Bkon Plus Czs

Uses

Chromium is an ingredient found in a variety of supplements and vitamins.

Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms .

Mecobalamin is used for-

• Peripheral Neuropathies
• Diabetic Neuropathy
• Verteberal Syndrome
• Nerve Compression Syndrome
• Multiple sclerosis
• Amyotrophic lateral sclerosis
• Parkinson’s disease
• Alzheimer’s disease
• Diabetic retinopathy
• Entrapment neuropathy
• Drug induced neuropathy
• Megaloblastic anemia due to Vitamin B12 deficiency

Pyridoxine (vitamin B6) is used to prevent or treat low levels of vitamin B6 in people who do not get enough of the vitamin from their diets. Most people who eat a normal diet do not need extra vitamin B6. However, some conditions (such as alcoholism, liver disease, overactive thyroid, heart failure) or medications (such as isoniazid, cycloserine, hydralazine, penicillamine) can cause low levels of vitamin B6. Vitamin B6 plays an important role in the body. It is needed to maintain the health of nerves, skin, and red blood cells.

Pyridoxine has been used to prevent or treat a certain nerve disorder (peripheral neuropathy) caused by certain medications (such as isoniazid). It has also been used to treat certain hereditary disorders (such as xanthurenic aciduria, hyperoxaluria, homocystinuria).

Selenium is an ingredient found in a variety of supplements and vitamins.

For the supplementation of total parenteral nutrition to prevent hyposelenemia .

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 .

Bkon Plus Czs is also used to associated treatment for these conditions: Mineral supplementationVitamin B12 Deficiency, Nutritional supplementationBackache, Dizziness, Fever, Headache, Hepatic; Functional Disturbance, Hepatitis, Iron Deficiency Anemia (IDA), Ketosis, Macrocytic anemia, Menière's Disease, Menstrual Distress (Dysmenorrhea), Metabolic Acidosis, Motion Sickness, Nausea and vomiting, Neuralgia, Sciatic, Neuritis, Neurological Conditions caused by B Vitamin Deficiency, Secondary anemia, Soreness, Muscle, Toothache, Toxinfectious state, Trigeminal Neuralgia (TN), Vitamin B1 deficiency, Vitamin B12 Deficiency, Vitamin B6 Deficiency, Vitamin Deficiency, Minor aches and pains, Minor pain, Nutritional supplementation, Supplementation, Vitamin supplementation, Wellness of the LiverNutritional 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 Bkon Plus Czs works

Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules . Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake . Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt.

Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein . As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells . Chromium attenuates the activity of PTP-1B in vitro, which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling . Transient upregulation of AMPK by chromium also leads to increased glucose uptake .

Vitamin B6 is the collective term for a group of three related compounds, pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM), and their phosphorylated derivatives, pyridoxine 5'-phosphate (PNP), pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP). Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).

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 .

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

Bkon Plus Czs dosage

Tablet: The usual adult dosage is one 500 mcg tablet three times daily. The dosage should be adjusted according to the age of patient and the severity of symptoms.

Injection:

• Peripheral neuropathies: The usual adult dosage is one ampoule equivalent to 500 mcg of Mecobalamin, administered intramuscularly or intravenously three times a week.The dosage should be adjusted according to the age of patient and the severity of symptoms.
• Megaloblastic anemia: The usual adult dosage is one ampoule equivalent to 500 mcg of Mecobalamin, administered intramuscularly or intravenously three times a week. After about two months of administration, dosage should be changed to one ampoule equivalent to 500 mcg of Mecobalamin every one to three months as maintenance therapy

ADULTS:

BY MOUTH:

• For hereditary sideroblastic anemia: Initially, 200-600 mg of vitamin B6 is used. The dose is decreased to 30-50 mg per day after an adequate response.
• For vitamin B6 deficiency: In most adults, the typical dose is 2.5-25 mg daily for three weeks then 1.5-2.5 mg per day thereafter. In women taking birth control pills, the dose is 25-30 mg per day.
• For abnormally high levels of homocysteine in the blood: For reducing high levels of homocysteine in the blood after childbirth, 50-200 mg of vitamin B6 has been taken alone. Also, 100 mg of vitamin B6 has been taken in combination with 0.5 mg of folic acid.
• For preventing macular degeneration: 50 mg of vitamin B6 in the form of pyridoxine has been used daily in combination with 1000 mcg of vitamin B12 (cyanocobalamin) 1000 mcg and 2500 mcg of folic acid for about 7 years.
• For hardening of the arteries (atherosclerosis): A specific supplement (Kyolic, Total Heart Health, Formula 108, Wakunga) containing 250 mg of aged garlic extract, 100 mcg of vitamin B12, 300 mcg of folic acid, 12.5 mg of vitamin B6, and 100 mg of L-argininedaily for 12 months.
• For kidney stones: 25-500 mg of vitamin B6 has been used daily.
• For nausea during pregnancy: 10-25 mg of vitamin B6 taken three or four times per day has been used. In people who don't respond to vitamin B6 alone, a combination product containing vitamin B6 and the drug doxylamine (Diclectin, Duchesnay Inc.) is used three or four times per day. Also, another product containing 75 mg of vitamin B6, 12 mcg of vitamin B12, 1 mg of folic acid, and 200 mg of calcium (PremesisRx, KV Pharmaceuticals) is used daily.
• For symptoms of premenstrual syndrome (PMS): 50-100 mg of vitamin B6 is used daily, alone or along with 200 mg of magnesium.
• For treating tardive dyskinesia: 100 mg of vitamin B6 per day has been increased weekly up to 400 mg per day, given in two divided doses.

INJECTED INTO THE MUSCLE:

• Hereditary sideroblastic anemia: 250 mg of vitamin B6 daily, reduced to 250 mg of vitamin B6 weekly once adequate response is achieved.

CHILDREN:

BY MOUTH:

• For kidney stones: Up to 20 mg/kg daily in children aged 5 years and up.

INJECTED INTO THE VEIN OR MUSCLE:

• For seizures that respond to vitamin B6 (pyridoxine-dependent seizures): 10-100 mg is recommended.

The daily recommended dietary allowances (RDAs) of vitamin B6 are:

• Infants 0-6 months, 0.1 mg
• Infants 7-12 months, 0.3 mg
• Children 1-3 years, 0.5 mg
• Children 4-8 years, 0.6 mg
• Children 9-13 years, 1 mg
• Males 14-50 years, 1.3 mg
• Males over 50 years, 1.7 mg
• Females 14-18 years, 1.2 mg
• Females 19-50 years, 1.3 mg
• Females over 50 years, 1.5 mg
• Pregnant women, 1.9 mg
• Breast-feeding women, 2 mg
• Some researchers think the RDA for women 19-50 years should be increased to 1.5-1.7 mg per day.

The recommended maximum daily intake is:

• Children 1-3 years, 30 mg
• Children 4-8 years, 40 mg
• Children 9-13 years, 60 mg

Adults, pregnant and breast-feeding women:

• 14-18 years, 80 mg
• over 18 years, 100 mg

Side Effects

Generally Mecobalamin is well tolerated. However, a few side effects like GI discomfort (including anorexia, nausea or diarrhea) & rash may be seen after administration of Mecobalamin.

Pyridoxine usually has no side effects when used in recommended doses.

If your doctor has prescribed this medication, remember that he or she has judged that the benefit to you is greater than the risk of side effects. Many people using this medication do not have serious side effects.

Pyridoxine can cause side effects when taken in large doses for a long time. Tell your doctor right away if any of these unlikely but serious side effects occur: headache, nausea, drowsiness, numbness/tingling of arms/legs.

A very serious allergic reaction to this drug is rare. However, seek immediate medical attention if you notice any symptoms of a serious allergic reaction, including: rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing.

This is not a complete list of possible side effects. If you notice other effects not listed above, contact your doctor or pharmacist.

Toxicity

Oral LD50 for Cr (VI) is 135 - 175 mg/kg in mouse and 46 - 113 mg/kg in rat . Oral LD50 for Cr (III) in rat is >2000 mg/kg . LD50 of chromium (III) oxide in rats is reported to be > 5g/kg . Other LD50 values reported for rats include: 3.5 g/kg (CI 3.19-3.79 g/kg) for chromium sulphate; 11.3 g/kg for chromium (III) acetate; 3.3 g/kg for chromium nitrate; and 1.5 g/kg for chromium nitrate nonahydrate .

Acute overdose of chromium is rare and seriously detrimental effects of hexavalent chromium are primarily the result of chronic low-level exposure . In case of overdose with minimal toxicity following acute ingestion, treatment should be symptomatic and supportive . There is no known antidote for chromium toxicity.

Hexavalent chromium is a Class A carcinogen by the inhalation route of exposure and Class D by the oral route . The oral lethal dose in humans has been estimated to be 1-3 g of Cr (VI); oral toxicity most likely involves gastrointestinal bleeding rather than systemic toxicity . Chronic exposure may cause damage to the following organs: kidneys, lungs, liver, upper respiratory tract . Soluble chromium VI compounds are human carcinogens. Hexavalent chromium compounds were mutagenic in bacteria assays and caused chromosome aberrations in mammalian cells. There have been associations of increased frequencies of chromosome aberrations in lymphocytes from chromate production workers . In human cells in vitro, Cr (VI) caused chromosomal aberrations, sister chromatid exchanges and oxidative DNA damage .

Oral Rat LD50 = 4 gm/kg. Toxic effects include convulsions, dyspnea, hypermotility, diarrhea, ataxia and muscle weakness.

Oral LD50 of 6700mg/kg in rats . Selenium exposure is teratogenic and can result in fetal death as tested in mice. Chronic toxicity is characterized by hair loss, white horizontal streaking on fingernails, paronchyia, fatigue, irritability, hyperreflexia, nausea, vomiting, garlic odor on breath, and metallic taste . Serum selenium correlates weakly with symtoms. Blood chemistry as well as liver and kidney function are normally unnaffected. Acute toxicity presents as stupor, respiratory depression, and hypotension. ST elevations and t-wave changes characteristic of myocardial infarction may be observed.

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

The medicine should not be used for months if there is no response at all after its use for a certain period of time.

Before taking pyridoxine, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.

During pregnancy, this vitamin has been found to be safe when used in recommended doses.

This vitamin passes into breast milk and is considered to be safe during breast-feeding when used in recommended doses. Consult your doctor for more information.

Interaction

Decreased GI tract absorption with neomycin, aminosalicylic acid, H2-blockers and colchicine. Reduced serum concentrations with oral contraceptives. Reduced effects in anaemia with parenteral chloramphenicol.

The effects of some drugs can change if you take other drugs or herbal products at the same time. This can increase your risk for serious side effects or may cause your medications not to work correctly. These drug interactions are possible, but do not always occur. Your doctor or pharmacist can often prevent or manage interactions by changing how you use your medications or by close monitoring.

To help your doctor and pharmacist give you the best care, be sure to tell your doctor and pharmacist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products) before starting treatment with this product. While using this product, do not start, stop, or change the dosage of any other medicines you are using without your doctor's approval.

Some products that may interact with this vitamin include: altretamine, cisplatin, phenytoin.

This vitamin may interfere with certain laboratory tests (including urine test for urobilinogen), possibly causing false test results. Make sure laboratory personnel and all your doctors know you use this vitamin.

Volume of Distribution

Absorbed chromium is distributed to all tissues of the body and its distribution in the body depends on the species, age, and chemical form . Circulating Cr (III) following oral or parenteral administration of different compounds can be taken up by tissues and accumulates in the liver, kidney, spleen, soft tissue, and bone .

Pyridoxine main active metabolite, pyridoxal 5’-phosphate, is released into the circulation (accounting for at least 60% of circulating vitamin B6) and is highly protein bound, primarily to albumin.

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

Chromium compounds are both absorbed by the lung and the gastrointestinal tract. Oral absorption of chromium compounds in humans can range between 0.5% and 10%, with the hexavalent (VI) chromium more easily absorbed than the trivalent (III) form . Absorption of chromium from the intestinal tract is low, ranging from less than 0.4% to 2.5% of the amount consumed . Vitamin C and the vitamin B niacin is reported to enhance chromium absorption .

Most hexavalent Cr (VI) undergoes partial intragastric reduction to Cr (III) upon absorption, which is an action mainly mediated by sulfhydryl groups of amino acids . Cr (VI) readily penetrates cell membranes and chromium can be found in both erythrocytes and plasma after gastrointestinal absorption of Cr (IV). In comparison, the presence of chromium is limited to the plasma as Cr (III) displays poor cell membrane penetration . Once transported through the cell membrane, Cr (VI) is rapidly reduced to Cr (III), which subsequently binds to macromolecules or conjugate with proteins. Cr (III) may be bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF).

The B vitamins are readily absorbed from the gastrointestinal tract, except in malabsorption syndromes. Pyridoxine is absorbed mainly in the jejunum. The Cmax of pyridoxine is achieved within 5.5 hours.

Oral bioavailability of 90% when given as L-selenomethionine . Tmax of 9.17h.

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 elimination half-life of hexavalent chromium is 15 to 41 hours .

The total adult body pool consists of 16 to 25 mg of pyridoxine. Its half-life appears to be 15 to 20 days.

Half life was observed to increase with chronic dosing time . For day 1-2 half life was 1.7 days. For day 2-3 half life was 3 days. For day 3-14 half life was 11.1 days.

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

Clearance

Excretion of chromium is via the kidneys ranges from 3 to 50 μg/day . The 24-hour urinary excretion rates for normal human subjects are reported to be 0.22 μg/day .

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

Elimination Route

Absorbed chromium is excreted mainly in the urine, accounting for 80% of total excretion of chromium; small amounts are lost in hair, perspiration and bile . Chromium is excreted primarily in the urine by glomerular filtration or bound to a low molecular-weight organic transporter .

The major metabolite of pyridoxine, 4-pyridoxic acid, is inactive and is excreted in urine

Mainly excreted in urine as 1beta-methylseleno-N-acetyl-d-galactosamine and trimethylselenonium . The amount excreted as 1beta-methylseleno-N-acetyl-d-galactosamine plateaus at doses around 2microg after which the amount excreted as trimethylselenonium increases. Some selenium is also excreted in feces when given orally .

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 .

Pregnancy & Breastfeeding use

Not recommended during pregnancy & lactation.

Category A: Controlled studies in women fail to demonstrate a risk to the foetus in the 1st trimester (and there is no evidence of a risk in later trimesters), and the possibility of foetal harm remains remote.

Contraindication

Hypersensitivity to any component of this product.

Special Warning

Use in children: Not recommended.

Storage Condition

Oral: Store at room temperature. Protect from moisture and light.

Parenteral: Store at room temperature. Do not expose to direct light.

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