Fludeoxyglucose F 18 (Systemic)


VA CLASSIFICATION
Primary: DX201

Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).

Not commercially available in Canada.



Category:


Diagnostic aid, radioactive (brain disorders; cardiac disease; inflammation/infection; neoplastic disease)—

Indications

Note: The bracketed information and the use of the superscript 1 in this monograph reflect the lack of labeled (approved) indications for this product {93}.

Accepted

Brain imaging1—Positron emission tomography (PET) using FDG is used in the evaluation of cerebral glucose metabolism in various physiological and pathological states {03}{53}. FDG-PET is indicated for the identification of regions of abnormal glucose metabolism associated with foci of epileptic seizures{06}{12}{15}{16}{23}{39}{50}{57}{59}{93}{96}.
Note:  It is used to examine glucose metabolism in [ Alzheimer's-type dementia]1, providing means of detecting early- to late-stage dementia, and a differential diagnosis from confounding conditions, such as multi-infarct dementia, pseudodementia, thyroid disease, normal-pressure hydrocephalus, and normal aging{10}{11}{23}{50}{98}. FDG-PET is also used in [behavior-metabolism relationship studies]1, to test for normal function or deficits in motor, visual, sensory, memory, and cognitive functions in the brain{08}{23}{53}. FDG-PET can be used to determine the degree and extent of injury in acute and chronic stages of a [stroke]1, providing criteria for reversible injury and a means of establishing proper selection and evaluation of therapy{23}. Studies indicate that FDG-PET may be used in the evaluation of traumatic brain injury{101}{102}{103}. FDG-PET can be used in the diagnosis of [mental depression]1, to differentiate unipolar from bipolar depression, as well as to differentiate chronic depression (pseudodementia) from Alzheimer's disease{97}{07}{23}.



Cardiac imaging, positron emission tomographic (diagnostic)1—FDG-PET is indicated in coronary artery disease and left ventricular dysfunction, when used together with myocardial perfusion imaging, for the identification of viable and ischemic{97} left ventricular myocardium with residual glucose metabolism and reversible loss of systolic function.{14}{23}{26}{29}{39}{50}{55}{96}
Note: FDG-PET is used in conjunction with perfusion imaging agents{97} to predict, preoperatively, the presence of reversible regional [wall-motion abnormalities]1, which is helpful in the selection of patients in whom revascularization may lead to improved ventricular function{20}{21}{46}. These combinations are also used as a pre- and post-[aortocoronary bypass surgery assessment]1{21}{22}{50}and [percutaneous transluminal coronary angioplasty assessment]1{43}{50}.



Whole-body imaging, positron emission tomographic (diagnostic)1—FDG-PET is indicated for the assessment of abnormal glucose metabolism to assist in the detection and{97} evaluation of malignancy in patients with known or suspected abnormalities found by other testing modalities, or in patients with an existing diagnosis of cancer.{03}{13}{30}{31}{33}{34}{35}{36}{37}{38}{39}{42}{44}{45}{47}{50}{54}{58}{64}{65}{66}{67}{68}{69}{70}{72}{73}{74}{75}{76}{78}{82}{83}{84}{86}{88}{89}{92}{94}{95}{96}

Note: Whole-body FDG-PET is also used to diagnose malignancy versus benign conditions, stage malignant diseases, monitor therapeutic response, and detect residual or recurrent malignant disease.


Note: Whole-body FDG-PET is indicated for the assessment of abnormal glucose metabolism to assist in the detection and evaluation of [ inflammation or infection]1 in patients with fever of unknown origin or in patients with suspected infection of orthopedic prostheses.{104}{105}

1 Not included in Canadian product labeling.



Physical Properties

Nuclear data:



Radionu-
clide
(half-life)
Decay
constant
Mode
of
decay
Principal
photon
emissions
(keV)
Mean
number of
photons/
disintegration
F 18
(110 min)
0.0063
min -1
Positron
decay
Gamma*
(511)
1.94
* The 2 gamma rays emitted in opposite directions at the moment of positron annihilation are used for imaging purposes. Detection devices usually used are positron emission tomography (PET) units; however, conventional planar scintillation cameras have also been used for some studies. {13} {29} {50}


Pharmacology/Pharmacokinetics

Physicochemical characteristics:
Molecular weight—
    182 {23}

Mechanism of action/Effect:

FDG is transported from blood to tissues in a manner similar to glucose and competes with glucose for hexokinase phosphorylation to FDG-6-phosphate. However, since FDG-6-phosphate is not a substrate for subsequent glucose metabolic pathways and has a very low membrane permeability, the FDG-6-phosphate becomes trapped in tissue in proportion to the rate of glycolysis or glucose utilization of that tissue. {01} {09} {13} {14} {23} {25} {26} {39} {41} {55} {56}

Brain imaging (diagnosis)— Normal brain has metabolic reliance on glucose. Changes from the normal brain metabolic pattern may signal the existence of a specific pathological state. In epilepsy, the seizure foci may be hypermetabolic or hypometabolic depending on whether the FDG uptake phase occurred during an ictal or interictal state, respectively. Reductions in glucose metabolism in specific brain regions may be the result of pathological changes in that particular region or may be the metabolic consequence of disconnection due to damage in the other parts of the brain (i.e., diaschisis). {97}

Neoplastic disease (diagnosis)—The rate of anaerobic glycolysis in tumors increases with higher degree of malignancy {02} {54}. It is believed that increased FDG uptake is caused by a shift in energy metabolism within malignant tumors from high yield oxidative pathways to inefficient anaerobic glycolysis, resulting in an increase in glucose utilization for a given energy demand {09} {39}. Enhanced expression of glucose transporters in the membranes of malignant cells may also play a role. {97}Accumulation of FDG in malignant tissue not only helps to locate and differentiate tumors, but can also be used to help distinguish recurrent malignant cerebral tumors from foci of radiation necrosis and edema, since glucose uptake takes place in tumors and in normal brain tissue, while active uptake is absent in an area of necrosis and reduced in edema {03} {50}. {97}

Ischemia, myocardial (diagnosis)—The amount of FDG-6-phosphate accumulated in myocardial tissue is proportional to the rate of tissue {97} glucose consumption. Significant glucose consumption and uptake of FDG occurs in ischemic tissue because in severe oxygen-deprived states the primary source of energy for the myocardium shifts from fatty acids to anaerobic glucose metabolism. {26} {29} FDG uptake in normal myocardium is also dependent on insulin-dependent glucose transport.{97}

Distribution:

FDG accumulates throughout the body in proportion to glucose metabolism. Because of high glycolytic rates, the brain and heart, post-prandially generally exhibit the highest accumulations. Other tissues that exhibit the potential for moderate glucose metabolic rates and therefore FDG uptake, are the liver, spleen, thyroid, gut and bone marrow. Active skeletal muscle will accumulate FDG; therefore, a relaxed state, especially in the early uptake phases, is necessary to minimize this uptake. Because of the urinary excretion of FDG, the urinary tract (e.g., kidneys, ureters, bladder) may exhibit intense FDG accumulations. FDG has been shown to accumulate in primary and metastatic tumors throughout the body. Accumulation of FDG in tumors may be related to the degree of tumor differentiation, the number of viable cancer cells present in the tumor, and possibly, the tumor proliferation rate and may also be related to the concentration of glucose transporters in the cell membrane.{97}

Protein binding:

Minimal {02}.

Biotransformation:

FDG is phosphorylated to FDG-6-phosphate by hexokinase, with no further metabolism taking place throughout the remainder of the study {01} {13} {29} {56} {78}.

Half-life:

75% of the administered activity of FDG is retained with an effective half-life of 1.83 hours; 19% has an effective half-life of 0.26 hour; and the remaining 6% has an effective half-life of 1.53 hours {02} {52}.

Time to peak concentration:

Approximately 30 minutes to peak tissue concentration {02}in highly metabolic tissues such as the brain. Since the time to peak concentration is dependent on the glucose metabolic rate and whole-body clearance of FDG, less metabolically active tissues such as many tumors may not reach peak concentrations until nearly 2 hours. The time also depends on the balance between the uptake of FDG, FDG clearance from the blood, and radioactive decay{97}.

Time to peak diagnostic effect

Imaging of the brain can begin 30 to 60 minutes after injection. Tumor imaging can begin 45 to 60 minutes after injection, but delayed imaging beginning as late as 3 hours after injection has been advocated to improve tumor-to-background activity ratio.{104}

Radiation dosimetry:
{05}{27}{100}

Estimated absorbed radiation dose
Organ
mGy/MBq
mrad/mCi
Bladder wall
0.17
629
Heart
0.065
240
Brain
0.026
96
Kidneys
0.021
77
Uterus
0.02
74
Ovaries
0.015
55
Testes
0.015
55
Adrenals
0.014
51
Small intestine
0.013
48
Liver
0.012
44
Pancreas
0.012
44
Spleen
0.012
44
Red marrow
0.011
41
Lungs
0.011
41
Thyroid
0.0097
36
Other tissue
0.011
41
Effective dose: 0.027mSv/MBq (0.1 rem/mCi)  
 Data based on the International Commission on Radiological Protection (ICRP) Publication 53—Radiation Dose to Patients from Radiopharmaceuticals.

Elimination:
    Renal (approximately 20% of administered activity excreted within the first 2 hours) {13} {52}.


Precautions to Consider

Pregnancy/Reproduction

Pregnancy—
The possibility of pregnancy should be assessed in women of child-bearing potential. Clinical situations exist where the benefit to the patient and fetus, based on information derived from radiopharmaceutical use, outweighs the risks from fetal exposure to radiation. In this situation, the physician should use discretion and reduce the administered activity to the lowest practical amount. {17} {28}

Breast-feeding

FDG is distributed into breast milk at low concentrations, but a large amount of FDG is accumulated in lactating breast tissue. Hence the radiation exposure to the breast-fed infant is predominantly from external radiation emanating from the mother{104}. {99}Temporary discontinuation of nursing for a period of 12 to 24 hours is considered adequate. {28}

Pediatrics

Diagnostic studies performed to date have not demonstrated pediatric-specific problems that would limit the usefulness of FDG in children {77} {85}{97}.


Geriatrics


Diagnostic studies performed to date have not demonstrated geriatric-specific problems that would limit the usefulness of FDG in the elderly {58} {71} {84} {86}.

Drug interactions and/or related problems
See Diagnostic interference.

Diagnostic interference
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With results of cardiac and whole-body imaging

Due to other medications
Colony growth stimulators    (may cause increased uptake of FDG in marrow and spleen{97})


Dextrose    (concurrent administration may cause hyperglycemia and thus interfere with FDG uptake{97})


Dopamine and
Insulin    (concurrent intravenous administration of these medications with FDG may alter myocardial extraction of FDG; insulin may decrease FDG uptake in tumor cells {25} {60} {78} {81}due to removal of FDG from the blood via uptake by insulin-dependent tissues [e.g., skeletal muscle]{97})


Laxatives    (irritation and/or excessive muscle activity may result in increased uptake of FDG in the intestinal wall and thus interfere with abdominal imaging{97})

With results of cardiac imaging and whole body imaging{97}

Due to medical problems or conditions
Anxiety    (muscle tensing may result in increased uptake of FDG in these areas{97})


Diabetes mellitus    (patients with diabetes mellitus may require normalization of plasma glucose levels and insulin therapy for optimal image quality {26} {55} {59} {81})


Menstrual cycle    (uterine uptake may change during phases of the menstrual cycle{97})


Urinary tract obstruction    (excreted FDG retained in the renal collecting system may interfere with abdominal imaging{97})



Side/Adverse Effects
There are no known side/adverse effects associated with the use of FDG.



Patient Consultation
As an aid to patient consultation, refer to Advice for the Patient, Radiopharmaceuticals (Diagnostic) .

In providing consultation, consider emphasizing the following selected information (» = major clinical significance):

Description of use
Action in the body: Concentration of radioactivity in brain, heart, and other sites of high glucose utilization (e.g., certain tumors) allows images to be obtained

Small amounts of radioactivity used in diagnosis; radiation received is low and considered safe

Before having this test
»   Conditions affecting use, especially:

Pregnancy—Risk to fetus from radiation exposure as opposed to benefit derived from use should be considered





Breast-feeding—Temporary discontinuation of nursing recommended because of risk of radiation exposure to infant

Preparation for this test
Fasting is generally required; other special{97} preparatory instructions may be given; patient should inquire in advance

Precautions after having this test
No special precautions


General Dosing Information
Radiopharmaceuticals are to be administered only by or under the supervision of physicians who have had extensive training in the safe use and handling of radioactive materials and who are authorized by the appropriate Federal or State regulatory agency, if required, or, outside the U.S., the appropriate authority {51}.

For brain imaging
Fasting for about 4 to 6 hours prior to the examination is sometimes recommended to increase the amount of FDG delivered to the brain {03} {23}.

To minimize the influence of external stimulation on the brain uptake of FDG, prior to the injection of FDG and for 30 minutes thereafter, the patient should be kept lying or sitting still in a quiet, darkened room {02} {10} {11} {92}.

Imaging is usually performed 30 to 60 minutes after administration of FDG {03} {50}.


For cardiac imaging
Optimal cardiac FDG-PET (e.g., better image quality) may be obtained if patients are in a glucose-loaded state rather than in the fasting state. Under fasting conditions with normal plasma levels of nonesterified fatty acids, only the ischemic areas of the myocardium use glucose preferentially, and thus, only these areas will accumulate FDG. This renders an image in which the myocardial outline is not well seen, making it difficult to locate the ischemic area. {25} {29} {60}In some cases, insulin as well as glucose loading, may be required for patients with relative glucose intolerance or impaired insulin sensitivity{97}.

For whole-body imaging
Glucose and FDG compete for the same cell membrane receptors; thus, elevated glucose levels will cause a decrease in cellular FDG uptake {79} {80}. Additionally, postprandial hyperinsulinemia increases FDG uptake in skeletal muscle and adipose tissue, making less available for uptake in tumor deposits.{104}For this reason, fasting for at least 4 hours prior to the examination is recommended to increase the relative uptake of FDG by the tumor {50} {71} {79} {80} {84}.


Note: Because of the poor reliability of patient history concerning diabetes and hyperglycemia, all patients should have their blood glucose levels checked prior to FDG administration. Ideally, the blood glucose should be <150{104} mg/dL (ideally within the normal range of 60 to 120 mg/dL). Administration of FDG to patients with a blood glucose > 200{104} mg/dL should be done only upon careful medical judgement.{97}


Safety considerations for handling this radiopharmaceutical
Guidelines for the receipt, storage, handling, dispensing, and disposal of radioactive materials are available from scientific, professional, state, federal, and international bodies. Handling of this radiopharmaceutical should be limited to those individuals who are appropriately qualified and authorized {77}.


Parenteral Dosage Forms

Note: The bracketed information and the use of the superscript 1 in this monograph reflect the lack of labeled (approved) indications for this product{93}.

FLUDEOXYGLUCOSE F 18 INJECTION USP

Usual adult and adolescent administered activity
Brain imaging1
Cardiac imaging1or
Whole-body imaging1
Intravenous, 185 to 740{104} megabecquerels (5 to 20 millicuries) {65} {71} {83}for whole-body imaging of malignancy, cardiac imaging, and brain imaging of epilepsy{96}.


Usual pediatric administered activity
Brain imaging1
Cardiac imaging1or
Whole-body imaging 1
Intravenous, in proportion to adult dose based on body weight or surface area{97}


Note: Safety and effectiveness in the evaluation of whole-body imaging of malignancy or cardiac imaging have not been established in patients up to 16 years of age.{96}


Usual geriatric administered activity
See Usual adult and adolescent administered activity .

Strength(s) usually available
U.S.—
Supplied in a multi-dose vials or single-dose vials or syringes containing various concentrations and amounts.{97}. Prepared on site at various clinical facilities or available from some nuclear pharmacies.{92}

Canada—
Prepared on site at various clinical facilities or available from some nuclear pharmacies.{92}

Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F). Protect from freezing.

Store upright in a lead shielded container. Use within 8 hours from the time of the end of synthesis.{96}

Note: Caution—Radioactive material.




Revised: 01/09/2003



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  1. Steinert HC, Hauser M, Allemann F, et al. Non-small cell lung cancer: nodal staging with FDG-PET versus CT with correlative lymph node mapping and sampling. Radiology 1997 Feb; 202(2): 441-6.
  1. Eberling JL, Nordahl TE, Kusubov N, et al. Reduced temporal lobe glucose metabolism in aging. J Neuroimaging 1995 Jul; 5(3): 178-82.
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  1. Reviewers' comments as of monograph revision of 7/7/97.
  1. FDA labeling guidance provided for parties submitting an NDA for fluodeoxyglucose F 18 injection.
  1. Institute for clinical PET. Colorectal cancer recurrence: a retrospective study. Abstract from the 1994 ICP meeting.
  1. Jones DN, McCowage HD, Sostman DM, et al. Monitoring of neoadjuvant therapy response of soft-tissue and musculoskeletal sarcoma using fluorine-18-FDG PET. J Nucl Med 1996; 37: 1438-44.
  1. Product Information: Fludeoxyglucose F 18 injection [18F] FDG. PETNet Pharmaceutical Services, Peoria, IL, USA, Revised 6/2000.
  1. Expert Committee comment, 03/2002
  1. Hoffman JM, Welsh-Bohmer KA, Hanson M, et al. FDG PET imaging in patients with pathologically verified dementia. J Nucl Med 2000;41:1920-8.
  1. Hicks RJ, Binns D, Stabin MG. Pattern of uptake and excretion of 18F-FDG in the lactating breast. J Nucl Med 2001;42:1238-42.
  1. Hays MT, Watson EE, Thomas SR, et al. MIRD dose estimate report No. 19: Radiation absorbed dose estimates from 18F-FDG. J Nucl Med 2002;43:210-14.
  1. Bergsneider M, Hovda DA, Shalmon E, et al. Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study. J Neurosurg 1997;86:241-51.
  1. Alavi A, Mirot A, Newberg A, et al. Fluorine-18–FDG evaluation of crossed cerebellar diaschisis in head injury. J Nucl Med 1997;38:1717–20.
  1. Worley G, Hoffman JM, Paine SS, et al. 18–Fluorodeoxyglucose positron emission tomography in children and adolescents with traumatic brain injury. Devel Med Child Neurol 1995;37:213–20.
  1. Expert Committee comment, 12/2002
  1. Zhuang H, Alavi A. 18–Fluorodeoxyglucose positron emission tomographic imaging in the detection and monitoring of infection and inflammation. Sem Nuc Med 2002;32:47–59.
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