Sulfinpyrazone ~ Antigout
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An antigout drug that has a uricosuric and pronounced antiplatelet effect. By reducing the reabsorption of uric acid in the proximal tubules of the nephron, it increases its excretion by the kidneys, especially in the first stage of treatment. After several weeks of continuous treatment, there is a marked decrease in the intensity and frequency of gout attacks, arthralgia is significantly reduced and joint mobility is increased. After a few weeks or months, tophi and periarticular urate deposits disappear; The formation of new deposits is significantly prevented. Reduces platelet adhesiveness and their tendency to aggregate, weakens the platelet release reaction, inhibits the synthesis of thromboxane A in platelets, and has a protective effect on the vascular endothelium. The duration of action of a single dose of the drug is 8-12 hours. Read more about the drug »
ATTENTION! ALWAYS check with your doctor or pharmacist to see if the found analogue can serve as a full replacement for the drug prescribed to you or the drug you are looking for. This is due to the need to use the dosage forms and doses prescribed specifically for you, which may differ even among analogues (more about analogues of drugs).
Hypersensitivity, “aspirin” asthma, peptic ulcer of the stomach and duodenum (in the acute stage), liver and/or renal failure (creatinine clearance less than 30 ml/min), nephrourolithiasis (including a history), during excretion with urine more than 800 mg of urates/day, concomitant therapy with cytostatics, radiation therapy of the tumor, blood disorders, pregnancy, lactation, childhood. With caution. History of blood disorders and peptic ulcer of the stomach and duodenum, chronic renal failure (CC Side effects:
Allergic reactions (skin rash, dermatitis, hyperthermia), dyspepsia, nausea, vomiting, abdominal pain, diarrhea;
gastrointestinal bleeding, agranulocytosis, leukopenia, thrombocytopenia, aplastic anemia, pancytopenia, exacerbation of gout (massive excretion of uric acid or lituresis at the beginning of treatment), impaired renal function. Overdose. Symptoms: nausea, vomiting, epigastric pain, diarrhea, ataxia, convulsions, shortness of breath, acute renal failure, coma. Treatment: gastric lavage, symptomatic therapy, intravenous dextrose. There is no specific antidote. If necessary, hemodialysis. Interaction:
Strengthens the effect of anticoagulants, antiplatelet agents, fibrinolytics, hypoglycemic and antigout drugs;
increases T1/2 of oral hypoglycemic drugs, penicillin and sulfonamides. Ethanol, ethacrynic acid, thiazide diuretics reduce effectiveness. Salicylates exhibit antagonism to the uricosuric effect and increase the risk of bleeding; Saluretics increase plasma urate concentrations. Combination with allopurinol leads to an additive effect. Special instructions:
Treatment with sulfinpyrazone in patients with gouty arthritis begins 2-3 weeks after an acute attack of gout.
If an attack occurs while using the drug, treatment should be continued simultaneously with colchicine or NSAIDs. The drug increases the incidence of an acute attack of gout at the beginning of treatment; therefore, the listed drugs should be prescribed simultaneously during the first 3-6 months of treatment (however, this also does not prevent the occurrence of an acute attack of gout). The patient should receive a sufficient amount of fluid (at least 2-3 l/day); urine should be alkalinized (sodium bicarbonate 3-7.5 g/day or potassium citrate 7.5 g/day) since increased excretion of uric acid during acidic urine may contribute to the formation of stones (in the first few months of treatment) in the urinary tract. During the treatment period, it is recommended to determine the level of uric acid in the blood serum and urine for 24 hours in order to adjust the dose of the drug; in patients with chronic renal failure, renal function. Should be taken with food or antacid medications to reduce gastrointestinal side effects. When prescribed to patients who have recently suffered a myocardial infarction, it is recommended to regularly perform a general urine test and determination of creatinine and urea, especially at the beginning of therapy. During the treatment period, it is necessary to monitor the prothrombin index. When diagnosing urates, diuretics should be stopped 2-3 days before the start of the study. When simultaneously prescribing ASA or other drugs that can affect hemostasis, the patient should be advised of the need to immediately consult a doctor in case of any unusual bleeding. For children, the dosage regimen is not defined. Preparations containing the active substance Sulfinpyrazone:
Anturan, Apo-Sulfinpyrazone
The information provided in this section is intended for medical and pharmaceutical professionals and should not be used for self-medication. The information is provided for informational purposes only and cannot be considered official.
Fluxum®
Fluxum® cannot be administered intramuscularly.
Parnanapine-induced thrombocytopenia
It is known that Fluxum®, like heparin itself and other low molecular weight heparins, can cause thrombocytopenia. Heparin-induced thrombocytopenia usually develops 4-10 days after the start of treatment or earlier in case of repeated cases. In 10-20% of patients, early mild thrombocytopenia (platelets >100,000/μl) occurs, which may persist or regress with continued treatment. As a result of the formation of antibodies to the heparin/platelet factor 4 complex, in some cases a more severe immune form, heparin-induced thrombocytopenia type II, may develop, followed by thrombus formation and thromboembolism in the arteries of the brain, lungs, lower extremities, etc., often with a fatal outcome. These patients may develop a new thrombus associated with thrombocytopenia caused by irreversible heparin-induced platelet aggregation, so-called white clot syndrome.
During treatment with Fluxum®, patients should be carefully monitored. Therefore, in the event of thrombocytopenia or in the event of symptoms associated with a new thrombotic event, or in the event of worsening of a previous thrombotic event, low molecular weight heparin should be discontinued. Alternative anticoagulant therapy should be attempted after discontinuation of heparin. Immediate use of oral anticoagulant therapy should be avoided as exacerbation of thrombosis has been observed.
During long-term treatment, the platelet count should be determined before starting therapy with Fluxum® and 2 times a week for the first month, and then monitoring of the platelet count may be less frequent. Fluxum should be prescribed with extreme caution to patients with a history of thrombocytopenia caused by heparin or other low molecular weight heparin; their platelet count should be performed every day. If thrombocytopenia occurs during heparin treatment, low molecular weight heparin therapy may be an alternative treatment option. In this case, the platelet count should be determined daily and, if thrombocytopenia persists, then low molecular weight heparin should be discontinued as early as possible. If thrombocytopenia is less than 100,000/μl, if thrombosis occurs and progresses, Fluxum® must be discontinued and the patient transferred to another anticoagulant therapy. Switching to oral anticoagulant therapy in these cases is not recommended, since thrombosis progression is known.
If heparin-induced thrombocytopenia is suspected, in vitro platelet aggregation tests do not have much diagnostic value; specialist consultation is necessary.
Spinal/epidural anesthesia
Carrying out spinal or epidural anesthesia, spinal-epidural analgesia or lumbar puncture during the prophylactic use of Fluxum®, as well as other low-molecular-weight heparins, may be complicated by spinal or epidural hematoma with the development of persistent or irreversible paralysis. The risk of these complications increases with the use of epidural catheters, the use of concomitant NSAIDs, antiplatelet drugs or anticoagulants, trauma or repeated spinal punctures, the presence of underlying hemostatic disorders, or in elderly patients. If it is necessary to carry out anesthesia/analgesia of this type during the prophylactic use of the drug Fluxum®, the presence of these risk factors should be carefully checked before these interventions. Typically, spinal catheters are installed no earlier than 8-12 hours after the last administration of a prophylactic dose of low molecular weight heparin. Fluxum® should not be administered 2-4 hours before and after insertion/removal of a catheter. The injection should be delayed or canceled if blood is aspirated from the spinal canal during spinal or epidural anesthesia. The catheter should be removed as soon as possible after (8-12 hours) the last prophylactic administration of Fluxum®.
Particular attention should be paid to patients who received Fluxum® before or after epidural or spinal anesthesia, checking for the presence of neurological symptoms such as low back pain, sensory and motor disorders (numbness or weakness in the lower extremities), bowel or bladder dysfunction. Patients should be informed of the need to immediately consult a doctor if these symptoms appear. If an epidural or spinal hematoma is suspected, prompt diagnosis and treatment, including spinal cord decompression, is required.
Non-interchangeability of sodium parnaparin with other low molecular weight heparins and unfractionated heparin.
Parnaparin cannot be interchanged (unit for unit) with unfractionated heparin, with other low molecular weight heparins or with synthetic polysaccharides. Each of these drugs differs in their starting materials, manufacturing process, physicochemical, biological and clinical properties, resulting in differences in biochemical identity, dosage and possibly clinical efficacy and safety. Each of these medications is unique and has its own instructions for use. If skin necrosis occurs, treatment with Fluxum® must be interrupted.
Switching from Fluxum® to oral anticoagulants
— Switching from Fluxum® to vitamin K antagonists (VKA).
Since there is an interval before VKA reaches its maximum effect, treatment with Fluxum® should not be interrupted until the required INR (International Normalized Ratio) is achieved.
— Switching to direct oral anticoagulants (DOAs):
These drugs should not be prescribed simultaneously with Fluxum®.
Treatment with DOACs should be initiated at the end of the recommended parnaparin treatment period and at the exact time that subsequent parnaparin administration would have been scheduled if parnaparin treatment had been continued.
There is no experience with the use of Fluxum® in patients with mechanical prosthetic valves (including pregnant women).
Heparins may suppress adrenal aldosterone secretion, leading to hyperkalemia, especially in patients with diabetes mellitus, chronic renal failure, pre-existing metabolic acidosis, elevated plasma potassium levels, or taking potassium-sparing medications. The risk of hyperkalemia appears to increase with duration of therapy but is usually reversible. Plasma potassium levels should be measured in patients at risk before initiating heparin therapy and then monitored regularly, especially if treatment is extended beyond 7 days.
Children: the use of Fluxum® in patients under 18 years of age is included in the “Contraindications” because efficacy and safety have not been established. Elderly patients: Elderly patients (especially those over eighty years of age) may be at greater risk of bleeding complications, so close clinical monitoring is recommended. However, there is no need to reduce the recommended doses of Fluxum® unless renal function is seriously impaired.
Renal Impairment: As stated in the Precautions section of the Contraindications section, the use of Fluxum® in patients with renal impairment should be used with caution and is associated with increased drug exposure, which increases the risk of bleeding: therefore, careful clinical monitoring is recommended. In cases of severe renal impairment (creatine clearance <30 ml/min), an increased risk of bleeding may also be observed at recommended doses, so a reduction in the Fluxum® dose may be required in these patients and monitoring of plasma anti-Xa activity is recommended.
Hepatic impairment: As advised in the Precautions section of the Contraindications section, the use of Fluxum® should also be used with caution in patients with impaired liver function, again due to the increased risk of bleeding: careful clinical monitoring is also recommended. .
Busulfan (Busulfanum)
Before intravenous administration, the contents of the vial are diluted with 0.9% sodium chloride solution or 5% dextrose solution in a volume 10 times the volume of the vial, to a final concentration of at least 0.5 mg/ml. To do this, the required amount of busulfan is taken with a syringe with a needle and a filter with a pore size of 5 microns (supplied with the drug), after which the needle is changed and the contents of the syringe are introduced into a container with a previously prepared solution of 0.9% sodium chloride or 5% dextrose solution. In all cases, busulfan should be introduced into the solvent, and not vice versa. The resulting solution is stirred by inversion.
Rapid infusions of busulfan are not recommended. Infusion pumps should be used. Before and after each infusion, it is necessary to flush the catheter with 5 ml of 0.9% sodium chloride or 5% dextrose solution.
Patients with hyperuricemia and/or hyperuricosuria require correction of these conditions before starting treatment with busulfan.
If delayed myelotoxicity is possible, it is recommended to discontinue treatment with busulfan or reduce its dose at the first sign of a sudden marked decrease in the number of leukocytes (particularly granulocytes) in order to prevent irreversible myelosuppression.
Some patients may be more sensitive to busulfan and exhibit rapid myelosuppression. Frequent and careful monitoring of peripheral blood parameters is necessary. The decrease in the number of leukocytes is exponential in nature and the construction of a semi-logarithmic dependence of the weekly decrease in the number of leukocytes makes it possible to predict the time for their number to reach 15 × 109/l and discontinuation of the drug.
Cytological examinations of the lungs, bladder, breast, cervix, lymph nodes, pancreas and thyroid glands, adrenal glands, bone marrow - cell dysplasia induced by busulfan can be severe and complicate the interpretation of cytological preparations.
Busulfan causes myelosuppression, which increases the incidence of microbial infections, slows wound healing and increases gum bleeding. If possible, all dental work should be completed before starting chemotherapy and should only be resumed once myelosuppression has resolved.
Dimethylacetamide (a solvent included in the busulfan dosage form) can cause increased transaminase activity and neurological symptoms.
A diluted solution of busulfan is stable for less than 8 hours at room temperature (25°C) and less than 12 hours when stored in the refrigerator. The infusion should be completed by this time.
The tablet form of the drug is stored in a tightly sealed container at a temperature below 40 ° C (preferably 15-25 ° C), unless otherwise prescribed by the manufacturer.
The solution for intravenous administration is stored at a temperature of 2-8 °C.
Use is only possible under the supervision of a physician experienced in chemotherapy.
Before and during treatment (at short intervals), it is necessary to determine the level of hemoglobin or hematocrit, the number of leukocytes (total, differential), platelets, alanine aminotransferase activity, alkaline phosphatase, bilirubin level, uric acid concentration, constant monitoring of kidney and lung function is required.
If you experience the following symptoms: chills, fever, cough or hoarseness, pain in the lower back or side, painful or difficult urination, bleeding or bruising, black stools, blood in the urine or stool, consult your doctor immediately.
Leukopenia develops from 10-15 days after the start of therapy (before this there is a short-term increase in the number of leukocytes), the lowest level is observed on the 11-30th day of treatment (may decrease within 1 month after discontinuation of the drug), the level of leukocytes is restored over the next 12- 20 weeks (in case of severe myelosuppression, treatment should be discontinued until symptoms of hematotoxicity resolve). In case of myelodepression (pancytopenia), after stopping busulfan, the number of formed elements is restored to the normal level within 1 month - 2 years.
If nausea and vomiting occur, busulfan should be continued; at the first signs of interstitial pneumosclerosis, treatment should be stopped. Bronchopulmonary dysplasia with the development of pneumosclerosis, accompanied by a decrease in the vital function of the lungs and the elasticity of the lung tissue, can develop within 8 months - 10 years (on average 4 years) after the start of treatment, and death is possible within 6 months after diagnosis.
If thrombocytopenia occurs, extreme caution is recommended when performing invasive procedures, regular inspection of intravenous injection sites, skin and mucous membranes (to identify signs of bleeding), limiting the frequency of venipuncture and avoiding intramuscular injections, monitoring blood content in urine, vomit, and feces. Such patients need to be careful when shaving, doing manicures, brushing their teeth, using dental floss and toothpicks, and performing dental procedures; constipation should be prevented, falls and other injuries should be avoided, as well as alcohol and acetylsalicylic acid, which increase the risk of gastrointestinal bleeding.
In order to prevent nephropathy caused by increased formation of uric acid (occurs most often in the initial stage of treatment), it is necessary to consume a sufficient amount of fluid, increase diuresis, prescribe allopurinol (in some cases) and use drugs that cause urine alkalinization.
In patients with increased seizure activity, treatment should be carried out under the protection of anticonvulsants (preferably benzodiazepines, since enzyme inducers, such as phenytoin, can increase the clearance of busulfan and reduce its effectiveness).
If a dose is missed, the dose is not replaced, and the subsequent dose is not doubled.
The vaccination schedule should be delayed (not earlier than 3 months or even up to 1 year after completion of the last course of chemotherapy) for the patient and other family members living with him (immunization with oral polio vaccine should be avoided). Avoid contact with infectious patients or use non-specific measures for prevention (protective mask, etc.).
Use in pediatric practice should be avoided since the safety and effectiveness of its use in children have not been determined. During treatment, adequate contraception should be used.
In case of contact of the drug with skin or mucous membranes, thoroughly rinse with water (mucous membranes) or water and soap (skin).
