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Cancer Anorexia and the Central Nervous System

NCT01564693 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 15

Last updated 2015-08-18

Study results available
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Summary

The pathogenesis of cancer anorexia is complex and multifactorial. However, a number of consistent and robust evidence point to a prominent role for the central nervous system. In particular, the hyperactivation of the immune system, due to tumour growth, causes a systemic inflammatory response primarily mediated by pro-inflammatory cytokines. At the central level, inflammatory response profoundly alters the activity of the hypothalamic nuclei, which are involved in the regulation of energy homeostasis. In particular, pro-inflammatory cytokines inhibit prophagic neurons activity, while enhance the activation of the anorexigenic neurons. Although supported by compelling experimental evidence, it should be acknowledged that this pathogenic hypothesis has not been confirmed yet by human studies.

Aim of the present study is to determine the specific pattern(s) of the brain activation after assumption of a standard meal in both anorexic and non-anorexic cancer patients to reveal potential differences, which will be correlated with the levels of concurrently measured circulating pro-inflammatory cytokines. The results obtained would help in assessing the role of the central nervous system and, in particular of the hypothalamus, in the pathogenesis of cancer anorexia.

Conditions

  • Cancer Cachexia

Sponsors & Collaborators

  • University of Roma La Sapienza

    lead OTHER

Principal Investigators

  • Alessandro Laviano, MD · University of Roma La Sapienza

Eligibility

Min Age
18 Years
Max Age
85 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2010-04-30
Primary Completion
2014-12-31
Completion
2015-04-30

Countries

  • Italy

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT01564693 on ClinicalTrials.gov