Originally characterized as a growth factor for erythrocytes, erythropoietin (EPO) is used to treat anemia and fatigue in cancer patients receiving radiation therapy and chemotherapy.
Naturally occurring human mutations influence a wide range of CBG properties and point toward a role in hitherto unexplained chronic musculoskeletal pain and fatigue disorders as well as potentially affecting fertility outcomes including offspring gender.
Corticosteroid-binding globulin (CBG; SERPIN A6) gene mutations are rare; only four mutations have been described, often in association with fatigue and chronic pain, albeit with incomplete penetrance.
Rare kindreds with CBG mutations reducing CBG levels or altering binding affinity have been described, along with clinical manifestations encompassing fatigue, chronic pain, and hypotension.
To the best of our knowledge, this case represents the first de novo mutation reported for corticosteroid-binding globulin deficiency, implicating a pathogenic role of variants of SERPINA6 in some cases of muscle fatigue.
A mechanism for the effect of CBG mutations on fatigue is not readily apparent because free cortisol levels are normal, although we speculate that CBG may have an effect on cortisol-brain transport.
Although relative hypotension and fatigue have recently been associated with CBG deficiency in a family with two CBG mutations (null and Lyon), the two homozygous subjects in this kindred were both normotensive and only the proband presented with fatigue.
As idiopathic fatigue disorders are associated with relatively low plasma cortisol, abnormalities of corticosteroid-binding globulin may be pathogenic.
The aim of this study was to investigate the predictive factors of objective response rate (ORR) and progression-free survival (PFS), and the correlation of albumin-bilirubin (ALBI) grade with decreased appetite and fatigue in hepatocellular carcinoma patients treated with lenvatinib.
After adjustments of variables, female sex, younger age at diagnosis, and lower serum albumin level were independently associated with fatigue scores, while a longer follow-up period and lower serum albumin levels were associated with itch scores.
The improvement in pain and fatigue was supported by the ECOG performance status remaining stable with the highest score being equal to 2 throughout the study and a trend towards an improvement in GPS performance status and albumin levels.
We assessed fatigue using three fatigue scales-the Brief Fatigue Inventory (BFI), the Edmonton Symptom Assessment System (ESAS), and the European Organization for Research and Treatment of Cancer Quality of Life Core Questionnaire 30 (EORTC QLQ-C30)-and determined their association with objective assessments, including handgrip strength, maximal inspiratory pressure, lean body mass, phase angle, and albumin.
In addition, plasma LC levels in terminally ill patients showed no correlations with albumin or CRP values nor with other clinical parameters, such as fatigue or body weight loss.
Herein we explored three mechanisms (pharmacokinetics, serum albumin and pharmacogenetics) through which dexamethasone may cause debilitating fatigue and disrupted sleep.
Serum IL-10 concentrations, relationship assessment scale, and fatigue severity scale values were found to be correlated with depression among the SLE patients (P = .036, P = .007, and P = .001, respectively).
Specifically, women with Lys_Glu or Glu_Glu genotype in the IL-10 gene had a 0.49 times lower risk of severe fatigue compared with those with Lys_Lys genotype (OR = 0.49, 95% CI = 0.25-0.92, P = 0.027).
These data indicate that increased activity of pro-inflammatory transcription factors may contribute to persistent cancer-related fatigue and provide insight into potential mechanisms for tonic increases in NF-κB activity, specifically decreased expression of GR anti-inflammatory transcription factors.
The aims of the present pilot study were to assess abnormalities in glucocorticoid receptor expression and to relate these abnormalities to the development of fatigue and to disease activity and severity in autoimmune cholestatic liver disease.
Further, the mutations at the hydrophobic amino acids primarily promote the aggregation tendency of SOD1 protein through different destabilizing mechanisms including changes in hydrophobic free energy, loss of electrostatic interactions in the protein's surface and loss of hydrogen bonds that bridges the protein core and surface.