CHLORHEXIDINE MOUTH WASH

JAN AUSHADHI KOTTIYAM PRICE - RS 16.25

CHLORHEXIDINE MOUTH WASH 

Chlorhexidine gluconate is a germicidal mouthwash that reduces bacteria in the mouth.

Chlorhexidine gluconate oral rinse is used to treat gingivitis (swelling, redness, bleeding gums). Chlorhexidine gluconate is usually prescribed by a dentist.

Chlorhexidine gluconate oral rinse is not for treating all types of gingivitis. Use the medication only to treat the condition your dentist prescribed it for. Do not share this medication with another person, even if they have the same gum symptoms you have.

Chlorhexidine gluconate may also be used for purposes not listed in this medication guide.

BAD BREATH?

Bad breath can be caused by a decreased flow of saliva. Saliva plays an important part in digestion and helps to remove odor-causing particles in the mouth.

Bad breath when you wake up is considered normal. This happens because the saliva that regularly washes away decaying food and odors during the day diminishes at night while you sleep. Your mouth becomes dry and dead cells stick to your tongue and inside of your cheek. Bacteria use these cells as a food source and expel foul-smelling gases.

How should I use chlorhexidine gluconate?

Follow all directions on your prescription label. Do not use this medicine in larger or smaller amounts or for longer than recommended.

Rinse your mouth with chlorhexidine gluconate twice daily after brushing your teeth.

Measure your dose using the cup provided with the medication. Swish the medicine in your mouth for at least 30 seconds, then spit it out. Do not swallow the mouthwash.

Do not add water to the oral rinse. Do not rinse your mouth with water or other mouthwashes right after using chlorhexidine gluconate.

Chlorhexidine gluconate may leave an unpleasant taste in your mouth. Do not rinse your mouth to remove this taste after using the medication. You may rinse the medicine away and reduce its effectiveness.

Use this medication for the full prescribed length of time. Your symptoms may improve before your gingivitis is completely cleared. Chlorhexidine gluconate will not treat a viral or fungal infection such as cold sores, canker sores, or oral thrush (yeast infection).

Visit your dentist at least every 6 months for preventive tooth and gum care.

Store chlorhexidine gluconate at room temperature away from moisture and heat.

Usual Adult Dose for Mucositis:

Usual dose: 15 mL (approximately 0.5 fluid ounces) swished in the mouth undiluted for 30 seconds and spit out 2 times a day

Comments:

-To decrease medicinal taste, patients should not rinse with water immediately after use.

-The mouthwash should be used after meals (e.g., after breakfast and dinner).

Use:

-Use between dental visits to treat gingivitis (characterized by redness and swelling of the gingivae and gingival bleeding upon probing)

Usual Adult Dose for Periodontitis:

Usual dose: 2.5 mg (1 periodontal chip) inserted into a periodontal pocket with probing pocket depth (PD) of 5 mm or more every 3 months

Maximum dose: Up to 8 periodontal chips/visit

What is the most important information I should know about chlorhexidine gluconate?

Chlorhexidine gluconate can cause a rare but serious allergic reaction that may be life-threatening. Get emergency medical help if you have: hives, severe skin rash; wheezing, difficult breathing; cold sweats, feeling light-headed; swelling of your face, lips, tongue, or throat.

Do not give this medication to a child or teenager without a doctor's advice. This medicine may cause severe irritation or chemical burns in young children.

 STRUCTUTE

 C₂₂H₃₀Cl₂N₁₀

 1,6-bis(4-chloro-phenylbiguanido)hexane

 Space-filling model of the chlorhexidine molecule, an antiseptic. Colour code:   Carbon, C: black   Hydrogen, H: white   Nitrogen, N: blue   Chlorine, Cl: green

DEHYDROEPIANDROSTERONE 25 mg capsules

JAN AUSHADHI KOTTIYAM

Used to treat male Hypogonadizam

Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone. It is one of the most abundant circulating steroids in humans, in whom it is produced in the adrenal glands,the gonads, and the brain, where it functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids. However, DHEA also has a variety of potential biological effects in its own right, binding to an array of nuclear and cell surface receptors, and acting as a neurosteroid and neurotrophin.

FUNCTIONS

As an androgen

DHEA and other adrenal androgens such as androstenedione, although relatively weak androgens, are responsible for the androgenic effects of adrenarche, such as early pubic and axillary hair growth, adult-type body odor, increased oiliness of hair and skin, and mild acne. Women with complete androgen insensitivity syndrome (CAIS), who have a non-functional androgen receptor (AR) and are immune to the androgenic effects of DHEA and other androgens, have absent or only sparse/scanty pubic and axillary hair and body hair in general, demonstrating the role of DHEA, testosterone, and other androgens in body hair development at both adrenarche and pubarche.

As a neurosteroid

As a neurosteroid and neurotrophin, DHEA has important effects in the central nervous system.

BIOLOGICAL ACTIVITY

Hormonal activity

Androgen receptor

Although it functions as an endogenous precursor to more potent androgens such as testosterone and DHT, DHEA has been found to possess some degree of androgenic activity in its own right, acting as a low affinity (Ki = 1 μM), weak partial agonist of the androgen receptor (AR). However, its intrinsic activity at the receptor is quite weak, and on account of that, due to competition for binding with full agonists like testosterone, it can actually behave more like an antagonist depending on circulating testosterone and dihydrotestosterone (DHT) levels, and hence, like an antiandrogen. However, its affinity for the receptor is very low, and for that reason, is unlikely to be of much significance under normal circumstances.

Estrogen receptors

In addition to its affinity for the androgen receptor, DHEA has also been found to bind to and activate the ERα and ERβ estrogen receptors with Ki values of 1.1 μM and 0.5 μM, respectively, and EC50 values of >1 μM and 200 nM, respectively. Though it was found to be a partial agonist of the ERα with a maximal efficacy of 30–70%, the concentrations required for this degree of activation make it unlikely that the activity of DHEA at this receptor is physiologically meaningful. Remarkably however, DHEA acts as a full agonist of the ERβ with a maximal response similar to or actually slightly greater than that of estradiol, and its levels in circulation and local tissues in the human body are high enough to activate the receptor to the same degree as that seen with circulating estradiol levels at somewhat higher than their maximal, non-ovulatory concentrations; indeed, when combined with estradiol with both at levels equivalent to those of their physiological concentrations, overall activation of the ERβ was doubled. As such, it has been proposed that DHEA may be an important and potentially major endogenous estrogen in the body.

Other nuclear receptors

DHEA does not bind to or activate the progesterone, glucocorticoid, or mineralocorticoid receptors.Other nuclear receptor targets of DHEA besides the androgen and estrogen receptors include the PPARα, PXR, and CAR. However, whereas DHEA is a ligand of the PPARα and PXR in rodents, it is not in humans. In addition to direct interactions, DHEA is thought to regulate a handful of other proteins via indirect, genomic mechanisms, including the enzymes CYP2C11 and 11β-HSD1 – the latter of which is essential for the biosynthesis of the glucocorticoids such as cortisol and has been suggested to be involved in the antiglucocorticoid effects of DHEA – and the carrier protein IGFBP1.

Neurosteroid activity

Neurotransmitter receptors

DHEA has been found to directly act on several neurotransmitter receptors, including acting as a positive allosteric modulator of the NMDA receptor, as a negative allosteric modulator of the GABAA receptor, and as an agonist of the σ1 receptor.
Neurotrophin receptors

In 2011, the surprising discovery was made that DHEA, as well as DHEA-S, directly bind to and activate the TrkA and p75NTR, receptors of neurotrophins like nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), with high affinity. DHEA was subsequently also found to bind to the TrkB and TrkC with high affinity, though it notably activated the TrkC but not the TrkB. DHEA and DHEA-S bound to these receptors with affinities that were in the low nanomolar range (around 5 nM), although the affinities were nonetheless approximately two orders of magnitude lower relative to highly potent polypeptide neurotrophins like NGF (0.01–0.1 nM). In any case, DHEA and DHEA-S both circulate at requisite concentrations to activate these receptors and were thus identified as important endogenous neurotrophic factors. They have since been labeled "steroidal microneurotrophins", due to their small-molecule and steroidal nature relative to their polypeptide neurotrophin counterparts.Subsequent research has suggested that DHEA and/or DHEA-S may in fact be phylogenetically ancient "ancestral" ligands of the neurotrophin receptors from early on in the evolution of the nervous system. The findings that DHEA binds to and potently activates neurotrophin receptors may explain the positive association between decreased circulating DHEA levels with age and age-related neurodegenerative diseases.
Microtubule-associated protein 2
Similarly to pregnenolone, its synthetic derivative 3β-methoxypregnenolone (MAP-4343), and progesterone, DHEA has been found to bind to microtubule-associated protein 2 (MAP2), specifically the MAP2C subtype (Kd = 27 µM). However, it is unclear whether DHEA increases binding of MAP2 to tubulin like pregnenolone.

DIACEREIN 50

JAN AUSHADHI KOTTIYAM PRICE - RS - 36.11 / 10 CAP

Diacerein blocks the chemicals that cause inflammation and pain. It builds cartilage (the hard connective tissue in the bones near the joints) in the body.

Diacerein is also known as diacetylrhein, is a slow-acting medicine of the class anthraquinone used to treat joint diseases such as osteoarthritis (swelling and pain in the joints).It works by inhibiting interleukin-1 beta. An updated 2014 Cochrane review found diacerein had a small beneficial effect on pain.Diacerein-containing medications are registered in some European Union and Asian countries and included as a treatment option on several international therapeutic guidelines.

PHARMACOLOGY
 Diacerein works by blocking the actions of interleukin-1 beta, a protein involved in the inflammation and destruction of cartilage that play a role in the development of symptoms of degenerative joint diseases such as osteoarthritis. Due to its specific mode of action, which does not involve the inhibition of prostaglandin synthesis, diacerein has been shown to have anti-osteoarthritis and cartilage stimulating properties in vitro and animal models.

 DOSAGE AND ADMINISTRATION
The recommended starting dose is 50 mg once daily with evening meal for the first 2 to 4 weeks of treatment, after which the recommended daily dose is 50mg twice daily.The treatment should be taken with food, one with breakfast and the other with evening meal. The capsules must be swallowed intact, without opening them, together with a glass of water.

Special Warning
In 2014 the European Medicines Agency (EMA’s) Pharmacovigilance and Risk Assessment Committee (PRAC) performed a review of diacerein-containing medicines over concerns about its gastrointestinal and liver effects. As a result, the PRAC has introduced additional proposals to manage diacerein’s risks and was satisfied that with new restrictions diacerein’s benefit on pain outweighs the side effects for osteoarthritis treatment.The following recommendations have been made around the use of diacerein:

    Due to the potential complications that can occur as a result of diarrhea in older adults, diacerein is no longer recommended in patients aged 65 years and above.
    It is also advised that patients start treatment on half the normal dose (i.e. 50 mg daily instead of 100 mg daily), and should stop taking diacerein if diarrhea occurs.
    It should not be used in any patient with liver disease or a history of liver disease, and doctors should be monitoring their patients for early signs of liver problems.
    The use of diacerein is to be limited to treating symptoms of osteoarthritis affecting the hip or knee.
    Diacerein should not be administered during pregnancy and lactation.

The PRAC concluded that the benefit-risk balance of diacerein-containing medicinal products remained favourable in the symptomatic treatment osteoarthritis, subject to the agreed changes to the product information and conditions.

 

BRAND	COMPANY	MRP For 10 S
JAS KOTTIYAM	JAN USHADHI KOTTIYAM	36.11
DYCERIN 50	GLENMARK	101.60
ARTHOCERIN 50	PULSE	79.00
ORCERIN 50	MACLEODS	87.70
OSTEOGARD 50	MICRO	90.00
DURAJOINT 50	ABOTT	91.00

C₁₉H₁₂O₈
 Diacetylrhein; Diacerhein;