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1515 on Drugs and Therapeutics Auvi-Q Epinephrine Auto-Injector Returns ...p 33 Crisaborole Eucrisa for Atopic Dermatitis ...p 34 Anticoagulation of Elderly Patients at High Risk for Fal

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ISSUE

1433

Volume 56

Published by The Medical Letter, Inc • A Nonprofi t Organization

ISSUE No

1515

on Drugs and Therapeutics

Auvi-Q Epinephrine Auto-Injector Returns p 33

Crisaborole (Eucrisa) for Atopic Dermatitis p 34

Anticoagulation of Elderly Patients at High Risk for Falls with Atrial Fibrillation p 35

Extended-Release Calcifediol (Rayaldee) for Secondary Hyperparathyroidism p 36

Kyleena – Another Hormonal IUD p 38

Drug Interaction: Clopidogrel and PPIs p 39

Atezolizumab (Tecentriq) for Bladder Cancer and NSCLC online only

ALSO IN THIS ISSUE

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33

on Drugs and Therapeutics

Take CME Exams

ISSUE

1433

Volume 56

ISSUE No

1515 Crisaborole (Eucrisa) for Atopic DermatitisAnticoagulation of Elderly Patients at High Risk for Falls with Atrial Fibrillation p 34p 35

Extended-Release Calcifediol (Rayaldee) for Secondary Hyperparathyroidism p 36

Kyleena – Another Hormonal IUD p 38

Drug Interaction: Clopidogrel and PPIs p 39

Atezolizumab (Tecentriq) for Bladder Cancer and NSCLC online only

ALSO IN THIS ISSUE

Auvi-Q (Kaléo; previously manufactured and

marketed by Sanofi ), the epinephrine auto-injector

approved by the FDA in 2012 for emergency treatment

of anaphylaxis and voluntarily withdrawn in 2015

due to potential inaccurate dosage delivery,1 has

become available once more According to Kaléo,

improvements in the manufacturing process have

addressed the concerns that led to its recall

THE DEVICE — No changes were made to the device

itself, which is about the length and width of a credit card and as thick as a smartphone It has an automatic needle retraction system and a red safety guard at the needle-end of the device Removal of the outer case initiates visual signals and an audio recording that provides step-by-step instructions and a 5-second countdown during the injection process The shelf-life

of the epinephrine in the auto-injector is 18 months; the shelf-life of the battery is longer

Auvi-Q’s needle length, gauge, and injection force are

similar to those of EpiPen In a randomized, crossover,

bioavailability study, injection of epinephrine 0.3 mg

from Auvi-Q and EpiPen resulted in similar peak

epinephrine levels and total epinephrine exposure.2 In

one study, patients and caregivers found Auvi-Q easier

to use than other epinephrine auto-injectors.3,4

CONCLUSION — Auvi-Q, which is being reintroduced

after having been voluntarily withdrawn from the market in 2015, is a smaller epinephrine auto-injector that provides visual signals and audio instructions as

it is being used It appears to be more convenient to

carry and easier to use than EpiPen

Auvi-Q Epinephrine Auto-Injector

Returns

Table 1 Epinephrine Auto-Injectors

Epinephrine injection, USP –

generic (Mylan)3 0.15 mg/0.3 mL, $300.00

EpiPen Jr (Mylan) 0.15 mg/0.3 mL 608.60

EpiPen 0.3 mg/0.3 mL 608.60

Epinephrine injection, USP 4 –

generic (Impax) 0.15 mg/0.15 mL, 395.20 5,6

Adrenaclick (Impax)7 0.3 mg/0.3 mL 460.90 5

Epinephrine injection, USP – 0.15 mg/0.15 mL, 4500.00 9

Auvi-Q (Kaléo)8 0.3 mg/0.3 mL 4500.00 9

1 The dose of epinephrine is 0.15 mg for patients who weigh 15-30 kg and

0.3 mg for those who weigh ≥30 kg.

2 Approximate WAC for one package containing two auto-injectors WAC =

wholesaler acquisition cost or manufacturer’s published price to

whole-salers; WAC represents a published catalogue or list price and may not

represent an actual transactional price Source: AnalySource® Monthly

February 5, 2017 Reprinted with permission by First Databank, Inc All

rights reserved ©2017 www.fdbhealth.com/policies/drug-pricing-policy.

3 Interchangeable with EpiPen and EpiPen Jr.

4 Adrenaclick and its generic equivalent are similar to EpiPen and EpiPen Jr

in size and functionality, but they are not considered interchangeable due to

differences in device design and instructions for use.

5 Both strengths cost the same

6 Both strengths are available at CVS for a cash price of $110.00 for two

auto-injectors.

7 Adrenaclick is no longer being manufactured; its generic equivalent will

continue to be marketed after supplies of Adrenaclick are depleted.

8 Auvi-Q is not interchangeable with other currently available epinephrine

auto-injectors.

9 Manufacturer's list price for insurers Insurers and pharmacy benefi t

managers may negotiate with the manufacturer for a lower price or decide

not to pay for Auvi-Q at all According to the manufacturer, the

out-of-pocket cost is $0 for all commercially insured patients, whether or not their

insurer covers the device The cash price for patients without government

or commercial insurance is $360 for those with a household income

≥$100,000/year and $0 for those with a household income <$100,000/year

1 FDA Updated: Sanofi US issues voluntary nationwide recall of all Auvi-Q due to potential inaccurate dosage delivery Available at www.fda.gov/Safety/Recalls/ucm469980.htm Accessed Feb

-ru ary 6, 2017.

2 ES Edwards et al Bioavailability of epinephrine from Auvi-Q compared with EpiPen Ann Allergy Asthma Immunol 2013; 111:132.

3 CA Camargo Jr et al Auvi-Q versus EpiPen: preferences of adults, caregivers, and children J Allergy Clin Immunol Pract 2013; 1:266.

4 T Umasunthar et al Patients’ ability to treat anaphylaxis using adrenaline autoinjectors: a randomized controlled trial Allergy 2015; 70:855.

Pronunciation Key

Epinephrine: ep" i nef' rin Auvi-Q: aw vee' cue

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Crisaborole (Eucrisa) for Atopic

Dermatitis

Pronunciation Key

Crisaborole: kris” a bor’ ole Eucrisa: you kris’ a

The FDA has approved crisaborole 2% ointment

(Eucrisa – Pfi zer) for topical treatment of mild to

moderate atopic dermatitis in patients ≥2 years old It

is the fi rst phosphodiesterase type-4 (PDE4) inhibitor

to be approved in the US for this indication

ATOPIC DERMATITIS — Atopic dermatitis (also known

as atopic eczema) is a chronic pruritic inflammatory

skin disease that commonly presents in infancy or early

childhood and is frequently associated with other atopic

disorders such as allergic rhinitis and asthma It has a

relapsing course, often improving by adolescence In

in-fants, atopic dermatitis typically involves the face, scalp,

and extensor surfaces of the limbs In older patients, it

characteristically involves the flexural areas

STANDARD TREATMENT — Application of moisturizers,

emollients, and barrier creams can reduce the need

for pharmacologic therapy Low-potency topical

corticosteroids are generally used for treatment of

mild atopic dermatitis when lesions fail to respond

to nonpharmacologic therapy, and medium- to

high-potency topical corticosteroids are used for moderate

to severe disease For maintenance treatment,

the lowest potency topical corticosteroid that is

effective should be used Long-term use of topical

corticosteroids can cause skin atrophy, purpura,

telangiectasias, and permanent striae.1,2

The topical calcineurin inhibitors tacrolimus (Protopic,

and generics) and pimecrolimus (Elidel) can be used

for topical corticosteroid-resistant atopic dermatitis

and for cases involving the face or intertriginous

areas where corticosteroid adverse effects can be

troublesome Calcineurin inhibitors are similar in

effi cacy to low- to medium-potency corticosteroids,

and they do not cause skin atrophy or other

corticosteroid adverse effects Skin malignancies

and lymphomas have been reported rarely in patients

treated with a topical calcineurin inhibitor; the labels of

tacrolimus and pimecrolimus include a boxed warning

about the risk of malignancy, but a causal relationship

has not been established.3

PHARMACOLOGY — Crisaborole inhibits PDE4,

resulting in increased levels of cyclic adenosine

monophosphate (cAMP) Its exact mechanism of

action for treatment of atopic dermatitis is unclear,

but increased cAMP levels suppress production of

proinflammatory cytokines.4 Systemic absorption of crisaborole is minimal after topical administration.5

CLINICAL STUDIES — In two identically-designed

randomized, double-blind trials in a total of 1522 patients ≥2 years old with mild (investigator’s static global assessment [ISGA] score of 2) to moderate (ISGA score of 3) atopic dermatitis, crisaborole 2% ointment applied twice daily for 28 days was compared

to its vehicle alone A signifi cantly higher percentage

of patients using crisaborole achieved the primary endpoint, an ISGA score at day 29 of 0 (clear) or 1 (almost clear) with a ≥2-grade improvement from baseline, compared to those using the vehicle alone (32.8% vs 25.4% in trial 1 and 31.4% vs 18.0% in trial 2).6

ADVERSE EFFECTS — The most common adverse

effect of crisaborole in the two clinical trials was burning or stinging at the application site, mainly on the fi rst day of treatment Contact urticaria occurred in

<1% of patients

PREGNANCY AND LACTATION — There are no adequate

studies of crisaborole in pregnant or lactating women

No adverse effects on embryofetal development were observed in pregnant rabbits and rats administered crisaborole orally at doses up to 3 and 5 times, respectively, the maximum recommended human dose

DOSAGE AND ADMINISTRATION — Eucrisa is available

in 60- and 100-g tubes A thin layer of crisaborole 2% ointment should be applied to the affected area twice daily Patients should be advised to wash their hands immediately after applying the drug

CONCLUSION — Crisaborole 2% ointment (Eucrisa)

appears to be modestly effective for short-term treatment of mild to moderate atopic dermatitis How

it compares in effi cacy to topical corticosteroids or calcineurin inhibitors remains to be established, and its long-term effi cacy and safety are unknown ■

Table 1 Some Topical Nonsteroidal Drugs for Atopic Dermatitis

Calcineurin Inhibitors

Pimecrolimus 1% cream – Elidel (Valeant) $517.70 Tacrolimus 0.03%, 0.1% ointment – generic 416.70 2

Protopic (Astellas) 486.20 2

PDE4 Inhibitor

Crisaborole 2% ointment – Eucrisa (Pfi zer) 580.00

PDE4 = phosphodiesterase type-4

1 Approximate WAC for a 60-g tube WAC = wholesaler acquisition cost or manufacturer’s published price to wholesalers; WAC represents a pub-lished catalogue or list price and may not represent an actual transac-tional price Source: AnalySource® Monthly February 5, 2017 Reprinted with permission by First Databank, Inc All rights reserved ©2017 www fdbhealth.com/policies/drug-pricing-policy

2 Both strengths cost the same.

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1 LF Eichenfi eld et al Guidelines of care for the management of

atopic dermatitis: section 2 Management and treatment of

atopic dermatitis with topical therapies J Am Acad Dermatol

2014; 71:116.

2 Drugs for allergic disorders Treat Guidel Med Lett 2013; 11:43.

3 WW Carr Topical calcineurin inhibitors for atopic dermatitis:

review and treatment recommendations Paediatr Drugs 2013;

15:303.

4 K Jarnagin et al Crisaborole topical ointment, 2%: a

nonsteroi-dal, topical, anti-inflammatory phosphodiesterase 4 inhibitor in

clinical development for the treatment of atopic dermatitis J

Drugs Dermatol 2016; 15:390.

5 LT Zane et al Crisaborole topical ointment, 2% in patients ages

2 to 17 years with atopic dermatitis: a phase 1b, open-label,

maximal-use systemic exposure study Pediatr Dermatol 2016;

33:380.

6 AS Paller et al Effi cacy and safety of crisaborole ointment, a

novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for

the topical treatment of atopic dermatitis (AD) in children and

adults J Am Acad Dermatol 2016; 75:494.

Anticoagulation of Elderly

Patients at High Risk for Falls

with Atrial Fibrillation

With the widespread adoption of the CHA2DS2-VASc

scoring system,1 oral anticoagulation therapy is

now recommended for all patients ≥75 years old

with nonvalvular atrial fi brillation.2,3 Atrial fi brillation

has, however, been associated with an increased

risk of falls, and older patients starting warfarin for

atrial fi brillation have a high rate of hospitalization

for intracranial bleeding.4,5 Many practitioners are

reluctant, therefore, to prescribe an oral anticoagulant

for elderly patients who are at high risk for falls

Most data on this subject come from patients who

were treated with warfarin The newer direct oral

anticoagulants dabigatran etexilate (Pradaxa),

rivarox-aban (Xarelto), apixrivarox-aban (Eliquis), and edoxrivarox-aban

(Savaysa) have been shown to be at least as effective

as warfarin in preventing ischemic stroke or systemic

embolism in patients with nonvalvular atrial fi brillation

and less likely to cause intracranial bleeding.6,7

CLINICAL STUDIES — Warfarin – Three large studies

of warfarin anticoagulation offer some useful

information, but only one was conducted specifi cally

in elderly patients at high risk for falls, and only one

was randomized

A chart review of 1245 elderly Medicare patients at high

risk for falls who were hospitalized with atrial fi bril lation

(mean age 83.0) and 18,261 other patients hospitalized

with atrial fi brillation (mean age 79.3) examined the

risk of subsequent intracranial hemorrhage About

33% of the patients at high risk for falls and 49% of the other patients were treated with warfarin at the time of hospital discharge Patients at high risk for falls were older and had more comorbidities They had a higher rate of intracranial hemorrhage than the other patients (2.8 vs 1.1 per 100 patient-years), especially traumatic intracranial hemorrhage (2.0 vs 0.34 per 100 patient-years), and they also had a higher rate of ischemic stroke (13.7 vs 6.9 per 100 patient-years) The patients at high risk for falls who were treated with warfarin and had risk factors other than age had a lower risk of a composite endpoint of out-of-hospital death or hospitalization for stroke, myocardial infarction, or any hemorrhage compared to those at high risk for falls who were not treated with warfarin (HR 0.75; 95% CI 0.61-0.91).8

In a randomized trial in 973 patients ≥75 years old with atrial fi brillation, warfarin (target INR 2-3) was compared to aspirin 75 mg/day After a mean

follow-up of 2.7 years, there were 21 fatal or disabling strokes (ischemic or hemorrhagic), two other intracranial hemorrhages, and one systemic embolus in patients taking warfarin, and 44 strokes, one other intracranial hemorrhage, and three systemic emboli in those taking aspirin The annual risk of a primary event was 1.8% with warfarin and 3.8% with aspirin.9

In the Swedish Atrial Fibrillation Cohort study, 90,706 patients who never took warfarin were compared to 68,306 patients who took the drug The patients who were not anticoagulated with warfarin were generally older and more likely to have a history of previous bleeding, dementia, or frequent falls With the exception

of patients with a CHA2DS2-VASc score of 0 (low stroke risk; no therapy preferred), the risk of ischemic stroke without anticoagulant treatment was greater than the risk of intracranial bleeding with anticoagulation.10

Low-Dose Apixaban – No randomized trial has

compared a direct oral anticoagulant with placebo

in elderly patients at high risk for falls with atrial

fi brillation In a trial (ARISTOTLE) comparing apixaban with warfarin in patients with atrial fi brillation, a subgroup of 831 patients received a low dose of apixaban (2.5 mg bid) approved by the FDA for use in patients with at least two of the following risk factors:

≥80 years old; weight ≤60 kg; serum creatinine ≥1.5 mg/dL In this subgroup, patients taking apixaban, compared to those taking warfarin, had lower incidences of stroke or systemic embolism (1.7% vs 3.3%) and major bleeding (3.3% vs 6.7%).11 None of the other direct oral anticoagulants has an FDA-approved lower dose for elderly patients

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CONCLUSION — No prospective randomized trial has

evaluated the risks and benefi ts of anticoagulation

in elderly patients at high risk for falls with atrial

fi brillation Available data suggest that the benefi ts

may outweigh the risks ■

1 Treatment of atrial fi brillation Med Lett Drugs Ther 2014;

56:53.

2 CT January et al 2014 AHA/ACC/HRS guideline for the

man-agement of patients with atrial fi brillation: executive summary:

a report of the American College of Cardiology/American Heart

Association Task Force on practice guidelines and the Heart

Rhythm Society Circulation 2014; 130:2071.

3 P Kirchhof et al 2016 ESC guidelines for the management of

atrial fi brillation developed in collaboration with EACTS Rev

Esp Cardiol (Engl Ed) 2017; 70:50.

4 WT O’Neal et al Effect of falls on frequency of atrial fi brillation

and mortality risk (from the REasons for Geographic and Racial

Differences in Stroke [REGARDS] Study) Am J Cardiol 2015;

116:1213.

5 JA Dodson et al Incidence and determinants of traumatic

in-tracranial bleeding among older veterans receiving warfarin for

atrial fi brillation JAMA Cardiol 2016; 1:65.

6 Which oral anticoagulant for atrial fi brillation? Med Lett Drugs

Ther 2016; 58:45.

7 M Sharma et al Effi cacy and harms of direct oral

anticoagu-lants in the elderly for stroke prevention in atrial fi brillation and

secondary prevention of venous thromboembolism:

system-atic review and meta-analysis Circulation 2015; 132:194.

8 BF Gage et al Incidence of intracranial hemorrhage in patients

with atrial fi brillation who are prone to fall Am J Med 2005;

118:612.

9 J Mant et al Warfarin versus aspirin for stroke prevention in

an elderly community population with atrial fi brillation (the

Birmingham Atrial Fibrillation Treatment of the Aged Study,

BAFTA): a randomised controlled trial Lancet 2007; 370:493.

10 L Friberg et al Net clinical benefi t of warfarin in patients with

atrial fi brillation: a report from the Swedish atrial fi brillation

co-hort study Circulation 2012; 125:2298.

11 CB Granger et al Apixaban versus warfarin in patients with

atrial fi brillation N Engl J Med 2011; 365:981.

Extended-Release Calcifediol

(Rayaldee) for Secondary

Hyperparathyroidism

The FDA has approved extended-release (ER)

calcifediol (25-hydroxyvitamin D3; Rayaldee –

Opko), a prohormone of calcitriol, the active form of

vitamin D3 It is indicated for treatment of secondary

hyperparathyroidism (SHPT) in adults with stage 3 or

4 chronic kidney disease (CKD) who have serum total

25-hydroxyvitamin D levels <30 ng/mL

Pronunciation Key

Calcifediol: kal” sif e dye’ ol Rayaldee: ray al’ dee

TREATMENT OF SHPT — Secondary

hyper-parathyroidism is a common complication of CKD;

it develops in response to declining renal function,

impaired phosphate excretion, and the inability

of the kidneys to convert vitamin D to calcitriol (1,25-dihydroxyvitamin D3) Reduced synthesis of calcitriol leads to low levels of serum calcium and elevated levels of serum phosphorus, which results in increased parathyroid hormone (PTH) secretion.1 Nutritional (inactive) vitamin D is effective in repleting vitamin D stores, but it is inferior to calcitriol and other active vitamin D analogs (see Table 2) in reducing PTH levels Calcimimetic agents increase sensitivity of calcium-sensing receptors on the parathyroid gland

to extracellular calcium, decreasing PTH and serum

calcium levels Cinacalcet (Sensipar) is FDA-approved

for oral treatment of SHPT in patients with CKD on dialysis.2 Etelcalcetide (Parsabiv), an IV calcimimetic

agent, was recently approved by the FDA for the same indication; it will be reviewed in a future issue

Whether reductions in PTH levels decrease cardiovascular risk, bone fractures, and mortality in patients with CKD remains to be established.3,4 When SHPT fails to respond to pharmacologic therapy, parathyroidectomy may be considered

PHARMACOKINETICS — Even though calcifediol is a

prodrug of calcitriol, the ER formulation may be more effective than calcitriol itself in lowering PTH levels because the slower rise in calcitriol levels causes less induction of the catabolic enzyme that degrades calcitriol.5

CLINICAL STUDIES — Approval of ER calcifediol was

based on the results of two similarly designed, double-blind trials in a total of 429 patients with stage 3 or

4 CKD who had SHPT and vitamin D insuffi ciency.6 Patients were randomized to take ER calcifediol or placebo once daily for 26 weeks The percentage

of patients who achieved a mean reduction of ≥30% from baseline in plasma intact parathyroid hormone (iPTH) during weeks 20-26, the primary endpoint, was signifi cantly higher with ER calcifediol than with placebo in both trials (33% vs 8% in trial 1 and 34% vs 7% in trial 2) Serum total 25-hydroxyvitamin D

Table 1 Pharmacology of ER Calcifediol

Class Vitamin D3 analog Mechanism of action Conversion to calcitriol, which binds to

vitamin D receptors Route Oral

Formulation 30 mcg ER capsules Metabolism CYP27B1 to calcitriol; CYP24A1 to inactive metabolites

Elimination half-life ~25 days in patients with stage 3 or 4 CKD Excretion Primarily biliary fecal route

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1 J Cunningham et al Secondary hyperparathyroidism: patho-genesis, disease progression, and therapeutic options Clin J

Am Soc Nephrol 2011; 6:913.

2 Cinacalcet (Sensipar) Med Lett Drugs Ther 2004; 46:80.

3 SN Salam et al Pharmacological management of secondary hyperparathyroidism in patients with chronic kidney diseases Drugs 2016; 76:841.

4 H Komaba et al Management of secondary hyperparathyroid-ism: how and why? Clin Exp Nephrol 2017 Jan 2 (epub).

5 M Petkovich et al Modifi ed-release oral calcifediol corrects vitamin D insuffi ciency with minimal CYP24A1 upregulation J Steroid Biochem Mol Biol 2015; 148:283.

6 SM Sprague et al Use of extended-release calcifediol to treat secondary hyperparathyroidism in stages 3 and 4 chronic kid-ney disease Am J Nephrol 2016; 44:316

7 Inhibitors and inducers of CYP enzymes and P-glycoprotein Med Lett Drugs Ther 2016 Aug 2 (epub) Available at: secure medicalletter.org/downloads/CYP_PGP_Tables.pdf Accessed February 16, 2017.

concentrations ≥30 ng/mL occurred in 80% and 83% of

patients taking ER calcifediol compared to 3% and 7%

of those taking placebo

ADVERSE EFFECTS — Among patients taking ER

calcifediol in the clinical trials, 2% developed

hyper-calcemia and 0.4% developed hyperphosphatemia,

compared to none of those taking placebo Adverse

reactions that occurred in at least 4% of patients treated

with ER calcifediol and more frequently than with

placebo were anemia (4.9% vs 3.5%), nasopharyngitis

(4.9% vs 2.8%), increased serum creatinine (4.9% vs

1.4%), and dyspnea (4.2% vs 2.8%)

DRUG INTERACTIONS — Coadministration of thiazide

diuretics, which reduce excretion of calcium in the

urine, and ER calcifediol may cause hypercalcemia

Cholestyramine may reduce the absorption of ER

calcifediol Phenobarbital and other anticonvulsants

can reduce plasma concentrations of ER calcifediol

by increasing its metabolism Strong CYP3A

inhibitors may inhibit enzymes involved in vitamin

D metabolism, and may alter serum levels of ER

calcifediol.7 Patients taking ER calcifediol with

digoxin (Lanoxin, and others) should be monitored for

high serum calcium levels because hypercalcemia

increases the risk of digitalis toxicity

PREGNANCY AND LACTATION — There are no adequate

studies of ER calcifediol in pregnant women Teratogenic

effects were seen in rabbits given calcifediol at doses

Table 2 Some Vitamin D Analogs for SHPT

Drug Some Available Formulations Initial Adult Oral Dosage Cost 1

Inactive

Cholecalciferol (vitamin D3) – generic 1000 IU tabs 1000 IU/d $0.50 Ergocalciferol (vitamin D2) – generic 50,000 IU caps 50,000 IU/wk 2.40

Active

Calcifediol ER − Rayaldee (Opko) 30 mcg ER caps 30 mcg once/d at bedtime 2 928.00 Calcitriol − generic 0.25, 0.5 mcg caps; 0.25 mcg once/d 3 30.70

Paricalcitol − generic 1, 2 mcg caps; 2, 5 mcg/mL Baseline iPTH: 152.40 6

Zemplar (Abbvie) IV soln ≤500 pg/mL: 1 mcg once/d or 2 mcg 3x/wk 4,5 390.30 6

>500 pg/mL: 2 mcg once/d or 4 mcg 3x/wk 4,5

Doxercalciferol − generic 0.5, 1, 2.5 mcg caps; 2 mcg/mL, 1 mcg once/d 7 736.50

ER = extended release; iPTH = intact parathyroid hormone; SHPT = secondary hyperparathyroidism; soln = solution

1 Approximate WAC cost for 30 days’ treatment at the lowest initial adult oral dosage WAC = wholesaler acquisition cost or manufacturer’s published price to wholesalers; WAC represents a published catalogue or list price and may not represent an actual transactional price Source: AnalySource® Monthly February

5, 2017 Reprinted with permission by First Databank, Inc All rights reserved ©2017 www.fdbhealth.com/policies/drug-pricing-policy.

2 Serum calcium level should be <9.8 mg/dL before starting treatment with calcifediol After 3 months, the dosage can be increased to 60 mcg once/d if iPTH is above treatment goal and if serum calcium is <9.8 mg/dL, phosphorus is <5.5 mg/dL, and total 25-hydroxyvitamin D is <100 ng/mL Monitor serum calcium, phosphorus, total 25-hydroxyvitamin D, and iPTH levels 3 months after initiating therapy or changing dosage and every 6-12 months thereafter.

3 Dosage for predialysis patients Can be increased to 0.5 mcg daily if necessary Serum calcium levels should be checked twice weekly during the titration

period, then monthly once the optimal dosage has been determined.

4 Dosage for patients with stage 3 or 4 CKD Thrice-weekly regimens should not be administered more frequently than every other day.

5 If iPTH levels relative to baseline remain unchanged or increase or decrease by <30%, the initial dosage should be increased by 1 mcg daily (or 2 mcg 3x/wk) at 2-4 week intervals If iPTH levels relative to baseline decrease by >60% or if iPTH is <60 pg/mL, the initial dosage should be decreased by 1 mcg daily (or 2 mcg 3x/wk).

6 Cost based on dosage of 1 mcg once/d A dosage of 2 mcg once/d costs $332.20 for the generic formulation and $780.60 for Zemplar.

7 Dosage for predialysis patients The dose can be increased by 0.5 mcg every 2 weeks to reach target levels of iPTH, as summarized in the package insert

Maximum dosage is 3.5 mcg once/d.

equivalent to 8-16 times the human dose of 60 mcg/ day The drug was not teratogenic in rabbits at a dose

of 5 mcg/kg/day or in rats at doses ≤60 mcg/kg/day Limited evidence suggests that calcifediol is poorly excreted in breast milk

CONCLUSION — Extended-release calcifediol

(Rayaldee) can lower concentrations of parathyroid

hormone and correct vitamin D insuffi ciency in adults with secondary hyperparathyroidism and stage 3

or 4 chronic kidney disease (CKD) It has not been compared to other vitamin D analogs that cost much less Randomized, controlled trials showing that any of these drugs improve morbidity or decrease mortality in patients with CKD are lacking ■

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Kyleena – Another Hormonal IUD

Pronunciation Key Levonorgestrel: lee" voe nor jes' trel Kyleena: kye lee’ nah

The FDA has approved Kyleena (Bayer), an intrauterine

device (IUD) that releases the synthetic progestin

levonorgestrel, for prevention of pregnancy It is the

fourth levonorgestrel-releasing IUD to be approved in

the US Like Mirena, which has been available since

2000, Kyleena is approved for up to 5 years of use.

IUDs — IUDs provide convenient, long-term

contra-ception and a rapid return to fertility after removal;

they are considered safe for use in most women,

including adolescents and nulliparous women.1 All

levonorgestrel-releasing IUDs, which are approved for

3 or 5 years of use, can reduce menstrual bleeding and

dysmenorrhea Amenorrhea can occur, especially with

devices that contain more levonorgestrel.2 ParaGard

T380A, a copper-containing IUD, is FDA-approved for

up to 10 years of use

THE NEW DEVICE — Kyleena has a 30x28-mm T-shaped

polyethylene frame with a drug reservoir containing 19.5

mg of levonorgestrel It is the same size as Skyla3 and

smaller than Mirena and Liletta,4 which are both 32x32

mm Kyleena is packaged with an inserter device that

is narrower than the Mirena inserter (3.8 vs 4.4 mm)

The release rate of levonorgestrel from Kyleena into

the uterine cavity is about 17.5 mcg/day after 24 days;

it gradually declines to 9 mcg/day after 1 year and 7.4

mcg/day after 5 years Unlike Mirena, Kyleena and other

levonorgestrel-releasing IUDs do not have restrictions in their labeling that limit use to women who have had at least one child

MECHANISM OF ACTION — The mechanism by which

levonorgestrel produces a contraceptive effect has not been conclusively established Local progestogenic ef-fects that interfere with conception include thicken ing

of the cervical mucus, inhibition of sperm capacitation, and changes in the endometrial lining The device itself causes inflammatory changes in the endometrium that can affect sperm survival and impair implantation

CLINICAL STUDY — In an unpublished, open-label

trial, 1452 women 18-35 years old (40% nulliparous)

received the Kyleena IUD The results of the trial

are summarized in the package insert The primary endpoint was the pregnancy rate calculated as the Pearl Index (number of pregnancies per 100 woman-years) A total of 870 women (60%) completed 3 years

of the trial Among 707 patients (49%) who enrolled in

an extension phase, 550 (38%) completed 5 years of use The annual pregnancy rates for years 1-5 were 0.16, 0.38, 0.45, 0.15, and 0.37, respectively The 5-year estimated cumulative pregnancy rate was 1.45 About 71% of 163 women who desired to become pregnant after stopping the trial conceived within 12 months of removing the device

Table 1 Comparison of Intrauterine Devices (IUDs)

IUD of Use 1 Rate 2 Content Some Advantages Some Disadvantages Cost 3

Copper-Containing IUD

ParaGard T380A 10 years 0.8 4 None ▶ Nonhormonal ▶ Irregular/heavy bleeding $739.00

▶ Lack of protection against STIs

Levonorgestrel-Releasing IUDs

(Allergan/Actavis)

LNG = levonorgestrel; STIs = sexually transmitted infections

1 FDA-approved maximum duration of use.

2 Pearl Index (number of pregnancies per 100 woman-years) for the first year of use, according to results of clinical trials summarized in the package insert for each IUD product.

3 Approximate WAC for one IUD Cost of insertion not included WAC = wholesaler acquisition cost or manufacturer’s published price to wholesalers; WAC

represents a published catalogue or list price and may not represent an actual transactional price Source: AnalySource® Monthly February 5, 2017 Reprinted with permission by First Databank, Inc All rights reserved ©2017 www.fdbhealth.com/policies/drug-pricing-policy.

4 Percent unintended pregnancy during first year of use Source: J Trussel in RA Hatcher et al Contraceptive Technology, 20th ed revised, New York, NY: Ardent

Media, 2011.

5 According to the FDA-approved labeling, Mirena is recommended only for women who have had at least one child.

▶ Decreased menstrual bleeding and dysmenorrhea

▶ Amenorrhea after one

year in 6% with Skyla,

in 12% with Kyleena,

in 19% with Liletta, and

in 20% with Mirena

▶ Smaller T-frame and narrower insertion

tube with Kyleena and

Skyla

▶ Irregular bleeding in first 3-6 months

▶ Progestin-related adverse effects such as headache, nausea, and acne

▶ Ovarian cysts

▶ Lack of protection against STIs

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1 KM Curtis and JF Peipert Long-acting reversible contraception

N Engl J Med 2017; 376:461.

2 Choice of contraceptives Med Lett Drugs Ther 2015; 57:127.

3 A new low-dose levonorgestrel-releasing IUD (Skyla) Med Lett Drugs Ther 2013; 55:21.

4 Liletta – a third levonorgestrel-releasing IUD Med Lett Drugs Ther 2015; 57:99

5 EN Berry-Bibee et al The safety of intrauterine devices in breastfeeding women: a systematic review Contraception 2016; 94:725.

6 KM Curtis et al U.S selected practice recommendations for contraceptive use, 2016 MMWR Recomm Rep 2016; 65:1.

ADVERSE EFFECTS — The most common adverse

effects reported in Kyleena users were vulvovaginitis

(24%), ovarian cysts (22%), abdominal/pelvic pain

(21%), headache/migraine (15%), acne/seborrhea

(15%), dysmenorrhea/uterine spasm (10%), breast

pain or discomfort (10%), and increased bleeding (8%)

Women using Kyleena can experience altered bleeding

patterns, especially during the fi rst 3-6 months after

insertion Amenorrhea developed in 12%, 20%, and 23%

of patients by the end of years 1, 3, and 5, respectively

Uterine perforation can occur during insertion of

Kyleena and may not be detected until a later date.

During clinical trials, the incidence of perforation

was <0.1% A systematic review of IUD safety found

an increased risk of uterine perforation among

breastfeeding women.5 Severe infection or sepsis,

including Group A streptococcal sepsis, and pelvic

inflammatory disease have been reported rarely

following insertion of levonorgestrel-releasing IUDs

Partial or complete expulsion of the device can occur;

in Kyleena clinical trials, the 5-year expulsion rate was

3.5% The risk of expulsion is higher when the device is

placed immediately postpartum

If an intrauterine pregnancy occurs with Kyleena in

place, the device should be removed; failure to remove

it could result in miscarriage, sepsis, or premature

labor and delivery About 50% of pregnancies that

occur with Kyleena in place are likely to be ectopic

In Kyleena clinical trials, the incidence of ectopic

pregnancy was 0.2% per year

TIMING OF INSERTION — Pregnancy must be ruled

out before inserting an IUD The manufacturer of

Kyleena recommends insertion of the IUD within 7

days of the start of the menstrual cycle or immediately

after a fi rst-trimester abortion Postpartum insertion

and insertion following a second-trimester abortion

should be postponed for a minimum of six weeks or

until the uterus is fully involuted to reduce the risk of

expulsion

Practice guidelines generally recommend abstaining

from sexual intercourse or using backup contraception

for 7 days after insertion of a levonorgestrel-releasing

IUD unless the device is inserted within 7 days of the

start of menstrual bleeding.6

CONCLUSION — Kyleena, a new

levonorgestrel-releasing intrauterine device (IUD), provides effective

contraception for at least 5 years It is smaller in size

and contains less levonorgestrel than the Mirena IUD

Drug Interaction: Clopidogrel and PPIs

The antiplatelet drug clopidogrel (Plavix, and others)

reduces major cardiovascular events, but can cause bleeding Proton pump inhibitors (PPIs) are often used with clopidogrel to prevent gastrointestinal bleeding, however, some evidence suggests that PPIs may interfere with the activation of clopidogrel and diminish its antiplatelet effect.1 FDA-approved labeling recommends avoiding concurrent use of the PPIs omeprazole and esomeprazole with clopidogrel

Table 1 Oral Proton Pump Inhibitors

OTC = over the counter

1 The lower end of the range is generally used for initial treatment of GERD

Higher or more frequent doses may be needed for patients with erosive esophagitis, peptic ulcer disease, hypersecretory conditions such as

Zollinger-Ellison syndrome, or for treatment of Helicobacter pylori infection.

2 PPIs are generally taken 30-60 minutes before the fi rst meal of the day

Taking one before the evening meal or taking the drug twice daily may be more effective for nocturnal acid control PPIs should generally be swallowed whole and should not be crushed or chewed Omeprazole/sodium

bicarbon-ate (Zegerid) should be taken on an empty stomach at least 1 hour before a meal Dexlansoprazole (Dexilant) can be taken with or without food.

3 Approximate WAC for 30 days’ treatment with the lowest usual adult dosage WAC = wholesaler acquisition cost or manufacturer’s published price to wholesalers; WAC represents a published catalogue or list price and may not represent an actual transactional price Source: AnalySource® Monthly February 5, 2017 Reprinted with permission by First Databank, Inc All rights reserved ©2017 www.fdbhealth.com/policies/drug-pricing-policy.

4 Approximate cost for 28 tablets or capsules.

5 Also available generically.

6 Immediate-release formulation that contains sodium bicarbonate as a buffer; it should be used with caution in patients on a low-sodium diet.

7 Approximate cost for 5-mg sprinkle capsules.

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POSSIBLE MECHANISM — Clopidogrel is a prodrug; the

CYP2C19 isozyme appears to be mainly responsible

for its bioactivation.2 Concurrent use of clopidogrel and

drugs that inhibit CYP2C19 could inhibit conversion

of clopidogrel to its active form Among the PPIs,

omeprazole and esomeprazole appear to be the

strongest inhibitors of CYP2C19 and pantoprazole

appears to be the weakest.3,4

CLINICAL STUDIES — Some pharmacodynamic and

pharmacokinetic studies have reported reductions

in platelet inhibition and the AUC of the clopidogrel

active metabolite in patients taking clopidogrel with

omeprazole or esomeprazole Similar effects were

not reported with pantoprazole, lansoprazole, or

dexlansoprazole.5-8

Whether concurrent use of clopidogrel and PPIs

results in clinically significant adverse cardiovascular

outcomes is not clear The results of several (mostly

observational) studies have been inconsistent.9,10

In a case-control study in patients ≥66 years old

who were started on clopidogrel after an acute MI,

concurrent use of a PPI (other than pantoprazole)

was associated with an increased risk of recurrent

MI within 90 days.11 In a retrospective cohort study

in 8205 patients with acute coronary syndrome

(ACS), use of a PPI with clopidogrel after hospital

discharge was associated with a higher risk of death

or rehospitalization due to ACS.12

In a retrospective cohort study of patients who were

prescribed clopidogrel after hospitalization for acute

MI, coronary artery revascularization, or unstable

angina, concurrent use of a PPI was not associated

with a statistically significant increased risk of

serious cardiovascular disease.13

In a randomized, placebo-controlled trial (COGENT),

use of omeprazole in patients taking clopidogrel

and aspirin decreased the incidence of GI bleeding

without increasing the risk of a cardiovascular event.14

The FDA concluded, however, that because of study

design limitations and a low number of reported

cardiovascular events, the results do not prove that

concurrent use of clopidogrel and omeprazole is safe.15

In addition, the fi xed-dose combination of omeprazole

and clopidogrel used in the trial was specifi cally

developed to delay absorption of omeprazole in order

to minimize an interaction.16

Some studies have suggested that PPI use is a

confounder associated with, rather than the cause of,

adverse cardiovascular outcomes in patients taking

clopidogrel.17,18

CONCLUSION — Concurrent use of clopidogrel and a

proton pump inhibitor (PPI) may result in decreased

levels of the clopidogrel active metabolite, and possibly

its antiplatelet activity, but whether it results in

clinically signifi cant adverse cardiovascular outcomes

is not clear Since omeprazole and esomeprazole appear to be most likely to affect the antiplatelet activity of clopidogrel and the FDA specifi cally warns against their concomitant use, it would be reasonable

to use another PPI such as pantoprazole in patients taking clopidogrel ■

document on the concomitant use of proton pump inhibitors and thienopyridines: a focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use A Report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents J Am Coll Cardiol 2010; 56:2051.

2 JL Mega et al Cytochrome P-450 polymorphisms and response

to clopidogrel N Engl J Med 2009; 360:354.

3 T Zvyaga et al Evaluation of six proton pump inhibitors as inhibi-tors of various human cytochromes P450: focus on cytochrome P450 2C19 Drug Metab Dispos 2012; 40:1698.

4 RS Wedemeyer and H Blume Pharmacokinetic drug interaction profi les of proton pump inhibitors: an update Drug Saf 2014; 37:201.

design study to assess the effects of dexlansoprazole, lansoprazole, esomeprazole, and omeprazole on the steady-state pharmacokinetics and pharmacodynamics of clopidogrel in healthy volunteers J Am Coll Cardiol 2012; 59:1304.

6 JM Siller-Matula et al Effects of pantoprazole and esomeprazole on platelet inhibition by clopidogrel. Am Heart J 2009;157:148.e1.

7 DJ Angiolillo et al Differential effects of omeprazole and pan-toprazole on the pharmacodynamics and pharmacokinetics of clopidogrel in healthy subjects: randomized, placebo-controlled, crossover comparison studies Clin Pharmacol Ther 2011; 89:65.

8 N Simon et al Omeprazole, pantoprazole, and CYP2C19 effects

on clopidogrel pharmacokinetic-pharmacodynamic relationships

in stable coronary artery disease patients Eur J Clin Pharmacol 2015; 71:1059.

9 SA Scott et al Antiplatelet drug interactions with proton pump inhibitors Expert Opin Drug Metab Toxicol 2014; 10:175.

10 SD Bouziana and K Tziomalos Clinical relevance of clopidogrel-proton pump inhibitors interaction World J Gastrointest Pharmacol Ther 2015; 6:17.

11 DN Juurlink et al A population-based study of the drug interac-tion between proton pump inhibitors and clopidogrel CMAJ 2009; 180:713.

12 PM Ho et al Risk of adverse outcomes associated with con-comitant use of clopidogrel and proton pump inhibitors following acute coronary syndrome. JAMA 2009; 301:937.

13 WA Ray et al Outcomes with concurrent use of clopidogrel and proton pump inhibitors: a cohort study Ann Intern Med 2010; 152:337.

14 DL Bhatt et al Clopidogrel with or without omeprazole in coronary artery disease N Engl J Med 2010; 363:1909.

15 MR Southworth and R Temple Interaction of clopidogrel and omeprazole N Engl J Med 2010; 363:1977.

16 DN Juurlink Comment on: Clopidogrel with or without omepra-zole in coronary artery disease N Engl J Med 2011; 364:681.

17 SP Dunn et al Impact of proton pump inhibitor therapy on the

ef-fi cacy of clopidogrel in the CAPRIE and CREDO trials J Am Heart Assoc 2013; 2:e004564.

18 SG Goodman et al Association of proton pump inhibitor use on cardiovascular outcomes with clopidogrel and ticagrelor Circula-tion 2012; 125:978.

Online Only Article

Atezolizumab (Tecentriq) for Bladder Cancer and NSCLC

www.medicalletter.org/TML-article-1515g

Trang 10

e40

The Medical Letter

on Drugs and Therapeutics

The FDA has approved the immune checkpoint

inhibitor atezolizumab (Tecentriq – Genentech) for

treatment of locally advanced or metastatic urothelial

carcinoma and metastatic non-small cell lung cancer

(NSCLC) that have progressed during or following

platinum-based chemotherapy Atezolizumab is the

fi rst programmed death-ligand 1 (PD-L1) blocking

antibody to become available in the US Two other

immune checkpoint inhibitors, the programmed death

receptor-1 (PD-1) inhibitors nivolumab (Opdivo) and

pembrolizumab (Keytruda), are also approved for

treatment of metastatic NSCLC, and nivolumab is

also approved for second-line treatment of locally

advanced or metastatic urothelial carcinoma

UROTHELIAL CARCINOMA — Urothelial carcinoma

(also known as transitional cell carcinoma) is the most common type of bladder cancer in the US Most urothelial cancers of the bladder are superfi cial and involve only the mucosa or submucosa with no muscular invasion Standard initial treatment for these cancers is transurethral resection with or without intravesical therapy (chemotherapy or BCG) About 10-15% of patients with superfi cial urothelial cancer will develop muscle-invasive or metastatic disease The standard treatment for these invasive cancers is radical cystectomy and platinum-based chemotherapy.1 Few options are available for treatment of metastatic urothelial cancer that has progressed after platinum-based chemotherapy, and none have improved survival.2

NSCLC — Standard initial treatment for patients with

metastatic NSCLC with no epidermal growth factor receptor (EGFR) mutations or anaplastic lymphoma kinase (ALK) translocations is generally platinum doublet therapy (a two-drug regimen that includes a platinum derivative such as carboplatin or cisplatin).3

If the disease progresses after platinum doublet therapy, nivolumab or pembrolizumab can be used

MECHANISM OF ACTION — Binding of PD-L1 to its

receptors on T cells and antigen presenting cells sup-presses cytotoxic T-cell activity, T-cell proliferation, and cytokine production Atezolizumab is a humanized IgG1 monoclonal antibody that binds to PD-L1 on tumor cells, preventing the ligand from interacting with its receptors and permitting the antitumor immune response

CLINICAL STUDIES — Urothelial Carcinoma – FDA

approval of atezolizumab for urothelial carcinoma was based on the results of a single-arm trial in 310 patients with inoperable locally advanced or metastatic urothelial cancer who had disease progression after a platinum-based regimen All patients were treated with atezolizumab 1200 mg IV once every 3 weeks The objec-tive response rate (ORR), the primary endpoint, was 15% (compared to a historical control ORR of 10% for second-line therapy) Increased PD-L1 expression on immune cells was associated with an increased response.4

In a single-arm trial in 119 cisplatin-ineligible patients with locally advanced or metastatic urothelial cancer

Atezolizumab (Tecentriq) for

Bladder Cancer and NSCLC

Pronunciation Key Atezolizumab: a” te zoe liz’ ue mab Tecentriq: te sen' trik

Table 1 Immune Checkpoint Inhibitors for Bladder Cancer and NSCLC

Drug Usual Adult Dosage Cost 1

PD-1 Inhibitors

Nivolumab – Bladder Cancer 2 :

Opdivo (BMS) 240 mg IV q2 wks $12,036.20

NSCLC 3,4 : 240 mg IV q2 wks 12,036.20

Pembrolizumab – NSCLC 4,5 : 200 mg IV q3 wks 8893.00

Keytruda (Merck)

PD-L1 Inhibitor

Atezolizumab – Bladder Cancer 2 :

Tecentriq (Genentech) 1200 mg IV q 3wks 8620.00

NSCLC 3,4 : 1200 mg IV q3wks 8620.00

NSCLC = non-small cell lung cancer

1 Approximate WAC for 30 days’ treatment WAC = wholesaler acquisition

cost or manufacturer’s published price to wholesalers; WAC represents a

published catalogue or list price and may not represent an actual

transac-tional price Source: AnalySource® Monthly February 5, 2017 Reprinted

with permission by First Databank, Inc All rights reserved ©2017 www.

fdbhealth.com/policies/drug-pricing-policy.

2 FDA-approved for locally advanced or metastatic urothelial carcinoma

that has progressed during or following platinum-based chemotherapy

or within 12 months of neoadjuvant or adjuvant platinum-based

chemo-therapy

3 FDA-approved for metastatic NSCLC with disease progression on or after

platinum-based chemotherapy

4 Patients with EGFR or ALK genomic tumor aberrations should receive

treatment with drugs specifi c for these aberrations before receiving a

PD-1 or PD-L1 inhibitor.

5 FDA-approved for fi rst-line treatment of metastatic NSCLC with

PD-L1 expression on ≥50% of tumor cells and no EGFR or ALK genomic

tumor aberrations, and metastatic NSCLC with PD-L1 expression on

≥1% of tumor cells and disease progression on or after platinum-based

chemotherapy.

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