a) Symptoms have included tearing, eye pain, foreign body sensation, photophobia, and blurred vision and begin about a week after systemic treatment is started. Symptoms have disappeared in 7 days without treatment. It has been speculated that these corneal changes resembled the corneal toxicity from topical cytarabine and were probably secondary to inhibition of DNA synthesis in the corneal epithelium (Hopen et al, 1981).

a) Cardiac disorders including pericarditis and fatal cardiomyopathy have been reported in patients with combination chemotherapies that have included cytarabine (Prod Info cytarabine IV, subcutaneous injection, 2002; Woods et al, 1999; Hermans et al, 1997; Gillis et al, 1992). Fatal cardiomyopathy was reported in 3 of 8 patients receiving high-dose cyclophosphamide and cytarabine, as well as whole body irradiation. Autopsies in all 3 demonstrated intramyocardial hemorrhage and necrosis and small pericardial effusions (Takvorian et al, 1985).
b) A 35-year-old woman with acute non-lymphoblastic leukemia receiving high-dose cytarabine during consolidation therapy developed sinoatrial blockade and bradycardia temporally related to the onset of therapy, although a causal relationship could not be established (Stamatopoulos et al, 1998).

a) Non-hematologic toxicity of cytarabine is likely related to CAPILLARY LEAK SYNDROME primarily involving the lung. The overall incidence of ARDS (adult respiratory distress syndrome) associated with cytarabine has been estimated to be 16%. Radiographically, diffuse interstitial or alveolar disease is usually evident; pleural effusion occurs in approximately 10% of cases. Some evidence indicates that continuous infusion may be more toxic than intermittent administration. High-dose methylprednisolone may be helpful for this syndrome (Kreisman & Wolkove, 1992).
b) Severe and sometimes fatal pulmonary toxicity has occurred following experimental high-dose schedules with cytarabine in some patients (Prod Info cytarabine IV, subcutaneous injection, 2002).
c) Fatal pulmonary edema, observed at autopsy, has been reported in patients treated with cytarabine for leukemia. Among 181 patients, 43 had massive edema, 59 had moderate edema and 79 had either no or slight edema. The pulmonary edema correlated to the GI lesions seen with cytarabine toxicity. The investigators believed that cytarabine-induced increased alveolar capillary permeability may have been responsible for these effects (Haupt et al, 1981).
d) Recovery after cytarabine-induced pulmonary edema in a 72-year-old woman with acute myeloid leukemia was attributed to the use of high-dose methylprednisolone. The authors, however, cautioned that further study was necessary before this therapy could routinely be recommended (Larouche et al, 2000).
e) The addition of high-dose cytarabine 24 g/m(2) to cyclophosphamide and single-dose total body irradiation or etoposide is very active, yet produced excessive pulmonary toxicity in 14 patients with lymphoma (Broun et al, 1990).
f) Anderson et al (1985) reported 16 of 72 patients (22%) developed subacute pulmonary failure secondary to high-dose cytarabine therapy in acute leukemia. Symptoms began 2 to 21 days (median, 6 days) after the first dose. Pulmonary toxicity increased with increasing number of doses.
g) Bronchiolitis obliterans organizing pneumonia (BOOP) with complete recovery was observed in 3 children with acute leukemias given cytarabine in combination with either idarubicin and daunorubicin (Battistini et al, 1997).

a) High-dose cytarabine therapy has been associated with cerebral and cerebellar dysfunction, including personality changes, somnolence, and coma, which are usually reversible (Prod Info cytarabine IV, subcutaneous injection, 2002). Toxicity is dose related. Intrathecal cytarabine doses have resulted in myelopathy (Watterson et al, 1994).
b) Patients with renal sufficiency have increased risk of cytarabine neurotoxicity (Damon et al, 1989; Smith et al, 1997).
c) Central nervous system (CNS) effects are not common with standard doses of cytarabine (100 to 200 mg/m(2)/day), but CNS toxicity may be the dose-limiting effect of high-dose therapy. Effects have included ataxia, dysphasia, nystagmus, seizures, and a decreased level of consciousness, with sometimes irreversible toxicity. These changes generally begin 3 to 34 days after the initiation of therapy (Herzig et al, 1987; Grossman et al, 1983; Baker et al, 1991).

a) Headache was one of the most common side effects (n=17 of 54) observed in patients who received liposomal cytarabine (Garcia-Marco et al, 2009).

a) The majority of cases experiencing neurotoxicity have received high-dose regimens of cytarabine. Lazarus et al (1981) reported CNS toxicity in 4 of 43 patients given total doses of up to 48 g/m(2) of cytarabine, none of which were life-threatening or irreversible. Four of 6 patients given 54 g/m2 developed neurotoxicity, which was fatal in one and irreversible in another (Lazarus et al, 1981).
b) INTRATHECAL: Intrathecal cytarabine, in high-dose or slow-release formulations, or in combination with methotrexate may cause spinal cord lesions, manifesting as tetraplegia, paraplegia, and cauda equina syndrome. In one study, 28 cases of spinal cord lesions (23 paraplegia (82%), 3 tetraplegia (11%), and 2 cauda equina (7%)) were reported. Six patients received high-dose (100 to 150 mg) or slow-release (50 mg liposomal form) cytarabine. The remaining 22 patients received concomitant or sequential methotrexate and cytarabine intrathecally. Symptoms developed 1 to 91 days (median, 10 days) following intrathecal chemotherapy. Patients with spinal cord lesions rarely recover, and are mostly left with residual motor and bowel or urinary disabilities. Complete recovery was reported in only 3 of the 28 reported cases (11%) (Kwong et al, 2009).
c) In a review of 153 records of patients with acute leukemia, 194 courses of high-dose cytosine arabinoside (HDAC) were administered. Two patients developed motor disability approximately 2 to 3 weeks after the start of therapy. The authors concluded, that therapy was associated with the development of a demyelinating polyneuropathy in approximately 1% of HDAC courses, and produced paresis, paralysis, and severe motor disability (Openshaw et al, 1996)
d) Progressive ascending paralysis was reported in 2 children following intrathecal and intravenous cytarabine treatment. Death resulted in one child. Necropsy findings included spinal cord demyelination characteristic of cytarabine neurotoxicity (Dunton et al, 1986). Rubinstein et al (1975) reported similar cases with necropsy findings of extensive symmetrical demyelinating and necrotizing lesions (Rubinstein et al, 1975).
e) Paraplegia following the intrathecal administration of cytarabine 100 mg/day for 5 days has been reported in a 27-year-old man with acute myelogenous leukemia (Wolff et al, 1979). The patient developed bilateral weakness, numbness, and paresthesia of the lower limbs at 2 months. He experienced ataxia, 3+ deep tendon reflexes, plantar dorsiflexion, and a moderate decrease in muscle strength.
f) Sensory peripheral neuropathy following cytarabine therapy has been reported in 2 patients with acute myelogenous leukemia (Russell & Powles, 1974). The first patient developed burning sensations in the feet after receiving a total of 2 g of cytarabine. Although symptoms improved following each subsequent course of treatment, neuropathy was still present 2.5 years after therapy.
g) Two patients with peripheral motor and sensory neuropathies following high-dose therapy with cytarabine, daunorubicin, and asparaginase has been reported. The combination of these drugs may potentiate the effects of induced neuropathy (Powell et al, 1986).
h) Three pediatric patients with acute myeloid leukemia, developed neuroophthalmological adverse events after administration of intrathecal liposomal cytarabine. A 13-year-old girl, developed lumbosacral pain, diplopic images and bilateral papilloedema after 3 doses of liposomal cytarabine and all symptoms resolved with supportive care. An 18-year-old male, developed a local inflammatory infiltrate, fever and highly elevated C-reactive protein after his first application of liposomal cytarabine. He developed diplopic images and papilloedema 12 days after his first dose. He also developed voiding and defecation difficulties attributed to acute cauda equina syndrome after dexamethasone therapy was completed; however, another round of dexamethasone therapy resolved all symptoms. Lastly, another 18-year-old male, developed severe headache behind his eye globes approximately 2 weeks after his third IT dose of liposomal cytarabine. The patient also developed bilateral papilloedema with small areas of hemorrhage. Dexamethasone was started for 10 days. A repeat eye exam showed worsening papilloedema. Six months after his cytarabine dose, the patient's symptoms resolved without sequela. In all 3 patients, MRI scans during the time of their symptoms revealed no abnormalities; no additional doses of cytarabine were given to any patient (Sommer et al, 2008).

a) Following an inadvertent intrathecal cytarabine overdose of 800 mg, no marked systemic or neurological adverse effects were noted; however, the patient suffered from severe paresthesias and complained of pain in the legs during intrathecal saline infusion for CSF exchange. No sequelae were noted after 3 months of follow-up (Ververs et al, 2000).

a) INTRATHECAL: Seizure has been reported in patients receiving slow-release liposomal cytarabine. An exact causal relationship was not clearly established, as seizure may be caused by other drugs, the underlying disease, or a variety of metabolic or infective conditions (Kwong et al, 2009).

a) INTRATHECAL: Encephalopathy manifesting as mental changes, motor deficits to higher mental function disorders and coma have been reported in patients receiving intrathecal cytarabine. An exact causal relationship was not clearly established, as encephalopathy may be caused by metabolic and infective conditions or toxic effects of systemic drugs (Kwong et al, 2009).
b) A 16-year-old male with Burkitt's lymphoma died of respiratory failure 18 months after his first dose of cytarabine intrathecal injection. Approximately 8 hours after receiving cytarabine 40 mg, the patient reported urinary retention and weakness and paraesthesia of both legs. On day 3, the patient developed dizziness, disorientation and vomiting. Spinal MRI revealed no apparent defects. On day 8, the patient developed tongue weakness, diminished facial sensations and ascending paraesthesia up to dermatome thoracal 2 were observed. Shortly after, the patient became quadriplegic. The patient was intubated on day 10. During the course of his illness, only a slight dilation of the ventricles, and low density in the cortex of the region adjacent to the lower part of the Sylvian fissure, in the interhemispheric fissure, in the vermis and superficial parts of the lateral cerebellum were noted on CT scan. The patient developed diabetes insipidus after 8 weeks, and a hydrocephalus internus was revealed by CT scan 11 weeks after the incident. The patient remained ventilated and continued to deteriorate. He died 18 months after the incident of respiratory insufficiency (Geissler et al, 1997).

a) CASE REPORT: Aseptic meningitis occurred in an 8-year-old girl with acute lymphoblastic leukemia (ALL) who received systemic high-dose cytarabine. Eleven days after her first dose of cytarabine (a total of 4 IV doses of cytarabine {500 mg/kg per dose} divided into 4 doses every 12 hours), she presented with fever and profound neutropenia. Blood cultures were positive (Streptococcus mitis) and vancomycin was started. Blood cultures were subsequently negative. Three days later, however, she developed a frontal-occipital headache, fever, and nuchal rigidity. Vancomycin was continued and symptoms resolved. Following a second course of cytarabine, similar symptoms developed after a third dose (375 mg/kg total). The first episode of meningitis and the cumulative dose of cytarabine in induction and consolidation phases may have predisposed the child to drug-induced meningitis after a second exposure (Pease et al, 2001).

a) The incidence of severe cerebellar toxicity from high-dose cytarabine regimens (36 to 48 g/m(2)) is approximately 8%. Irreversible or fatal cerebellar toxicity was reported in 1% of patients receiving high-dose regimens. Age older than 50 years and renal insufficiency are the greatest risk factors for the development of neurotoxicity; dosage reduction should be considered in these patients. Effects have included personality changes, somnolence, coma, dysarthria, nystagmus, ataxia and seizures. In one case, in addition to cerebellar ataxia and involuntary myoclonic jaw closures, a 38-year-old patient also experienced neuropsychological sequelae of impaired word generation and slower reading rate (Zawacki et al, 2000).
b) In a retrospective review of 53 patients who received high-dose cytarabine (2 to 3 g/m(2)), CNS toxicity developed in 37.7% of patients, with ocular and dermatologic toxicities occurring in 37.7% and 45.3% of patients, respectively. Cytarabine-induced neurotoxicity may involve irreversible cerebral and cerebellar damage; whereas, the ocular and dermatologic toxicity was reversible in this review (Graves & Hooks, 1989).
c) Neurotoxicity has also been reported with intrathecal administration (Marmont & Damasio, 1973; Breuer et al, 1977; Baker et al, 1991; Wolff et al, 1979).
d) Following the intrathecal administration of cytarabine 170 mg/day for 5 days, a 27-year-old man with acute myelogenous leukemia developed bilateral weakness, numbness, and paresthesia of the lower limbs at 2 months. He experienced ataxia, 3+ deep tendon reflexes, plantar dorsiflexion, and a moderate decrease in muscle strength. Electromyelogram indicated widespread denervation and nerve conduction studies showed slowing of the motor and sensory velocities. Symptoms completely resolved over the next 2 months following discontinuation of the therapy (Wolff et al, 1979).

a) Parkinsonian symptoms were associated with high-dose cytarabine therapy for acute myelogenous leukemia in a 64-year-old woman. The patient developed tremors approximately 3 weeks following completion of therapy (6 g IV every 12 hr for 6 days; total, 72 g); the patient had also received numerous courses of cytarabine several years previously. Parkinsonian symptoms responded partially to antiparkinson agents. Twelve weeks following the onset of tremor and rigidity, symptoms abated spontaneously without recurrence (Luque et al, 1987).
b) Another case of Parkinsonism was reported in a 9-year-old boy diagnosed with acute lymphocytic leukemia who had received high-dose cytosine arabinoside systemically and intrathecally over a 6-year period, in addition to cycles of other chemotherapy. Symptoms responded to levodopa/carbidopa and the disorder resolved within 9 months. However, imaging studies revealed both permanent and reversible structural changes in the brain (Chutorian et al, 2003).
c) Basal ganglia necrosis was reported in a 35-month-old toddler who received cytarabine therapy for treatment of acute lymphoblastic leukemia (Sirvent et al, 1998).

a) A case of pseudotumor cerebri in an 11-year-old boy following intermediate-dose cytarabine. Symptoms included headache, diplopia, photophobia, nausea and vomiting has been reported. Following lumbar puncture and prednisone and acetazolamide treatment, the boy recovered. An exact causal relationship was not clearly established (Fort & Smith, 1999).

a) The most significant adverse effect of intrathecal administration of liposomal cytarabine is chemical arachnoiditis, which can be fatal if left untreated (Prod Info DEPOCYT(R) intrathecal injection, 2003).

a) CASE REPORT: A patient with acute myelogenous leukemia developed neurotoxicity following 50 mg of intrathecal cytarabine. The patient developed a nonproductive cough and hoarseness within a few hours progressing to difficulty swallowing, complete dysphagia, and aphonia after 3 to 5 days. He later developed diplopia and accessory nerve paralysis. Complete recovery occurred in about 3 weeks except for moderate diplopia for an additional 2 months (Marmont & Damasio, 1973).

a) PARENTERAL Common gastrointestinal events reported with intravenous cytarabine include: anorexia, nausea, vomiting and diarrhea. Oral and anal inflammation or ulceration can also develop (Prod Info cytarabine IV, subcutaneous injection, 2002).
b) HIGH-DOSE: As with other antineoplastics, there is a relatively high incidence of gastrointestinal side effects associated with cytarabine therapy. Nausea and vomiting are common following high-dose cytarabine (Rudnick et al, 1979).
c) LIPOSOMAL: Nausea was reported as one of the most common side effects in patients (n=7 of 54) receiving liposomal cytarabine (Garcia-Marco et al, 2009).
d) LIPOSOMAL: Vomiting was reported as one of the most common side effects in patients (n=6 of 54) receiving liposomal cytarabine (Garcia-Marco et al, 2009).
e) Experimental (high) doses may be associated with severe gastrointestinal effects, including severe ulceration of the gastrointestinal tract, pneumatosis cystoides leading to peritonitis, necrotizing colitis and bowel necrosis (Prod Info cytarabine IV, subcutaneous injection, 2002).

a) Infusions may be commonly associated with diarrhea, ileus, abdominal pain, hematemesis and melena. Massive upper GI bleeding has been reported (Slavin et al, 1978)

a) A case of acute pancreatitis associated with cytarabine has been reported; however, it is unclear if concomitant medications with L-asparaginase played a role (Altman et al, 1982).
b) A 36-year-old man receiving a continuous 7 day infusion of cytarabine (200 mg/m(2)/day) developed acute pancreatitis. An association with cytarabine was suspected based on the temporal relationship and the absence of other known risk-factors for development of acute pancreatitis (McBride et al, 1996)
c) Pancreatitis was described as a complication of cytarabine therapy in 2 of 30 patients receiving the drug for leukemia and lymphoma (Siemers et al, 1985). Both patients received cytarabine in high doses (6.9 g IV every 12 hr for 11 doses and 5.25 g every 12 hr for 6 days). However, it is unclear if cytarabine was the actual cause of pancreatitis in these patients; in one patient, relapse of pancreatitis occurred 41 days following cytarabine therapy.

a) Parotitis occurred in 2 patients receiving AML induction therapy with cytarabine 200 mg/m(2)/day in continuous infusion for 7 days. Parotitis developed on day 5 and day 4, respectively. Symptomatology disappeared following drug discontinuation. Rechallenge with intermediate dose cytarabine failed to reproduce parotitis (Cetkovsky & Koza, 1994).

a) Acute pseudomembranous enterocolitis resulting from cytotoxic chemotherapy with hydroxydaunorubicin and cytarabine has been reported in 2 patients. Both patients underwent subtotal colectomy as treatment for this adverse effect (Lea et al, 1980).

a) Cholelithiasis and choledocholithiasis were diagnosed in a 3-year-old boy and a 6-year-old girl both with acute leukemia after receiving sequential high-dose cytarabine and asparaginase therapy. No other known risk factors were reported, and imaging studies (including CT) of the abdomen prior to initiation of therapy were negative for gallstones (Sandoval et al, 2003).

a) Jaundice and hepatic dysfunction have been reported to occur with cytarabine therapy. Liver damage with increased hyperbilirubinemia has been observed with high-dose cytarabine therapy (Prod Info cytarabine IV, subcutaneous injection, 2002).
b) Fatal veno-occlusive disease of the liver has been reported following the use of cytarabine (Woods et al, 1980).
c) Acute hepatitis and acute renal failure were reported in a 45-year-old woman with secondary myelodysplastic syndrome after receiving low-dose cytarabine therapy. Clinical effects resolved following drug cessation (Tanaka et al, 1999).

a) Urinary retention and renal dysfunction are less frequent genitourinary adverse effects of cytarabine (Prod Info cytarabine IV, subcutaneous injection, 2002).

a) Acute renal failure and acute hepatitis were reported in a 45-year-old woman with secondary myelodysplastic syndrome after receiving low-dose cytarabine therapy. Clinical effects resolved following drug cessation (Tanaka et al, 1999).
b) A 68-year-old woman with myelodysplastic syndrome developed acute interstitial nephritis (AIN) during low-dose cytarabine therapy, although the diagnosis was not confirmed by kidney biopsy. Symptoms resolved after methylprednisolone therapy was instituted (Nakatani et al, 2000).

a) A single case of hemorrhagic cystitis associated with cytarabine is reported in a 2-year-old with granulocytic leukemia. The patient received 22 to 44 mg daily IV for 10 days followed by 66 mg every 2 weeks IV for 2 months. The patient presented with gross hematuria after 3 months. Pyelogram showed left ureteral dilatation and external pressure effect of bladder and nodular defects in its left wall. The drug was discontinued and the hematuria stopped (Renert et al, 1973).

a) The major toxic effect following therapeutic doses of cytarabine is myelosuppression, manifest as leukopenia, particularly granulocytopenia, thrombocytopenia, and anemia, sometimes with striking megaloblastic changes and reticulocytopenia. Expect changes in the morphology of bone marrow and peripheral smears (Prod Info cytarabine IV, subcutaneous injection, 2002).
b) NADIR: Granulocytopenia demonstrates a biphasic nadir, first at 7 to 9 days with a second usually more sever nadir at 15 to 24 days. Platelet nadir occurs at 12 to 15 days (Prod Info cytarabine IV, subcutaneous injection, 2002).

a) Cytarabine was discontinued and the patient developed bruising and bleeding 2 days later. Over the next 2 weeks, the patient eventually recovered. This patient also received isoniazid during the episode, however, erythroid recovery occurred without alteration of isoniazid therapy (Lee et al, 1984).

a) An 11-year-old boy with nephrotic syndrome treated with prednisolone, cyclophosphamide, cytarabine and chlorambucil, was diagnosed with acute lymphocytic leukemia over 3 years after cessation of therapy. It was concluded that the chance of malignant disease increases when cytotoxic agents are applied to a non-malignant condition.

a) Rash is a frequent adverse effect of cytarabine (Prod Info cytarabine IV, subcutaneous injection, 2002). Cutaneous changes limited to the hands have been described in patients receiving cancer chemotherapy with regimens involving cytarabine (Burgdorf et al, 1982). A syndrome of pain and erythema of the palms and soles, progressing to bullae and desquamation, may occur following high-dose cytarabine. Alopecia has been reported (Prod Info cytarabine IV, subcutaneous injection, 2002).
b) Kantar et al (1999) reported maculopapular eruptions on the lower extremities and trunk in a 12-year-old following low-dose cytarabine therapy, which improved after stopping treatment, and recurred on drug rechallenge (Kantar et al, 1999).
c) Cutaneous small vessel necrotizing vasculitis has been reported following high-dose cytarabine therapy (Prod Info cytarabine IV, subcutaneous injection, 2002; Ahmed et al, 1998).
d) In a retrospective review of 53 patients who received high-dose cytarabine (2 to 3 g/m(2)), CNS toxicity developed in 37.7% of patients, with ocular and dermatologic toxicities occurring in 37.7% and 45.3% of patients, respectively. Cytarabine-induced neurotoxicity may involve irreversible cerebral and cerebellar damage; whereas, the ocular and dermatologic toxicity was reversible (Graves & Hooks, 1989).

a) A fatal case of toxic epidermal necrolysis resulting from high-dose cytarabine (2 g/m(2) IV every 12 hours for 4 days) was reported in a 13-year-old girl. The diagnosis was supported by clinical symptoms and histopathologic examination of a skin biopsy. The girl developed pancytopenia resistant to G-CSF therapy and died of septicemia (Ozkan et al, 2001).

a) High-dose cytarabine therapy has been associated with the occurrence of asymptomatic nonoliguric rhabdomyolysis (Truica & Frankel, 2002; Margolis et al, 1987). It is suggested that patients with malignancies can be predisposed to high-dose cytarabine-induced rhabdomyolysis as a result of concurrent fever, infections or electrolyte imbalance (Margolis et al, 1987).

a) the "cytarabine syndrome", consisting of fever, myalgia, bone pain, occasionally chest pain, diffuse maculopapular rash, conjunctivitis, and malaise has been reported. This syndrome usually occurs 6 to 12 hours after drug administration. Corticosteroids have been helpful for the treatment and prophylaxis of this syndrome. If this syndrome responds to corticosteroid therapy, cytarabine may be continued (Prod Info cytarabine IV, subcutaneous injection, 2002; Castleberry et al, 1981). While it was previous thought that the most likely explanation was drug hypersensitivity (Shah et al, 1983; Castleberry et al, 1981), more recently the role of the direct release of cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1ra, and interferon-gamma (IFN-gamma) have been described (Elk et al, 2001; Elk & Abrahamsson, 2004).

a) Acute anaphylaxis in a 5-year-old girl with leukemia following cytarabine administration has been reported. Specific IgE antibodies to cytarabine were demonstrated in the patient's serum by the ELISA technique (Berkowitz et al, 1987).

a) Infections (ie, viral, fungal, bacterial, parasitic or saprophytic) may be associated with the therapeutic use of cytarabine alone or in combination with other agents. Infections may be severe, even fatal in some patients (Prod Info cytarabine IV, subcutaneous injection, 2002).
b) A high incidence of streptococcal septicemia has been reported in patients with acute myelogenous leukemia following high-dose cytarabine therapy for remission induction or postremission intensive consolidation. Prophylactic regimens, including cotrimoxazole, were ineffective in preventing this complication. More studies are required to confirm these findings (Kern et al, 1987). Sepsis resulting in death has been reported following cytarabine therapy (Rudnick et al, 1979).

a) Cytarabine can obliterate primary and secondary antibody mediated immune responses after therapeutic administration (Prod Info cytarabine IV, subcutaneous injection, 2002).

a) In pregnant mice administered cytarabine during the period of organogenesis, decreased fetal weight was reported at a maternal dose of 0.5 mg/kg/day (about 0.05 times the recommended human dose). In addition, increased early and late resorptions and reduced live litter sizes were reported at 8 mg/kg/day (approximately equal to the recommended human dose) (Prod Info DEPOCYT(R) intrathecal injection, 2014).

a) Monitor for possible cardiac toxicity.
b) Monitor for cerebral and cerebellar toxic effects in severe overdoses.

a) INDUCTION THERAPY: 50 mg intrathecally every 14 days for 2 doses (weeks 1 and 3) (Prod Info DEPOCYT(R) intrathecal injection, 2014)
b) CONSOLIDATION THERAPY: 50 mg intrathecally every 14 days for 3 doses (weeks 5, 7, and 9), followed by an additional dose at week 13 (Prod Info DEPOCYT(R) intrathecal injection, 2014)
c) MAINTENANCE: 50 mg intrathecally every 28 days for 4 doses (weeks 17, 21, 25, and 29) (Prod Info DEPOCYT(R) intrathecal injection, 2014)

a) INDUCTION THERAPY: 100 mg/m(2)/day as a continuous IV infusion on days 1 through 7 or 100 mg/m(2) IV injection every 12 hr on days 1 through 7 (Prod Info cytarabine intravenous injection, intrathecal injection, subcutaneous injection, 2014)

a) INDUCTION THERAPY: 100 mg/m(2)/day as a continuous IV infusion on days 1 through 7 or 100 mg/m(2) IV injection every 12 hr on days 1 through 7 (Prod Info cytarabine intravenous injection, intrathecal injection, subcutaneous injection, 2014)
b) Cytarabine doses of 10 mg/kg, by 24 hr infusion, and followed by daunorubicin and adriamycin have been given to pediatric patients to achieve remission (Paton et al, 1982).

a) 3779 mg/kg

a) 3150 mg/kg

a) Greater than 10 g/kg

a) Greater than 5 g/kg

a) Greater than 5 g/kg

a) Greater than 5 g/kg