Study: causes cancer treatment cognitive impairments?

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Reference Vardy J., Dhillon HM, Pond Gr, et al. Cognitive function and fatigue after the diagnosis of colon cancer. Ann oncol. 2014; 25 (12): 2404-2412. EPUB September 11, 2014. Design prospective longitudinal study with jointly adapted controls participants The participants were divided into 3 groups. Group 1 had localized colon cancer (CRC), stadiums I to III (n = 291). Group 2 had a limited metastatic disease or a locally recurrent CRC (n = 72). Group 3 consisted of healthy controls (HC) from the community, which were adapted according to age and gender (n = 72). All participants had a good performance status according to the Eastern scale Cooperative Oncology Group. Exclusion criteria were ...
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Reference

Vardy J., Dhillon HM, Pond Gr, et al. Cognitive function and fatigue after the diagnosis of colon cancer. ann oncol. 2014; 25 (12): 2404-2412. EPUB September 11, 2014.

Design

prospective longitudinal study with jointly adapted checks

participant

The participants were divided into 3 groups. Group 1 had localized colon cancer (CRC), stadiums I to III (n = 291). Group 2 had a limited metastatic disease or a locally recurrent CRC (n = 72). Group 3 consisted of healthy controls (HC) from the community, which were adapted according to age and gender (n = 72). All participants had a good performance status according to the Eastern scale Cooperative Oncology Group. Exclusion criteria were previous malignancy; all comorbidities that could affect cognition; History of alcohol abuse or psychiatric disorders; Norormal hematological, kidney or liver function; Or bad knowledge of English.

target parameter

primary endpoints were the cognitive function assessed using the Global Deficit Score (GDS) and the fatigue evaluated using the Functional Assessment of Cancer Therapy-Fatigue (FACT-F). The GDS consisted of several cognitive tests, including the computer -aided Cambridge Neuropsychology Tested Automated Battery and the modified Six Elements Test. All participants were evaluated with the fact cogitives in order to assess the perception of their cognitive function. Quality of life and fatigue were rated with the subscales Fact-F and Fact-General. Fear and depression were recorded on the basis of the 12-point questionnaire on general health. The blood parameters were measured in group 1 and HC and included 10 cytokines, coagulation factors, sex hormones, carcinoembryonal protein (CEA) and apolipoprotein e genotype.

important knowledge

The primary result of the result, GDS, showed significant differences between CRC in early stages (group 1) and metastatic CRC (group 2) vs. HC (group 3). Group 3 had a cognitive impairment rate of 15 % (11/72) compared to 45 % (126/281) of the participants in group 2 (odds ratio [or]: 4.51, 95 % confidence interval [CI]: 2.28-8.93; p <0.001) and 47 % (31/66) of group 3 (OR: 4.51, KI: 2.20-10.97; Women in group 1 had a stronger cognitive impairment than men in the same group (55/105 [52%] against 71/176 [40%]; p <. 050). Fatigue was given by 52 % (149/287) of Group 1 and 26 % (19/72) of Group 3 ( p <. 001). Overall, women gave more exhaustion than men ( p =. 005). The cognitive function was not connected to measured blood parameters, including cytokines, sex hormones, coagulation factors, CEA or apolipoprotein-e genotype.

Comment

cognitive deficits in connection with cancer treatment were mainly documented in women with breast cancer. However, there are only a few studies that have evaluated cognitive function before treatment. This first prospective study that evaluates fatigue and cognition before treatment for CRC patients suggests that cognitive deficits could be part of the disease process itself.
chemotherapy-related cognitive impairments, more often referred to as "chemo brain", have been reported anecdotically since the emergence of chemotherapy.
Today we have a much better assessment of the participation of cytokines in the promotion and progression of cancer ulcers. Since many of these cytokines both increase inflammation and reduce blood flow, it is not surprising that cancer with our understanding of cognitive expiry that uses the same paths gets to a crossroads. 2.3 This idea that cancer can lead to systemic biological aberrations that can cause cognitive degeneration, more than 15 years old. 4
chemotherapy-related cognitive impairments, more often referred to as "chemo brain", have been reported anecdotically since the emergence of chemotherapy. The latest research results confirm that cognitive deficits are not only real, but can last a few decades. Another explanation that attracts attention is the effect of pro -inflammatory cytokines that result from chemotherapy. Such immunzytokines such as interleukin (IL) -1 and IL-6 and tumor necrosis factor alpha were associated with the inflammatory effects of treatment. Interestingly, these are the same cytokines that are produced in cancer processes. They are also the same family of cytokines that are involved in causing cognitive degeneration. 6 It is now assumed that the presence of cognitive deficits before the start of chemotherapy plays at least a certain role in what patients perceive as "chemo brain". Since the cancer and chemotherapy share this inflammatory tendency, 7 the extent to which the cancer itself and chemotherapy each contribute to the "chemo brain", it is difficult to estimate.
Several small prospective studies have shown that the cognitive decline is preceded by chemotherapy and/or radiation. Fifty patients with leukemia or myelodyplastic syndrome showed that before the beginning of chemotherapy, cognitive impairment, together with an increase in inflammatory cytokines (especially IL-6), occurred. 8 In another study with small cell lung cancer, cognitive deficits existed before chemotherapy and/or operation Prophylactic irradiation of the brain. 9.10 Another study in which various cognitive parameters were examined in 84 women with non -metastatic primary breast cancer, showed that the majority had an impairment before the start of chemotherapy.
While the current study did not show any significant increases in cytokines among those with the greatest cognitive deficits, the authors found that "the middle values ​​of most cytokines were significantly higher in cancer patients than with healthy control persons" and tends to climb the severity of the disease. The lack of a direct connection between cytokine mirrors and cognitive decay implies a more complex mechanism as simple inflammation. In addition, confounder such as nutritional status, sleep disorders, comedications, comorbidities and blood flow have influenced cognitive functional tests.
It is important to emphasize that the presence of cognitive deficits before treatment does not remove the possible worsening of these deficits through the treatment. It is only emphasized that the underlying biology of inflammation and the impaired cognitive function should be tackled at all points along the cancer supply continuum.

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