Reactions 1680, p271 - 2 Dec 2017
Neuropathy: case report
A man developed [age at the time of reaction onset not
clearly stated] developed neuropathy during therapy with
oxaliplatin [route, dosage and duration of treatment to reaction
onset not stated].
The man with a history of metastatic colon cancer,
presented for further care in May 2016 at the age of 62 years.
Eleven years before the presentation, in August 2005, he was
diagnosed with stage III colon cancer. On 23 August 2005, he
underwent a subtotal colectomy. In 2005, he received
treatment with FOLFOX regimen that included fluorouracil
[5-fluorouracil], folinic acid [leucovorin] and oxaliplatin.
However, he developed grade 1 neuropathy due to oxaliplatin
and intermittent haematuria of unknown aetiology. In
April 2015, he developed new liver lesions consistent with
metastatic colon adenocarcinoma. From April 2015 to
December 2015, he was treated with FOLFIRI regimen
consisting of fluorouracil [5-fluorouracil], folinic acid
[leucovorin] and irinotecan with bevacizumab. However, the
FOLFIRI regimen was stopped due to disease progression in
the liver. He was then treated with Irinotecan and Cetuximab
from December 2015 to April 2016, but therapy was
discontinued due to disease progression in the liver and lymph
nodes, as well as new hydroureteronephrosis. To evaluate the
hydronephrosis, he underwent bilateral retrograde
pyelograms, which revealed bilateral large mid-ureteral filling
defects suggestive of bilateral upper tract urothelial carcinoma.
He had bilateral ureteral stent placements. A urine cytology
from the right ureter confirmed urothelial carcinoma with
absence of MSH-2 and MSH-6 expression.
At the time of current presentation (in May 2016), the man’s
neuropathy from prior oxaliplatin use persisted. Given the
presence of mismatch repair deficiency in the primary colon
cancer, he was treated with pembrolizumab on compassionate
use basis in June 2016. Following the initiation of
pembrolizumab, his carcinoembryonic antigen (CEA)
declined. However, from November 2016 to February 2017,
the CEA began to increase and accompanied by worsening of
the liver lesions on the PET scan (performed in March 2017).
Therefore, in March 2017, pembrolizumab was switched to
atezolizumab. As of June 2017, he was continued on therapy
with atezolizumab with decreasing CEA. Due to mismatch
repair deficiency and a family history of cancers, he underwent
germ-line testing for Lynch syndrome, which confirmed a
diagnosis of MSH-2 related Lynch syndrome.
Author comment: "When the patient presented to our
clinic in May 2016, he had grade 1 neuropathy from prior
oxaliplatin and intermittent hematuria."
Ghatalia P, et al. Mismatch repair deficient metastatic colon cancer and urothelial
cancer: A case report of sequential immune checkpoint therapy. Cancer Biology
and Therapy 18: 651-654, No. 9, 2 Sep 2017. Available from: URL: http://
doi.org/10.1080/15384047.2017.1356506 - USA
Reactions 2 Dec 2017 No. 16800114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved