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BACKGROUND: Plasma cell myeloma (PCM) is characterized by hypercalcemia, renal impairment, anemia, and bone destruction. While pleural effusion, ascites, abdominal pain, and bloody stool are common manifestations of lung disease or gastrointestinal disorders, they are rarely observed in patients with PCM. CASE SUMMARY: A 66-year-old woman presented with complaints of recurrent chest tightness, wheezing, and abdominal bloating accompanied by bloody stools. Computed tomography revealed pleural effusion and ascites. Pleural effusion tests showed inflammation, but the T-cell spot test and carcinoembryonic antigen were negative. Endoscopy showed colonic mucosal edema with ulcer formation and local intestinal lumen stenosis. Echocardiography revealed enlarged atria and reduced left ventricular systolic function. The diagnosis remained unclear. Further testing revealed elevated blood light chain lambda and urine immunoglobulin levels. Blood immunofixation electrophoresis was positive for immunoglobulin G lambda type. Smear cytology of the bone marrow showed a high proportion of plasma cells, accounting for about 4.5%. Histopathological examination of the bone marrow suggested PCM. Flow cytometry showed abnormal plasma cells with strong expression of CD38, CD138, cLambda, CD28, CD200, and CD117. Fluorescence in situ hybridization gene testing of the bone marrow suggested 1q21 gene amplification, but cytogenetic testing showed no clonal abnormalities. Colonic mucosa and bone marrow biopsy tissues were negative for Highman Congo red staining. The patient was finally diagnosed with PCM. CONCLUSION: A diagnosis of PCM should be considered in older patients with pleural effusion, ascites, and multi-organ injury.
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BACKGROUND: Pathogenesis and effective therapeutics of chronic pancreatic inflammation and fibrosis remain uncertain. PURPOSE: To investigate the effects of sulfasalazine (SF) on pancreatic inflammation and fibrogenesis. METHODS: Chronic pancreatic injury in rats was induced by diethyldithiocarbamate (DDC) and interfered by SF through intraperitoneal injection. The rats were divided into five groups: group N, normal control group, rats were treated with dilated water only; group DS1, rats received SF (10 mg/kg) 2 hours before DDC treatment; group DS2, rats were treated with DDC and then SF (100 mg/kg, twice a week); group DS3, rats were treated with DDC, then SF (100 mg/kg, thrice a week); and group DDC, rats were treated with DDC only. Pancreatic inflammation and fibrosis were determined by hematoxylin and eosin staining and Sirius red staining. The genes and proteins related to NF-κB pathway and fibrogenesis including NF-κB/p65, TNF-α, ICAM-1, α-SMA, and Con 1 were detected by immunohistochemical staining, reverse transcription polymerase chain reaction, and Western blotting. RESULTS: Rats in the DDC and DS1 groups showed the highest histological scores after DDC treatment, but the scores of DS2 and DS3 groups decreased significantly when compared with the DDC group. Sirius red staining showed collagen formation clearly in DDC and DS1 rats rather than in DS2 and DS3 rats. NF-κB/p65, ICAM-1, and α-SMA were strongly expressed in DDC and DS1 rats, while DS2 and DS3 rats showed mild to moderate expression by immunohistochemistry. Reverse transcription polymerase chain reaction showed increased levels of NF-κB/p65, ICAM-1, TNF-α, α-SMA, and Con 1 mRNA in DDC and DS1 rats in comparison to normal controls. The mRNA levels of these molecules in DS2 and DS3 rats were significantly lower than those in DS1 and DDC rats. Western blotting demonstrated that the NF-κB/p65, ICAM-1, and α-SMA expressions in pancreatic tissues of the rats of the DDC group were more clear than those of the normal control, DS2, and DS3 rats. CONCLUSION: SF inhibits pancreatic inflammation and fibrogenesis via NF-κB signaling pathway.
Asunto(s)
Inflamación/tratamiento farmacológico , FN-kappa B/metabolismo , Estrés Oxidativo , Páncreas/efectos de los fármacos , Páncreas/patología , Sulfasalazina/farmacología , Sulfasalazina/uso terapéutico , Animales , Fibrosis/tratamiento farmacológico , Inyecciones Intraperitoneales , Páncreas/metabolismo , Ratas , Ratas Wistar , Transducción de Señal/efectos de los fármacos , Sulfasalazina/administración & dosificaciónRESUMEN
Hepatocellular carcinoma (HCC) typically originates from HBV or HCV associated liver cirrhosis. Primary Sjögren's syndrome (pSS) is a kind of autoimmune disease. A sixty-two year old female patient with mild liver damage was diagnosed with pSS after excluding viral, alcoholic and drug-induced hepatitis according to serum immunological detection and liver biopsy. But when she was hospitalized for a second time two years later, a CT scan revealed liver neoplasm. Surgery confirmed HCC and liver cirrhosis by pathology. The elevated level of AFP recovered to normal after tumorectomy. In conclusion, HCC might be a candidate outcome in patients with pSS; it is the doctors' responsibility to keep this kind of patient under surveillance.
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Carcinoma Hepatocelular/etiología , Neoplasias Hepáticas/etiología , Síndrome de Sjögren/complicaciones , Biopsia , Carcinoma Hepatocelular/sangre , Carcinoma Hepatocelular/diagnóstico , Carcinoma Hepatocelular/cirugía , Quimioterapia Adyuvante , Femenino , Hepatectomía , Humanos , Cirrosis Hepática/etiología , Neoplasias Hepáticas/sangre , Neoplasias Hepáticas/diagnóstico , Neoplasias Hepáticas/cirugía , Persona de Mediana Edad , Síndrome de Sjögren/diagnóstico , Tomografía Computarizada por Rayos X , Resultado del Tratamiento , alfa-Fetoproteínas/metabolismoRESUMEN
BACKGROUND/AIMS: High-fat diets contribute to pancreatic fibrogenesis, but the pathogenesis remains unclear. This study investigated the role of nuclear factor kappa B (NF-κB) in high-fat diet-induced pancreatic fibrosis in rats. METHODS: Male Wistar rats were fed a high-fat diet or standard normal chow for 20 weeks. Pancreatic fibrosis was determined by Sirius red staining. Immunohistochemical staining, reverse transcription-polymerase chain reaction and Western blotting were used to identify NF-κB-associated genes or protein expressions. RESULTS: Inflammation, fat deposition, pancreatic stellate cell activation and fibrosis were observed in the pancreases of the high-fat diet group. NF-κB subunit p65 (NF-κB/p65) expression was localized to the nucleus, and intercellular adhesion molecule 1 (ICAM-1) was over-expressed. Pancreatic gene expression levels of NF-κB/p65, ICAM-1 and tumor necrosis factor α were all elevated significantly in rats fed a high-fat diet compared with control rats. Western blotting also revealed significantly increased levels of ICAM-1 and nuclear NF-κB/p65 in rats fed high-fat diets comparison with control rats. CONCLUSIONS: NF-κB is involved in high-fat diet-related pancreatic fibrosis.
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Epigallocatechin gallate (EGCG), a major component of green tea extracts, is known to have anti-fibrotic properties in many organs. The aim of present study was to investigate effects of EGCG on rat pancreatic fibrosis induced by diethyldithiocarbamate (DDC). Oral gavages of different dose of EGCG (50, 100 and 200 mg/kg daily for 8 weeks) ameliorated histological changes and significantly suppressed collagen deposition in a dose-dependent manner. Meanwhile, administration of EGCG inhibited overexpression of TGF-beta1 and alpha-smooth muscle actin (a symbol of activation of pancreatic stellate cells). Moreover, EGCG has a potent influence on expression of Smads (downstream transcription factor of TGF-beta1). EGCG suppressed the expression of Smad3 and enhanced the expression of Smad7. In conclusion, our results demonstrated that EGCG attenuated rat pancreatic fibrosis induced by DDC and therefore may be an anti-fibrogenic candidate in the pancreatic fibrosis.
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Catequina/análogos & derivados , Enfermedades Pancreáticas/tratamiento farmacológico , Enfermedades Pancreáticas/patología , Actinas/antagonistas & inhibidores , Administración Oral , Animales , Catequina/administración & dosificación , Catequina/química , Catequina/farmacología , Catequina/uso terapéutico , Colágeno/metabolismo , Ditiocarba/toxicidad , Relación Dosis-Respuesta a Droga , Fibrosis/tratamiento farmacológico , Fibrosis/patología , Histocitoquímica , Inmunohistoquímica , Masculino , Estructura Molecular , Peso Molecular , Músculo Liso/química , Enfermedades Pancreáticas/inducido químicamente , ARN Mensajero/metabolismo , Distribución Aleatoria , Ratas , Ratas Wistar , Proteína smad3/antagonistas & inhibidores , Proteína smad7/metabolismo , Factores de Tiempo , Factor de Crecimiento Transformador beta1/antagonistas & inhibidoresRESUMEN
Relations between hyperlipidemia and chronic pancreatitis remain unclear. Microcirculatory disturbances and oxidative stress are involved in pathogeneses of a high numbers of diseases. The objective of this study was to induce hyperlipidemia in rats by long-term high-fat diet intake, then investigate the biochemical, microcirculatory, and histological alterations in blood and pancreatic tissues of these animals, and discuss their potential significances. Pancreatic blood flow was detected by intravital microscope; malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured in pancreatic tissues for assessment of oxidative stress and alpha-smooth muscle actin (alpha-SMA) expression was determined by immunohistochemical staining and RT-PCR. The results showed that the velocity of pancreatic microvascular blood flow of rats with hyperlipidemia decreased significantly as compared to control value (p = 0.008). Pancreatic MDA content increased whereas SOD activity decreased in these rats (p = 0.022; p = 0.039, respectively). Histologically, microvesicles in acinar and islet cells, dilated rough endoplasmic reticulum, swollen mitochondrion and modified vascular endothelial cells were observed under light microscope and transmission electron microscope. In addition, alpha-SMA expression was up-regulated significantly (p < 0.05). These results suggest that long-term high-fat diet can induce chronic pancreatic injuries which could be considered as "nonalcoholic fatty pancreatic disease", and pancreatic microcirculatory disturbances and oxidative stress may play an important part in the underlying pathogenesis.
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Grasas de la Dieta/efectos adversos , Microcirculación/fisiopatología , Enfermedades Pancreáticas/inducido químicamente , Enfermedades Pancreáticas/fisiopatología , Especies Reactivas de Oxígeno/metabolismo , Adaptación Fisiológica/efectos de los fármacos , Animales , Hiperlipidemias , Masculino , Microcirculación/efectos de los fármacos , Microcirculación/patología , Estrés Oxidativo/efectos de los fármacos , Páncreas/irrigación sanguínea , Páncreas/efectos de los fármacos , Páncreas/patología , Páncreas/fisiopatología , Enfermedades Pancreáticas/patología , Ratas , Ratas Wistar , Factores de TiempoRESUMEN
BACKGROUND: It has been reported that serum soluble E-selectin (sE-selectin) may be increased in some inflammatory liver diseases. The purpose of our study was to investigate changes of sE-selectin, T lymphocyte subsets, natural killer (NK) cells, and HBV load in patients with chronic hepatitis B (CHB), analyze the relationship between them, and discuss their significances. METHODS: Fifty-four patients with chronic hepatitis B and fourteen controls were studied. Serum sE-selectin, T lymphocyte subsets, NK cells, and hepatitis B virus (HBV) load were detected by enzyme-linked immunosorbent assay (ELISA), flow cytometry (FCM), and fluorescence quantitative polymerase chain reaction (FQ-PCR), respectively. RESULTS: sE-selectin level in patients with CHB increased significantly than that in controls (p<0.01). The percentages of CD4 positive cells and NK cells decreased while the percentage of CD8 positive cells increased significantly in CHB patients than in controls (p<0.01, respectively). sE-selectin level significantly related to levels of T lymphocyte subsets, NK cells, serum alanine aminotransferase (sALT) and aspartate aminotransferase (sAST) (p<0.01, respectively), but had no relationship with HBV level. CONCLUSION: The sE-selectin levels in patients with chronic hepatitis B increase significantly and correlate to liver inflammation, suggesting that sE-selectin can be considered as an additional useful marker of CHB inflammatory activity, and E-selectin may play part of role in pathogenesis of chronic hepatitis B.
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OBJECTIVE: To study the pathogenesis of abnormal bone metabolism in patients with HBV liver cirrhosis. METHODS: NM-300 signal-energy X-ray absorptiometry system was used to measure the bone mineral density (BMD) in 61 liver cirrhosis patients and 30 age-matched healthy controls. The serum levels of 1,25(OH)2D3, parathyroid hormone (PTH), calcitonin (CT), bone gamma-carboxyglutamic acid-containing protein (BGP), IL-1beta, IL-6, tumor necrosis factor (TNF)alpha and urine crosslaps were also detected in these patients. RESULTS: BMD in patients with HBV liver cirrhosis was lower than those of the controls. The serum levels of 1,25(OH)2D3 and BGP in cirrhosis patients were lower than those in the controls, and they were much lower in the osteoporosis (OP) group than in the non-osteoporosis (NOP) group. The PTH and CT were higher significantly in the patients than in the controls. The changes of serum 1,25(OH)2D3 and BGP were correlated with the changes of BMD. The serum levels of IL-1beta, IL-6, TNFalpha and urine crosslaps in cirrhosis patients were higher than those of the controls, and they were much higher in the OP group than in the NOP group. We also found that the serum levels of IL-1beta, IL-6, TNFalpha and urine crosslaps had a negative correlation with BMD. CONCLUSIONS: These data suggest that bone formation is weakened and bone resorption is increased in patients with HBV liver cirrhosis, 1,25(OH)2D3 plays an important role in abnormal bone formation. Elevation of serum IL-1beta, IL-6, TNFalpha can accelerate bone resorption and cause hepatic bone disease (HBD). Taking 1,25(OH)2D3 and reducing the level of IL-1beta, IL-6, TNFalpha may be very important in preventing and treating HBD.