INVITED REVIEW
CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY
AND MALIGNANCY: A SYSTEMATIC REVIEW
YUSUF A. RAJABALLY, MD, FRCP ,1,2 and SHAHRAM ATTARIAN, MD, PhD3,4
1
School of Life and Health Sciences, Aston Brain Centre, Aston University, Aston Triangle, Birmingham, B4 7ET, United Kingdom
2
Regional Neuromuscular Service, University Hospitals Birmingham, Birmingham, United Kingdom
3
Reference Centre for Neuromuscular Diseases and ALS, Centre Hospitalier Universitaire La Timone, Marseille, France
4
Aix-Marseille University, Inserm, GMGF, Marseille, France
Accepted 28 November 2017
ABSTRACT: A systematic review of the literature was per-
formed on the association of chronic inflammatory demyelinat-
ing polyneuropathy (CIDP) with malignancy. Hematological
disorders are the most common association, particulalry non-
Hodgkin lymphoma. CIDP frequently precedes the malignancy
diagnosis, and there is a favorable CIDP response to treatment
more than 70% of the time. Melanoma is the second most com-
mon association and may be accompanied by antiganglioside
antibodies; CIDP shows a good response to immunotherapy.
Other cancers are rare, with variable timings and presentations
but good responses to immunomodulation and/or cancer ther-
apy. Unusual neurological features such as ataxia, distal/upper
limb predominance, or cranial/respiratory/autonomic involve-
ment may suggest associated malignancy as may abdominal
pain, diarrhea/constipation, poor appetite/weight loss, dermato-
logical lesions, and lymphadenopathy. In the appropriate clinical
and electrophysiological setting, CIDP associated with cancer
should be considered. Immunomodulatory therapy, cancer treat-
ment alone, or a combination may be effective.
Muscle Nerve 57: 875–883, 2018
Chronic inflammatory demyelinating polyneurop-
athy (CIDP) is an autoimmune peripheral neurop-
athy of increasing prevalence with age.1,2 CIDP has
been described in association with various disor-
ders and may be more difficult to recognize in cer-
tain clinical settings, such as in concurrent cancer.
Most reports describe isolated cases or small case
series. CIDP has been best and most frequently
described in the context of hematological malig-
nancies. However, limited epidemiologic data are
available on the association.
The issue of the association of CIDP and malig-
nancy is important. In patients found to have
CIDP, knowledge of the clinical features suggesting
an associated malignancy will lead to the evalua-
tion required for prompt diagnosis and treatment
Abbreviations: CIDP, chronic inflammatory demyelinating polyneurop-
athy; CLL, chronic lymphocytic leukemia; CRMP5, collapsin response
mediator protein 5; CSF, cerebrospinal fluid; GBS, Guillain-Barre  syn-
drome; HL, Hodgkin lymphoma; IVIg, intravenous immunoglobulin; MAG,
myelin-associated glycoprotein; NHL, Non-Hodgkin lymphoma; PE,
plasma exchanges; WM, Waldenstro €m macroglobulinemia
Key words: cancer; carcinoma; chronic inflammatory demyelinating poly-
neuropathy; lymphoma; malignancy; melanoma
Conflicts of Interest: The authors have no conflicts of interest.
Correspondence to: Y. A. Rajabally; e-mail: y.rajabally@aston.ac.uk
C 2017 Wiley Periodicals, Inc.
V
Published online 1 December 2017 in Wiley Online Library (wileyonlinelibrary.
com). DOI 10.1002/mus.26028
CIDP and Malignancy: a Review
of an underlying malignancy. Conversely, in
patients with a known malignancy, identifying asso-
ciated CIDP will be helpful in determining the use
of immunotherapy in addition to cancer treatment
for optimal treatment.
In this Review on the association of CIDP and
malignancy, we sought to identify publications relat-
ing to the association and to extract relevant clinical,
electrophysiological, biological, and histopathologi-
cal information. Treatments and responses were also
evaluated. Our main objectives were to try to deter-
mine the best approaches for identifying an associa-
tion and to review therapeutic options.
METHODS
A systematic literature review was conducted from a
Medline search from 1966 through October 2017 on reports
describing the association of chronic inflammatory neuropa-
thy with malignancy of any type. Only papers published in
English and French were considered. Our search methodol-
ogy followed the standard guidelines for systematic litera-
ture reviews outlined in the PRISMA (Preferred Reporting
Items for Systematic Reviews and Meta-Analyses) statement.3
Abstracts were excluded. For the search, we used MeSH terms
“cancer,” “inflammatory,” “chronic inflammatory demyelinat-
ing polyradiculoneuropathy,” “chronic inflammatory demye-
linating polyneuropathy,” “CIDP,” “demyelinating,”
“hematological,” “haematological,” Lewis-Sumner syndrome,”
“malignancy,” and “neuropathy.” Additional searches were
based on results of initial searches and included “lymphoma,”
“Hodgkin’s Lymphoma,” “HL,” “non-Hodgkin’s Lymphoma,”
“NHL,” “myeloma,” “Waldenstr€ oms Macroglobulinemia,”
“chronic lymphocytic leukemia,” “CLL,” “adenocarcinoma,”
“carcinoma,” “melanoma,” “hepatocarcinoma,” “pancreatic
carcinoma,” “prostatic carcinoma,” “breast carcinoma,” “lung
cancer,” “small cell lung carcinoma,” “renal carcinoma,”
“seminoma,” and “sarcoma”. Cases describing direct malig-
nant nerve infiltration were excluded as were those with axo-
nal mononeuritis multiplex, with or without confirmed
paraneoplastic peripheral nerve microvasculitis. Similarly,
descriptions of non-CIDP, classical paraneoplastic, neuropa-
thies/neuronopathies associated with cancer were excluded.
Cases with paraneoplastic antibodies were included if the clini-
cal and electrophysiological picture met requirements for a
diagnosis of CIDP per existing criteria.4 Presentations
described as subacute were included. Described associations
with Guillain-Barre syndrome (GBS) or other clearly acute
neuropathies were excluded as was POEMS (polyneuropathy,
organomegaly, endocrinopathy, M-protein skin) syndrome.
MUSCLE & NERVE June 2018 875

RESULTS
Articles which had descriptions of patients
considered to have at least possible CIDP, per cur-
rent criteria,4 associated with malignancy were
retrieved. This included a clinical course consistent
with the diagnosis, demyelinating electrophysiology
per existing criteria or as described in the paper as
compatible with CIDP, and fulfilment of support-
ive diagnostic features, including cerebrospinal
fluid (CSF) findings, imaging, and therapeutic
response to immunotherapy. Cases with undetailed
electrophysiology were included if the diagnosis
was specified as CIDP as were the few reports in
which the physiology was described as axonal but
the clinical picture consistent with CIDP and at
least 1 supportive diagnostic feature were present.
Inflammatory Neuropathies Associated with Hematological
Malignancies. Neuropathies may frequently occur
in lymphoma without a definite explanation. Such
neuropathies are usually mild, mostly sensory, and
axonal in type. The cause is not known, but meta-
bolic and toxic mechanisms are generally sus-
pected and are sometimes treatment related.
Neuropathy in this context may otherwise be
related to direct lymphomatous infiltration of
peripheral nerves, resulting in neurolymphomato-
sis, with variable clinical presentations. The electro-
physiology may occasionally misleadingly be
demyelinating and lead to an erroneous CIDP
diagnosis. Infiltration may occur by lymphocytes
from neighbouring blood vessels into the endo-
neurial space, resulting in segmental demyelin-
ation and axonal loss.5 Dysimmune neuropathies
such as CIDP and GBS may occur with lymphoma.
The cause is unclear but may presumably be
related to the immune perturbations accompany-
ing lymphomatous disease. Such inflammatory
neuropathies may precede the identification of
lymphoma or occur during its course.
CIDP has been reported in association with
lymphoma of different subtypes (Table 1). There
have been a few large series. In a French cohort of
150 patients with lymphoma, 13 patients (8.7%)
had a demyelinating neuropathy consistent with
CIDP.6 Four of these patients (31%) had Hodgkin
lymphoma (HL). It is noteworthy, however, that
HL in this series was associated exclusively with a
CIDP phenotype but not the other associated
described phenotypes (i.e., radiculopathy or multi-
ple mononeuropathy). The remaining 9 patients
(69%) had non-Hodgkin lymphoma (NHL). Of
those, 2 had a NH T-cell lymphoma and 7 had NH
B-cell lymphoma. In an international multicentre
study, 2 of 24 (8.3%) patients with HL and 7 of 29
(24.1%) with NHL had CIDP.7 Another French
report described 5 cases of CIDP from a cohort of
876 CIDP and Malignancy: a Review
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40 patients with Waldenstr€ om macroglobulinemia
(WM) with neuropathy.8 An additional 6 patients
were described in this report with a pure motor
neuropathy without electrophysiological demyelin-
ation. Four of those patients had antiganglioside
(anti-GM1, anti-GD1b, and/or anti-GM2) anti-
bodies of immunoglobulin (Ig)M subtype,
responding to various immunomodulatory/chemo-
therapy treatments. Because these 4 patients could
also have had a motor CIDP, the potential total
was 9 CIDP cases in this WM series with neuropa-
thy (22.5% of the whole cohort). An additional 12
cases of NHL of various types9–18 have been
described in contrast to only 2 with HL.19,20 There-
fore, in total, 8 cases of CIDP associated with HL
have been reported versus 37 associated with NHL,
suggesting a much more frequent association with
the latter.
Onset of CIDP frequently preceded that of lym-
phoma. Four of the reported cases of HL had
CIDP onset before the hematological diagnosis
and the remaining 4 after the hematological diag-
nosis. Patients with NHL usually had, in the larger
series, CIDP onset preceding the hematological
diagnosis (17/21, 81%). This was confirmed by
individual case reports and small case series in
which CIDP preceded the lymphoma diagnosis in
9 of 13 cases, corresponding to a combined figure
of 76.5%.
Identification of lymphoma required extended
follow-up, but reported early features were cranial
and respiratory involvement and dysautonomia, all
unusual for CIDP, as well as skin changes, lymph-
adenopathy, abnormalities of blood count, serum
protein electrophoresis, and immunofixation, lead-
ing to bone marrow/lymph node biopsy.
Limited information about treatment is avail-
able, although CIDP associated with HL appears to
have a poor prognosis, with 4 of 7 patients deterio-
rating despite hematological treatment. Use of
additional immunomodulatory therapies was not
described. Two patients improved with treatment
for HL, and 1 improved with corticosteroid ther-
apy. Patients with NHL appeared to do better, with
improvement reported in 24 of 33 cases (72.7%).
An additional 3 patients were described as having
stabilized with treatment. The effective treatments
used were varied and consisted of monotherapy
with steroids in 4 (16.7%) patients, plasma
exchange (PE) in 2 (8.3%), and intravenous Ig
(IVIg) in 4 (16.7%). Fourteen (58.3%) patients
received chemotherapy alone or in combination
with steroids, IVIg, or PE, with half of those cases
(B-cell NHL) reportedly responsive to rituximab.
Hence, about 40% of treatment-responsive patients
with lymphoma were treated with classical immu-
nomodulatory therapy only, and the remaining
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Table 1. Association of CIDP with hematological malignancies reported in the literature
Timing of
Hematological malignancy
malignancy Patients, in relation Clinical CSF protein, Treatment
Reference subtype n to CIDP features EDX mg/dl and response

15 Histiocytic lymphoma 2 9 mo after; Typical; asymmetrical D; NA 202; 91 Corticosteroids

1; CLL 1 6 mo after upper limb effective in both
19 HL 1 Before NA D NA NA
21 MDS 3 NA Dysautonomia NA NA MDS treatment effective in 2
24 HCL; MDS 2 NA NA NA NA PE ineffective
10 NHL 1 3 y before Typical D 150 PE effective
20 HL 1 1 y before Multifocal D 138 Steroids effective
11 EBV-associated 1 Concurent Lower limbs D 79 Chemotherapy 1
B-cell lymphoma steroids effective
17 T-cell lymphoma 1 3 y after Distal D 79 Steroids effective
6 HL: 4; T-cell NHL: 2; 13 Before: 9; after: 4 5 sensory D NA IVIg and steroids less
B-cell NHL: 7 predominant, effective than PE;
3 motor most efficacious:
predominant chemotherapy 1 IVIg
or PE; 70% favorable prognosis
18 T-cell lymphoma 1 3 mo after Lower limbs 1 D 264 Steroids effective
right facial
weakness
23 Chronic myelomonocytic 1 6 y after Lower limbs D 111 IVIg ineffective and steroids
leukaemia effective
7 HL: 2; NHL: 7 9 HL: 6 mo after and NA D Raised in all IVIg: improved in 4/5; steroids:
12 mo after; improved
NHL: after in 6 in 0/2; RTX: improved in 2/2
(both B-cell lymphoma)
14 T-cell lymphoma 1 10 mo after Typical D 164 Improved with IVIg
13 CLL: 2; NHL: 1 3 Concurrent DADS D NHL: improved IVIg 1 RTX; CLL:
dramatic
response to IVIg follwed by
RTX 1 FLU 1 CYC;
CLL: improved IVIg and PE
8 WM 5 After in 4/5 Typical D NA IVIg improvement in 1; IVIg
stabilized in 1;
IVIg 1 RTX improved in 1
8 WM 4 NA Pure motor; with Axonal 80;76; NA;40 1 IVIg improved; 1 improved after
antiganglioside (motor) FLU 1 PE; 1 unresponsive to
antibodies IVIg 1 RTX; 1 untreated
12 PTCL-NOS 1 Concurrent Typical D 72 Improved with chemotherapy
(CHOP)
16 NHL (AILT, WM, MF) 3 AILT: 44 mo Typical D AILT: 120; IVig response in 1; steroid
before; WM: WM: 191 response in 1;
12 mo after; MF: chemotherapy response in 1
132 mo before
9 WM 1 Concurrent Multifocal 1 cranial D 400 Steroid responsive
22 MM 1 30 m after Distal D Raised IVIg 1 chemotherapy: slight effect

A, axonal; AILT, angio-immunoblastic T-cell lymphoma; CA, carcinoma; CHOP, Cyclophsphamide, Doxorubicin, Oncovin, Prednisone; CIDP, chronic
inflammatory demyelinating polyneuropathy; CLL, chronic lymphocytic leukemia; CSF, cerebrospinal fluid; CYC, Cyclophosphamide; D, demyelinating;
DADS, distal acquired demyelinating sensory and motor neuropathy; EBV, Epstein–Barr virus; EDX, electrophysiology; FLU, Fludarabine; HCL, hairy cell
leukemia; HL, Hodgkin lymphoma; IVIg, intravenous immunoglobulins; MDS, myelodysplastic syndrome; MF, mycosis fungoides; MM, multiple myeloma;
NA, not available; NHL, non-Hodgkin lymphoma; PE, plasma exchanges; PTCL-NOS, peripheral T-cell lymphoma, not otherwise specified; RTX, ; WM,
Waldenstro€m macroglobulinemia.

60% were treated with chemotherapy, often in
combination with immunomodulation.
Other hematological malignancies have rarely
been reported in association with CIDP. These are
detailed in Table 1 and include single cases of
myelodysplastic syndrome, hairy cell leukemia,
chronic myelomonocytic leukemia, chronic lym-
phocytic leukemia, and myeloma.13,21–24 Chemo-
therapy was the main treatment administered, on
occasion with IVIg or steroids, with variable
efficacy.
CIDP and Malignancy: a Review
Chronic Inflammatory Neuropathies Associated With
Melanoma. Table 2 details reports of associated
melanoma and CIDP. There are a dozen reported
cases of CIDP and melanoma, excluding patients
who developed CIDP as a result of melanoma
immunotherapy,19,25–32 vaccination by melonoma
lysates,33 interferon a-2b,34 and, more recently,
immune check-point inhibitors.35,36 With mela-
noma lysates and interferon a-2b, implication of
the melanoma appeared possible, particularly in
the latter case because the patient had been
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Table 2. Association of CIDP with melanoma reported in the literature
Patients, Timing of malignancy CSF protein, Treatment
Reference n in relation to CIDP Clinical features EDX mg/dl and response
19 1 10 y after NA D NA NA
27 3 6 mo after; 4 mo after; Facial weakness in 1, D (all) 104;86; 60 Steroids 1 PE effective;
12 mo before lower limb exclusive in 2 steroids effective;
treatment declined
32 1 3 y before Typical D 62 NA
26 1 10 y after Mild, indolent D >800 NA
25 1 18 mo before Typical D 287 IVIg, steroids effective
30 1 Concurrent Motor weakness of 4 limbs, A (motor) 190 IVIg unresponsive,
ophthalmoplegia steroids effective
33 1 22 mo before (CIDP after Typical D 25 Steroids unresponsive,
vaccinal melanoma lysates) PE effective
31 1 5 mo after Typical D 36 IVIg effective
34 1 14 mo before (CIDP after Typical D 52 IVIg effective
interferon a-2a)
29 2 6 y before; concurrent Typical D (both) NA Steroids effective; fatal
outcome despite chemotherapy
28 1 Concurrent Typical D 249 IVIg 1 Steroids effective

A, axonal; CIDP, chronic inflammatory demyelinating polyneuropathy; CSF, cerebrospinal fluid; D, demyelinating; EDX, electrophysiology; NA, not available;
IVIg, intravenous immunoglobulins; PE, plasma exchanges..

untreated for 40 weeks before neurological presen-
tation. In contrast, treatment was highly likely to
be the cause of CIDP with the use of immune
check-point inhibitors. These reports were not, for
those reasons, included in Table 2. In half of the
treatment-unrelated cases, CIDP occurred before
the diagnosis of melanoma, whereas, in the other
half, the inflammatory neuropathy appeared later.
Antiganglioside antibodies to GM1, GM2, or GM3
were present in about half of the reported cases,
although there were no other characteristic diag-
nostic features. All 9 patients who were treated
with immunotherapy improved; 3 improved with
steroids, 2 with IVIg, 1 with PE, and 3 with combi-
nation therapies.
Chronic Inflammatory Neuropathies Associated With
Intra-abdominal Cancers. Gastrointestinal/Hepatic
Carcinoma. Table 3 provides a summary of
chronic inflammatory neuropathies associated with
intra-abdominal cancers. We found 2 cases of
CIDP associated with gastric and esophageal ade-
nocarcinoma with the neuropathy either preceding
or following the cancer diagnosis.37,38 No specific
diagnostic features were reported. Treatment
response to steroids was favorable in 1 patient, but
the other patient was unresponsive to both steroids
and IVIg.
Three cases of colorectal carcinoma have been
described, 2 in patients with a distal acquired
demyelinating sensory and motor neuropathy-
CIDP phenotype, with associated anti–myelin-
associated glycoprotein (MAG) antibodies.39,40 In 1
of these patients, predominant upper limb involve-
ment was reported. In both patients, CIDP
878 CIDP and Malignancy: a Review
preceded the malignancy diagnosis, and associated
symptoms such as constipation and abdominal
pains led to additional investigations. In 1 patient,
surgical cancer treatment led to resolution of
CIDP. The other patient was transiently responsive
to IVIg but then unresponsive to immunomodula-
tory treatment that included steroids and PE. Sub-
sequent cancer treatment was not effective. In a
third case of concomittant, upper limb-
predominant CIDP, with abdominal pain and diar-
rhea revealing the malignancy, spontaneous neuro-
logical recovery occurred postcancer treatment
without additional immunotherapy.41
Associated pancreatic adenocarcinoma has
been the subject of 3 case reports, with CIDP pre-
ceding the cancer diagnosis in 2 cases.24,41,42 Neu-
ropathic pain, unusual for CIDP, was present in 1
case, although no other atypical clinical features
were described. IVIg was successful in 1 case. PE
failed in another case but was effective in the third
after a partial response to a combination of IVIg
and steroids.
Hepatocellular carcinoma (HCC) and cholan-
giocarcinoma were reported in 3 cases,41,43,44 with
an unconfirmed diagnosis in another patient.45
CIDP preceded or was concurrent with the malig-
nancy diagnosis in 2 patients, and all 3 patients
were steroid responsive.
Renal Carcinoma. Three cases of renal carci-
noma have been described in association with
CIDP.46–48 Neuropathy preceded or followed the
carcinoma diagnosis. CIDP was of asymmetric
onset in 1 case, exclusively sensory in 1, and
involved cranial nerves in 2. Anti-ganglioside
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Table 3. Association of CIDP with intra-abdominal malignancies reported in the literature
Patients, Malignancy Timing of malignancy Clinical CSF protein, Treatment and
Reference n type in relation to CIDP features EDX mg/dl response
37 1 Gastric CA 1 y before Typical D 70 Steroid responsive
41 1 Pancreatic CA Concurrent Typical D 127 IVIg responsive
41 1 Rectosigmoidal CA Concurrent Pure upper limb D 90 Recovery with cancer treatment
41 1 Cholangiocarcinoma 5 mo after Typical D 130 IVIg responsive, then
steroid responsive
21 1 HCC NA NA NA NA Unresponsive to PE
44 1 HCC Concurrent Typical D 68 Steroid resonsive
43 1 HCC NA Typical D High Steroid responsive
45 1 HCC 2 mo before Typical A NA IVIg responsive
38 1 Esophageal CA Concurrent Pure motor Motor 101 IVIg/steroid unresponsive
conduction
blocks
42 1 Pancreatic CA Concurrent Typical D 107 IVIg/Steroids/PE partially
effective; additional
improvement after resection
39 1 Colorectal CA 1 mo after DADS-CIDP D NA Improved with tumor resection
40 1 Rectosigmoidal CA 4 y after DADS-CIDP D 140 Mild initial IVIg-response, then
IVIg/steroid/PE unresponsive
47 1 Renal CA 2 mo before Multifocal, asymetric, NA NA Untreated
cranial 1 respiratory
46 1 Renal CA 2 mo after Sensory D 28 Improved with tumor resection
48 1 Renal CA Concurrent Lower limb D 150 Improved with tumor resection

A, axonal; CA, carcinoma; CIDP, chronic inflammatory demyelinating polyneuropathy; CSF, cerebrospinal fluid; D, demyelinating; DADS, distal acquired
demyelinating sensory and motor neuropathy; EDX, electrophysiology; HCC, hepatocellular carcinoma; IVIg, intravenous immunoglobulins; NA, not avail-
able; PE, plasma exchanges.

antibodies were reported in 1 case. Nephrectomy
resulted in neurological improvement in 2 cases,
and neurological improvement was virtually com-
plete in 1 case. IVIg had an uncertain effect in
another case.
Chronic Inflammatory Neuropathies Associated With
Breast Cancer. Chronic inflammatory neuropa-
thies associated with breast cancer are detailed in
Table 4. We identified 6 published cases of CIDP
associated with breast cancer.24,37,49–51 In all of 5
cases with documented history, the neuropathy
preceded the cancer diagnosis by months to years.
Sensory ataxia predominated in 2 cases, and cra-
nial nerve involvement was reported in 1. Among 5
patients treated with conventional therapies for
CIDP, 3 responded, 2 to PE and 1 to steroids. One
patient was unresponsive to PE, and 1 patient
responded remarkably to cancer treatment. In the
patient who had a sensory ataxic phenotype, anti-
collapsin response mediator protein 5 (CRMP5)
antibodies were present initially but became unde-
tectable after treatment.
Chronic Inflammatory Neuropathies Associated With
Respiratory Tract and Lung Cancer. Chronic inflam-
matory neuropathies associated with respiratory
tract and lung cancer are detailed in Table 4.
Three cases of CIDP have been described with
lung carcinoma, which occurred years before the
cancer diagnosis in 2 of the cases.19,24 PE appeared
CIDP and Malignancy: a Review
to have some effect in 2 cases, although the
responses were not well documented. Rare cases of
demyelinating neuropathy associated with anti-Hu
and/or anti-CRMP5 antibodies and associated with
small cell lung carcinoma and with clinical courses
consistent with CIDP have also been reported.
Ataxia and encephalopathy were described in 1
case, with pathologically concurrrent inflammatory
changes in the dorsal root ganglia and demyelin-
ation in peripheral nerves.52,53 One case of CIDP
that developed 2 years before a diagnosis of laryn-
geal cancer has also been reported.19
Chronic Inflammatory Neuropathies Associated With
Other Rarely Reported Forms of Cancer. Chronic
inflammatory neuropathies associated with other
rarely reported forms of cancer are detailed in
Table 4. Rarely, other forms of cancer reported
with CIDP include seminoma, uterine sarcoma,
prostate cancer, mediastinal neuroendocrine
tumor, Kaposi sarcoma, and orbital neurogenic
tumor.52,54–56 Neuropathy occurred as frequently
before cance diagnosis as it did after cancer diag-
nosis. No specific diagnostic features were
described. All 4 patients who were treated with ste-
roids were reported to be improved.
DISCUSSION
The most commonly reported malignancies in
association with CIDP are hematological. These
can be of different subtypes, although lymphoma
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Table 4. Association of CIDP with other malignancies reported in the literature
Patients, Timing of malignancy Clinical CSF protein,
Reference n Malignancytype in relation to CIDP features EDX mg/dl Treatment and response
37 1 Breast CA 6 y before NA D 55 NA
24 1 Beast CA NA NA D NA PE unresponsive
50 2 Breast CA (both) 9 mo after, 4 mo after Typical D (both) 53, 120 Both PE responsive
49 1 Breast CA 2 mo after Sensory D 75 IVIg unresponsive,
predominant 1 steroid responsive
myelopathy
51 1 Breast CA 2 y after Sensory D 166 Considerable improvement
anti-CRMP5 1 with resection, radio-/
chemo-/hormone therapy
19 1 Larynx CA 2 years after NA D NA NA
19 1 Lung CA 5 y after NA D NA NA
24 2 Lung CA NA NA D NA Moderate/mild, transient
improvement
53 1 Lung CA anti-Hu 1 3 mo after Painful sensory, D 162 Untreated for neuropathy
then motor 1
cerebellar features,
encephalopathy
52 5 Lung CA anti-CRMP5 1 NA Typical D NA NA
55 1 Seminoma 3 mo after Typical D 267 Steroid responsive
52 1 Uterine sarcoma NA NA D NA NA
52 2 Prostatic CA NA NA D NA NA
(1 with associated
renal CA)
52 1 Mediastinal NA NA D NA NA
neuroendocrine
tumor
54 1 Kaposi sarcoma 5 mo after Typical D 235 Steroid responsive
56 1 Orbital neurogenic tumor 12 mo before Distal predominant D 101 Steroid responsive

CA, carcinoma; CIDP, chronic inflammatory demyelinating polyneuropathy; CRMP5; collapsin response mediator protein 5; CSF, cerebrospinal fluid; D,
demyelinating; EDX, electrophysiology; IVIg, intravenous immunoglobulins; NA, not available; PE, plasma exchange.

appears to be the most frequent. CIDP appears to
have been reported more commonly with NHL
than with HL, with the former having an incidence
more than fourfold that of the latter. In more
than three-quarters of cases, CIDP preceded the
diagnosis of NHL. CIDP associated with HL
appears to have a poor prognosis. However, CIDP
associated with NHL appears to be as responsive to
immunomodulatory treament as the idiopathic
form (i.e., > 70% of cases).57 Globally, effective
treatment consisted of immunomodulatory therapy
only in 40% of patients and of chemotherapy,
often in association with steroids, IVIg, or PE, in
the remaining 60%. This is of importance because
treatment may not always be deemed necessary
from the hematological point of view (e.g., in
WM) and suggests that this should be considered
in the presence of associated CIDP. Rituximab was
commonly used with good effect in cases with NH
B-cell disease. There have been numerous cases of
associations reported with WM, which, although
more commonly presenting with anti-MAG neurop-
athy, can also be associated with CIDP, which is a
more disabling but also more treatable entity. This
is highly relevant clinically in view of therapeutic
options that may be considered. It is important to
880 CIDP and Malignancy: a Review
note that there also appears to be a subset of
patients with motor predominant CIDP-like neu-
ropathy who fail to display electrophysiological
demyelination but who may have antiganglioside
antibodies and who may do well with immunomod-
ulatory therapy. In addition, published series
appear to suggest that 20%–25% of patients with
NHL with a paraneoplastic syndrome may have
CIDP.7 Over 20% of patients with WM and neurop-
athy of primarily unknown cause may also have
CIDP.8 These findings may have major implica-
tions for clinical management for these patients.
With other malignancies, associated CIDP
appears responsive to immunotherapy in the
majority of cases. Specifically, 23 of 26 treated
patients (88.5%) were described as improving with
immune treatment. Melanoma and breast cancer
appear to be associated with the most treatment-
responsive forms of CIDP. Monotherapy with ste-
roids was the most commonly described (9 cases)
treatment form, followed by PE (5 cases) and IVIg
(3 cases). Combination therapies were used in the
remainder. Cancer treatment alone was effective in
all 5 cases in which it was attempted, occasionally
with complete remission. In practice, this may indi-
cate that immunomodulatory therapy requires
MUSCLE & NERVE June 2018

consideration shortly after chemotherapy if the lat-
ter alone proves ineffective on CIDP or even ear-
lier and concurrently in case of severe, disabling,
or rapidly progressive neuropathy.
The currently reviewed literature suggests that
a progressive neuropathy developing over more
than 2 months and affecting function requires
investigation for CIDP in patients with any preex-
isting hematological disease because treatment
with conventional therapies appears to be fre-
quently effective. Conversely, because a majority of
reported cases identified CIDP prior to the diagno-
sis of cancer, as has been well illustrated in the
cases of NHL (>75%), melanoma (50%), and
breast cancer (100%), adequate investigations for
underlying malignancies are essential to diagnostic
evaluation of CIDP. Recognition of suggestive neu-
rological features such as marked ataxia; cranial,
respiratory, or autonomic involvement; and distal
predominance, asymmetric disease, and neuro-
pathic pain is essential at an early stage. Systemic
features that should be particularly noted are loss
of appetite and weight; abdominal pain, diarrhea,
and/or constipation; dermatological signs; and
lymphadenopathy. Standard testing requires regu-
lar and repeated serum and urine electrophoresis
and immunofixation. It is noteworthy that >50%
of patients with lymphoma and CIDP have been
described as having a monoclonal gammopathy
compared with <20% of those with B-cell NHL or
idiopathic CIDP.6 Additional investigations to be
considered include skeletal X-ray survey, bone mar-
row study, and/or lymph node biopsy. Whole-body
computed tomography scanning and positron
emmission tomography require careful consider-
ation as do upper and lower gastrointestinal endos-
copy and mammography. It is noteworthy that,
although these tests are generally considered in
absence of treatment response, most reports of
cases of successful initial therapy, despite the pres-
ence of an associated cancer, suggest that treat-
ment unresponsiveness alone is insufficient
information on which to base a decision regarding
additional investigations.
The total number of cases reported remains rel-
atively low, perhaps because of underreporting or
nonrecognition of CIDP. Cancer types are quite
varied, and it is appropriate to be mindful of this
heterogeneity to avoid focusing only on some. The
requirement for adequate history taking and exten-
sive initial and follow-up general clinical examina-
tions should be kept in mind, as illustrated by
some of the lymphoma and melanoma cases
reported. We have been unable to identify specific
patterns of electrophysiological, CSF, or imaging
abnormalities to suggest the asociation. This con-
trasts with what has been recenty reported in
CIDP and Malignancy: a Review
10974598, 2018, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/mus.26028 by Cochrane Oman, Wiley Online Library on [20/12/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
patients with GBS and malignancy, for instance,
who may frequently have normal CSF protein lev-
els.58 Finally, the presence of onconeural anti-
bodies, although exceptional, does not appear to
exclude a diagnosis of CIDP in cases of known or
undiagnosed cancer and not should lead to a fail-
ure to consider the use of immunomodulatory
therapy in selected cases.
From the pathophysiological point of view, the
mechanisms of malignancy-associated CIDP remain
uncertain. Molecular mimicry has been suggested
in some cases of melanoma.32 Strong and highly
specific IgM immunoreactivity to GM2, sulfoglucur-
onyl lactosaminyl paragloboside, and sulfatide were
reported, suggesting that they may have been gen-
erated in response to melanoma antigens. Further-
more, immunofluorescent staining of melanoma
tissue from the affected patient showed IgM reac-
tivity, and antiserum to GM2 reacted to the same
cells. Gangliosides including GM2 have otherwise
previously been reported on melanoma cells.59
CIDP occurring after vaccination with melanoma
lysates also supports similar mechanisms.33 The
absence of antibody detection in all reported cases
of melanoma-associated CIDP may be due to the
requirement for expression of specific histocom-
patibility antigens for generation of such anti-
bodies.32 Whether molecular mimicry may explain
cases of CIDP associated with other malignancies is
unknown. The processes involved in lymphoma-
associated CIDP, especially NHL, are of particular
interest because of the higher frequencies
described and require additional study. Finally, in
some patients, particularly those presenting with
typical CIDP, with good immunotherapy response,
and with only exceptionally reported cancers, coin-
cidental association remains possible.
This Review has a number of limitations. First,
the diagnosis of CIDP was clearly provided and
documented in only a proportion of cases and was
deduced from the clinical data, electrophysiology
and CSF results, and immunomodulatory treat-
ment response in others. In this regard, we fol-
lowed the latest guidelines on CIDP management,
but the reliance on a number of often insuffi-
ciently documented parameters may reduce the
level of diagnostic certainty. For example, deter-
mining whether the patients in the articles that
were reviewed met clinical criteria for typical CIDP
per current diagnostic guidelines4 proved difficult
for many reports. Second, the interpretation of
electrophysiological abnormalities relied on incom-
plete descriptions and in some cases was per-
formed without supporting figures and/or
normative values for the individual laboratories.
Third, response to treatment often was anecdotal
and qualitative, particularly in papers published in
MUSCLE & NERVE June 2018 881

the nonneurological literature, lacking appropriate
outcome measures, again, limiting the validity of
authors’ conclusions.
In conclusion, CIDP occurring in conjunction
with cancer is well described. It is a diagnostic
challenge and likely remains underrecognized,
although probably relatively rare. Reliable epidemi-
ological data on the association are not available.
Just as is true for its other associations,60 awareness
of the connection between CIDP and malignancy
is essential for the adequate holistic approach to
clinical management for this patient subgroup.
The reporting of new cases will help improve our
understanding of the pathophysiological mecha-
nisms involved and should help to guide the devel-
opment of more effective treatments.
Ethical Publication Statement: We confirm that we have read the
Journal’s position on issues involved in ethical publication and
affirm that this report is consistent with those guidelines.
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