Sarcopenia, which is defined as a decrease in skeletal muscle mass and strength with aging, is an important risk factor in clinical medicine that is associated with mortality, and poor surgical and nonsurgical outcomes. Sarcopenia is now recognized as a multifactorial geriatric syndrome. Cachexia is defined as a metabolic syndrome with inflammation as the key feature, so cachexia can be an underlying condition of sarcopenia. Recently, cachexia has been defined as a complex metabolic syndrome associated with an underlying illness and characterized by the loss of muscle mass with or without a loss of fat mass. These two conditions overlap but are not the same. In clinical practice, many factors related to sarcopenia (decreased food intake, inactivity, and decreased hormones) are reported frequently in patients with cachexia. On the contrary, systemic inflammation, the core feature of cachexia, can also be present in apparently healthy older sarcopenic patients. This suggests that new therapeutic approaches, alone or in combination, may be appropriate in both conditions.
Aging ; Cachexia* ; Clinical Medicine ; Eating ; Humans ; Inflammation ; Mortality ; Muscle, Skeletal ; Nutrition Therapy ; Risk Factors ; Sarcopenia*

Cachexia is a common complication in patients with lung cancer. It aggravates the toxic and side effects of chemotherapy, hinders the treatment plan, weakens the responsiveness of chemotherapy, reduces the quality of life, increases complications and mortality, and seriously endangers the physical and mental health of patients with lung cancer. The causes and pathogenesis of tumor cachexia are extremely complex, which makes its treatment difficult and complex. Controlling cachexia in lung cancer patients requires many means such as anti-tumor therapy, inhibition of inflammatory response, nutritional support, physical exercise, and relief of symptoms to exert the synergistic effect of multimodal therapy against multiple mechanisms of tumor cachexia. To date, there has been a consensus within the discipline that no single therapy can control the development of cachexia. Some therapies have made some progress, but they need to be implemented in combination with multimodal therapy after fully assessing the individual characteristics of lung cancer patients. This article reviews the application of drug therapy and nutritional support in lung cancer patients, and looks forward to the research direction of cachexia control in lung cancer patients.
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Cachexia/therapy* ; Combined Modality Therapy ; Humans ; Lung Neoplasms/drug therapy* ; Neoplasms/complications* ; Nutritional Support/adverse effects* ; Quality of Life

Cancer is a catabolic inflammatory disease that causes patients to often experience weight loss, or even cachexia in severe cases. Undernourishment in patients with cancer impairs the quality of life and therapeutic response, further leading to poor prognosis. Active and frequent nutritional screening and assessment using valid tools are important for fast and appropriate nutritional intervention. Additionally, a suitable individualized nutritional intervention strategy should be established based on the nutritional assessment result. In general, nutritional intervention begins with nutritional counseling of patients diagnosed with cancer, and a well-planned nutritional counseling improves the treatment adherence and nutritional status. When planning nutritional supplementation for cancer patients, specific nutrients, including amino acids and fatty acids, should be considered. However, there has been no consistent result showing that any particular nutrient significantly improves the prognosis of cancer patients. Hence, continuous attention from clinical physicians is needed to plan nutritional improvement in patients with cancer.
Amino Acids ; Cachexia ; Counseling ; Fatty Acids ; Humans ; Mass Screening ; Nutrition Assessment ; Nutrition Therapy ; Nutritional Status ; Prognosis ; Quality of Life ; Weight Loss

OBJECTIVE: The aim of this study is to summarize preclinical studies on herbal medicines used to treat cancer cachexia and its underlying mechanisms. METHODS: We searched four representing databases, including PubMed, EMBASE, the Allied and Complementary Medicine Database, and the Web of Science up to December 2016. Randomized animal studies were included if the effects of any herbal medicine were tested on cancer cachexia. The methodological quality was evaluated by the Collaborative Approach to Meta-Analysis and Review of Animal Data from Experimental Studies (CAMARADE) checklist. RESULTS: A total of fourteen herbal medicines and their compounds were identified, including Coptidis Rhizoma, berberine, Bing De Ling, curcumin, Qing-Shu-Yi-Qi-Tang, Scutellaria baicalensis, Hochuekkito, Rikkunshito, hesperidin, atractylodin, Sipjeondaebo-tang, Sosiho-tang, Anemarrhena Rhizoma, and Phellodendri Cortex. All the herbal medicines, except curcumin, have been shown to ameliorate the symptoms of cancer cachexia through anti-inflammation, regulation of the neuroendocrine pathway, and modulation of the ubiquitin proteasome system or protein synthesis. CONCLUSIONS This study showed that herbal medicines might be a useful approach for treating cancer cachexia. However, more detailed experimental studies on the molecular mechanisms and active compounds are needed.
Animals ; Cachexia/etiology* ; Herbal Medicine/trends* ; Medicine, East Asian Traditional/trends* ; Neoplasms, Experimental/drug therapy* ; Phytotherapy/trends*

Cachexia ; etiology ; Cough ; Delayed Diagnosis ; Fever ; Humans ; Hypercalcemia ; etiology ; Male ; Middle Aged ; Radiography ; Renal Dialysis ; Renal Insufficiency ; etiology ; therapy ; Tuberculosis, Pulmonary ; complications ; diagnostic imaging

OBJECTIVETo study the leptin resistance mechanism of Xiaoyan Decoction (XD) in lung cancer cachexia (LCC) rats.

METHODSAn LCC rat model was established. Totally 40 rats were randomly divided into the normal control group, the LCC model group, the XD group, and the positive control group, 10 in each group. After LCC model was set up, rats in the LCC model group were administered with normal saline, 2 mL each time. Rats in the XD group were administered with XD at the daily dose of 2 mL. Those in the positive control group were administered with Medroxyprogesterone Acetate suspension (20 mg/kg) by gastrogavage at the daily dose of 2 mL. All medication lasted for 14 days. The general condition and tumor growth were observed. Serum levels of leptin and leptin receptor in the hypothalamus were detected using enzyme-linked immunosorbent assay. Contents of neuropeptide Y (NPY) and anorexia for genomic POMC were detected using real-time PCR technique.

RESULTSSerum leptin levels were lower in the LCC model group than in the normal control group with statistical significance (P < 0.05). Compared with the LCC model groups, serum leptin levels significantly increased in the XD group (P < 0.01). Leptin receptor levels in the hypothalamus increased significantly in the LCC model group (P < 0.01). Increased receptor levels in the LCC model group indicated that either XD or Medroxyprogesterone Acetate could effectively reduce levels of leptin receptor with statistical significance (P < 0.01). There was also statistical difference between the XD group and the positive control group (P < 0.05). Contents of NPY was higher in the LCC model group than in the other groups with statistical difference (P < 0.05). There was no statistical difference in NPY between the normal control group and the rest 2 treatment groups (P > 0.05). There was statistical difference in POMC between the normal control group and the LCC model group (P < 0.05). POMC could be decreased in the XD group and the positive control group with statistical significance (P < 0.05), and it was more obviously decreased in the XD group (P < 0.05).

CONCLUSIONSLeptin resistance existed in LCC rats. XD could increase serum leptin levels and reduce leptin receptor levels in the hypothalamus. LCC could be improved by elevating NPY contents in the hypothalamus and reducing POMC contents, promoting the appetite, and increasing food intake from the periphery pathway and the central pathway.

Animals ; Cachexia ; drug therapy ; etiology ; Drugs, Chinese Herbal ; therapeutic use ; Eating ; Humans ; Hypothalamus ; metabolism ; Leptin ; metabolism ; Lung Neoplasms ; complications ; Neuropeptide Y ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

There are concerns whether megestrol acetate (MA) stimulates the growth of prostate cancer in castration-resistant prostate cancer (CRPC). We evaluated the effect of cumulative doses of MA on the disease-specific survival (DSS) in patients with CRPC who were receiving Docetaxel-based chemotherapy. From July 2003 through June 2009, we identified 109 consecutive patients with CRPC and who had received docetaxel-based chemotherapy. Of these patients, 68 (62.4%) have not received MA, whereas 21 patients (19.3%) and 20 patients (18.3%) had received low dose MA (total < or = 18,400 mg) and high dose MA (total > 18,400 mg), respectively. We assessed the effect of several variables on DSS. None of the clinicopathological variables differed among the three groups. When comparing DSS using Kaplan-Meier analysis, there was no statistically significant survival differences among the three groups (P = 0.546). Using multivariate Cox proportional analyses with backward elimination, the number of docetaxel cycles was only significant factor predicting DSS (HR: 0.578, 95% CI: 0.318-0.923, P = 0.016). Cumulative doses of MA as adjuvant treatment for patients with CRPC and who are receiving docetaxel-based chemotherapy, did not affect their DSS. Therefore, MA can be safely administered in cachexic patients with CRPC.
Aged ; Aged, 80 and over ; Anorexia/complications/*drug therapy ; Antineoplastic Agents/therapeutic use ; Antineoplastic Agents, Hormonal/*therapeutic use ; Cachexia/complications/*drug therapy ; Castration ; Humans ; Kaplan-Meier Estimate ; Male ; Megestrol Acetate/*therapeutic use ; Middle Aged ; Proportional Hazards Models ; Prostatic Neoplasms/complications/*drug therapy/mortality ; Taxoids/therapeutic use

We investigated the role of fasting hormones and pro-inflammatory cytokines in cancer patients. Hormones (ghrelin, adiponectin, and leptin) and cytokines (TNF-alpha, IFN-gamma, and IL-6) were measured by ELISA or RIA in lung cancer and colorectal cancer patients before the administration of cancer therapy, and measurements were repeated every 2 months for 6 months. From June 2006 to August 2008, 42 patients (19 with colorectal cancer and 23 with lung cancer) were enrolled. In total, 21 patients were included in the cachexia group and the others served as a comparison group. No significant difference in the initial adiponectin, ghrelin, TNF-alpha, IFN-gamma, or IL-6 level was observed between groups, although leptin was significantly lower in cachectic patients than in the comparison group (15.3 +/- 19.5 vs 80.9 +/- 99.0 pg/mL, P = 0.007). During the follow-up, the patients who showed a > 5% weight gain had higher ghrelin levels after 6 months. Patients exhibiting elevated IL-6 levels typically showed a weight loss > 5% after 6 months. A blunted adiponectin or ghrelin response to weight loss may contribute to cancer cachexia and IL-6 may be responsible for inducing and maintaining cancer cachexia.
Adiponectin/analysis ; Aged ; Antineoplastic Agents/therapeutic use ; Cachexia/*physiopathology ; Colorectal Neoplasms/drug therapy/*metabolism/mortality ; Cytokines/*analysis ; Female ; Follow-Up Studies ; Ghrelin/analysis ; Humans ; Interferon-gamma/analysis/physiology ; Interleukin-6/analysis ; Leptin/analysis ; Lung Neoplasms/drug therapy/*metabolism/mortality ; Male ; Middle Aged ; Peptide Hormones/*analysis ; Prognosis ; Prospective Studies ; Survival Rate ; Tumor Necrosis Factor-alpha/analysis ; Weight Gain ; Weight Loss

OBJECTIVE: To describe the nutritional status of women with peritoneal metastasis (PM) from recurrent ovarian, fallopian, or peritoneal cancer and to assess longitudinal variations of the cachexia-anorexia syndrome (CAS) during palliative pressurized intraperitoneal aerosol chemotherapy (PIPAC). METHODS: Nutritional assessment included body mass index (BMI), bioelectrical impedance analysis (BIA), and blood chemistry. CAS presence/absence was recorded before and during repeated cycles (1–11) of PIPAC. RESULTS: Eighty-four patients with peritoneal cancer (n=5) or PM from recurrent ovarian (n=77) or fallopian tube (n=2) cancer were included. At baseline, resting metabolism (RM) (1,432±172 kcal/day), visceral fat level (7.5±3.2), skeletal muscle mass (27.2%±4.6%), upper arm circumference (27.9±4.6 cm), lower leg circumference (35.1±3.9 cm), serum parameters (albumin [3.5±0.7 g/dL], total protein [6.3±0.9 g/dL], and transferrin [202±60 mg/dL]) were below normal limits. C-reactive protein (CRP) (4.3±6.8 mg/dL), caliper body fat (35.7%±6.3%), and total body fat mass (35.6%±8.5%) were above normal limits. Nineteen/84 (23%) patients had CAS at baseline. Deterioration or stabilization/improvement of CAS was observed in 9/55 (16.4%) and 46/55 (83.6%) patients with follow-up data, respectively. Baseline body fat mass, visceral fat level, skeletal muscle mass, caliper body fat, BMI, ascites, Karnofsky index, RM, and CRP, as well as tumor response were not predictive of CAS deterioration. CONCLUSION: Nutritional decline and onset or deterioration of CAS are difficult to predict. Careful measuring and monitoring of nutritional parameters and CAS in all patients seems to be necessary in order to identify those patients in need of enteral/parenteral nutrition support.
Adipose Tissue ; Anorexia* ; Arm ; Ascites ; Body Mass Index ; C-Reactive Protein ; Cachexia* ; Chemistry ; Drug Therapy* ; Electric Impedance ; Fallopian Tubes ; Female ; Follow-Up Studies ; Humans ; Intra-Abdominal Fat ; Karnofsky Performance Status ; Leg ; Metabolism ; Muscle, Skeletal ; Neoplasm Metastasis* ; Nutrition Assessment ; Nutritional Status* ; Ovarian Neoplasms ; Transferrin

OBJECTIVETo assess the putative involvement of NF-kappaB and pro-inflammatory cytokines in the pathogenesis of cancer cachexia and the therapeutic efficacy of indomethacin (IND) on cachexia.

METHODSThirty young male BALB/c mice were divided randomly into five groups: A, control; B, tumor-bearing plus saline; C, tumor-bearing plus IND (0.25 mg/kg); D, tumor-bearing plus IND (0.5 mg/kg); and E, tumor-bearing plus IND (2.0 mg/kg). Colon 26 adenocarcinoma cells of murine were inoculated subcutaneously to induce cachexia. Saline and IND were given intraperitoneally daily for 7 days from the onset of cachexia to sacrifice. Food intake and body composition were documented, serum TNF-alpha and IL-6 levels and activity of NF-kappaB in spleen were investigated in all animals.

RESULTSCachexia was observed in all tumor-bearing mice. No difference was found between groups in food intake (P > 0.05). By day 16, body weights of non-tumor mice were about 82.0% of healthy controls (P < 0.01), and the weight of gastrocnemius was decreased by 28.7% (P < 0.01). Gastrocnemius weight was increased markedly (P < 0.01) after treatment of IND (0.5 mg/kg). Tumor-bearing caused a significant increase in serum TNF-alpha and IL-6 levels (P < 0.01). The concentration of TNF-alpha (P < 0.05) and IL-6 (P < 0.01) in tumor-bearing mice was reduced after administration of 0.5 mg/kg IND for 7 days. NF-kappaB activation in the spleen was increased in tumor-bearing mice in comparison with controls. NF-kappaB activity was reduced in mice treated with IND. The maximal inhibition was observed at an dosage of 0.5 mg/kg (P < 0.01). Liner positive correlation was found between NF-kappaB activity and cytokine levels (r(TNF-alpha) = 0.918, P(TNF-alpha) = 0.028; r(IL-6) = 0.884, P(IL-6) = 0.046).

CONCLUSIONSCachexia induced by colon 26 adenocarcinoma cells may be partially attributed to the enhanced TNF-alpha and IL-6 levels which is controlled by NF-kappaB. IND may inhibit the activation of NF-kappaB, decrease serum TNF-alpha and IL-6 levels and thus alleviate the cachexia.

Adenocarcinoma ; complications ; metabolism ; Animals ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Cachexia ; drug therapy ; etiology ; metabolism ; Colonic Neoplasms ; complications ; metabolism ; Indomethacin ; pharmacology ; Interleukin-6 ; metabolism ; Male ; Mice ; Mice, Inbred BALB C ; NF-kappa B ; metabolism ; Neoplasm Transplantation ; Tumor Necrosis Factor-alpha ; metabolism