0355 Extracorporeal Immunoadsorption (Prosorba Column) · 2020. 9. 8. · Extracorporeal...

Extracorporeal Immunoadsorption (Prosorba Column) - Medical Clinical Policy Bulletins... of 22

(https://www.aetna.com/)

Extracorporeal Immunoadsorption (ProsorbaColumn)

Number: 0355

Policy *Please see amendment for Pennsylvania Medicaid at the end of this CPB.

Aetna considers extracorporeal immunoadsorption (ECI)

medically necessary for any of the following indications:

1. Hemolytic uremic syndrome, with clinical evidence of

serious bleeding with platelet count below 50,000 or the

potential for serious bleeding with platelet count below

20,000; or

2. Idiopathic thrombocytopenic purpura, with clinical evidence

of serious bleeding with platelet count below 50,000 or the

potential for serious bleeding with platelet count below

20,000; or

3. Last resort treatment of life-threatening systemic lupus

erythematosus when conventional therapy has failed to

prevent clinical deterioration; or

4. Moderate-to-severe rheumatoid ar thritis, for reduction of signs and symptoms in members who have failed other

treatments (e.g., non-steroidal anti-inflammatory drugs,

methotrexate); or

Policy History

Last Review

05/28/2019

Effective: 11/08/1999

Next

Review: 03/27/2020

Review History

Definitions

Additional Information

Clinical Policy Bulletin

Notes

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https://www.aetna.com/


5. Myasthenic crisis when conventional therapy (e.g.,

intravenous immunoglobulin or plasmas exchange) has

failed; or

6. Pemphigus vulgaris that is resistant to standard therapy,

including dapsone, corticosteroids, and

immunosuppressants (e.g., azathioprine or cyclosporine).

Aetna considers ECI experimental and investigational for all

other indications because its effectiveness for indications other

than the ones listed above has not been established (not an all-

inclusive list):

▪ Allergic asthma

▪ Atopic dermatitis

▪ Anti-phospholipid syndrome

▪ Dermatomyositis

▪ Elevated lipoprotein(a)

▪ Epidermolysis bullosa acquisita

▪ Heart failure

▪ Hepatitis B.

See

CPB 0206 - Parenteral Immunoglobulins,

also (../200_299/0206.html)

CPB 0285 - Plasmapheresis/Plasma Exchange/Therapeutic

Apheresis (../200_299/0285.html)

, CPB 0315 - Enbrel (Etanercept) (0315.html)

, CPB 0341 - Infliximab (0341.html),

and CPB 0595 - Anakinra (Kineret) (../500_599/0595.html).

Background

Extra-corporeal immunoadsorption (ECI), also referred to as

protein immunoadsorption therapy or by the trade name

Prosorba Column (Cypress Bioscience), consists of a highly

purified protein A (isolated from staphylococcus aureus) that is

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bonded to a silica matrix. Plasma is collected from the patient

in a pheresis procedure and then passed over the column.

Circulating immune complexes and IgG bind to the protein A

and are thus selectively removed from plasma. The plasma

can then be returned to the patient, thus eliminating the need

for a plasma exchange.

Idiopathic thrombocytopenic purpura (ITP) is characterized by

rapid platelet destruction and typically appears in young

women and also in male patients who are sero-positive for HIV

infection. It is usually a relatively benign disorder in its chronic

form and there is no indication to treat when the platelet count

is above 50,000. In cases involving more serious bleeding or

with platelet counts less than 20,000, ECI has successfully

reversed the immune thrombocytopenia by removal and

modulation of platelet-specific IgG and circulating immune

complexes.

Extra-corporeal immunoadsorption has also been used in the

treatment of hemolytic uremic syndrome (HUS), which is

characterized by thrombocytopenia, microangiopathic

hemolytic anemia, and progressive renal failure. It may occur

in patients with malignancies treated with mitomycin C and

cisplatin. This syndrome is known to be associated with

circulating immune complexes that may play a role in its

pathogenesis. A number of patients treated with protein A

columns have achieved a definite increase in platelet count,

decrease of hemolysis, and stabilization of renal function.

More recently, the Food and Drug Administration (FDA) has

approved extra-corporeal immunoadsorption for the treatment

of rheumatoid arthritis (RA). It is indicated for use in

therapeutic reduction of signs and symptoms of moderate-to-

severe RA in adult patients with long-standing disease who

have failed or are intolerant of disease-modifying anti-

rheumatic drugs. The FDA stressed that the machine was for

use in a small proportion of patients, those with moderate-to-

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severe symptoms who have failed other treatments; it is not

first-line therapy. The machine offers a 30 % chance of

improving the swelling and pain that cripples patient's joints.

For HUS and ITP, treatment is typically given 6 times over the

course of 2 to 3 weeks. For RA, patients are typically treated

once-weekly for 12 weeks.

Ruocco et al (2005) stated that pemphigus vulgaris (PV) is a

rare autoimmune bullous dermatosis with a high mortality rate

if untreated. The disease results from autoimmunity to normal

components of keratinocyte cell membrane (desmogleins 3

and 1) belonging to the cadherin super-gene family. Standard

treatment for PV entails combination of glucocorticoids (high

dosage) and immunosuppressants. In patients with severe, life-

threatening, or refractory PV, stronger therapies should be

considered (e.g., "pulse-therapy" with discontinuous

intravenous infusion of mega doses of immunosuppressants

over a short-time, plasmapheresis, and ECI of pathogenic

autoantibodies using the extracellular domain of the PV main

antigen (desmoglein 3) produced by baculovirus or, more

recently, a tryptophan-linked polyvinyl alcohol adsorber.

Braun et al (2000) noted that reduction of pathological

autoantibodies (Abs) as well as circulating immune complexes

(IC) can be beneficial in the treatment of autoimmune

disease. Plasmapheresis has been shown to reduce Abs in

systemic lupus erythematosus (SLE), but its effect on health

outcome was not better compared with conventional

immunosuppression in the past. These investigators

evaluated immunoadsorption (IAS) as rescue therapy in

patients suffering from SLE. A total of 8 patients with severe,

therapy-resistant SLE underwent immunoadsorption onto

protein A sepharose without concomitant

immunosuppressants. Remission of the disease was achieved

in 7 patients. Therapy had to be stopped in 1 patient because

of side-effects. The best results were obtained when IAS was

performed daily, without supplementary intravenous

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immunoglobulin therapy. Oral cyclophosphamide for 3 to 6

months during follow-up was used to suppress relapse.

Circulating IC and Abs were effectively eliminated regardless

of their IgG subclass. The authors concluded that IAS onto

protein A might be used as an extra-corporeal treatment option

in SLE when other therapies are ineffective.

Stummvoll et al (2009) stated that IAS with various methods is

used as a rescue therapy in severely ill SLE patients who are

refractory to conventional therapeutic procedures. The

method aims at the rapid and extensive removal of

pathogenic IC and Abs. Long-term observational studies

suggested efficacy and have not seen an increase in the risk

of infections (as were seen in other extracorporeal

procedures). However, randomized controlled trials (RCT) are

lacking. Recently, biologicals aiming at tumor necrosis factor-

blockade or B-cell depletion have been used to treat severe

SLE. They are easier to apply since they do not necessitate

additional hardware or specially trained staff. While there is

emerging evidence for efficacy from uncontrolled observations,

no RCT could so far demonstrate benefit in SLE. Under these

circumstances, IAS still has a role in treating severe SLE,

when other therapies are ineffective or are contraindicated (as

in pregnancy).

Biesenbach et al (2009) stated that pathogenic Abs are a

hallmark of SLE and their rapid removal is beneficial in active

SLE. Immunoadsorption is effective in removing serum levels

of all classes of immunoglobulin (Ig), IC and anti-dsDNA Abs

and appears superior to plasmapheresis with respect to side

effects. Immunoadsorption can be performed with different

columns, which use different ligands to bind their target. In

particular, high affinity columns are in the focus of interest.

Their ligands are either sheep IgG directed against human Ig

(Ig-column, Ig-Therasorb((R))), or staphylococcal Protein A

(ProtA-column, Immunosorba((R))), or the synthetic peptide

Gam146 (GAM-column, Globaffin((R))). In the

authors' experience, Ig-columns have been effective in treating

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active renal SLE. However, no analysis has so far been

published on which column type should be preferred in treating

SLE patients. Among the authors' SLE patients maintained on

prolonged IAS therapy, those with stable renal SLE and low-

to-moderate disease activity who were successfully treated by

using Ig-columns were identified. Six of these patients were

switched to ProtA-columns, keeping the rest of the protocol

and the medication constant. In addition, 2 patients were

switched from Ig- to GAM-columns. All types of columns

significantly lowered the serum levels of IgG, IgM, and anti-

dsDNA Abs. Disease activity was constantly low before and

after the switch, as were parameters of renal function. In

addition, patients with highly active disease were effectively

treated when ProtA- (n = 6) or GAM-columns (n = 1) were

used as first-line extracorporeal treatment. The authors

concluded that these findings demonstrated that all columns

are adequately effective in controlling key parameters of SLE.

Thus, it is not the type of the ligand, but only the outcome, i.e.,

the successful removal of Ig, IC, and auto-Abs that is needed

for controlling SLE activity.

Gürcan and Ahmed (2011) noted that long-term remission in

patients with epidermolysis bullosa acquisita (EBA) is difficult

to achieve. Patients who are resistant or develop side effects

to conventional immuno-suppressive therapy (CIST) have

been treated with several other agents. These investigators

focused on the clinical outcome in patients treated with a

single drug or combination, and determined if long-term

remission can be induced. Data on 71 patients were

analyzed. There are no controlled trials. The regimens used

included colchicine, cyclosporine, daclizumab, dapsone,

intravenous immunoglobulin, mesalazine, mycophenolic acid,

rituximab, extra-corporeal photochemotherapy, and

plasmapheresis. The use of CIST, especially in widespread

and recalcitrant patients, usually does not produce a

prolonged clinical remission and can have hazardous side

effects. The authors stated that intravenous immunoglobulin,

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rituximab and immunoadsorption have been successfully used

in some, but the benefits from their use may require addi tional

studies.

Lagoumintzis and colleagues (2010) noted that current

medications for myasthenia gravis (MG) are non-specific and

include acetylcholinesterase inhibitors, immunosuppressants,

plasma exchange (PE), intravenous immunoglobulin

(IVIG) administration and thymectomy. Treatments that

selectively target the anti-acetylcholine receptor (AChR) auto-

Abs may prove to be more effective and free of side-effects.

These investigators reviewed 2 approaches aimed at the

development of antigen-specific therapies for MG. The first is

specific apheresis of Abs from patients' sera using immobilized

recombinant AChR domains as immunoadsorbents. These

researchers had shown that the combined recombinant

extracellular domains of all human AChR subunits are capable

of specifically immunoadsorbing the majority of pathogenic auto-

Abs from several MG sera. The second therapeutic approach is

the development of non-pathogenic anti-AChR monoclonal Abs

that could potentially be used as protective agents by blocking

the binding of patients' auto-Abs to the AChR.

Blaha et al (2011) described their experience with PE

and IAS in patients with MG. The group of 27 patients

consists of 21 patients treated with PE and 6 patients who

received IAS. Plasma exchange led to stabilization in 20

patients. In patients treated with IAS, therapy could be

discontinued in 2 patients after 13 months of therapy, and the

other 4 patients were stabilized without myasthenic crises after

6 to 9 years of therapy.Extra-corporeal elimination therapy

through PE or IAS is effective and sometimes life-saving and is

safe in the hands of an experienced team (6 % complication

rate).

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Kohler et al (2011) noted that myasthenic crisis is the most

serious life-threatening event in patients with MG, affecting up

to 27 % within the first 2 years following onset of disease.

Extra-corporeal removal of circulating Abs against the nicotinic

acetylcholine receptor (AChRAb) by methods of therapeutic

apheresis, such as PE and IAS had been demonstrated as

effective treatment especially in acute situations of myasthenic

crisis. These investigators presented the results of a

prospective, randomized controlled clinical trial, investigating

19 patients with myasthenic crisis, who were randomized to

receive either PE (n = 10) or IAS (n = 9) in addition to

combined drug treatment. Patients received 3 to 5 (mean

of 3.5 for PE, and 3.4 for IAS) treatments over a period of 7

days with a pre-defined treatment volume of 1.5 L plasma (i.e.,

20 to 25 ml/kg plasma representing 0.5 to 0.6 patients' plasma

volumes). Clinical courses were monitored using disease

specific clinical scores. After initiation of IAS or PE, the mean

value of myasthenia scores decreased equally until day 14 of

the post-treatment phase. Patients from both treatment

groups improved to a stable clinical status of Oosterhuis

Classes 1 and 2. Substantial reduction of AChRAb was

documented after each session of PE or IAS. During the

treatment period, 16 adverse effects (7 serious adverse

events, SAE) in the PE and 10 (1 SAE) in the IAS group were

observed. The authors concluded that IAS proved to be

equally effective compared with PE treatment in patients with

myasthenic crisis; 3 to 5 treatment sessions using low plasma

volume dosage of 20 to 25 ml/kg were adequate to improve

clinically relevant symptoms significantly in mostpatients.

Felix and colleagues (2015) stated that dilated cardiomyopathy

is a common myocardial disease characterized by ventricular

chamber enlargement and systolic dysfunction that result in

heart failure. In addition to genetic predisposition, viral

infection and myocardial inflammation play a causal role in the

disease process of dilated cardiomyopathy. Experimental and

clinical studies suggested that activation of the humoral

immune system, with production of circulating cardiac

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autoantibodies, plays an important functional role in the

development and progression of cardiac dysfunction in

patients with dilated cardiomyopathy. Small open-controlled

studies showed that removal of circulating antibodies by

immunoadsorption resulted in improvement of cardiac function

and decrease in myocardial inflammation. The authors

concluded that currently immunoadsorption is an experimental

treatment option for improvement of cardiac function -- therapy

that calls for confirmation by a placebo-controlled multi-center

study.

Also, an UpToDate review on “Possibly effective emerging

therapies for heart failure” (Colucci, 2015) states that

“Immunoadsorption -- Antibodies against cardiac cell proteins,

including mitochondrial proteins, contractile proteins, and beta-

receptors, have been identified in dilated cardiomyopathy. If

cardiac autoantibodies contribute to myocardial dysfunction,

their removal with immunoadsorption might improve left

ventricular hemodynamics. Several studies have

demonstrated the potential benefit of this approach …. Various

types of immunotherapy [including immunoadsorption] have

been investigated in patients with HF but such therapy does

not have an established clinical benefit except for specific

indications in patients with myocarditis”.

Atopic Dermatitis

Zink et al (2016) stated that patients with atopic dermatitis

(AD) tend to have greatly elevated levels of serum

immunoglobulin E (IgE). However, the role of IgE in the

pathogenesis of AD is debated. In an open-label, pilot study,

these researchers evaluated an anti-IgE-treatment approach

by combining extracorporeal IAS and anti-IgE antibody

omalizumab in 10 patients with severe, therapy-refractory AD.

IgE levels decreased after IAS and decreased continuously in

all patients during anti-IgE therapy. The reverse trend was

observed during 6 months follow-up without treatment. In

parallel with these observations, an improvement in AD was

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Extracorporeal Immunoadsorption (Prosorba Column) - Medical Clinical Policy Bulleti... of 22

observed during the treatment period, with aggravation during

follow-up. The authors concluded that further research is

needed, based on the principle of reducing IgE levels in order

to improve clinical symptoms, using a combination anti-IgE

treatment approach, adjusted according to IgE levels. The

main drawback of this study was the combinational use of IAS

and omalizumab. The findings of this pilot study need to be

validated by well-designed studies.

Anti-Phospholipid Syndrome

Kronbichler et al (2016) stated that extracorporeal treatments

have been used since the 1970s in the management of SLE.

A RCT comparing the effectiveness of standard of care (SOC)

combined with PE against SOC alone in patients with lupus

nephritis revealed no difference in terms of renal outcome.

Subsequently, initial expectations have been dampened and

further experience with PE is mainly limited to observational

studies and single-case reports. Beneficial effects have been

reported in patients with refractory disease course or in

pregnancy with prior complications due to SLE and anti-

phospholipid syndrome (APS). A more specific form of

extracorporeal treatment, IAS, has emerged as a valuable

option in the treatment of SLE. In line with the PE experience,

IAS appeared to have beneficial effects in patients with

refractory disease, contraindications to standard

immunosuppression or during pregnancy. The mechanism

IAS relates to autoantibody removal but for PE removal of

activated complement components, coagulation factors,

cytokines and micro-particles may also be relevant. Both

treatments have good safety profiles although reactions to

blood product replacement in PE and procedure-related

complications (e.g., bleeding or catheter-related infections)

have occurred. The authors concluded that there is a need to

more clearly define the clinical utility of PE and IAS in

refractory lupus and APS subgroups.

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Elevated Lipoprotein(a)

Waldmann and Parhofer (2016) noted that an elevated plasma

concentration of lipoprotein(a) (Lp(a)) is an independent risk

factor for cardiovascular disease. Life style modification and

currently available drugs either fail to effectively lower plasma

Lp(a) levels or do not result in clinical benefit. However,

lipoprotein apheresis is very efficient in decreasing Lp( a)

concentrations. A single apheresis session c an acutely

decrease Lp(a) by approximately 60 to 75 % and weekly or bi-

weekly performed apheresis resulted in considerably

decreased mean i nterval concentrations (approximately 25 to

40 % reduction). While most apheresis systems (HELP,

heparin induced extracorporeal LDL precipitation; DALI, direct

adsorption of lipoproteins; lipoprotein apheresis with dextran-

sulfate; lipid filtration; IAS) decrease LDL and Lp(a), Lipopac is

specific and only decreases Lp(a). The authors stated that Lp

(a) apheresis is an expensive and time-consuming process,

but is associated with very few side effects. They stated that 2

RCTs gave conflicting c onsults with respect to the effect on

angiographic changes; retrospective analyses indicated that

regular apheresis translates into clinical benefit in patients with

elevated Lp(a); but adequate RCTs are lacking.

Allergic Asthma

In a randomized, controlled, open-label, pilot trial, Lupinek and

colleagues (2017) evaluated the safety and efficacy of a single-

use IgE immunoadsorber column (IgEnio) regarding the

selective depletion of IgE in patients with allergic asthma; and

examined if IgEnio can bind IgE-omalizumab immune

complexes. A total of 15 subjects were enrolled and randomly

assigned to either the treatment group (n = 10) or to the

control group (n = 5). Immunoadsorption was done by veno-

venous approach, processing the 2-fold calculated plasma

volume during each treatment. A minimum average IgE-

depletion of 50 % after the last cycle in the intention-to-treat

population was defined as primary end-point. Safety of the

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treatment was studied as secondary end-point. In addition,

possible changes in allergen-specific sensitivity were

investigated, as well as clinical effects by peak flow

measurement and symptom-recording. The depletion of IgE-

omalizumab immune complexes was studied in-vitro. IgE

immunoadsorption with IgEnio selectively depleted 86.2 % (±

5.1 % SD) of IgE until the end of the last cycle (p < 0.0001).

Removal of pollen allergen-specific IgE was associated with a

reduction of allergen-specific basophil-sensitivity and

prevented increases of allergen-specific skin-sensitivity and

clinical symptoms during pol len s easons. IgEnio also depleted

IgE-omalizumab immune complexes in-vitro. The therapy

under investigation was safe and well-tolerated. During a total

of 81 aphereses, 2 SAE were recorded, one of which, an

episode of acute dyspnea, possibly was related to the

treatment and resolved after administration of anti-histamines

and corticosteroids. The authors concluded that the findings

of this pilot study indicated that IgE immunoadsorption with

IgEnio may be used to treat patients with pollen-induced

allergic asthma. Furthermore, the treatment could render

allergic patients with highly elevated I gE-levels eligible for the

administration of omalizumab and facilitate the desorption of

IgE-omalizumab complexes. Moreover, they stated that

additional clinical investigations with a higher number of

participants are planned to confirm these findings and to

further improve treatment efficacy.

These investigators also noted that a drawback of this study

was that, due to the uneven distribution of allergic co-

morbidities (i.e., rhinitis, dermatitis) in the study groups and

due to the low number of study participants (n = 15), effects of

the treatment on co-morbidities could not be investigated. The

effects of treatment with IgEnio on clinical endpoints will be

assessed in follow-up studies. Likewise, effects of long-term

treatment will be analyzed in future studies.

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Furthermore, an UpToDate review on “Treatment of moderate

persistent asthma in adolescents and adults” (Peters et al,

2018) does not mention extracorporeal immunoadsorption as

a therapeutic option.

Treatment of Hepatitis B

Han and colleagues (2018) established a novel HBV specific

immunoadsorbent for the removing of HBV particles. The anti-

HBsAg monoclonal antibody was immobilized on sepharose

beads to produce a sepharose anti-HBs column. Then the

immunoadsorbent was evaluated and characterized by

scanning electron microscopy. In addition, time-dependent

effects of the eradication capacity of anti-HBsAg functionalized

sepharose beads against HBV were investigated. Proposed

immunoadsorbents exhibited a favorable biocompatibility as

well as specificity. With the optimized recycle time, the

decontamination performance of HBV particles and quantity of

HBsAg were assessed either by real-time quantitative PCR or

ELISA, which showed that the immunoadsorbent could

remove approximately 90 % of the HBV and 90 % of the

HBsAg from human plasma samples. The authors concluded

that anti-HBsAg functionalized adsorbents introduced in this

work exhibited potential for HBV removal and this approach

could establish a novel therapeutic option or at least as a

combination supplementary therapy strategy with anti-viral

drugs for the treatment regimen of HBV.

CPT Codes / HCPCS Codes / ICD-10 Codes

Information in the [brackets] below has been added for clarification purposes. Codes requiring a 7th character are represented by "+":

Code Code Description

CPT codes covered if selection criteria are met:

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36516 Therapeutic apheresis; with extracorporeal

immunoadsorption, selective ads orption or

selective filtration and plasma reinfusion

O ther HCPCS codes related to the CPB:

J7500 Azathioprine, oral 50 mg

J7501 Azathioprine, parenteral, 100 mg

J7502 Cyclosporine, oral, 100mg

J7515 Cyclosporine, oral, 25 mg

J7516 Cyclosporine, parenteral, 250 mg

ICD-10 codes covered if selection criteria are met:

D59.3 Hemolytic-uremic syndrome [with clinical

evidence of serious bleeding with platelet count

below 50,000 or the potential for serious

bleeding with platelet count below 20,000]

D69.3 Immune thrombocytopenic purpura [idiopathic

thrombocytopenic purpura (ITP) with clinical

evidence of serious bleeding with platelet count

below 50,000 or the potential for serious

bleeding with platelet count below 20,000]

G70.01 Myasthenia gravis with (acute) exacerbation

L 10.0 -

L 10.9

Pemphigus [resistant to standard therapy,

including dapsone, corticosteroids, and

immunosuppressants (e.g., azathrioprine or

cyclosporine)]

M05.00 -

M06.9

Rheumatoid arthritis with rhuematoid f actor

[moderate to severe rheumatoid ar thritis (RA),

for reduction of signs and symptoms in

members who have failed ot her treatments

(e.g., NSAIDS, methotrexate)]



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M32.10 -

M32.9

Systemic lupus erythematosus (SLE) [severe

for whom other interventions have been

unsuccessful, have become intolerable, or are

contraindicated]

ICD-10 codes not covered for indications listed in the CPB ( no t all inclusive):

B16.0 -

B16.9

Acute hepatitis B

B18.0 Chronic viral hepatitis B with delta-agent

B18.1 Chronic viral hepatitis B without delta-agent

B19.10 -

B19.11

Unspecified viral hepatitis B

D68.61 Antiphospholipid syndrome

E78.89 Other lipoprotein metabolism disorders

[elevated lipoprotein(a)]

I50.1 -

I 50.9

Heart failure

J45.20 -

J45.998

Asthma [allergic]

L 20.0 -

L 20.9

Atopic dermatitis

M33.00 -

M33.99

Dermatopolymyositis

Q81.9 Epidermolysis bullosa, unspecified

[epidemolysis bullosa acquisita]



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The above policy is based on the following references:

1. Handelsman H. Protein A columns for immune

thrombocytopenia. Health Technology Assessment

Reports, 1990 No. 7. AHCPR Pub. No. 91-0008.

Rockville, MD: Agency for Health Care Policy and

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2. Snyder HW, Cochran SK, Balint JP, et al. Experience

with protein A-immunoadsorption in treatment-

resistant adult immune thrombocytopenic purpura.

Blood. 1992;79(9):2237-2245.

3. Mittelman A, Bertram J, Henry DH, et al. Treatment of

patients with HIV thrombocytopenia with hemolytic

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1):15-18.

4. Korec S, Schein PS, Smith FP, et al. Treatment of

cancer-associated hemolytic uremic syndrome with

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5. Snyder HW, Mittelman A, Oral A, et al. Treatment of

cancer chemotherapy-associated thrombotic

thrombocytopenic purpura/hemolytic uremic

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Cancer. 1993;71:1882-1892.

6. Balint JP. Immune modulation associated with

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913.

7. Weisenhutter CW, Irish BL, Bertram JH. Treatment of

patients with refractory rheumatoid arthritis with

extracorporeal protein A immunoadsorption columns:

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8. Kunz K, Kuppermann M, Bowe T, et al. Protein A

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treatment of steroid-resistant immune

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thrombocytopenic purpura. Int J Technol Assess

Health Care. 1996;12(3):436-449.

9. Nakaji S. Current topics on immunoadsorption

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controlled trial of the Prosorba column for treatment

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11. Bueno D Jr, Sevigny J, Kaplan AA. Extracorporeal

treatment of thrombotic microangiopathy: A ten year

experience. Ther Apher. 1999;3(4):294-297.

12. Felson DT, LaValley MP, Baldassare AR, et al. The

Prosorba column for treatment of refractory

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13. Kwaan HC, Gordon LI. Thrombotic microangiopathy in

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56.

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for the treatment of rheumatoid arthritis: Final results

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apheresis in myasthenia gravis. Ther Apher. 2000;4

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18. Cypress Biosciences, Inc. Prosorba Column.

Professional Labeling. San Diego, CA: Cypress

Bioscience; March 18, 1999.

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indications for protein A-based extracorporeal

immunoadsorption. Ther Apher. 2001;5(5):394-403.

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20. Saydain G, George L, Raoof S. New therapies:

Plasmapheresis, intravenous immunoglobulin, and

monoclonal antibodies. Crit Care Clin. 2002;18(4):957-

975.

21. Alberta Heritage Foundation for Medical Research

(AHFMR). Prosorba treatment for rheumatoid arthritis.

Technote TN 30. Edmonton, AB: AHFMR; 2001.

22. Hailey D, Topfer LA. Extracorporeal immunoadsorption

treatment for rheumatoid arthritis. Issues in Emering

Health Technologies Issue 28. Ottawa, ON: Canadian

Coordinating Office for Health Technology Assessment

(CCOHTA); 2002.

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disorders. Therap Apher Dial. 2003;7(2):197-205.

24. Kiprov DD, Golden P, Rohe R, et al. Adverse reactions

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Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan

benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial,

general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care

services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors

in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely

responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is

subject to change.

Copyright © 2001-2020 Aetna Inc.

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AETNA BETTER HEALTH® OF PENNSYLVANIA

Amendment to Aetna Clinical Policy Bulletin Number: 0355 Extracorporeal

Immunoadsorption (Prosorba Column)

There are no amendments for Medicaid.

www.aetnabetterhealth.com/pennsylvania annual 06/01/2020

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http://www.aetnabetterhealth.com/pennsylvania

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