scholarly journals Systemic lupus erythematous presenting with hemorrhagic shock caused by gastric penetration of pancreatic pseudocyst: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Hideya Itagaki ◽  
Suzuki Katuhiko
Keyword(s):  
Computed Tomography ◽  
Chronic Pancreatitis ◽  
Pleural Effusion ◽  
Disease Activity ◽  
Pancreatic Pseudocyst ◽  
High Disease Activity ◽  
Amylase Level ◽  
Systemic Lupus Erythematous ◽  
Systemic Lupus ◽  
Left Pleural Effusion

Abstract Background Systemic lupus erythematous that causes various organ damage is rarely associated with pancreatic lesion. To the best of our knowledge, no cases presenting with hemorrhage shock caused by gastric penetration of pancreatic pseudocyst due to lupus pancreatitis have been reported. Herein, we report a case of hemorrhage shock caused by gastric penetration of pancreatic pseudocyst due to lupus pancreatitis. Case presentation A 53-year-old Japanese man with a history of systemic lupus erythematous, pancreatic pseudocyst, and chronic pancreatitis complained of epigastric pain and had hematemesis. He visited our emergency room and was admitted in our hospital. Upper endoscopy showed that hemostasis was obtained; however, computed tomography scan was performed since he was suspected to have gastric penetration into hollow viscera. The computed tomography revealed accumulation of fluid around the pancreas and gastric penetration of pancreatic cyst. Blood test showed increased serum amylase level. These results suggest that the exacerbation of chronic pancreatitis causes the penetration. Surgery was considered; however, we took a wait-and-see approach since hemostasis was obtained. After that, he was in stable condition, although he suffered from fever and accumulation of left pleural effusion was observed by computed tomography. However, he had massive hematemesis and melena 9 days after hospitalization and died in spite of several treatments including blood transfusion. Autopsy revealed that he actually had pleural thickening, which is not caused by accumulation of left pleural effusion but by severe pleural inflammation. We therefore performed additional blood and urinary tests on the same day. The test results showed that he had a high titer of anti-double-stranded deoxyribonucleic acid (DNA) antibody, hypocomplementemia, and erythrocyturia, indicating that he had systemic lupus erythematous with high disease activity considering his fever and pleural inflammation. Conclusions Patients who have systemic lupus erythematous with high disease activity have the potential to develop fatal complications due to pancreatitis, so appropriate treatments are required for such patients.

scholarly journals Impacts of FcγRIIB and FcγRIIIA gene polymorphisms on systemic lupus erythematous disease activity index

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Mansoor Karimifar ◽  
Khosro Akbari ◽  
Reza ArefNezhad ◽  
Farshid Fathi ◽  
Mohammad Moosaeepour ◽  
...  
Keyword(s):  
Disease Activity ◽  
Activity Index ◽  
Clinical Manifestations ◽  
Disease Activity Index ◽  
Unknown Etiology ◽  
Systemic Lupus Erythematous ◽  
Nucleotide Polymorphisms ◽  
Systemic Lupus ◽  
Single Nucleotide ◽  
Chronic Autoimmune Disease

Abstract Objective Systemic lupus erythematous (SLE) disease is a chronic autoimmune disease with unknown etiology that can involve different organs. Polymorphisms in Fcγ receptors have been identified as genetic factors in susceptibility to SLE. This study was aimed to investigate effects of two single nucleotide polymorphisms (SNPs) within FcγRIIB and FcγRIIIA genes on systemic lupus erythematous disease activity index (SLEDAI) in an Iranian population. Results Our findings indicated TT and GG genotypes were the common genotypes of FcγRIIB and FcγRIIIA SNPs in SLE patients, respectively. There were no significant differences in genotype and allele frequencies of FcγRIIB and FcγRIIIA SNPs in SLE and healthy subjects. However, the frequencies of genotypes and alleles of FcγRIIB and FcγRIIIA SNPs were significantly associated with some clinical manifestations used to determine SLEDAI (P < 0.001–0.5).

Clinical, neuroimaging and immunological phenotype of South African neuropsychiatric systemic lupus erythematosus patients

Lupus ◽  
2019 ◽  
Vol 28 (5) ◽  
pp. 685-694
Author(s):  
N Mvambo ◽  
A I Bhigjee ◽  
G M Mody
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cerebrovascular Disease ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Large Vessel ◽  
High Disease Activity ◽  
Small Vessel ◽  
Systemic Lupus ◽  
Vessel Disease ◽  
Large Vessel Disease

Neuropsychiatric systemic lupus erythematosus (NPSLE) is an important cause of morbidity and mortality. We undertook this observational retrospective study of patients with NPSLE who had brain magnetic resonance imaging (MRI) to determine the indications for MRI and the correlation of clinical and laboratory findings with MRI. We identified 83 NPSLE patients (84.3% women) seen at Inkosi Albert Luthuli Central Hospital in Durban, South Africa, between June 2003 and May 2017. The mean age at SLE diagnosis was 26.24 ± 12.81 years and the median interval to NPSLE was 11.0 (interquartile range, 4.0–39.0) months. The most common indications for MRI were seizures (45.8%), psychosis (18.1%) and cerebrovascular disease (18.1%). The MRI was abnormal in 68 (81.9%) with small-vessel disease in 65 (78.3%) and large-vessel disease in eight (9.6%). The small-vessel abnormalities were white-matter hyperintensities (WMH) (59.0%), atrophy (55.4%) and lacunae (4.6%). Our patients had high disease activity at NPSLE. Cerebrovascular disease was associated with an abnormal MRI ( p = 0.018) and large-vessel disease ( p = 0.014) on MRI. Our NPSLE patients were younger and had high disease activity, and seizures were more common compared with other studies. The most common MRI abnormalities were WMH and cortical atrophy, in agreement with other studies.

Myeloid-derived suppressor cells contribute to systemic lupus erythaematosus by regulating differentiation of Th17 cells and Tregs

2016 ◽  
Vol 130 (16) ◽  
pp. 1453-1467 ◽  
Author(s):  
Jianjian Ji ◽  
Jingjing Xu ◽  
Shuli Zhao ◽  
Fei Liu ◽  
Jingjing Qi ◽  
...  
Keyword(s):  
Disease Activity ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Suppressor Cells ◽  
Cell Polarization ◽  
High Disease Activity ◽  
Myeloid Derived Suppressor Cells ◽  
Systemic Lupus ◽  
And Function

Although major advancements have made in investigating the aetiology of SLE (systemic lupus erythaematosus), the role of MDSCs (myeloid-derived suppressor cells) in SLE progression remains confused. Recently, some studies have revealed that MDSCs play an important role in lupus mice. However, the proportion and function of MDSCs in lupus mice and SLE patients are still poorly understood. In the present study, we investigated the proportion and function of MDSCs using different stages of MRL/lpr lupus mice and specimens from SLE patients with different activity. Results showed that splenic granulocytic (G-)MDSCs were significantly expanded by increasing the expression of CCR1 (CC chemokine receptor 1) in diseased MRL/lpr lupus mice and in high-disease-activity SLE patients. However, the proportion of monocytic (M-)MDSCs remains similar in MRL/lpr lupus mice and SLE patients. G-MDSCs produce high levels of ROS (reactive oxygen species) through increasing gp91phox expression, and activated TLR2 (Toll-like receptor 2) and AIM2 (absent in melanoma 2) inflammasome in M-MDSCs lead to IL-1β (interleukin 1β) expression in diseased MRL/lpr mice and high-disease-activity SLE patients. Previous study has revealed that MDSCs could alter the plasticity of Th17 (T helper 17) cells and Tregs (regulatory T-cells) via ROS and IL-1β. Co-culture experiments showed that G-MDSCs impaired Treg differentiation via ROS and M-MDSCs promoted Th17 cell polarization by IL-1β in vitro. Furthermore, adoptive transfer or antibody depletion of MDSCs in MRL/lpr mice confirmed that MDSCs influenced the imbalance of Tregs and Th17 cells in vivo. Our results indicate that MDSCs with the capacity to regulate Th17 cell/Treg balance may be a critical pathogenic factor in SLE.

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