|LETTER TO EDITOR
|Year : 2022 | Volume
| Issue : 1 | Page : 56-58
A rare paraneoplastic finding of the breast cancer and chronic inflammatory demyelinating polyneuropathy
Basak Elcin Ates1, Kezban Aslan-Kara1, Melek Ergin2, Hacer Bozdemir1
1 Department of Neurology and 1Pathology, Faculty of Medicine, Cukurova University, Adana, Turkey
2 Department of Pathology, Faculty of Medicine, Cukurova University, Adana, Turkey
|Date of Submission||22-Jun-2021|
|Date of Decision||08-Dec-2021|
|Date of Acceptance||20-Dec-2021|
|Date of Web Publication||31-Mar-2022|
Basak Elcin Ates
Department of Neurology, Faculty of Medicine, Cukurova University, Adana 01330
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Ates BE, Aslan-Kara K, Ergin M, Bozdemir H. A rare paraneoplastic finding of the breast cancer and chronic inflammatory demyelinating polyneuropathy. Neurol Sci Neurophysiol 2022;39:56-8
|How to cite this URL:|
Ates BE, Aslan-Kara K, Ergin M, Bozdemir H. A rare paraneoplastic finding of the breast cancer and chronic inflammatory demyelinating polyneuropathy. Neurol Sci Neurophysiol [serial online] 2022 [cited 2022 Jun 28];39:56-8. Available from: http://www.nsnjournal.org/text.asp?2022/39/1/56/342359
Chronic inflammatory demyelinating polyneuropathy (CIDP) is a chronic, progressive, or relapsing disease secondary to immune-mediated inflammation of the peripheral nerves. The incidence of CIDP is on average 2–3/100,000.
It is known that peripheral nerves are affected in 1.7%–16% of cancer patients. In malignancies, tumor infiltration or compression, applied treatments, viral infections, etc., cause peripheral nerves to be affected., Breast cancer is one of the most common malignancies that cause paraneoplastic syndrome (PNS). In the literature, breast cancer-associated PNS has been reported very rarely (1%).,,
CIDP in breast cancer-associated PNS has not been reported so far. We present a case diagnosed with CIDP and found to have breast cancer.
A 75-year-old female patient without a known systemic disease was admitted to our clinic in January with the complaints of numbness in the hands and feet, difficulty in walking for 15 days, and frequent falls while walking. Electromyography (EMG) showed sensorimotor polyneuropathy (PNP) with acute signs of axonal destruction and segmental demyelination [Table 1]. She did not have any past history. Neurological examination (NE) revealed quadriparesis (upper extremities: 4/5, lower extremities proximal: 4/5, knee flexion: 4/5, knee extension: 5/5, ankle flexion: 2/5, and ankle extension: 3/5), DTR losted, deep sensation was lost in the lower extremities, and a glove-sock-style sensory defect was described. Romberg +/-. Subacute PNP was primarily considered in the case. In etiology, hemogram and blood biochemistry were within the normal limits. Hemoglobin A1C level, lipid profile, and B12 level were normal. Infectious tests were negative. ANA: 32.50 (range 20–60 low positive). Carcinoembryonic antigen (CEA): 4.61 ng/mL, (N: 0–3 ng/mL). Cryoglobulin test was negative, protein electrophoresis was normal. Serum kappa and lambda-free light chain levels were 21.7 mg/L (N: 3.30–19.40) and 26.7 mg/L (N: 5.7–26.3). Radiologic evaluation was made. There was no pathological finding on posterior–anterior chest radiography. Spinal magnetic resonance imaging did not show any signs in favor of a space-occupying lesion or inflammation that could explain the findings of quadriparesis. Abdomen ultrasonography (USG) was within the normal limits, thorax computed tomography showed one solitary pulmonary nodule in the left lung, and ejection fraction level was 62% on echocardiography. Breast USG showed a lesion suspicious for malignancy in the upper outer quadrant of the right breast and a calcified fibroadenoma in the right outer half midline. Superposed nodular opacities and diffuse calcifications were seen in the bilateral parenchyma and were reported as BIRADS 4. She had no family history of breast cancer. In the cerebrospinal fluid (CSF) examination, protein was 88 mg/dl (>40 mg/dl), glucose was 67 mg/dL, and lactate was 1.93. CSF cytology was normal.
As a result of NE and EMG findings, five sessions of apheresis were performed. Due to partial recovery, 1 week after apheresis, 0.4 g/kg/day intravenous immunoglobulin (IVIG) was given in five doses. After IVIG treatment was completed, investigations for breast cancer continued. Physiotherapy was applied at this interval. The examination findings had completely resolved at the time of first discharge. After the treatment, there was no motor deficit in the past NE. Two months after discharge, invasive ductal carcinoma was detected in biopsy [Figure 1], and right subcutaneous mastectomy was performed. She presented with the same complaints in the lower extremities 1.5 months after mastectomy. Her NE revealed quadriparesis at the level of 4/5 muscle strength, and the patient was diagnosed with paraneoplastic CIDP. Five sessions of apheresis followed by 5 days of IVIG treatment. After the treatment, motor deficit in the upper extremities was completely resolved, the muscle strength of the lower extremities was 4/5. She could walk without support while being discharged.
|Figure 1: Invasive component of breast cancer (perineural invasion is indicated by an arrow in the lower right corner)|
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| Discussion|| |
The patient, who presented with sensorimotor findings due to recurrent peripheral neuropathy involvement, had a history of progression longer than 8 weeks. The presence of acute damage of thick myelinated nerve fibers in NE and EMG and the presence of albuminocytological dissociation in the CSF, the patient was diagnosed with CIDP according to the diagnosis and treatment guidelines criteria of the European Federation of Neurologic Societies. In the etiological examination, a suspicious lesion belonging to the BIRADS 4 score was detected in the upper outer quadrant of the right breast. In her clinical follow-up, invasive ductal carcinoma was detected. The patient was diagnosed with CIDP secondary to breast cancer as a result. Steroid/immunosuppressive treatment was planned for the patient, but she was followed up in an oncology clinic in another province.
The coexistence of breast cancer and CIDP may have been coincidental, yet we cannot exclude this. Although both diseases were so much frequent, we could not find so much coexistent case report in the literature as mentioned in the article.
For the diagnosis of PNS, other etiological reasons should be excluded, malignancy should be screened, and finally, neurological syndrome should be included in the group of syndromes associated with malignancy. Paraneoplastic antibodies do not have to be positive for a diagnosis of PNS. In our case, there were no any metabolic-systemic diseases and no toxic substance exposure that could cause PNP (statins, amiodarone, etc.).
In the literature, it is seen that breast cancer rarely presents with paraneoplastic neurological findings. That's why we wanted to publish this case. Murphy et al. reported that only 56 of 17,725 breast cancer patients developed PNS, only 38 (67.9%) of 56 patients were diagnosed with invasive ductal carcinoma. Among the PNS reported in this series, CIDP has not been mentioned in the peripheral nervous system involvement.
Positive antibodies support PNS in the diagnosis of paraneoplastic sensorimotor neuropathy. Anti-Hu antibodies can be detected in 85% of these patients. However, it has been reported that anti-Yo and anti-Ri can also be detected in serum. Paraneoplastic antibodies were positive in only 36% of motor and sensory neuropathies developed in patients diagnosed with breast cancer. In our case, paraneoplastic antibodies could not be screened for technical reasons. It is known that primary malignancy treatment contributes to the treatment of neurological symptoms in these patients. In the treatment guidelines of PNSs, IVIG, plasmapheresis, and steroid are recommended. The same treatment was prescribed in patients defined as CIDP or Guillain-Barré syndrome. With these treatment methods, it is recommended that IVIG can be administered again to a patient who does not improve clinically within 1–2 weeks (2 g/kg, within 5 days) and plasmapheresis or cyclophosphamide treatments can be initiated in the case of no response.
In conclusion, malignancies should be considered while investigating the etiology of PNP. Even if the tests are negative, if the clinical suspicion continues, the patient should be followed closely or the tests should be repeated. Similarly, as seen in our case, breast cancer screening in women over the age of 50 years should definitely be done annually.
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Conflicts of interest
There are no conflicts of interest.
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