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This entry may involve drug content, and any online drug advice cannot replace the doctor's advice.
Triamcinolone acetonide and econazole cream Triamcinolone acetonide is white or white-like crystalline powder; Tasteless. This product is soluble in acetone, slightly soluble in chloroform, slightly soluble in ethanol and slightly soluble in water. Take the specific rotation of this product, accurately weigh it, add dioxane to dissolve it and dilute it quantitatively to make a solution containing 10mg per 1ml, and measure it according to law (Appendix ⅵ E), and the specific rotation is+10/to+107. Its effect is similar to that of triamcinolone acetonide, and its anti-inflammatory and anti-allergic effects are strong and lasting. It takes effect within a few hours after intramuscular injection, and reaches the maximum effect after 1 ~ 2 days, and the effect can last for 2 ~ 3 weeks.
Chinese name
triamcinolone acetonide
Foreign name
triamcinolone acetonide
Another name
Triamcinolone acetonide; triamcinolone acetonide
CAS number
76-25-5
EINECS number
200-948-7
structural formula
C24H3 1FO6
molecular weight
434.5
content
99%
use
It is an adrenocortical hormone.
catalogue
1 User Manual
2 identification
3 check
4 content determination
5 determination method
Six signs
7 Usage and dosage
Eight preventive measures
9 Adverse reactions
10 treatment of eczema
1 1 Toxicity of the substance
explain
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Chinese alias: triamcinolone acetonide; Triamcinolone acetonide; Relieve inflammation and relaxation; Triamcinolone acetonide; Triamcinolone acetonide-a; Triamcinolone acetonide-a; 9- fluoro-1 1b, 2 1- dihydroxy-16a, 17-[( 1- methyl ethylene) bis (oxygen)]-progesterone-/kloc.
Si Nuo. : 76-25-5
EINECSno。 : 200-948-7
Molecular formula: C24H3 1FO6.
Molecular weight: 434.5
Content: 99%
Quality standard: EP5
Physical and chemical properties: white or white-like crystalline powder; Odorless, almost tasteless, soluble in acetone, insoluble in water, slightly soluble in chloroform, stable in nature.
Function: It is an adrenocortical drug used for neurodermatitis, eczema, psoriasis, joint pain, bronchial asthma and other diseases.
Packing specification: 5KG/ aluminum foil bag
This product is white or white-like crystalline powder; Tasteless. The preparation is triamcinolone acetonide injection. Its effect is similar to that of triamcinolone acetonide, and its anti-inflammatory and anti-allergic effects are strong and lasting. It takes effect within a few hours after intramuscular injection, and reaches the maximum effect after 1 ~ 2 days, and the effect can last for 2 ~ 3 weeks. basis
This product is soluble in acetone, slightly soluble in chloroform, slightly soluble in ethanol and slightly soluble in water.
Take this product for specific rotation, accurately weigh it, add dioxane to dissolve it and dilute it quantitatively to make a solution containing 10mg per 1ml, and determine it according to the law (Appendix ⅵ E), and the specific rotation range is+10/to+107.
distinguish
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(1) Accurately weigh this product 10mg, dissolve it in ethanol and dilute it to 100ml, accurately measure it in a measuring bottle from 10ml to 100ml, dilute it to scale with ethanol, and use spectrophotometry (Appendix Ⅳ a) at the wavelength of 225.
(2) The infrared absorption spectrum of this product should be consistent with the control spectrum (spectrum group 603).
cheque
edit
triamcinolone acetonide
According to the fluorine inspection method (Appendix VIII E), the fluorine content of this product should be 4.0% ~ 4.75%.
For other steroids, add chloroform-methanol (9: 1) to make a solution of 1.0% as the test solution;
Accurately measure an appropriate amount, add chloroform-methanol (9: 1) and dilute it to 0.02% solution as control solution. Take a thin layer of color.
Spectroscopic test (Appendix ⅴ b): Absorb the above two solutions 10μl, respectively spot them on the same silica gel GF254nm thin-layer plate, and use dichloromethane-ether-methanol-water (77: 15:8: 1.2) as developing agent, spread them out, and dry them.
Loss on drying takes this product and dries it to constant weight at 65438 005℃, and the weight loss shall not exceed 65438 0.5% (Appendix VIII L).
Residue on ignition shall not exceed 0.2% (Appendix VIII n).
The selenium content is 0. 10g, which should meet the requirements (0.0050%) after inspection according to law (Appendix VIII D).
Content determination
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This product is adrenocortical hormone. 9- fluoro-1 1β, 2 1- dihydroxy-1 6alpha, 17[( 1- methylethylene) bis (oxygen)]-progesterone-/kloc.
The content of alkene-3,20-dione should be 97.0% ~ 102.0% based on dry product.
According to high performance liquid chromatography (appendix ⅴ d).
Octadecylsilane bonded silica gel is used as a filler for chromatographic conditions and system suitability test. The mobile phase was methanol-water (70:30), and the detection wavelength was 240nm. The theoretical plate number calculated by triamcinolone acetonide peak should be not less than 2500, and the separation degree between triamcinolone acetonide peak and internal standard peak should be greater than 2.0.
The internal standard solution is a solution containing 0.65438 0.05 mg per 65438 0 ml with fluocinolone acetate and methanol.
Determination method Take an appropriate amount of triamcinolone acetonide reference substance, accurately weigh it, add methanol to dissolve it, and dilute it quantitatively to make a solution containing about 0.65438±0.3mg per 65438±0ml; Accurately measure 5ml solution and 5ml internal standard solution, put them into 25ml volumetric flask, dilute them to scale with methanol, shake them evenly, inject them into 25μl liquid chromatograph, and record the chromatogram; Take an appropriate amount of this product and determine it by the same method. Calculate the peak area according to the internal standard method.
assay method
edit
Method Name: Triamcinolone acetonide-Triamcinolone acetonide-HPLC
Scope of application: This method uses high performance liquid chromatography to determine the content of triamcinolone acetonide in triamcinolone acetonide bulk drug.
This method is suitable for triamcinolone acetonide bulk drug.
Methods: The sample was dissolved in methanol and diluted quantitatively, and then separated by HPLC. The peak area of triamcinolone acetonide was detected at the wavelength of 240nm by ultraviolet absorption detector, and its content was calculated.
Reagent: methanol
Instruments and equipment: 1. tool
1. 1 HPLC
1.2 column
Using octadecylsilane bonded silica gel as filler, the theoretical plate number should be not less than 5000 according to triamcinolone acetonide peak calculation.
1.3 ultraviolet absorption detector
2. Chromatographic conditions
2. 1 mobile phase: methanol and water =525 475.
2.2 Detection wavelength: 240 nm
2.3 column temperature: room temperature
Sample preparation:
1. Preparation of reference solution
Accurately weigh an appropriate amount of triamcinolone acetonide reference substance, dissolve it in methanol, and quantitatively dilute it to about 30? In each 1 ml. The solution of g is the reference solution.
2. Preparation of test solution
Accurately weigh a proper amount of sample, dissolve it with methanol and dilute it quantitatively to about 30? Triamcinolone acetonide per 1 ml. The solution of g is the solution to be tested.
Note: "Accurate weighing" means that the weighing should be accurate to one thousandth of the weighing. "Precise measurement" means that the accuracy of measuring volume should meet the accuracy requirements of volume pipette in national standards.
Operating steps: Accurately absorb 20mL of control solution and 20 ml of test solution respectively, inject them into high performance liquid chromatograph, measure the peak area of triamcinolone acetonide (C24H3 1FO6) at the wavelength of 240nm with ultraviolet absorption detector, and calculate its content.
References: China Pharmacopoeia, edited by National Pharmacopoeia Committee, Chemical Industry Press, 2005, Part II, p. 200.
indicate
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Is suitable for various dermatoses (such as neurodermatitis, eczema, psoriasis, etc.). ), joint pain, bronchial asthma, scapulohumeral periarthritis, tenosynovitis, acute sprain, chronic low back pain, and ophthalmic inflammation.
dosage
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Intramuscular injection: 20- 100 mg once a week; Subcutaneous or intra-articular injection, generally 2.5-5mg, no more than 30mg per day and no more than 75mg per week. Ointment can also be used externally. Eye drops, 1-4 times a day. Aerosol 3-4 times a day. Intra-articular injection may cause joint injury. Long-term use of eye drops will lead to an increase in intraocular pressure.
Matters needing attention
edit
Storage: sealed from light.
Indications: Suitable for various skin diseases (such as neurodermatitis, eczema, psoriasis, etc.). ), joint pain, bronchial asthma, scapulohumeral periarthritis, tenosynovitis, acute sprain, chronic low back pain, and ophthalmic inflammation.
Administration and dosage: intramuscular injection, 20- 100mg once a week; Subcutaneous or intra-articular injection, generally 2.5-5mg, no more than 30mg per day and no more than 75mg per week. Ointment and eye drops can also be used externally, 1-4 times a day. Aerosol is injected 3-4 times a day. Intra-articular injection may cause joint injury. Long-term use of eye drops will lead to an increase in intraocular pressure.
Contraindications: Viral, tuberculous and acute suppurative eye diseases are not allowed. Pregnant women should not use it for a long time.
counteraction
edit
Triamcinolone acetonide and econazole cream
High dose of this product is easy to cause diabetes, digestive tract ulcer and Cushing-like syndrome, and has a strong inhibitory effect on hypothalamus-pituitary-adrenal axis. Concurrent infection is the main adverse reaction.
1. Long-term use of high-dose corticosteroids can cause metabolic disorders of water, salt, sugar, protein and fat: centripetal obesity, full moon face, hirsutism, weakness, hypokalemia, edema, hypertension and diabetes. , clinically known as Cushing's syndrome. These symptoms can be cured without special treatment. Generally, it will gradually subside after stopping the drug and return to normal after several months or a long time. If necessary, antihypertensive and hypoglycemic drugs can be used, and symptomatic treatments such as low pressure, low sugar and high protein diet and potassium supplementation can be given. Therefore, patients with hypertension, arteriosclerosis, renal insufficiency and diabetes should be properly supplemented with vitamin D and calcium, and corticosteroids should be used with caution.
2. Induce or aggravate infection: Corticosteroids have anti-inflammatory effect, but no antibacterial effect, which can reduce the body's anti-infection ability and is conducive to the growth, reproduction and spread of bacteria. Therefore, long-term use of glucocorticoids can induce infection or expand or spread the potential infection focus in vivo, and also spread the original static tuberculosis focus. Attention should be paid to the change of illness and whether there is any phenomenon of inducing infection during medication, and anti-infection treatment should be given at the same time.
3. Induce or aggravate peptic ulcer: Glucocorticoid can not only hinder tissue repair and delay tissue healing, but also increase gastric acid and pepsin secretion, reduce gastric mucus secretion, reduce gastric mucosal resistance, induce or aggravate gastric and duodenal ulcer bleeding, and even cause digestive tract perforation.
4, nervous system symptoms: excitement, insomnia, individual patients can induce psychosis, epilepsy patients can induce seizures. Therefore, psychotic patients, mental patients and epileptic patients should be banned.
5. Adrenal cortex atrophy or dysfunction: Long-term use of such drugs will affect the secretion of adrenocorticotropic hormone in hypothalamus and anterior pituitary gland, reduce the secretion of endogenous glucocorticoid or lead to adrenal cortex dysfunction, thus causing negative feedback. Once you encounter stress, such as bleeding and infection, you may experience dizziness, nausea, vomiting, hypotension, hypoglycemia or hypoglycemia coma.
6, rebound phenomenon and withdrawal symptoms: long-term use of hormonal drugs, when the symptoms are basically controlled, if the reduction is too large or suddenly stop taking drugs, the original symptoms or rapid aggravation can occur, this phenomenon is called rebound phenomenon. This is because the patient is dependent on hormones or the symptoms are not completely controlled. The treatment is to restore the dosage of hormone, and then gradually reduce it after the symptoms are controlled.
Treatment of eczema
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The World Health Organization (WHO) clearly pointed out in its guidance document on immune desensitization therapy that "immune desensitization therapy is the only fundamental therapy that can completely treat allergic eczema". The authoritative organization of international allergy research also puts forward that "high-quality standardized desensitizer should be used, and the best allergy treatment scheme should be adopted at the same time, including removing eczema allergen, immune repair of patients, symptomatic drug treatment of allergic eczema complicated with skin inflammation, and standardized desensitizer immunotherapy, which is referred to as" four in one and four therapy "scheme.
First, we should try to find allergens. Sometimes allergens are difficult to find, and they may not be clear, because people are exposed to too many things. You can record what you ate three days ago when you get sick from your mouth. If you eat something many times, your rash will get worse. Remember not to eat in the future. In addition, we should pay attention to environmental factors. Don't go where there are many flowers and pollen. Wear a mask when going out in pollen season. There are also common allergies, such as allergies to frames and allergies to the decoration of belts, which should be avoided. Because you start to feel itchy after using a cosmetic, it generally means that you are allergic to the ingredients in the cosmetic, so don't use this cosmetic. This is prevention first, try to find the reason. Can't find the reason. Try to avoid some allergic factors in life.
Second, eczema can be itchy, and scratching often aggravates skin lesions. In fact, dermatitis tickles more and more, causing a vicious circle. So, don't scratch when it itches, it tends to tickle more and more.
Third, see a doctor. You can take some antiallergic drugs for rash and chlorpheniramine and antihistamine for severe itching. Doctors will prescribe some drugs for external use, the most common being corticosteroids. There are more than 20 kinds of hormone drugs, and the hormones are strong and weak. We advocate not using the strongest medicine at first. The strongest medicine is not suitable for long-term use and has side effects. You can also use some topical ointments and potions.
Substance toxicity
edit
Experimental data of toxic effects reported in literature and periodicals
figure
Toxicity type
test method
test object
Dosage used
toxic effect
1
acute toxicity
intramuscular injection
Adult male
57 1 μ g/kg
1. Vascular toxicity-shock
2. Toxicity of skin and accessories-dermatitis (after systemic contact)
3. Immune system toxicity-anaphylactic shock
2
acute toxicity
Parenteral
Adult female
4 mg/kg
1. Behavioral toxicity-muscle weakness
2. Vascular toxicity-high blood pressure, no autonomic ganglia.
three
acute toxicity
Subcutaneous/subcutaneous injection
mouse
13 100 μ g/kg
Except for lethal dose, no other values were reported for detailed effects.
four
acute toxicity
take orally
mouse
5 mg/kg
Except for lethal dose, no other values were reported for detailed effects.
five
acute toxicity
Intraperitoneal injection
mouse
105mg/kg
Except for lethal dose, no other values were reported for detailed effects.
six
acute toxicity
Subcutaneous/subcutaneous injection
mouse
132mg/kg
Except for lethal dose, no other values were reported for detailed effects.
seven
Mutation toxicity
Human cells
1 nmol/l
eight
Mutation toxicity
Human cells
10 nmol/l
nine
Mutation toxicity
Skin surface
mankind
5000 ppm
10
Mutation toxicity
Skin surface
mankind
5000 ppm
1 1
Mutation toxicity
Mouse cells
1 nmol/l
12
Mutation toxicity
Mouse leukocytes
10 nmol/l
13
Reproductive toxicity
Skin surface
Adult female
10 1 mg/kg, 12- 29 weeks after pregnancy.
1. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
2. Reproductive toxicity-abnormal development of gastrointestinal system
14
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
450 ug/kg, female 1 1- 19 days after conception.
1. Reproductive toxicity-affecting delivery
2. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
3. Reproductive toxicity-decrease of neonatal weight gain.
15
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
900 mg/kg, 1 1- 19 days after pregnancy.
1. Reproductive toxicity-Embryo or fetal death
16
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
1 mg/kg, female 14- 15 days after conception.
1. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
17
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
2 mg/kg, female 14- 15 days after conception.
1. Reproductive toxicity-increased mortality after implantation
18
Reproductive toxicity
intramuscular injection
mouse
375 ug/kg, female 12- 14 days after conception.
1. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
19
Reproductive toxicity
intramuscular injection
mouse
500 μ g/kg, after female conception 14 days.
1. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
2. Reproductive toxicity-affecting the fetus
20
Reproductive toxicity
intramuscular injection
mouse
750 ug/kg, 12- 14 days after female conception.
1. Reproductive toxicity-affecting newborns
2 1
Reproductive toxicity
intramuscular injection
mouse
1500 ug/kg, 12- 14 days after female conception.
1. Reproductive toxicity-abnormal development of urinary system
22
Reproductive toxicity
intramuscular injection
mouse
750 ug/kg, 12- 14 days after female conception.
1. Reproductive toxicity-increased mortality after implantation
2. Reproductive toxicity-affecting litter size
3. Reproductive toxicity-Embryo or fetal death
23
Reproductive toxicity
Intraperitoneal injection
mouse
13 mg/kg, 12 days after female conception.
1. Affect the reproductive toxicity of the fetus.
24
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
12800 ug/kg, female pregnancy 1 1- 14 days later.
1. Reproductive toxicity-increased mortality after implantation
25
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
960 ug/kg, 1 1- 14 days after female conception.
1. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
26
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
2500 μ g/kg, after female conception 12 days.
1. Reproductive toxicity-increased mortality after implantation
2. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
27
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
10 mg/kg, female pregnancy 1 1 day.
1. Reproductive toxicity-Embryo or fetal death
2. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
28
Reproductive toxicity
Subcutaneous/subcutaneous injection
mouse
12800 ug/kg, female pregnant 1 1 days.
1. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
29
Reproductive toxicity
intramuscular injection
mouse
480 ug/kg, 1 1- 14 days after female conception.
1. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
30
Reproductive toxicity
intramuscular injection
mouse
10 mg/kg, female pregnancy 1 1 day.
1. Affect the reproductive toxicity of the fetus.
3 1
Reproductive toxicity
intramuscular injection
mouse
5 mg/kg, 1 1 day after female conception.
1. Reproductive toxicity-increased mortality after implantation
2. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
32
Reproductive toxicity
intramuscular injection
mouse
10 mg/kg, female pregnancy 1 1 day.
1. Reproductive toxicity-genetic material that affects fetal or embryonic cells
33
Reproductive toxicity
intramuscular injection
mouse
10 mg/kg, female pregnancy 1 1 day.
1. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
2. Reproductive toxicity-Embryo or fetal death
3. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
34
Reproductive toxicity
Inflow in endlessly.
mouse
650 μ g/kg, 6- 18 days after female conception.
1. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
35
Reproductive toxicity
Inflow in endlessly.
mouse
6500 ug/kg, 6- 18 days after female conception.
1. Reproductive toxicity-increased mortality before embryo implantation
36
Reproductive toxicity
intramuscular injection
monkey
50 mg/kg, 23-3 1 day after female conception.
1. Reproductive toxicity-abnormal development of central nervous system
2. Reproductive toxicity-abnormal ear/eye development
3. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
37
Reproductive toxicity
intramuscular injection
monkey
60 mg/kg, 465438+ 0-44 days after female conception.
1. Reproductive toxicity-abnormal development of skull and face (including nose/tongue)
2. Reproductive toxicity-abnormal development of musculoskeletal system
3. Reproductive toxicity-abnormal development of blood and lymphatic system (including spleen and bone marrow)
38
Reproductive toxicity
intramuscular injection
monkey
60 mg/kg, 465438+ 0-44 days after female conception.
1. Reproductive toxicity-fetal toxicity (such as fetal dysplasia, but not death)
2. Reproductive toxicity-Embryo or fetal death
39
Reproductive toxicity
intramuscular injection
monkey
50 mg/kg, 23-3 1 day after female conception.
1. Reproductive toxicity-abnormal steady-state development of the body
40
Reproductive toxicity
intramuscular injection
monkey
3 mg/kg, 63-65 days after female conception.
1. Reproductive toxicity-abnormal development of respiratory system
4 1
Reproductive toxicity
intramuscular injection
hamster
500 μ g/kg, 9 days after female conception.
1. Reproductive toxicity-increased mortality after implantation
2. Reproductive toxicity-abnormal development of central nervous system
3. Reproductive toxicity-other developmental abnormalities
Forty two.
Reproductive toxicity
intramuscular injection
hamster
100 ug/kg, female pregnancy 1 1 days.
1. Reproductive toxicity-abnormal development of endocrine system
2. Reproductive toxicity-affecting the biochemistry and metabolism of newborns.
[ 1-30]
reference data
1. Yearbook of Drug Treatment. (Harvey Whitney Books, Cincinnati, Ohio, 42696, 45242) v. 26- 1992-: 28, 13 10, 1994.
2. Dutch medical journal. (Elsevier Science, POB 2 1 1, 1000 AE Amsterdam. Netherlands)
3. Future drugs. (J.R. Prous, S.A., Apartado de Correos 540,08080, Barcelona, Spain) v.1-1975/76-:6,44, 198 1
4. Gegen Yakuji. Medicine monthly. (Yakugyo Jihosha, Inaoka Mansion, No.2-36, Hamamachi, Kanda Town, Chiyoda District, Tokyo, Japan, zip code:101) v.1959-:21,21.
5. Japanese drugs (ethical drugs). (Yakugyo Jiho Co., Ltd., Tokyo, Japan): 65 16 1982
6. Cancer research. (Public Ledger Building, Room 8 16, 6th floor & chestnuts Sts. Philadelphia, Pennsylvania19106) v.1-1941-:43,2664, 1983.
7. Archives of Dermatology. (AMA, No.535 dearborn Street, Chicago, Illinois, 606 10) Phone number: 82-1960-:103,39, 197 1
8. Psoriasis, Proceedings of the International Symposium, Stanford, California, 197 1, edited by Farber, E.M. and A.J. Cox. , Stanford University Press, Stanford, California, 197 1:-335, 197 1
9.Arzneimittel-Forschung。 Drug research. (Editio Cantor Press, postal code 1255, W-7960 Aulendorf, Federal Reserve. The representative of Germany. )V. 1- 195 1- : 36， 1782， 1986
10. Cancer research. (Public Ledger Building, Room 8 16, 6th floor & chestnuts Sts. Philadelphia, Pennsylvania19106) v.1-1941-:43,2536, 1983.
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