Nizoral Drug Uses

Nizoral is a medicine used for the treatment of systemic fungal infections or for other conditions determined by your physician. You should not use Nizoral Tablets for fungal meningitis.

How Taken

It is recommended that you use Nizoral once daily until the infection has disappeared. If the infection is serious, your doctor may increase the daily dosage.

Nizoral Warnings/Precautions

You should report to your doctor any signs and symptoms which may indicate liver dysfunction so that appropriate biochemical testing can be done. Such signs and symptoms may include unusual fatigue, anorexia, nausea and/or vomiting, jaundice, dark urine or pale stools. Nizoral tablets may alter your metabolism.

Nizoral Missed Dose

If you miss a dose, use it as soon as you remember. If it is near the time for the next dose, skip the missed dose and resume your usual dosing schedule. Do not double the dose to catch up.

Nizoral Possible Side Effects

Stop taking this medicine and check with your doctor if any of these side effects occur: fever and chills; skin rash or itching; dark or amber urine; fever and sore throat; loss of appetite; pale stools; reddening.

Nizoral Storage

Store at controlled room temperature 15°-25°C (59°-77°F). Protect from moisture.

Nizoral Overdose

Seek emergency medical attention if you suspect an overdose. Symptoms of a Nizoral overdose may include: constipation; diarrhea; dizziness; drowsiness; headache; nausea; vomiting.

More Information

If your symptoms do not improve within a few weeks (or months for some infections), or if they become worse, check with your doctor.

Disclaimer

This drug information is for your information purposes only, it is not intended that this information covers all uses, directions, drug interactions, precautions, or adverse effects of your medication. This is only general information, and should not be relied on for any purpose. It should not be construed as containing specific instructions for any particular patient. We disclaim all responsibility for the accuracy and reliability of this information, and/or any consequences arising from the use of this information, including damage or adverse consequences to persons or property, however such damages or consequences arise. No warranty, either expressed or implied, is made in regards to this information.

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Tretinoin, also known as all-trans-retinoic acid (ATRA), is a naturally occurring derivative of vitamin A (retinol). Retinoids such as tretinoin are important regulators of cell reproduction, proliferation, and differentiation and are used to treat acne and photodamaged skin and to manage keratinization disorders such as ichthyosis and keratosis follicularis. Tretinoin also represents the class of anticancer drugs called differentiating agents and is used in the treatment of acute promyelocytic leukemia (APL). For the the induction of remission in patients with acute promyelocytic leukemia (APL), French-American-British (FAB) classification M3 (including the M3 variant); For the topical treatment of acne vulgaris, flat warts and other skin conditions (psoriasis, ichthyosis congenita, icthyosis vulgaris, lamellar icthyosis, keratosis palmaris et plantaris, epidermolytic hyperkeratosis, senile comedones, senile keratosis, keratosis follicularis (Darier's disease), and basal cell carcinomas.); For palliative therapy to improve fine wrinkling, mottled hyperpigmentation, roughness associated with photodamage. Tretinoin binds to alpha, beta, and gamma retinoic acid receptors (RARs). RAR-alpha and RAR-beta have been associated with the development of acute promyelocytic leukemia and squamous cell cancers, respectively. RAR-gamma is associated with retinoid effects on mucocutaneous tissues and bone. Although the exact mechanism of action of tretinoin is unknown, current evidence suggests that the effectiveness of tretinoin in acne is due primarily to its ability to modify abnormal follicular keratinization. Comedones form in follicles with an excess of keratinized epithelial cells. Tretinoin promotes detachment of cornified cells and the enhanced shedding of corneocytes from the follicle. By increasing the mitotic activity of follicular epithelia, tretinoin also increases the turnover rate of thin, loosely-adherent corneocytes. Through these actions, the comedo contents are extruded and the formation of the microcomedo, the precursor lesion of acne vulgaris, is reduced. Tretinoin is not a cytolytic agent but instead induces cytodifferentiation and decreased proliferation of APL cells in culture and in vivo. When Tretinoin is given systemically to APL patients, tretinoin treatment produces an initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission (CR). The exact mechanism of action of tretinoin in APL is unknown.

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