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High Pulse and Tegretol

I would like to know if there is any known connection between high pulse (90-100) and Tegretol taking.
Tegretol is a drug prescribed for avouding ephyleptic atacks.

I would also want to know if there is any contraindication of taking a Beta Blocker together with Tegretol.

Thank you.
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238668 tn?1232735930
Dear Nori,
An increased heart rate is not a typical reaction to Tegretol.  Calcium channel blockers should be closely monitored with tegretol but beta-blockers are generally safe to take at the same time.  I have attached some drug information from the AHFS for you info.  Not all will apply to your case.


Chemistry and Stability


Carbamazepine is an iminostilbene derivative that is used as both an anticonvulsant and for the relief of pain associated with trigeminal neuralgia (tic douloureux). Carbamazepine is structurally related to the tricyclic antidepressants such as amitriptyline and imipramine. Carbamazepine occurs as a white to off-white powder and is practically insoluble in water and soluble in alcohol and in acetone.

The multi-compartment, extended-release capsule formulation of carbamazepine (Carbatrol) contains 3 different types of beads: immediate-, extended-, and enteric-release beads. The 3 bead types are combined in a specific ratio to allow for twice-daily dosing.


Carbamazepine tablets, extended-release tablets, and chewable tablets should be stored in tight, light-resistant containers at temperatures not exceeding 30DGC. Carbamazepine extended-release capsules should be stored in tight, light-resistant containers at 15-25DGC. Because dissolution characteristics and associated oral bioavailability of carbamazepine tablets may be affected substantially by moisture, patients should be cautioned to keep containers of the tablets tightly closed and in a dry location, away from areas with excessive moisture (e.g., showers, bathrooms, humidifiers). Carbamazepine tablets may lose one-third or more of their oral bioavailability when exposed to excessive moisture. Tablets continuously exposed to 97% relative humidity at room temperature for 2 weeks become hardened and dissolve poorly.

Carbamazepine oral suspension should be stored in tight, light-resistant containers at temperatures not exceeding 30DGC; freezing of the oral suspension should be avoided.

Testing has shown that mixing carbamazepine oral suspension either with chlorpromazine oral solution or with liquid thioridazine preparations results in a rubbery, orange precipitate. (See Cautions: Precautions and Contraindications.) It is not known whether the development of this precipitate results in decreased bioavailability of either carbamazepine or the other drugs. The extent to which this interaction occurs with other liquid preparations also is not known. Therefore, the manufacturer recommends that carbamazepine oral suspension not be administered simultaneously with other liquid preparations.


The pharmacologic actions of carbamazepine appear to be qualitatively similar to those of the hydantoin-derivative anticonvulsants. The anticonvulsant activity of carbamazepine, like phenytoin, principally involves limitation of seizure propagation by reduction of posttetanic potentiation (PTP) of synaptic transmission. Carbamazepine appears to provide relief of pain in trigeminal neuralgia by reducing synaptic transmission within the trigeminal nucleus. The drug has also demonstrated sedative, anticholinergic, antidepressant, muscle relaxant, antiarrhythmic, antidiuretic, and neuromuscular transmission-inhibitory actions. Carbamazepine has only slight analgesic properties.


The pharmacokinetic parameters of carbamazepine disposition are similar in children and in adults; however, there is a poor correlation between dosage and plasma concentrations of carbamazepine in children. The effects of race and gender on carbamazepine pharmacokinetics have not been systematically evaluated.


Carbamazepine is slowly absorbed from the GI tract. Following chronic oral administration of carbamazepine tablets, suspension, extended-release tablets, or extended-release capsules, peak plasma concentrations are reached in 4.5, 1.5, 3-12, or 4.1-7.7 hours, respectively. The oral bioavailabilities of carbamazepine tablets and suspension reportedly are equivalent, although the rate of absorption is faster for the suspension. The bioavailability of the extended-release tablets is reportedly 89% of that of the suspension, and the absorption of the extended-release tablets is slightly slower than that of the conventional tablets. Peak plasma concentrations of the drug are higher and trough concentrations are lower for the suspension compared with tablets when the drug is administered once or twice daily, but steady-state concentrations reportedly are comparable when the suspension is administered in 3 divided doses daily and the tablets are administered in 2 divided doses daily. Following oral administration of carbamazepine extended-release capsules or tablets every 12 hours, steady-state plasma carbamazepine concentrations were comparable to those achieved with corresponding dosages of the conventional (immediate-release) tablets every 6 hours. Although one manufacturer states that peak plasma concentrations may be higher with chewable tablets than with conventional tablets, a crossover study employing this manufacturer's tablets in adults with seizure disorders showed no such difference. In this study, the oral pharmacokinetics, including bioavailability, and peak and trough plasma concentrations, were comparable for conventional and chewable tablets of the drug, although individual patients may have achieved somewhat higher concentrations for one or the other tablet formulation.

Two to 4 days of therapy may be required to achieve steady-state plasma concentrations. Although optimal therapeutic plasma concentrations suitable for all patients have not yet been determined, therapeutic plasma concentrations of carbamazepine (for both anticonvulsant effects and relief of pain of trigeminal neuralgia) are usually 3-14 ug/mL. Some investigators have noted that nystagmus frequently occurs when plasma concentrations are greater than 4 ug/mL and that ataxia, dizziness, and anorexia often occur when plasma concentrations are 10 ug/mL or greater. There appears to be a wide variation in steady-state plasma concentrations produced by specific daily dosages of carbamazepine (e.g., daily dosages of 800 mg, 1.2 g, or 1.6 g may produce plasma concentrations of 2-10 ug/mL).

In one study, when carbamazepine extended-release capsules (Carbatrol) were administered as a single 400-mg dose with a high-fat meal, the rate, but not the extent, of carbamazepine absorption was increased when compared with administration of the capsules in the fasting state. Results of a multiple-dose study of the extended-release capsules indicate that when these capsules are administered after a meal, peak steady-state plasma concentrations are within the therapeutic range. When the extended-release capsules of carbamazepine (Carbatrol) are broken and the beads sprinkled over applesauce prior to administration, the pharmacokinetic profile of the drug is similar to that following oral administration of the intact capsule to fasting individuals. The manufacturer of carbamazepine extended-release capsules states that the elimination half-life of the drug does not differ substantially between fasted and nonfasted conditions of administration.


Carbamazepine is widely distributed in the body; the drug has been detected in CSF (approximately 15-22% of serum concentrations), the brain (at autopsy), duodenal fluids, bile, and saliva. A major metabolite, carbamazepine 10,11-epoxide, has also been detected in CSF. Carbamazepine rapidly crosses the placenta (i.e., 30-60 minutes) and accumulates in fetal tissues, with higher concentrations in the liver and kidney than in brain and lungs. Carbamazepine and its epoxide metabolite are distributed in breast milk. The ratio of the concentration in breast milk to that in plasma is approximately 0.4 for the drug and 0.5 for the epoxide metabolite.

In vitro studies indicate that at plasma concentrations of 1-50 ug/mL, 75-90% of the drug is bound to plasma proteins.


Carbamazepine has a relatively long plasma half-life, variously reported to be 8-72 hours. The variability results in part because carbamazepine can induce its own metabolism; autoinduction of metabolism usually is completed after 3-5 weeks of a fixed dosing regimen. The plasma half-life generally ranges from 25-65 hours initially and from 12-17 hours with multiple dosing.

The metabolic fate of carbamazepine has not been completely elucidated. A major metabolic pathway appears to be oxidation by microsomal enzymes in the liver (principally cytochrome P-450 isoform 3A4) to form carbamazepine 10,11-epoxide (CBZ-E), which is almost completely metabolized to trans-10,11-dihydroxy-10,11-dihydrocarbamazepine (trans-CBZ-diol) and excreted in urine mainly unconjugated. CBZ-E has anticonvulsant activity in animals and potent analgesic activity in patients with trigeminal neuralgia. CBE-E also has been implicated as contributing to adverse neurologic effects of the drug. Carbamazepine is more rapidly metabolized to CBZ-E in children than in adults. In children younger than 15 years of age, there is an inverse relationship between the CBZ-E/CBZ ratio and increasing age; this ratio was reported to be 0.44 in children younger than 1 year old and 0.18 in children 10-15 years of age. Carbamazepine also undergoes aromatic hydroxylation to form 2-hydroxycarbamazepine and 3-hydroxycarbamazepine. The pathway is not clearly determined, but the drug also undergoes metabolism to form 9-hydroxymethyl-10-carbamoyl-acridan. Carbamazepine and its metabolites are excreted in urine. Only about 1-3% of the drug is excreted in urine unchanged. Carbamazepine induces liver microsomal enzymes and thus may accelerate its own metabolism and that of other concomitantly administered drugs that are metabolized by these enzymes. (See Drug Interactions.)


Seizure Disorders

Carbamazepine is used in adults and children in the prophylactic management of partial seizures with complex symptomatology (psychomotor or temporal lobe seizures), generalized tonic-clonic (grand mal) seizures, and mixed seizure patterns that include partial seizures with complex symptomatology, generalized tonic-clonic seizures, or other partial or generalized seizures. Patients with partial seizures with complex symptomatology appear to show greater improvement during carbamazepine therapy than patients with other types of seizures. Although the drug is useful in the management of mixed seizures, the response in patients with mixed seizures may be variable. The drug is ineffective in the management of absence (petit mal) seizures or myoclonic and akinetic seizures. Carbamazepine may be administered concomitantly with other anticonvulsants such as phenytoin, phenobarbital, or primidone. However, the drug should be administered with caution in conjunction with those anticonvulsants that produce toxic effects similar to carbamazepine such as phenacemide (no longer commercially available in the US), mephenytoin, or trimethadione or paramethadione (both no longer commercially available in the US).

Trigeminal Neuralgia

Carbamazepine is used in the symptomatic treatment of pain associated with true trigeminal neuralgia. Carbamazepine is not a simple analgesic and should not be administered casually for relief of trivial facial pain. Although some patients with glossopharyngeal neuralgia may respond to carbamazepine, the drug usually does not provide relief in facial pain from causes other than trigeminal neuralgia. Some patients with trigeminal neuralgia who did not respond to carbamazepine have been successfully treated with combined carbamazepine-phenytoin therapy.

Other Uses

Carbamazepine has been used in the symptomatic management of the acute phase of schizophrenia+, as an adjunct to therapy with an antipsychotic agent in patients who fail to respond to an adequate trial of the antipsychotic agent alone. The American Psychiatric Association recommends that adjunctive therapy with carbamazepine be reserved for patients whose disease is resistant to treatment but for whom clozapine is not appropriate because of inadequate response to or adverse effects of clozapine, preference of the patient, or likelihood of inadequate compliance with the schedule of monitoring necessary for therapy with clozapine. For such adjunctive therapy, carbamazepine generally is administered at the same range in dosage and therapeutic plasma concentrations as in the management of seizure disorders. For additional information on the management of schizophrenia, see Uses: Psychoneurologic Disorders, in the Phenothiazines General Statement 28:16.08.

In some patients unable to tolerate or who had an inadequate therapeutic response to standard therapy (e.g., lithium, antipsychotic agents), carbamazepine has been used effectively alone or in combination with other drugs (e.g., lithium, antipsychotic agents) for the management of acute mania+, for maintenance therapy of bipolar affective disorder+ to prevent or attenuate recurrences of bipolar episodes, and for the management of aggression (e.g., uncontrolled rage outbursts) and/or loss of control (dyscontrol) in patients with or without an underlying seizure disorder (e.g., as features of intermittent explosive disorder, conduct disorder, antisocial personality disorder, borderline personality disorder, dementia)+. Carbamazepine also has been used in the management of alcohol withdrawal syndrome+.

Carbamazepine has been used for the relief of neurogenic pain and/or control of seizures in a variety of conditions including "lightning" pains of tabes dorsalis+, pain and control of paroxysmal symptoms of multiple sclerosis+, paroxysmal kinesigenic choreoathetosis+, Kluver-Bucy syndrome+, post-hypoxic action myoclonus+, acute idiopathic polyneuritis+ (Landry-Guillain-Barre syndrome), pain of posttraumatic paresthesia+, pain of diabetic neuropathy+, and, in children, hemifacial spasm+ and dystonia+. The drug has also been used for its antidiuretic effects in the management of neurohypophyseal diabetes insipidus+; however, other less toxic agents are available, and patients with primary polydipsia and polyuria have shown signs of water intoxication during carbamazepine therapy.


Hematologic Effects

While transient or persistent, minor hematologic changes (e.g., decreased leukocyte counts) are not uncommon, the risk of serious carbamazepine-induced hematologic toxicity appears to be low. Deaths from aplastic anemia have occurred rarely following carbamazepine therapy. Other hematopoietic complications associated with the drug include leukopenia, agranulocytosis, eosinophilia, leukocytosis, thrombocytopenia, pancytopenia, hyponatremia, bone marrow depression, and purpura. Although data from a population-based, case-control study indicate that the risk of developing aplastic anemia or agranulocytosis in patients receiving carbamazepine is 5-8 times greater than that in the general population, the overall risk of these reactions in the untreated general population is low (about 6 cases per million population per year for agranulocytosis and about 2 cases per million population per year for aplastic anemia.) Transient or persistent decreases in platelet or leukocyte counts are not uncommonly associated with carbamazepine use, but currently available data do not permit accurate estimates of the incidence or outcome of these effects; however, the vast majority of cases of leukopenia reportedly have not progressed to aplastic anemia or agranulocytosis. In addition, because the apparent frequency of minor hematologic changes progressing to agranulocytosis and aplastic anemia is very low, the vast majority of such changes observed during routine, periodic hematologic monitoring of carbamazepine-treated patients are unlikely to be signaling the impending development of either abnormality. Nonetheless, determination of baseline hematologic function should be performed prior to initiation of carbamazepine therapy, and patients exhibiting abnormalities during therapy with the drug should be monitored closely. (See Cautions: Precautions and Contraindications.)

Cardiovascular Effects

Adverse cardiovascular effects (some of which may be fatal), including congestive heart failure, aggravation of hypertension, hypotension, syncope and collapse, edema, thrombophlebitis, thromboembolism, aggravation of coronary artery disease, arrhythmias, and AV block, have been reported. Myocardial infarction has been associated with tricyclic compounds.

Hepatic Effects

Hepatic complications associated with the long-term administration of carbamazepine include abnormalities in liver function test results, cholestatic and hepatocellular jaundice, and hepatitis.

Genitourinary Effects

Genitourinary complications associated with carbamazepine include urinary frequency, acute urinary retention, oliguria with elevated blood pressure, azotemia, renal failure, and impotence. Albuminuria, glycosuria, elevated BUN concentrations, and microscopic deposits in the urine have also been reported.

Nervous System Effects

Adverse neurologic and sensory effects of carbamazepine include dizziness, vertigo, drowsiness, fatigue, ataxia, disturbances of coordination, confusion, headache, nystagmus, blurred vision, transient diplopia, visual hallucinations, hyperacusis, oculomotor disturbances, speech disturbances, and abnormal involuntary movements. Rarely, peripheral neuritis and paresthesia, depression with agitation, talkativeness, and tinnitus may occur. Reports of associated paralysis and other symptoms of cerebral arterial insufficiency have been made, but the exact relationship of these reactions to the administration of carbamazepine has not been established.

Initiation of carbamazepine for the management of complex partial seizures has been associated with exacerbation of seizures, principally atypical absence and/or generalized convulsive seizures, in some children with mixed seizure disorders. In one group of children, video-EEG monitoring revealed a generalized paroxysmal spike-and-wave discharge in all of the children in whom exacerbation of seizures occurred during carbamazepine therapy. Children who developed frequent generalized convulsive seizures had a pattern of spikes and slow waves with a frequency of 1-2 cycles/second, and those who developed more frequent and severe atypical absence seizures had a generalized spike-and-wave discharge of 2.5-3 cycles/second. Although the mechanism is not known, it was suggested that exacerbation of seizures in these children may result from carbamazepine-induced activation of epileptiform discharges. It has been suggested that carbamazepine be used with caution for the management of complex partial seizures in children with mixed seizure disorders, particularly those who have a generalized absence or atypical absence component, and that the drug be avoided when there is generalized, synchronous, spike-and-wave discharges of 2.5-3 cycles/second in association with clinical seizures regardless of their clinical manifestation. The possibility that a worsening of atypical absence and/or generalized convulsive seizures following initiation of carbamazepine therapy may be drug-induced rather than the natural history of the child's epilepsy should be considered.

GI Effects

Adverse GI effects of carbamazepine include nausea, vomiting, gastric distress, abdominal pain, diarrhea, constipation, anorexia, dryness of the mouth and pharynx, glossitis, and stomatitis.

Dermatologic and Sensitivity Reactions

Adverse dermatologic effects of carbamazepine include pruritic and erythematous rashes, urticaria, photosensitivity reactions, alterations in skin pigmentation, toxic epidermal necrolysis, and exfoliative dermatitis. In addition, erythema multiforme (including Stevens-Johnson syndrome), erythema nodosum, and development of a lupus erythematosus-like syndrome or aggravation of systemic lupus erythematosus have been reported. Alopecia may also occur. Although a causal relationship has not been established, hirsutism has been reported rarely in patients receiving carbamazepine.

Hypersensitivity reactions, including fever, rash, peripheral eosinophilia, and reversible aseptic meningitis (manifested by confusion, myoclonus, and CSF pleocytosis), have been reported rarely in patients receiving carbamazepine.

Other Adverse Effects

Other adverse effects reported during carbamazepine therapy include diaphoresis, fever and chills, adenopathy or lymphadenopathy, acute intermittent porphyria, aching joints and muscles, leg cramps, and conjunctivitis. Decreased plasma calcium concentrations have been reported. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cases of frank water intoxication, with hyponatremia and confusion, have also been reported. Pulmonary hypersensitivity, characterized by fever, dyspnea, pneumonitis, or pneumonia, also has occurred. Isolated cases of neuroleptic malignant syndrome have been reported with concomitant use of carbamazepine and psychotropic drugs.

Although scattered, punctate lens opacities have occurred only rarely in patients receiving carbamazepine, other drugs such as the phenothiazines have caused various ocular changes.

Precautions and Contraindications

Carbamazepine may produce dangerous and alarming adverse effects, principally consisting of hematopoietic, cardiovascular, hepatic, and renal disturbances. The drug also shares the toxic potentials of the hydantoin-derivative anticonvulsants, and the usual precautions of anticonvulsant administration should be observed. When serious adverse effects occur requiring discontinuance of the drug, it is important to remember that abrupt withdrawal of any anticonvulsant drug may precipitate seizures or status epilepticus. Patients must be carefully examined prior to initiation of carbamazepine therapy and should remain under close medical supervision throughout therapy with the drug. Carbamazepine should be prescribed only after careful benefit-to-risk evaluation in patients with a history of cardiac, hepatic, or renal damage or adverse hematologic reaction to other drugs or who have had interrupted therapy with carbamazepine.

Close attention by the patient and clinician to signs and symptoms of the possible development of hematologic toxicity is important in patients receiving carbamazepine. Patients should be informed of the early signs and symptoms of a potential hematologic problem, such as fever, sore throat, infection, mouth ulcers, easy bruising, and petechial or purpuric hemorrhage, and should be instructed to report to their physician immediately if any such sign or symptom occurs. While the manufacturers previously recommended initial frequent (possibly weekly during the first 3 months of therapy) and then less frequent, periodic (monthly for at least 2-3 years) testing of hematologic function in any patient receiving carbamazepine, they currently state that, since the frequency of minor hematologic changes progressing to aplastic anemia and agranulocytosis is very low, the vast majority of such changes observed during routine, periodic monitoring are unlikely to be signaling the impending development of either abnormality. Therefore, the manufacturers currently recommend that complete blood counts, including platelet and possibly reticulocyte counts and serum iron determinations, be performed prior to initiating carbamazepine therapy and that subsequent monitoring be individualized by the clinician. Guidelines for periodic monitoring of hematologic function have been suggested by some clinicians, and clinicians experienced in the use of carbamazepine and knowledgeable about the drug's potential toxicity can be consulted for more specific information. Patients exhibiting baseline abnormalities and those receiving other potentially myelotoxic drugs or with a history of adverse hematologic reactions to any drug should be considered at special risk, and carbamazepine therapy should be monitored closely or avoided in these patients. The manufacturers recommend that patients with a history of bone marrow depression not receive the drug. Patients who exhibit low or decreased leukocyte or platelet counts during the course of carbamazepine therapy should be monitored closely. Discontinuance of carbamazepine therapy should be considered if any evidence of significant bone marrow depression develops. In addition, if such evidence develops, particularly if it occurs as a result of overdosage, it has been suggested that complete blood counts, platelet counts, and reticulocyte counts be performed daily and bone marrow aspiration and trephine biopsy be done immediately and repeated as often as necessary to monitor recovery. Alternatively, one manufacturer suggests that the frequency of this monitoring in patients who develop evidence of significant bone marrow depression during the usual course of carbamazepine therapy (i.e., not resulting from overdosage) may be individualized by the clinician. Other special periodic hematologic studies may also be helpful in patients with evidence of significant bone marrow depression. Fully developed aplastic anemia requires appropriate, intensive monitoring and therapy for which specialized consultation should be sought. Some clinicians also advise hematologic consultation if neutropenia and depressed platelet and reticulocyte counts occur during therapy with the drug.

Carbamazepine should be administered with caution to patients with a history of cardiac damage. Liver function tests should be performed prior to carbamazepine therapy, particularly in patients with a history of liver disease, and periodically thereafter. Carbamazepine should be immediately discontinued if evidence of aggravated liver dysfunction or active liver disease is observed. Complete urinalysis and BUN determinations should also be performed prior to and periodically during carbamazepine therapy.

Carbamazepine may exacerbate seizures in some children with mixed seizure disorders. Some clinicians recommend that prolonged video-EEG monitoring be performed prior to initiating carbamazepine therapy in children with mixed seizure disorders in an attempt to identify those children who may be at risk for carbamazepine-induced exacerbation of seizures. (See Cautions: Nervous System Effects.)

Persons who perform hazardous tasks requiring mental alertness or physical coordination should be warned about the possible adverse neurologic and sensory effects of carbamazepine. Because of the relationship of carbamazepine to other tricyclic compounds, the possibility of activation of a latent psychosis or, in geriatric patients, confusion or agitation should be kept in mind.

Baseline and periodic eye examinations including slit-lamp, funduscopy, and tonometry are recommended in patients receiving carbamazepine. Carbamazepine has shown mild anticholinergic activity; therefore, patients with increased intraocular pressure should be closely observed during carbamazepine therapy.

Because a rubbery, orange substance was noticed in the stool of a patient who ingested chlorpromazine oral solution immediately after ingesting carbamazepine oral suspension and subsequent testing has shown that mixing carbamazepine oral suspension with chlorpromazine or thioridazine oral solution results in a rubbery, orange precipitate, the manufacturer recommends that carbamazepine oral suspension not be administered with other liquid preparations. In addition, it is not known whether the development of this precipitate results in decreased bioavailability of carbamazepine or the other drugs.

Carbamazepine should not be administered to patients with a history of previous bone marrow depression and/or hypersensitivity to the drug or to patients who have demonstrated sensitivity to any of the tricyclic antidepressants (e.g., amitriptyline, desipramine, imipramine, nortriptyline, protriptyline). Carbamazepine should be administered with extreme caution, if at all, concurrently with other drugs which may increase the possibility of toxic reactions.

Pediatric Precautions

Efficacy of carbamazepine for management of seizures in children is based on extrapolation of the demonstrated efficacy of carbamazepine in adults and also on in vitro studies that confirmed that the pathogenetic mechanisms associated with seizure propagation in adults are essentially the same as those in children; in addition, mechanism of action of carbamazepine in the treatment of seizures is the same in adults and children. The therapeutic range for plasma carbamazepine concentrations (i.e., 4-12 ug/mL) is the same in children and adults. Safety of carbamazepine in children is based on clinical studies in which the drug was administered for up to 6 months. Data from long-term clinical studies in children are not available.

Mutagenicity and Carcinogenicity

Bacterial and mammalian mutagenicity studies using carbamazepine have shown no evidence of mutagenicity. Carbamazepine has produced dose-related increases in the incidence of hepatocellular tumors in female rats and benign interstitial cell adenomas in male rats. The clinical importance of these findings is not known.

Pregnancy and Lactation

Safe use of carbamazepine during pregnancy has not been established. Adverse fetal effects have been observed in reproduction studies in rats. Although several reports suggest an association between use of anticonvulsants in pregnant, epileptic women and an increased incidence of birth defects in children born to these women, a causal relationship to many of these drugs has not been established.
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