Find information on thousands of medical conditions and prescription drugs.

Flucytosine

Flucytosine, a fluorinated pyrimidine analogue, is a synthetic antimycotic drug. Chemically it is referred to as 4-amino-5-fluoro-2(1H)-pyrimidinon. The sum formula is C4H4FN3O. Fucytosine has the CAS-Number 2022-85-7. It is structurally related to the cytostatic flourouracil and to floxuridine. It is available in oral and in some countries also in injectable form. A common brand name is AncobonĀ®. The drug is dispensed in capsules of 250 mg and 500 mg strength. The injectable form is diluted in 250ml NaCl-solution to contain 2.5 grams totally (10mg per ml). more...

Home
Diseases
Medicines
A
B
C
D
E
F
Captagon
Famohexal
Famotidine
Faslodex
Faslodex
Fasoracetam
Felbamate
Felbatol
Felodipine
Felypressin
Femara
Femara
Fempatch
Femring
Fenfluramine
Fenofibrate
Fentanyl
Fexofenadine
Filgrastim
Filipin
Finasteride
Fioricet
Fiorinal
Flagyl
Flarex
Flavoxate
Flecainide
Flexeril
Flomax
Flonase
Flovent
Floxuridine
Fluacizine
Flucloxacillin
Fluconazole
Flucytosine
Fludarabine
Fludrocortisone
Flumazenil
Flunisolide
Flunitrazepam
Fluocinonide
Fluohexal
Fluorometholone
Fluorouracil
Fluoxetine
Fluphenazine
Flurazepam
Flutamide
Fluticasone
Fluvastatin
Fluvoxamine
FML
Focalin
Folic acid
Follutein
Fomepizole
Formoterol
Fortamet
Fortovase
Fosamax
Fosinopril
Fosinoprilat
Fosmidomycin
Fosphenytoin
Frova
Frovatriptan
Frusehexal
Fulvestrant
Fumagillin
Furazolidone
Furosemide
Furoxone
Fusafungine
Fusidic acid
Fuzeon
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

The solution is physically incompatible with other drugs including Amphotericin B.

Pharmacology

Mechanisms of action

Two major mechanisms of acton have been elucidated, one is that the drug is intrafungally converted into the cytostatic flourouracil that undergoes further steps of activation and finally interacts as 5-fluorouridinetriphosphate with RNA-biosynthesis and disturbs therefore the building of certain essential proteins. The other mechanism is the conversion into 5-flourodeoxyuridinemonophosphate which inhibits fungal DNA-synthesis.

Spectrum of susceptible fungi and Resistance

Flucytosine is as well in vitro and in vivo active against some strains of Candida and Cryptococcus. Limited studies demonstrate that Flucytosine may be of value against infections with Sporothrix, Aspergillus, Cladosporium, Exophila, and Phialophora. Resistance is quite commonly seen as well in treatment naive patients and under current treatment with Flucytosine. In different strains of Candida resistance has been noted to occur in 1 to 50% of all specimen obtained from patients.

Pharmacokinetic data

Flucytosine is well absorbed (75 to 90%) from the GI-Tract. Intake with meals slows the resorption, but does not decrease the amount resorbed. Following an oral dose of 2 grams peak serum levels are reached after approximately 6 hours. The time to peak level decreases with continued therapy. After 4 days peak levels are measured after 2 hours. The drug is eliminated renally. In normal patients Flucytosine has reportedly a half-life of 2.5 to 6 hours. In patients with impared renal function higher serum levels are seen and the drug tends to cumulate in these patients. The drug is mainly excreted unchanged in the urine (90% of an oral dose) and only traces are metabolized and excreted in the feces. Therapeutic serum levels range from 25 to 100mcg/ml. Serum levels in exceed of 100mcg are associated with a higher incidence of side-effects. Periodic measurements of serum levels are recommended for all patients and are a must in patients with renal damage.

Human overdose

Symptoms and their severities are unknown, because Flucytosine is used under close medical supervision, but expected to be an excess of the usually encountered side-effects on bone-marrow, GI-Tract, liver, and kidney-function. Vigouros hydration and hemodialysis may be helpful to remove the drug from the body. Hemodialysis is particular useful in patients with impaired renal function.

Human carcinogenity

It is not known, if Flucytosine is a human carcinogen. The issue has been raised because traces of 5-fluorouracil, which is a known carcinogen, are found in the colon resulting from the metabolization of Flucytosine.

Read more at Wikipedia.org


[List your site here Free!]


Pseudoallescheria boydii breast implant infection in a lung transplant recipient
From CHEST, 10/1/05 by Hina Sahi

INTRODUCTION: Pseudoallescheria boydii is a ubiquitous fungus present in soil, sewage and polluted waters. Although the clinical spectrum is wide, the most frequent disease in immunocompetent individuals is a mycetoma. An increasing number of cases of disseminated infections are reported in immunocompromised patients yet a review of the lung transplant literature yields relatively few cases of disseminated infection. The clinical and histopathological presentation of Psedoallescheria boydii infection is similar to Aspergillus spp and Fusarium spp; therefore culture is necessary to make the correct diagnosis. This is especially relevant since infection due to Psedoallescheria boydii is often resistant to antimycotic drugs such as Amphoterecin B and Flucytosine, which are commonly used to treat Aspergillus infections.

CASE PRESENTATION: A 57-year-old female patient, status post a right single lung transplant 14 months ago for COPD, presented to the hospital with complaints of severe left mastalgia. She had bilateral silicone breast implants placed twenty five years ago. She was maintained on routine triple drug therapy consisting of Tacrolimus, Mycophenolate mofetil and Prednisone. She was also on routine opportunistic infection prophylaxis with Itraconazole, Valgancyclovir and Trimethoprim-Sulfamethaoxazole. Recently the patient was diagnosed with Grade A1B0 acute rejection on surveillance bronchoscopy which had not resolved inspite of two treatments with pulse steroids. The patient reported a one week history of severe, continuous left breast pain with concomitant tight sided pleuritic chest pain. In addition she had developed painful skin lesions on both thighs and blurting of vision. On examination the left breast was swollen, warm and exquisitely tender to touch around the implant capsule.

She had multiple skin lesions which were approximately one centimeter in diameter, red, warm, tender and nonblanching. Neurological exam revealed ptosis of the left eyelid and third cranial nerve palsy. CT scan chest showed a loculated right pleural effusion suggestive of empyema and a persistent right lower lobe parenchymal nodule. Skin biopsy from the thigh lesion revealed a fungal abscess with pseudohyphae consistent with Pseudoallescheria spp. An MRI breast revealed marked inflammatory enhancement around the left silicone breast implant. Bilateral breast implants were emergently surgically removed. Microscopic evaluation of the left implant capsule demonstrated evidence of invasion by fungal hyphae. MRI brain revealed multiple ring enhancing lesions in the parenchyma suggestive of a hematogenously disseminated infection. The patient was treated with high dose intravenous Voriconazole. Multiple tissue cultures grew Pseudoallescheria boydii. We suspect that the initial nidus was the pulmonary nodule, with hematogenous dissemination at a time of increased immunosuppression. We were unable to identify a definite exposure inspite of extensive questioning. This makes it difficult to predict any future re-infection.

DISCUSSIONS: P.boydii may cause life-threatening illness in the lung transplant population. Early diagnosis should be done by fungal culture so that adequate therapy may be initiated. In the pre Voriconazlole era, disseminated infection in the lung transplant population was uniformly fatal. However in recent years there have been some treatment successes with the use of Voriconazole. To our knowledge this is the first reported case of breast implant infection with Psedoallescheria boydii in the lung transplant population. This raises questions regarding the safety of these foreign bodies in an immunosuppressed population prone to opportunistic infections. There may be a case here for removal of such foreign bodies prior to transplant. We reviewed our lung transplant database but could not identify any other case of breast implant infection.

CONCLUSION: Cosmetic foreign bodies in a lung transplant recipient have the potential to be infected, due to the immune suppressed nature of the patient. There should be a low threshold to remove such implants during the pre-transplant work up, if agreeable to the patient.

DISCLOSURE: Hina Sahi, None.

Hina Sahi MD * Marie Budev DO Robin Avery MD Cleveland Clinic Foundation, Cleveland, OH

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

Return to Flucytosine
Home Contact Resources Exchange Links ebay