Administration of the drug for 8 days did not effectively shorten the recovery period compared with the average reported in the literature without the drug and may. A complicating factor is that several commonly used anti-cancer drugs are prone to cause agranulocytosis thus interfering with treatment.
One is characterised by sudden destruction of large numbers of leucocytes in peripheral blood by antibodies elicited in.
Drug induced agranulocytosis treatment. An unexpected precipitous fall in peripheral leucocyte count may occur during treatment of certain sensitised individuals with drugs usually well tolerated by most people. Three basic mechanisms for drug sensitivity have been found. One is characterised by sudden destruction of large numbers of leucocytes in peripheral blood by antibodies elicited in.
The application of granulocyte-macrophage and granulocyte colony stimulation factors GM-CSF and G-CSF has been progressively increased in the treatment of patients with agranulocytosis. The aim of our study was to compare the time of neutrophil recovery in patients with severe agranulocytosis treated with G-CSF or GM-CSF and the historical control group. We have studied 6 patients with agranulocytosis treated.
Drugs most often associated with neutropenia or agranulocytosis include dipyrone diclofenac ticlopidine calcium dobesilate spironolactone antithyroid drugs eg propylthiouracil carbamazepine sulfamethoxazole- trimethoprim 3-lactam antibiotics clozapine levamisole and vancomycin. A third type involves development of agranulocytosis following a latent period during which a sensitive patient is treated with large amounts of chlorpromazine. This type of reaction is associated with production of bone marrow insufficiency in a patient who is believed to have a limited proliferative potential of bone marrow cells which limit compensatory bone marrow response during treatment with.
Any patient with suspected drug-induced agranulocytosis should be admitted immediately to a hospital with facilities for isolation monitoring and treatment by a medical and nursing team experienced in the management of neutropenia. A full drug history including over-the-counter medicines should be taken. A 48-year-old woman who was treated for thyrotoxicosis with methimazole developed agranulocytosis.
The methimazole was stopped and treatment with subcutaneous granulocyte colony-stimulating factor G-CSF was initiated. Administration of the drug for 8 days did not effectively shorten the recovery period compared with the average reported in the literature without the drug and may. G-CSF was applied in three patients with acute iatrogenic immunological agranulocytosis after ticlopidine thimazol and aminoglutethimide complicated by severe infections.
Before this treatment was started no improvement had been achieved despite the administration of antibiotics and corticosteroids for 4 to 9 days. Two patients had anaemia and one–thrombocytopenia probably due to the damage to. To demonstrate that drug-induced agranulocytosis can occur after a very prolonged period of low-dose treatment with antithyroid medications.
We present the history and long-term follow-up of a patient with Graves disease including clinical and laboratory findings and provide a brief review of the related literature. Nine patients with drug-induced agranulocytosis received recombinant human granulocyte colony-stimulating factor rhG-CSF to accelerate myeloid recovery because of life-threatening infections related to neutropenia. All patients showed a quick recovery of their granulocyte counts.
Side effects were substantial however. Three patients two with a severe infection and one with preexisting pulmonary. Góra-Tybor J Krykowski E Robak T.
Treatment of drug-induced agranulocytosis with colony stimulating factors G-CSF or GM-CSF. Arch Immunol Ther Exp Warsz 1996. Arch Immunol Ther Exp Warsz 1996.
Agranulocytosis may be caused by many drugs. High-risk drugs include antithyroid drugs clozapine ticlopidine sulfasalazine dipyrone trimethoprimsulfamethoxazole carbamazepine and probably rituximab. Suspect drugs should be stopped immediately.
If you have an infection your healthcare provider will prescribe antibiotics and other medications to. Granulocyte colony-stimulating factor G-CSF. Your provider may recommend injections of a drug to help your body.
Agranulocytosis is a serious side effect of antithyroid drugs. To ascertain the knowledge of patients and review the quality of information available on the internet. A questionnaire survey was performed for patients receiving antithyroid drugs.
Patients attending endocrine clinics who were receiving antithyroid drug treatment group A n 33 were interviewed. Under an Elsevier user license. Antithyroid drugs are widely used to treat hyperthyroidism especially Graves disease but they tend to cause agranulocytosis which increases the mortality rate.
Granulocyte colony-stimulating factor decreases. Other drugs that interfere with or inhibit granulocyte colony formation may induce agranulocytosis. Drugs with this characteristic include valproic acid carbamazepine and the beta-lactam antibiotics.
A complicating factor is that several commonly used anti-cancer drugs are prone to cause agranulocytosis thus interfering with treatment. Morbidity and perhaps mortality of antithyroid drug-induced agranulocytosis. 1 Introduction Antithyroid drug ATD therapy is one option for the treatment of hyperthyroidism together with surgery and radioactive iodine.
Long-term remission of hyperthy-roidism can be achieved in about 50 of patients with Graves disease treated with ATDs 1. Rine-induced agranulocytosis by re-exposing them to the drug 4. Within 2 hr a drop in leukocyte count was observed con-firming the relationship between drug and reaction.
Another experiment showed that blood transfused from agranulocyto-sis patient to normal controls resulted in a rapid drop in neu-trophil count 5. It also suggested mechanisms involving pre-.