Severe Weight Loss and Its Association with Fatigue in Old Patients at Discharge from a Geriatric Hospital

Although malnutrition is frequent in the old, little is known about its association with fatigue. We evaluated the relation of self-reported severe weight loss with fatigue and the predictors for fatigue in old patients at hospital discharge. Severe weight loss was defined according to involuntary weight loss ≥5% in the last three months. We determined fatigue with the validated Brief Fatigue Inventory questionnaire. The regression analyses were adjusted for age, sex, number of comorbidities, medications/day, and BMI. Of 424 patients aged between 61 and 98 y, 34.1% had severe weight loss. Fatigue was higher in patients with severe weight loss (3.7 ± 2.3 vs. 3.2 ± 2.3 points, p = 0.021). In a multinomial regression model, weight loss was independently associated with higher risk for moderate fatigue (OR:1.172, CI:1.026-1.338, p = 0.019) and with increased risk for severe fatigue (OR:1.209, CI:1.047-1.395, p = 0.010) together with the number of medications/day (OR:1.220, CI:1.023-1.455, p = 0.027). In a binary regression model, severe weight loss predicted moderate-to-severe fatigue in the study population (OR:1.651, CI:1.052-2.590, p = 0.029). In summary, patients with self-reported severe weight loss at hospital discharge exhibited higher fatigue levels and severe weight loss was an independent predictor of moderate and severe fatigue, placing these patients at risk for impaired outcome in the post-hospital period

Iron deficiency in chronic heart failure: case-based practical guidance

In patients with chronic heart failure, iron deficiency, even in the absence of anaemia, can aggravate the underlying disease and have a negative impact on clinical outcomes and quality of life. The 2016 European Society of Cardiology guidelines for the diagnosis and treatment of acute and chronic heart failure recognize iron deficiency as a co-morbidity in chronic heart failure and recommend iron status screening in all newly diagnosed patients with chronic heart failure. Furthermore, the guidelines specifically recommend considerations of intravenous iron therapy, ferric carboxymaltose, for the treatment of iron deficiency. However, in spite of these recommendations, iron deficiency remains often overlooked and undertreated. This may be due, in part, to the lack of clinical context and practical guidance accompanying the guidelines for the treating physician. Here, we provide practical guidance complemented by a case study to assist and improve the timely diagnosis, treatment, and routine management of iron deficiency in patients with chronic heart failure

Neurological and endocrinological disorders: orphans in chronic obstructive pulmonary disease

SummaryPatients with chronic obstructive pulmonary disease (COPD) are often characterised by a range of characteristic co-morbidities that interfere with their pulmonary disease. In addition to a mere association with co-morbidities, a complex pathophysiological interaction and mutual augmentation occurs between COPD and its co-morbidities that may result in disease progression and increased morbidity and mortality. An interdisciplinary approach is required both for diagnosis and treatment to target co-morbidities early in the course of the disease. This review summarizes the current knowledge of the interaction with cerebrovascular disease and endocrinological co-morbidities in COPD patients. There is growing evidence that COPD is an independent risk factor for ischemic stroke, increasing the risk about twofold. Stroke risk in COPD patients increases with the severity of the disease as measured by the degree of airflow limitation. The presence of cardiovascular risk factors is of particular importance for stroke prevention in COPD patients. Endocrinological co-morbidities are also important and many are associated with increased cardiovascular risk. Impaired glucose metabolism ranges from insulin resistance to overt diabetes mellitus, which is a frequent finding and is associated with worse outcome

Ursodeoxycholic acid treatment in a rat model of cancer cachexia

UDCA treatment in the Yoshida hepatoma model showed a trend towards attenuation of tissue loss in animals with progressive weight loss in cancer cachexia. Tumor growth and activity indicators were not altered. Both doses of UDCA tended to reduce the mortality rates in tumor-bearing animals. Larger studies with longer follow-up are required to verify these findings

IGF-1 treatment reduces weight loss and improves outcome in a rat model of cancer cachexia

Background: A hallmark symptom of cancer cachexia is the loss of skeletal muscle. This is at least partially due to a deregulation of the growth hormone/IGF-1 axis and a subsequently impaired protein synthesis in skeletal muscle. Here, we investigated the effect of IGF-1 supplementation in a rat model of cancer cachexia. Methods: Juvenile rats were inoculated with the Yoshida AH-130 hepatoma and treated once daily with 0.3 mg kg−1 day−1 (low dose) or 3 mg kg−1 day−1 (high dose) IGF-1 or placebo for a period of maximal 16 days. Body weight and body composition (by NMR) were assessed at baseline and at the end of the study or day of death. Locomotor activity and food intake were assessed at baseline and day 10/11 after tumour inoculation for 24 h. Results: Untreated tumour-bearing rats lost 55.3 ± 2.14 g body weight, which was reduced by low-dose to −39.6 ± 11.1 g (p = 0.0434) and high-dose IGF-1 to −42.7 ± 8.8 g (p = 0.057). Placebo-treated rats lost 41.4 ± 2.0-g lean mass, which was attenuated by low-dose IGF-1 (−28.8 ± 8.3 g, p = 0.041) and high-dose IGF-1 (−30.9 ± 7.4, p = 0.067). Spontaneous activity and food intake were improved by low-dose IGF-1 only. No effect on fat mass was observed. Low-dose IGF-1 significantly reduced mortality (HR = 0.45, 95%CI = 0.21–0.93, p = 0.0315), whilst the high dose did not reach significance (HR = 0.68, 95%CI = 0.26–1.74, p = 0.42). Conclusion: Low-dose IGF-1 reduced mortality and attenuated loss of body weight as well as muscle mass in the Yoshida hepatoma rat model. Moreover, an improved quality of life was observed in these animals. Further experiments using different doses are necessary

Impact of chronic inflammatory airway disease on stroke severity and long-term survival after ischemic stroke - a retrospective analysis

Background Chronic inflammatory airway disease (CIAD) has emerged as independent risk factor for cardiovascular mortality and ischemic stroke but the impact of co-existing CIAD in patients with ischemic stroke is less clear. Methods We retrospectively analyzed 1013 patients with acute ischemic stroke who were consecutively admitted to the Department of Neurology, Charité - Universitätsmedizin Berlin, Germany within one year. Mean follow-up was 80 months (IQR 32–85 months). Using multivariable regression models we analyzed the impact of CIAD (defined as chronic obstructive pulmonary disease or asthma bronchiale) on stroke severity and outcome. Results Co-existing CIAD was evident in 7.1 % (n = 72) of all patients with acute ischemic stroke. Baseline characteristics of stroke patients with CIAD did not differ significantly from ischemic stroke patients without CIAD. Age (OR 1.17 [95 % CI 1.03-1.37] per decade), atrial fibrillation (OR 3.43 [95 % CI 2.47-4.78]) and coronary artery disease (OR 1.51 [95 % CI 1.07–2.14]) but not a history of CIAD (p = 0.30) were associated with severe stroke (NIHSS≥11) on hospital admission. Age (HR 1.70 [95 % CI 1.53-1.87] per decade), peripheral artery disease (HR 1.91 [95 % CI 1.35-2.7]), stroke severity at hospital admission (NIHSS per point HR 1.08 [95 % CI 1.06-1.10]), and history of CIAD (HR 1.43 [95 % CI 1.02-2.00]) were independently associated with mortality during long-term follow-up. However, CIAD was not significantly associated with short-term mortality after stroke. Conclusion Co-existing CIAD showed no significant association with stroke severity at hospital admission and early mortality after ischemic stroke. CIAD was negatively associated with long-term survival after ischemic stroke

Body weight changes and incidence of cachexia after stroke

Background: Body weight loss is a frequent complication after stroke, and its adverse effect on clinical outcome has been shown in several clinical trials. The purpose of this prospective longitudinal single-centre observational study was to investigate dynamical changes of body composition and body weight after ischemic stroke and an association with functional outcome. Methods: Sixty-seven consecutive patients (age 69 ± 11 years, body mass index 27.0 ± 4.1 kg/m2, 42% female patient, mean ± SD) with acute ischemic stroke with mild to moderate neurological deficit (National Institute of Health Stroke Scale median 4, ranged 0–12) were analysed in the acute phase (4 ± 2 days) and at 12 months (389 ± 26 days) follow-up. Body composition was examined by dual energy X-ray absorptiometry. Cachexia was defined according to the consensus definition by body weight loss ≥5% within 1 year and additional clinical signs. Lean tissue wasting was considered if a ratio of upper and lower limbs lean mass sum to squared height (kg/m2) was ≤5.45 kg/m2 for female patient and ≤7.25 kg/m2 for male patient. Results: According to the body weight changes after 12 months, 42 (63%) patients had weight gain or stable weight, 11 (16%) patients had moderate weight loss, and 14 (21%) patients became cachectic. A relative decline of 19% of fat tissue and 6.5% of lean tissue was observed in cachectic patients, while no changes of lean tissue were observed in non-cachectic patients after 12 months. The modified Rankin Scale was 48% higher (2.1 ± 1.6, P < 0.05), Barthel Index was 22% lower (71 ± 39, P < 0.01), and handgrip strength was 34% lower (21.9 ± 13.0, P < 0.05) in cachectic compared to non-cachectic patients after 12 months. The low physical performance if defined by Barthel Index <60 points was linked to the lean tissue wasting (OR 44.8, P < 0.01), presence of cachexia (OR 20.8, P < 0.01), and low body mass index <25 kg/m2 (OR 11.5, P < 0.05). After adjustment for cofounders, lean tissue wasting remained independently associated with the low physical performance at 12 months follow-up (OR 137.9, P < 0.05). Conclusions: In this cohort study, every fifth patient with ischemic stroke fulfilled the criteria of cachexia within 12 months after index event. The incidence of cachexia was 21%. Cachectic patients showed the lowest functional and physical capacity

Hand grip strength and fatigability: correlation with clinical parameters and diagnostic suitability in ME/CFS

Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease accompanied by muscular fatigue and pain. A functional measure to assess muscle fatigability of ME/CFS patients is, however, not established in clinical routine. The aim of this study is to evaluate by assessing repeat maximum handgrip strength (HGS), muscle fatigability as a diagnostic tool and its correlation with clinical parameters. Methods: We assessed the HGS of 105 patients with ME/CFS, 18 patients with Cancer related fatigue (CRF) and 66 healthy controls (HC) using an electric dynamometer assessing maximal (Fmax) and mean force (Fmean) of ten repetitive measurements. Results were correlated with clinical parameters, creatinine kinase (CK) and lactate dehydrogenase (LDH). Further, maximum isometric quadriceps strength measurement was conducted in eight ME/CFS patients and eight HC. Results: ME/CFS patients have a significantly lower Fmax and Fmean HGS compared to HC (p < 0.0001). Further, Fatigue Ratio assessing decline in strength during repeat maximal HGS measurement (Fmax/Fmean) was higher (p <= 0.0012). The Recovery Ratio after an identical second testing 60 min later was significantly lower in ME/CFS compared to HC (Fmean2/Fmean1; p <= 0.0020). Lower HGS parameters correlated with severity of disease, post-exertional malaise and muscle pain and with higher CK and LDH levels after exertion. Conclusion: Repeat HGS assessment is a sensitive diagnostic test to assess muscular fatigue and fatigability and an objective measure to assess disease severity in ME/CFS