysfunction. Because IL-2 production (Th(1) cytokine) is decreased, this causes decreased activity of natural-killer-cell (NK cell) and T cytolytic cells, normally involved in killing viruses, bacteria, and malignant cells [A3424].

In humans, zinc deficiency may lead to the generation of new CD4+ T cells, produced in the thymus. In cell culture studies (HUT-78, a Th(0) human malignant lymphoblastoid cell line), as a result of zinc deficiency, nuclear factor-kappaB (NF-kappaB) activation, phosphorylation of IkappaB, and binding of NF-kappaB to DNA are decreased and this results in decreased Th(1) cytokine production .

In another study, zinc supplementation in human subjects suppressed the gene expression and production of pro-inflammatory cytokines and decreased oxidative stress markers [A3424]. In HL-60 cells (a human pro-myelocytic leukemia cell line), zinc deficiency increased the levels of TNF-alpha, IL-1beta, and IL-8 cytokines and mRNA. In such cells, zinc was found to induce A20, a zinc finger protein that inhibited NF-kappaB activation by the tumor necrosis factor receptor-associated factor pathway. This process decreased gene expression of pro-inflammatory cytokines and oxidative stress markers .

The exact mechanism of zinc in acne treatment is poorly understood. However, zinc is considered to act directly on microbial inflammatory equilibrium and facilitate antibiotic absorption when used in combination with other agents. Topical zinc alone as well as in combination with other agents may be efficacious because of its anti-inflammatory activity and ability to reduce P. acnes bacteria by the inhibition of P. acnes lipases and free fatty acid levels .

Dosage

Trichoton At dosage

Acetylcysteine Tablet:

The dispersible tablet should be dissolved in 1/2 glass of water before use (preferably in the evening). The duration of treatment should be 5 to 10 days in the acute phase. It may be continued in the chronic state for up to 6 months or according to the advice of the physician.

As a mucolytic:

Adults: 600 mg daily as a single dose.
In Paracetamol overdose: Initially 140 mg/kg, followed by 70 mg/kg every 4 hours for an additional 17 doses. As an antidote, Acetylcysteine is reported to be very effective when administered within 8 hours of Paracetamol overdose, with the protective effect diminishing after this time. Initiation of treatment after a lapse of 15 hours has previously been thought to be ineffective, but recent studies suggest that beneficial results may still be obtained.

Acetylcysteine Respirator Solution:

The 20% solution may be diluted to a lesser concentration with either Sodium Chloride for injection, Sodium Chloride for inhalation, sterile water for injection, or sterile water for inhalation.

As a mucolytic:

Adult:

5-10 ml of 10% or 20% solution by nebulizer every 6-8 hr PRN.

Children:

1-11 months: 1-2 ml of 20% or 2-4 ml of 10% solution by nebulizer every 6-8 hr PRN.
12 months-11 years: 3-5 ml of 20% or 6-10 ml of 10% solution by nebulizer every 6-8 hr PRN.
Below 12 years: 5-10 ml of 10/20% solution by nebulizer every 6-8 hr PRN.

Diagnostic Bronchograms: 1-2 ml of 20% or 2-4 ml of 10% solution 2-3 times by nebulization or by instillation intratracheally prior to procedure.

Nebulization tent or croupette: This form of administration requires very large volumes of the solution, occasionally as much as 300 ml during a single treatment period. If a tent or croupette must be used, the recommended dose is the volume of acetylcysteine (using 20%) that will maintain a very heavy mist in the tent or croupette for the desired period. Administration for intermittent or continuous prolonged periods, including overnight, may be desirable.

Direct Instillation: When used by direct instillation, 1-2 ml of a 20% solution may be given as often as every hour. When used for the routine nursing care of patients with tracheostomy, 1-2 ml of a 20% solution may be given every 1-4 hours by instillation into the tracheostomy.

Side Effects

Generally, Acetylcysteine is well tolerated. However, mild effects such as nausea, headache, tinnitus, urticaria, stomatitis, rhinorrhoea, chills, fever, bronchospasm may be observed. Occasional cases of nausea and dyspepsia, rare cases of urticaria may be observed.

Toxicity

Patients experiencing an overdose may present with vomiting, nausea, bronchospasm, periorbital angioedema, and hypotension. Treat patients with symptomatic and supportive measures. Hemodialysis may remove some acetylcysteine from circulation as it is somewhat protein bound.

Prolonged skin contact may cause irritation.

Copper toxicity is belevied to be due to fenton-type redox reactions occuring with high copper concentrations which produce damaging reactive oxygen species .

According to the Toxnet database of the U.S. National Library of Medicine, the oral LD50 for zinc is close to 3 g/kg body weight, more than 10-fold higher than cadmium and 50-fold higher than mercury .

The LD50 values of several zinc compounds (ranging from 186 to 623 mg zinc/kg/day) have been measured in rats and mice .

Precaution

Acetylcysteine should be given in caution in asthma patients.

Interaction

After taking Acetylcysteine orally it increases the bioavailability of Amoxicillin, but shows no effect on Doxycycline and reduces the absorption of Cefalexin. Acetylcysteine seems to increase the effects of Nitroglycerin.

Volume of Distribution

The volume of distribution of acetylcysteine is 0.47 L/kg.

A pharmacokinetic study was done in rats to determine the distribution and other metabolic indexes of zinc in two particle sizes. It was found that zinc particles were mainly distributed to organs including the liver, lung, and kidney within 72 hours without any significant difference being found according to particle size or rat gender .

Elimination Route

An 11 g dose in the form of an effervescent tablet for solution reaches a mean C_max of 26.5 µg/mL, with a T_max of 2 hours, and an AUC of 186 µg*h/mL.

Systemic - approximately 50%

Copper absorption varies inversely with intake. Absorption range is 12-65%.

Zinc is absorbed in the small intestine by a carrier-mediated mechanism . Under regular physiologic conditions, transport processes of uptake do not saturate. The exact amount of zinc absorbed is difficult to determine because zinc is secreted into the gut. Zinc administered in aqueous solutions to fasting subjects is absorbed quite efficiently (at a rate of 60-70%), however, absorption from solid diets is less efficient and varies greatly, dependent on zinc content and diet composition .

Generally, 33% is considered to be the average zinc absorption in humans . More recent studies have determined different absorption rates for various populations based on their type of diet and phytate to zinc molar ratio. Zinc absorption is concentration dependent and increases linearly with dietary zinc up to a maximum rate [L20902].

Additionally zinc status may influence zinc absorption. Zinc-deprived humans absorb this element with increased efficiency, whereas humans on a high-zinc diet show a reduced efficiency of absorption .

Half Life

The mean terminal half life of acetylcysteine in adults is 5.6 hours and in pre-term neonates is 11 hours.

The half-life of zinc in humans is approximately 280 days .

Clearance

Acetylcysteine has a mean clearance of 0.11 L/hr/kg.

In one study of healthy patients, the clearance of zinc was found to be 0.63 ± 0.39 μg/min .

Elimination Route

An oral dose of radiolabelled acetylcysteine is 13-38% recovered in the urine in the first 24 hours, while 3% is recovered in the feces.

Copper appears to be eliminated primarily through bile .

The excretion of zinc through gastrointestinal tract accounts for approximately one-half of all zinc eliminated from the body .

Considerable amounts of zinc are secreted through both biliary and intestinal secretions, however most is reabsorbed. This is an important process in the regulation of zinc balance. Other routes of zinc excretion include both urine and surface losses (sloughed skin, hair, sweat) .

Zinc has been shown to induce intestinal metallothionein, which combines zinc and copper in the intestine and prevents their serosal surface transfer. Intestinal cells are sloughed with approximately a 6-day turnover, and the metallothionein-bound copper and zinc are lost in the stool and are thus not absorbed .

Measurements in humans of endogenous intestinal zinc have primarily been made as fecal excretion; this suggests that the amounts excreted are responsive to zinc intake, absorbed zinc and physiologic need .

In one study, elimination kinetics in rats showed that a small amount of ZnO nanoparticles was excreted via the urine, however, most of the nanoparticles were excreted via the feces .