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Review
. 2024 Apr 27;16(9):1696.
doi: 10.3390/cancers16091696.

Updates in Cancer Cachexia: Clinical Management and Pharmacologic Interventions

Sudeep Pandey  1 , Lauren Bradley  1 , Egidio Del Fabbro  2
Affiliations
Review

Updates in Cancer Cachexia: Clinical Management and Pharmacologic Interventions

Sudeep Pandey et al. Cancers (Basel). .

Abstract

Despite a better understanding of the mechanisms causing cancer cachexia (CC) and development of promising pharmacologic and supportive care interventions, CC persists as an underdiagnosed and undertreated condition. CC contributes to fatigue, poor quality of life, functional impairment, increases treatment related toxicity, and reduces survival. The core elements of CC such as weight loss and poor appetite should be identified early. Currently, addressing contributing conditions (hypothyroidism, hypogonadism, and adrenal insufficiency), managing nutrition impact symptoms leading to decreased oral intake (nausea, constipation, dysgeusia, stomatitis, mucositis, pain, fatigue, depressed mood, or anxiety), and the addition of pharmacologic agents when appropriate (progesterone analog, corticosteroids, and olanzapine) is recommended. In Japan, the clinical practice has changed based on the availability of Anamorelin, a ghrelin receptor agonist that improved lean body mass, weight, and appetite-related quality of life (QoL) compared to a placebo, in phase III trials. Other promising therapeutic agents currently in trials include Espindolol, a non-selective β blocker and a monoclonal antibody to GDF-15. In the future, a single therapeutic agent or perhaps multiple medications targeting the various mechanisms of CC may prove to be an effective strategy. Ideally, these medications should be incorporated into a multimodal interdisciplinary approach that includes exercise and nutrition.

Keywords: cachexia; cancer; cancer cachexia; wasting syndrome.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 2
Figure 2
A framework for the management of patients with cancer cachexia in daily practice. (ESAS, Edmonton Symptom Assessment Scale; PG-SGA, Patient-Generated Subjective Global Assessment; SPPB, Short Physical Performance Battery) [44].
Figure 1
Figure 1
Proposed stages of cachexia [6].
Figure 3
Figure 3
Simplified theoretical model demonstrating the complex interplay of different mechanisms producing cachexia. These mechanisms should not be viewed in isolation, since they are all inter-related, e.g., proinflammatory cytokines have a profound effect on the endocrine system, but there is also reciprocal modulation. TNF: Tumor Necrosis Factor; IL: Interleukin; INF: Interferon; CRP: C-Reactive Protein; ROS: Role of Oxidative Stress; GDF: Growth Differentiation Factor; ZAG: Zinc-α2-Glycoprotein; LMF: Lipid-Mobilizing Factor; PTHrP: Parathyroid Hormone-Related Protein; NPY: Neuropeptide Y; AgRP: Agouti-Related Protein; POMC: Pro-opiomelanocortin; CART: Cocaine and Amphetamine-Regulated Transcript; ACP: Acid Phosphatase.
Figure 4
Figure 4
Simplified summary of multimodal management of cancer cachexia.
See this image and copyright information in PMC

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