High albumin level is a predictor of favorable response to immunotherapy in autoimmune encephalitis

Abstract Abstract 3832 Myelodysplastic syndromes (MDS) represent a heterogeneous group of clonal disorders characterized by reduced hematopoiesis and progression to leukemia. Albumin is a prognostic biomarker in many malignant and non-malignant conditions, including multiple myeloma, chronic inflammation and aging. Recently, one study (Yepez, M, ASH 2010, abst #4001) showed that hypoalbuminemia was an independent prognostic factor in MDS. However, serum albumin levels can vary with time and be influenced by nutrition, age and presence of other comorbidities which are prevalent in MDS. To have an accurate assessment, we took the average serum albumin level of MDS patients over a period of 6 months. We hypothesize low average albumin will confer worse outcomes We conducted a retrospective analysis of 237 MDS patients seen in Cleveland Clinic between 1999 and 2009 (RARS= 30, RCMD=25, RAEB1/2=61, 5q- syndrome= 4, CMML1/2=39, MDS/MPN-U=32, RARS-T=30, RCUD=26). A total of 194 patients were included since average albumin was able to be calculated. The median age is 66 (20–92) years. Median follow-up time is 15 months (0–81 months). Clinical information including age, SNP-A karyotyping results, hemoglobin and serum albumin at time of diagnosis, average serum albumin level over 6 months, absolute neutrophil count, platelet counts, bone marrow blasts, and metaphase cytogenetic results were obtained.Patients were divided based on IPSS into lower and higher risk disease. We analyzed a total of 123 patients in the lower risk and 71 patients in the higher risk group. Further, we subdivided patients into lower albumin level (<3.5) or higher (3.5 or greater) based on the average albumin over 6 months. The median overall survival (OS) of the cohort is 15 months. Categorical variables were analyzed using Fisher's exact test. The Cox-proportional hazards model was used to assess univariate and multivariate analyses for OS and progression free survival (PFS); factors assessed included age (≥60 vs. <60 years), disease grouping (MDS and MDS/MPN vs sAML), BM blasts (≥5 vs. <5 %), Hgb level (≥10 vs. <10 g/dL), metaphase cytogenetics (MC) risk groups using IPSS criteria (good, intermediate, poor), presence or absence of new SNP lesions and average albumin level. Each variable was retained in the multivariate model regardless of its statistical significance. Only variables with p<.05 in multivariate analysis were considered significant. Similar to the study by Yepez M et al, we also found that serum albumin level at the time of original diagnosis is prognostic in MDS and related disorders. Patients with low albumin levels at diagnosis (<3.5) have a worse OS compared to those with high albumin levels (6 vs 16 mos, p=.005). However, this was possible with a dichotomized albumin level. More importantly, we also found that the lower average serum albumin level [OS (8 vs 30 mos, p=.0001) and PFS (5 vs 20 mos, p=<.0001)] over 6 months can also be prognostic in MDS but not in MDS/MPN and sAML. Patients with low average albumin have poorer survival compared to patients with high albumin (OS: 6 vs 23 months, p=<.0001; PFS: 5 vs 15 months, p= <.0001). The same statistically significant findings were observed in patients stratified to lower (OS: 9 vs 37 mos, p=.001; PFS: 5 vs 24 mos, p=<.0001) or higher (5 vs 13 mos, p=.03) risk MDS by IPSS. Multivariate analysis showed that low average albumin level is an independent predictor of poor outcomes in MDS (OS: HR=2.12 CI:1.53–2.99, p=<.0001; PFS: HR=1.91 CI:1.31–2.76, p=.0009). Similarly, previously validated poor prognostic factors in MDS remained significant (Age ≥60 [HR:1.87, p=.0003], sAML disease grouping [HR:2.08, p=.0001], Hgb <10 g/dl [HR:1.42, p=.009], BM blasts [HR:1.44, p=.03], Poor risk cytogenetics [HR:2.22, p=.004], and presence of new SNP lesions [HR:1.59, p=.0008]. To identify factors that may result in worse outcomes in low average albumin patients, we assessed treatment response differences between patients which were not significant between low and high albumin levels. However AML transformation [(42/92 (45%) vs 111/150 (74%), p.002] and cytogenetics [Poor vs Good/Intermediate (21/43 (49%) vs 55/185 (30%), p=.02)] correlated with lower average albumin levels. In conclusion, low average serum albumin levels are an independent predictor of worse outcomes in MDS. Moreover, these data suggest that low average serum albumin is associated with poor risk karyotype and with progression to AML. Disclosures: No relevant conflicts of interest to declare.

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Serum Albumin Level < 32 g/l on Day 30 Can Predicts Higher Risk of Non-Relapse Mortality in Acute Lymphoblastic Leukemia Following Allogeneic Stem Cell Transplantation

Blood ◽

10.1182/blood.v124.21.5930.5930 ◽

2014 ◽

Vol 124 (21) ◽

pp. 5930-5930

Author(s):

Feras Alfraih ◽

Vikas Gupta ◽

John Kuruvilla ◽

Jeffrey H. Lipton ◽

Hans A. Messner ◽

...

Keyword(s):

Risk Factor ◽

Serum Albumin ◽

Acute Gvhd ◽

Serum Albumin Level ◽

Lymphoblastic Leukemia ◽

Chronic Gvhd ◽

Group Versus ◽

Albumin Level ◽

Grade 3 ◽

High Albumin

Introduction: It is extremely significant issue to predict hematopoietic stem cell transplant (HSCT) outcomes using a biomarker. In this study, we attempted to evaluate the impact of post-transplant serum albumin on outcomes in patients with acute lymphoblastic leukemia (ALL). Methods: 123 patients with ALL receiving HSCTs between 1999 and 2012 at our center were evaluated for post-transplant serum albumin levels and their correlation with transplant's outcome. The level of serum albumin was retrospectively retrieved in certain time point ± 3 days for following periods: 1 month pre HSCT and then weekly after transplantation for first 3 months. 100 patients had available serum albumin levels. The ROC analyses were used to determine the most statistically significant cutoff level of serum albumin level correlating with NRM at 1 year. The ROC analysis suggested the level of 32 g/l at 4 weeks post HSCT as the best cutoff level for further analysis. Thus patients were stratified into low versus high albumin level group according to that cutoff level. Results: Median age for all patients is 37 (range 17-61), 35% were female and related donors were 57%. Matched donors were 83%. 71% were in 1st complete remission. 37% were Philadelphia chromosome positive. GVHD prophylaxis was CSA/MTX 60%, CSA/MMF 22%. Conditioning regimen was myeloablative in 95%. 61% received peripheral blood stem cells. With a median follow-up among survivors of 60 months (range 21-100), 61% patients showed albumin level ³ 32g/l at day 30 while 39% showed dropped albumin level <32 g/l at day 30. The OS rate at 2 years was 61% in high albumin group versus 23% in low albumin group (p < 0.001). The NRM rate was 62% in high albumin group versus 17% in low albumin group (p < 0.001). However, no difference of relapse incidence was noted between the two groups. The cumulative incidence of overall acute GVHD, grades 2/4, grades 3/4 at day 120 and overall chronic GVHD at 2 years was 67%, 59%, 16% and 45% in high albumin group versus 72%, 70%, 49% and 39% in low albumin group, suggesting higher incidence of grade 3/4 acute GVHD in low albumin group vs high. In multivariate analysis, serum albumin level < 32 g/l at 4 weeks was confirmed as an independent adverse risk factor for NRM (p=0.04, HR 2.81) together with acute GVHD grades 3/4 (p 0.01, HR 3.79) and chronic GVHD (p²0.001, HR 0.21). For OS, albumin level was not confirmed as an independent risk factor, but acute GVHD grade 3/4 (p< 0.001, HR 3.36) and chronic GVHD (p <0.001, HR 0.008) were found to be independent factors. For relapse chronic GVHD grade 3-4 was the only independent prognostic factor (p <0.001, HR 0.27). Conclusion: The present study suggested that 1) serum albumin level less than 32 g/l at day 30 can predicts higher risk of non-relapse mortality and 2) dropped serum albumin might be affected by in part the occurrence of severe acute GVHD, and by independent mechanism of gut GVHD. Further study is strongly warranted to confirm the prognostic role of serum albumin level on transplant outcomes in a prospectively designed study. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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Serum albumin and beta-amyloid deposition in the human brain

Neurology ◽

10.1212/wnl.0000000000010005 ◽

2020 ◽

Vol 95 (7) ◽

pp. e815-e826

Author(s):

Jee Wook Kim ◽

Min Soo Byun ◽

Jun Ho Lee ◽

Dahyun Yi ◽

So Yeon Jeon ◽

...

Keyword(s):

Confidence Interval ◽

Serum Albumin ◽

Human Brain ◽

Odds Ratio ◽

Serum Albumin Level ◽

Continuous Variable ◽

Albumin Level ◽

Cerebral White Matter ◽

Low Serum ◽

High Albumin

ObjectivesTo investigate the relationships of serum albumin with in vivo Alzheimer disease (AD) pathologies, including cerebral β-amyloid (Aβ) protein deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMH), in the human brain.MethodsA total of 396 older adults without dementia underwent comprehensive clinical assessments, measurement of serum albumin level, and multimodal brain imaging, including [11C] Pittsburgh compound B-PET, 18F-fluorodeoxyglucose-PET, and MRI. Serum albumin was categorized as follows: <4.4 g/dL (low albumin), 4.4 to 4.5 g/dL (middle albumin), and >4.5 g/dL (high albumin; used as a reference category). Aβ positivity, AD-signature region cerebral glucose metabolism (AD-CM), AD-signature region cortical thickness (AD-CT), and WMH volume were used as outcome measures.ResultsSerum albumin level (as a continuous variable) was inversely associated with Aβ deposition and Aβ positivity. The low albumin group showed a significantly higher Aβ positivity rate compared to the high albumin group (odds ratio 3.40, 95% confidence interval 1.67–6.92, p = 0.001), while the middle albumin group showed no difference (odds ratio 1.74, 95% confidence interval 0.80–3.77, p = 0.162). Neither serum albumin level (as a continuous variable) nor albumin categories were related to AD-CM, AD-CT, or WMH volume.ConclusionsLow serum albumin may increase the risk of AD dementia by elevating amyloid accumulation. In terms of AD prevention, more attention needs to be paid to avoid a low serum albumin level, even within the clinical normal range, by clinicians.

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Serum albumin level can predict disease progression in patients with HIV infection

PsycEXTRA Dataset ◽

10.1037/e556822006-018 ◽

2000 ◽

Keyword(s):

Hiv Infection ◽

Serum Albumin ◽

Disease Progression ◽

Serum Albumin Level ◽

Albumin Level ◽

Predict Disease Progression

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Fibrin Polymerization Defect in HIV-infected Patients-Evidence for a Critical Role of Albumin in the Prolongation of Thrombin and Reptilase Clotting Times

Thrombosis and Haemostasis ◽

10.1055/s-0038-1653779 ◽

1995 ◽

Vol 73 (03) ◽

pp. 349-355 ◽

Cited By ~ 4

Author(s):

Pierre Toulon ◽

Elyane Frere ◽

Claude Bachmeyer ◽

Nathalie Candia ◽

Philippe Blanche ◽

...

Keyword(s):

Critical Role ◽

Human Albumin ◽

Albumin Level ◽

Final Concentration ◽

Albumin Concentration ◽

Clotting Time ◽

Fibrin Polymerization ◽

Small Series ◽

Group 1

SummaryThrombin clotting time (TCT) and reptilase clotting time (RCT) were found significantly prolonged in a series of 72 HIV-infected patients drawn for routine coagulation testing. Both TCT and RCT were highly significantly correlated with albumin (r = -0.64, and r = -0.73 respectively, p<0.0001). TCT and RCT were significantly higher (p<0.0001) in a series of 30 other HIV-infected patients selected on their albumin level below 30.0 g/l (group l) than in 30 HIV-infected patients with albumin level above 40.0 g/l or in 30 HIV-negative controls; the two latter groups were not different. In vitro supplementation of plasma from group 1 patients with purified human albumin up to 45.0 g/l (final concentration) lead to a dramatic shortening effect on both TCT and RCT, which reached normal values. The TCT and RCT of the purified fibrinogen solutions (2.0 g/l final concentration) were not different in the three groups, and normal polymerization curves were obtained in all cases. This further ruled out the presence of any dysfibrinogenemia in the plasma from group 1 patients. Using purified proteins, highly significant correlations were demonstrated between the albumin concentration and the prolongations of both TCT and RCT, which were of the same magnitude order than those found in the patients plasma. These results suggest that hypo-albuminemia is responsible for the acquired fibrin polymerization defect reported in HIV-infected patients. The pathophysiological implication of the low albumin levels was suggested by the finding of decreased albumin levels (associated with prolonged TCT and RCT) in a small series of the eight HIV-infected patients who developed thrombotic complications.

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