Oxaliplatin-Induced Neuropathy: A Long-Term Clinical and Neurophysiologic Follow-Up Study

Prospective Study of the Clinical, Electrophysiologic, and Sonographic Characteristics of Oxaliplatin‐Induced Neuropathy

“…Conroy et al reported an incidence of 9% six months after treatment begin but the monitoring included clinical examination only. Our electrophysiological and clinical data are, however, in line with data from previous longitudinal studies on patients with colorectal cancer . Burakgazi et al examined a group of 8 patients receiving oxaliplatin in cumulative doses lower than in our cohort at different time points (treatment begin, 1, 3, 6, and 12 months after) and showed a reduction of clinical neuropathy scores and sural/peroneal sNAP 6 months after treatment begin for 100% of the patients.…”

“…Nerve ultrasound is a patient‐friendly, noninvasive method to measure nerve damage that is much easier to be regularly and frequently used in a patient population with such a burdening disease compared to nerve conduction techniques. All three above‐mentioned longitudinal studies also point out this methodological compliance problem for the nerve conduction studies . This indicates the importance of investigating any potential use of nerve ultrasound in the diagnosis and monitoring of oxaliplatin‐induced neuropathy.…”

“…Longitudinal nerve conduction studies during oxaliplatin treatment for colorectal cancer (eg, the FOLFOX regimen) point to the development of a distal length‐dependent neuropathy at total doses of 540–850 mg/m 2 . Studies in patients with metastatic pancreatic cancer (mPC) are lacking . Only one ultrasound study investigating the morphological characteristics of peripheral nerves at the end of oxaliplatin‐induced polyneuropathy (OIPN) exists .…”

Incidence, severity, longitudinal trends and predictors of acute and chronic oxaliplatin‐induced peripheral neuropathy in Taiwanese patients with colorectal cancer

“…In contrast, earlier study (Baek et al, ) reported that the cumulative dose of OXAL was unrelated to the severity of OXAIPN. Other previous studies with OXAL dosages up to 750–800 mg were found to be associated with chronic OXAIPN (Lu, ; Sereno et al, ; Ventzel et al, ), whereas dosages above 864 mg were more likely to produce grade II or grade III OXAIPN (Kokotis, Schmelz, Kostouros, Karandreas, & Dimopoulos, ). Moreover, OXAIPN symptoms may be more serious among patients who received C/T in winter season, when patients with OXAIPN were more likely to experience OXAIPN symptoms of severity grade II ( n = 9) and grade III ( n = 2).…”

Searching for analgesic drug candidates alleviating oxaliplatin‐induced cold hypersensitivity in mice

“…Oxaliplatin is a third-generation, platinum-based cytotoxic derivative used to treat advanced colorectal cancer. Compared to other platinum-based drugs, it has a better safety profile featured by a lower incidence of hematological adverse effects and gastrointestinal toxicity but in ~95% of patients this drug causes severe neuropathic pain episodes characterized by increased cold hypersensitivity (cold allodynia; Ventzel et al, 2018) and mechanical sensory deficits (Binder et al, 2007;Kokotis, Schmelz, Kostouros, Karandreas, & Dimopoulos, 2016): mechanical hyperalgesia, (Binder et al, 2007) mechanical (tactile) allodynia (Hsieh et al, 2016), and dose-dependent touch threshold deficits (Nour, 1995). These mechanical sensory deficits may vary in the course of CIPN duration: In the acute phase, a greater than normal sense to touch and touch-evoked neuropathic pain episodes (tactile allodynia) of at least moderate intensity are observed (Hsieh et al, 2016;Ventzel et al, 2018), whereas in the chronic phase, patients treated with oxaliplatin report sensory loss (Ventzel et al, 2018).…”