scholarly journals Low serum levels of complement C3c at diagnosis indicate poor outcome in ANCA-associated glomerulonephritis

Author(s):  
Désirée Tampe ◽  
Eva Baier ◽  
Samy Hakroush ◽  
Björn Tampe
Keyword(s):  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jae Hwa Kim ◽  
Go-Tak Kim ◽  
Siyeoung Yoon ◽  
Hyun Il Lee ◽  
Kyung Rae Ko ◽  
...  

Abstract Background Vitamin B12 (Vit B12) deficiency results in elevated homocysteine levels and interference with collagen cross-linking, which may affect tendon integrity. The purpose of this study was to investigate whether serum Vit B12 levels were correlated with degenerative rotator cuff (RC) tear. Methods Eighty-seven consecutive patients with or without degenerative RC tear were enrolled as study participants. Possible risk factors (age, sex, medical history, bone mineral density, and serum chemistries including glucose, magnesium, calcium, phosphorus, zinc, homocysteine, Vitamin D, Vit B12, homocysteine, and folate) were assessed. Significant variables were selected based on the results of univariate analyses, and a logistic regression model (backward elimination) was constructed to predict the presence of degenerative RC tear. Results In the univariate analysis, the group of patients with degenerative RC tear had a mean concentration of 528.4 pg/mL Vit B12, which was significantly lower than the healthy control group (627.1 pg/mL). Logistic regression analysis using Vit B12 as an independent variable revealed that Vit B12 concentrations were significantly correlated with degenerative RC tear (p = 0.044). However, Vit B12 levels were not associated with tear size. Conclusion Low serum levels of Vit B12 were independently related to degenerative RC tear. Further investigations are warranted to determine if Vit B12 supplementation can decrease the risk of this condition.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jung-Lung Hsu ◽  
Ming-Feng Liao ◽  
Chun-Che Chu ◽  
Hung-Chou Kuo ◽  
Rong-Kuo Lyu ◽  
...  

AbstractOur study aimed to investigate the incidence, risk factors and time to occurrence of malignancy in patients with dermatomyositis (DM) and polymyositis (PM). The electronic medical records of 1100 patients with DM and 1164 patients with PM were studied between January 2001 and May 2019. Malignancies after myositis were diagnosed in 61 (5.55%) patients with DM and 38 (3.26%) patients with PM. The cumulative incidence of malignancies in patients with DM were significantly higher than patients with PM (hazard ratio = 1.78, log-rank p = 0.004). Patients with DM had a greater risk of developing malignancy than those with PM at 40–59 years old (p = 0.01). Most malignancies occurred within 1 year after the initial diagnosis of DM (n = 35; 57.38%). Nasopharyngeal cancer (NPC) was the most common type of malignancy in patients with DM (22.95%), followed by lung, and breast cancers. In patients with PM, colorectal, lung and hepatic malignancies were the top three types of malignancy. The risk factors for malignancy included old age (≥ 45 years old) and low serum levels of creatine phosphokinase (CPK) for patients with DM and male sex and low serum levels of CPK for patients with PM. Low serum levels of CPK in patients with myositis with malignancy represented a low degree of muscle destruction/inflammation, which might be attributed to activation of the PD-L1 pathway by tumor cells, thus inducing T-cell dysfunction mediating immune responses in myofibers. A treatment and follow-up algorithm should explore the occurrence of malignancy in different tissues and organs and suggested annual follow-ups for at least 5.5 years to cover the 80% cumulative incidence of malignancy in patients with DM and PM.


2021 ◽  
Author(s):  
Kárita Cláudia Freitas Lidani ◽  
Fabiana Antunes Andrade ◽  
Marcia Holsbach Beltrame ◽  
Indira Chakravarti ◽  
Maria Regina Tizzot ◽  
...  

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Inès Dufour ◽  
Alexis Werion ◽  
Leila Belkhir ◽  
Anastazja Wisniewska ◽  
Marie Perrot ◽  
...  

Abstract Background The severity of coronavirus disease 2019 (COVID-19) is highly variable between individuals, ranging from asymptomatic infection to critical disease with acute respiratory distress syndrome requiring mechanical ventilation. Such variability stresses the need for novel biomarkers associated with disease outcome. As SARS-CoV-2 infection causes a kidney proximal tubule dysfunction with urinary loss of uric acid, we hypothesized that low serum levels of uric acid (hypouricemia) may be associated with severity and outcome of COVID-19. Methods In a retrospective study using two independent cohorts, we investigated and validated the prevalence, kinetics and clinical correlates of hypouricemia among patients hospitalized with COVID-19 to a large academic hospital in Brussels, Belgium. Survival analyses using Cox regression and a competing risk approach assessed the time to mechanical ventilation and/or death. Confocal microscopy assessed the expression of urate transporter URAT1 in kidney proximal tubule cells from patients who died from COVID-19. Results The discovery and validation cohorts included 192 and 325 patients hospitalized with COVID-19, respectively. Out of the 517 patients, 274 (53%) had severe and 92 (18%) critical COVID-19. In both cohorts, the prevalence of hypouricemia increased from 6% upon admission to 20% within the first days of hospitalization for COVID-19, contrasting with a very rare occurrence (< 1%) before hospitalization for COVID-19. During a median (interquartile range) follow-up of 148 days (50–168), 61 (12%) patients required mechanical ventilation and 93 (18%) died. In both cohorts considered separately and in pooled analyses, low serum levels of uric acid were strongly associated with disease severity (linear trend, P < 0.001) and with progression to death and respiratory failure requiring mechanical ventilation in Cox (adjusted hazard ratio 5.3, 95% confidence interval 3.6–7.8, P < 0.001) or competing risks (adjusted hazard ratio 20.8, 95% confidence interval 10.4–41.4, P < 0.001) models. At the structural level, kidneys from patients with COVID-19 showed a major reduction in urate transporter URAT1 expression in the brush border of proximal tubules. Conclusions Among patients with COVID-19 requiring hospitalization, low serum levels of uric acid are common and associate with disease severity and with progression to respiratory failure requiring invasive mechanical ventilation.


1980 ◽  
Vol 94 (3) ◽  
pp. 341-345 ◽  
Author(s):  
Jens Faber ◽  
Carsten Kirkegaard ◽  
Ib Bo Lumholtz ◽  
Kaj Siersbæk-Nielsen ◽  
Thorkild Friis

Abstract. Serum levels of thyroxine, 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2), 3',5'-diiodothyronine (3',5'-T2) and TSH were measured in two clinical situations which are both known to induce a low serum T3 high serum rT3 syndrome: 1) during the early course of acute myocardial infarction (AMI) and after recovery, and 2) before and during one week's propranolol medication (20 mg 4 times a day). In 10 patients with AMI serum levels of the iodothyronines were unchanged on admission to hospital (in average 6.6 h after onset of symptoms). However, already 24 h after onset of symptoms serum T3 and 3,3'T2 were reduced whereas serum rT3 and 3',5'-T2 were increased. Serum T3 and 3,3'-T2 reached a nadir on day 4 and 3, respectively, whereas serum rT3 and 3',5'-T2 reached peak values 24 h after onset of symptoms. In eight healthy, euthyroid volunteers propranolol medication induced similar changes in iodothyronine concentration as AMI did. However, the alterations were more delayed. Serum T3 decreased slowly reaching statistically significantly reduced values on day 7. Serum rT3 and 3',5'-T2 were significantly enhanced from day 3 and 4, respectively. A close parallelism in alterations of serum T3 and 3,3'-T2 levels was observed. Our data suggest that T3 in the two situations studied is a major precursor for 3,3'-T2 probably as a consequence of reduced 5'-deiodinase activity. It seems possible that the mechanisms affecting the metabolism of the iodothyronines in AMI and during propranolol medication involved the same enzyme system. However, the late appearance of the alterations in serum iodothyronines levels during propranolol medication might indicate different modes of action.


2009 ◽  
Vol 4 ◽  
pp. BMI.S1115 ◽  
Author(s):  
Anthony J. Russo ◽  
Lauren Neville ◽  
Christine Wroge

Aim Deficiency of Alpha-1-antitrypsin (AAT) can be a genetic condition that increases the risk of developing liver, lung and possibly gastrointestinal disease. Since many autistic children also have gastrointestinal disorders, this study was designed to measure serum concentration of AAT and establish AAT genotypes in autistic children, age and gender matched non-autistic siblings, parents and controls. Subjects and Methods We used an indirect ELISA with monoclonal IgG to AAT to measure AAT serum concentrations in 71 members from 16 families of individuals with autism and 18 controls (no family history of autism). We used a duplex polymerase chain reaction to detect M, S and Z alleles for alpha-1 antitrypsin expression in 52 members of 12 of the above families. Results A significantly high number of autistic family members had lower than normal serum levels of AAT when compared to controls. Autistic children with regressive onset had significantly lower levels of AAT compared to controls, and a significant number of autistic children with low serum AAT also had hyperbilirubinemia, gastrointestinal disease and respiratory problems. We also found that a significantly high number of these individuals had the PiMZ genotype and correspondingly low levels of serum alpha-1 antitrypsin. Discussion Knowing that low levels of alpha-1 antitrypsin may be inherited, and that low levels of AAT may be associated with GI disease in autistic children, genotyping autistic children may help identify individuals susceptible to developing digestive problems.


2019 ◽  
Vol 109 ◽  
pp. 1411-1416 ◽  
Author(s):  
Paola Caroline Lacerda Leocádio ◽  
Penélope Lacrísio dos Reis Menta ◽  
Melissa Tainan Silva Dias ◽  
Júlia Rodrigues Fraga ◽  
Alessandra Carvalho Goulart ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Muhammad M. Aslam ◽  
Peter John ◽  
Attya Bhatti ◽  
Sidrah Jahangir ◽  
M. I. Kamboh

Rheumatoid arthritis (RA) is a systemic multifactorial autoimmune disorder. The interactions between diverse environmental and genetic factors lead to the onset of this complex autoimmune disorder. Serum levels of vitamin D (VD) are involved in the regulation of various immune responses. Vitamin D is a key signaling molecule in the human body that maintains calcium as well as phosphate homeostasis. It also regulates the functions of the immune system and, thus, can play a substantial role in the etiology of various autoimmune disorders, including RA. Low serum VD levels have been found to be associated with a higher risk of RA, although this finding has not been replicated consistently. The molecular mechanisms by which VD influences autoimmunity need to be further explored to understand how variation in plasma VD levels could affect the pathogenesis of RA. This mini-review focuses on the influence of VD and its serum levels on RA susceptibility, RA-associated complexities, treatment, and transcriptome products of key proinflammatory cytokines, along with other cytokines that are key regulators of inflammation in rheumatoid joints.


2011 ◽  
Vol 54 ◽  
pp. S449-S450
Author(s):  
M. Arciello ◽  
S. Petta ◽  
B. Conti ◽  
V. Leoni ◽  
G. Iannucci ◽  
...  

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