IgG4-related retroperitoneal fibrosis: a newly characterized disease.

Retroperitoneal fibrosis (RPF) is a rare disease characterized by chronic, nonspecific inflammatory and sclerotic or fibrotic tissue in the periaortic or periiliac retroperitoneum that encases adjacent structures. There will be a series of clinical manifestations once the proliferated fibrous tissues encase the abdominal aorta, iliac arteries and urinary duct. RPF is generally divided into two types: idiopathic retroperitoneal fibrosis (IRPF) without identified pathogenesis, making up about two-thirds of cases, and secondary retroperitoneal fibrosis. Recent studies on Immunoglobulin G4-related disease (IgG4-RD) reveal that abundant infiltration of IgG4 positive plasma cells is found in biopsies on the mass of RPF of some IRPF patients, which is identified as one spectrum of IgG4-RD and is named IgG4-related RPF. IgG4-related RPF is often misdiagnosed as retroperitoneal visceral malignancy and is treated with surgery. In addition, because of its good response to glucocorticoid, early detection and treatment is important. We review the definition, epidemiology, clinical features, diagnostic criteria, treatment and prognosis of IgG4-related RPF in this article to raise awareness of this newly characterized disease.

Relationship between uric acid and arterial stiffness in the elderly with metabolic syndrome components.

BACKGROUND: High uric acid (UA) levels and metabolic syndrome (MS) are risk factors for atherosclerotic diseases. Brachial-ankle pulse wave velocity (baPWV) is a valid and reproducible measurement by which to assess arterial stiffness and a surrogate marker of atherosclerosis. However, little is known about the relationship between them, especially in elderly Chinese with MS components who are at high risk for atherosclerotic diseases. METHODS: One thousand and twenty Chinese subjects (159 women) older than 60 years of age (mean age (70.6 ± 5.7) years) with at least one MS component underwent routine laboratory tests, and baPWV measurements were analyzed. RESULTS: Participants were divided into four groups by MS components. The mean age did not significantly differ among the MS component groups. We found that not only the diagnostic factors (blood pressure, body mass index (BMI), lipids, glucose) of MS but also baPWV, UA, insulin, homeostasis model of assessment for insulin resistence index (HOMAIR) levels increased, and high density lipoprotein (HDL)-C decreased with an increased number of MS components (test for trend P < 0.05). The association between UA and baPWV was observed after adjustment for gender, age, blood pressure, BMI, serum creatinine and high density lipoprotein, and insulin resistance (r = 0.186, P < 0.0001). There were increases in the odds ratios for the association between the number of components of MS, UA and baPWV, even after adjustment for traditional risk factors. However, after adjustment for insulin or HOMA-IR, there were no significant differences in the multivariate odds ratios among the number of MS components for UA. CONCLUSIONS: The UA level is positively associated with baPWV and MS, but the association between UA and MS is dependent on insulin resistance. Furthermore, baPWV is independently associated with MS in our study population.

The organ specificity in pathological damage of chronic intermittent hypoxia: an experimental study on rat with high-fat diet.

PURPOSE: It is known today that sleep apnea hypopnea syndrome and its characteristic chronic intermittent hypoxia can cause damages to multiple organs, including the cardiovascular system, urinary system, and liver. It is still unclear, however, whether the damage caused by sleep apnea hypopnea syndrome and the severity of the damage are organ-specific. METHODS: This research observed the pathological effects of chronic intermittent hypoxia on rat's thoracic aorta, myocardium, liver, and kidney, under the condition of lipid metabolism disturbance, through establishing the rat model of chronic intermittent hypoxia with high-fat diet by imitating the features of human sleep apnea hypopnea syndrome. In this model, 24 male Wistar rats were randomly divided into three groups: a control group fed by regular diet, a high-fat group fed by high-fat diet, and a high-fat plus intermittent hypoxia group fed by high-fat diet and treated with intermittent hypoxia 7 h a day. At the end of the ninth week, the pathological changes of rat's organs, including the thoracic aorta, myocardium, liver, and kidney are observed (under both optical microscopy and transmission electron microscopy). RESULTS: As the result of the experiment shows, while there was no abnormal effect observed on any organs of the control group, slight pathological changes were found in the organs of the high-fat group. For the high-fat plus intermittent hypoxia group, however, remarkably severer damages were found on all the organs. It also showed that the severity of the damage varies by organ in the high-fat plus intermittent hypoxia group, with the thoracic aorta being the worst, followed by the liver and myocardium, and the kidney being the slightest. CONCLUSIONS: Chronic intermittent hypoxia can lead to multiple-organ damage to rat with high-fat diet. Different organs appear to have different sensitivity to chronic intermittent hypoxia.

An experimental research on chronic intermittent hypoxia leading to liver injury.

PURPOSE: Sleep apnea-hypopnea syndrome and its chronic intermittent hypoxia component may cause multi-system-targeted injury. The latest finding shows that liver is one of the injured organs. The purpose of the study is to observe the dynamic process of the influence that chronic intermittent hypoxia plays on rat liver enzyme, hepatic histology, and ultrastructure based on lipid disorders. METHODS: A total of 72 male Wistar rats were randomly divided into three groups. The control group was fed with a regular chow diet, the high fat group with a high fat diet, and the high fat plus intermittent hypoxia group with a high fat diet with a 7-h/day intermittent hypoxia treatment. Changes were observed in rat liver enzyme, hepatic histology, and ultrastructure of the three groups on the third, sixth, and ninth weeks, respectively. The liver paraffin sections were detected with myeloperoxidase. RESULTS: The liver function and structure of the control group were found to be normal; the liver enzyme level of the high fat group was significantly higher than that of the control group on the sixth and ninth weeks; and the liver enzyme level of the high fat plus intermittent hypoxia group was significantly higher than that of the control group and the high fat group on the third, sixth, and ninth weeks (all P < 0.01). Observed by a light microscope and a transmission electron microscope, the high fat group and the high fat plus intermittent hypoxia group were all characterized by nonalcoholic fatty liver disease: the high fat group was characterized by simple fatty liver on the third and sixth weeks and by steatohepatitis on the ninth week; the damage of the high fat plus intermittent hypoxia group was significantly more severe than that of the high fat group in all the monitoring points, characterized by steatohepatitis on the sixth week and by obvious liver fibrosis on the ninth week; the myeloperoxidase level of the high fat plus intermittent hypoxia group was significantly higher than that of the control group and the high fat group (all P < 0.01). CONCLUSIONS: Under the conditions of high fat and intermittent hypoxia, the injury to the liver function, hepatic histology, and ultrastructure is more severe than that of the high fat group. The injury mainly was characterized by nonalcoholic fatty liver disease and becomes more severe with increased exposure time. Oxidative stress may play an important role in the mechanism.

[Effects of high-fat plus ethanol diet on myocardial ultrastructure in rats].

OBJECTIVE: To study the effects of high-fat plus ethanol diet on myocardial ultrastructure in rats. METHODS: 40 male SD rats in seventy-eight-week old were randomly divided into four groups: group A was control group, fed with common feedstuff; group B was high-fat diet group, freely foraging high-fat feedstuff; group C was ethanol group, the rats were intragastrically administered 60% ethanol solution twice a day by 1 ml/kg; group D was high-fat diet and ethanol group, the rats freely foraged high-fat feedstuff, and ethanol solution was intragastrically administered as before. After 12 weeks, blood samples were taken through jugular vein, the concentration of blood cholesterol (TG), triglycerides (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL) were determined. The cardiac index was also determined for all groups and the cardiac morphous were observed by high resolution Doppler ultrasound, and myocardial ultrastructure was observed by transmission electron microscope. RESULTS: After experiment, TG levels of groups A, B, C, D were (1.07 +/- 0.21), (2.34 +/- 0.72), (1.33 +/- 0.42) and (1.75 +/- 0.65) mmol/L, respectively (F = 8.323, P = 0.000); TC levels were (1.74 +/- 0.38), (5.66 +/- 1.74), (1.70 +/- 0.44) and (5.65 +/- 2.95) mmol/L, respectively (F = 13.670, P = 0.000); HDL levels were (0.65 +/- 0.11), (2.99 +/- 0.54), (0.52 +/- 0.13) and (2.06 +/- 0.26) mmol/L, respectively (F = 112.225, P = 0.000); LDL levels were (0.74 +/- 0.22), (1.87 +/- 0.90), (0.60 +/- 0.26) and (1.54 +/- 0.78) mmol/L, respectively (F = 7.318, P = 0.001); Apo-A1 levels were (0.25 +/- 0.10), (0.31 +/- 0.14), (0.21 +/- 0.05) and (0.36 +/- 0.11) g/L, respectively (F = 3.015, P = 0.047); Apo-B levels were (0.18 +/- 0.03), (0.11 +/- 0.04), (0.16 +/- 0.03) and (0.39 +/- 0.13) g/L, respectively (F = 15.621, P = 0.000); ALT levels were (111.25 +/- 20.18), (447.13 +/- 89.25), (173.13 +/- 44.01) and (198.25 +/- 39.81) U/L, respectively (F = 58.708, P = 0.000); AST levels were (105.50 +/- 9.99), (483.00 +/- 16.80), (120.75 +/- 5.09) and (276.88 +/- 10.48) U/L, respectively (F = 1906.624, P = 0.000);TBIL levels were (1.35 +/- 0.12), (1.66 +/- 0.18), (1.89 +/- 0.15) and (2.68 +/- 0.35)U/L, respectively (F = 55.006, P = 0.000); cardiac indexes were (3.02 +/- 0.22)%, (3.21 +/- 0.16)%, (3.26 +/- 0.26)% and (3.43 +/- 0.27)%, respectively (F = 16.150, P = 0.000). There were changes of cardiac morphous in group C and D, but not in group A and B; the myocardial ultrastructure was normal in Group A, but light to heavy changes were found in group B, C and D. CONCLUSION: High-fat diet and excessive intake of ethanol significantly induce abnormal lipid metabolism. High-fat diet induces the changes of myocardial ultrastructure before cardiac morphous and electrocardiogram, and intake of ethanol changes cardiac muscle in microstructure and macroscopy. High-fat diet plus ethanol may worsen this injury farther.

Sleep apnea hypopnea syndrome and liver injury.

OBJECTIVE: A general review was made of studies involving: (1) the relationship between sleep apnea hypopnea syndrome/sleep apnea style intermittent hypoxia and liver injury and (2) the mechanism that causes the liver injury. DATA SOURCES: The data used in this review were mainly from Medline and PubMed published in English from 1993 to February 2009. The search term was "sleep apnea hypopnea syndrome". STUDY SELECTION: (1) Clinical and laboratory evidence that sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia leads to liver injury; (2) the mechanism that causes the liver injury. RESULTS: The effect of sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia on the liver function is characterized by serum aminotransferase elevation. The liver histological injury includes hepatic steatosis, hepatocyte ballooning, lobular inflammation, lobular necrosis, and liver fibrosis. Sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia can cause insulin resistance and oxidative stress. CONCLUSIONS: Sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia can lead to chronic liver injury, which, in most cases, is shown as nonalcoholic fatty liver disease. Insulin resistance and oxidative stress caused by sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia play an important role in the mechanism of chronic liver disease development.

[A study on non-invasive indexes of atherosclerosis in obstructive sleep apnea-hypopnea syndrome patients].

OBJECTIVE: To investigate the relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and atherosclerosis through determining flow-mediated dilation (FMD), pulse wave velocity (PWV) and carotid intima-media thickness (CIMT). METHODS: FMD, PWV and CIMT were measured in 76 OSAHS patients (68 men/8 women) and 76 control subjects matched for age, sex and body mass index. FMD, PWV and CIMT were compared between the two groups. In the OSAHS group, correlations were calculated between apnea-hypopnea index (AHI) and FMD, PWV and CIMT. RESULTS: Compared to the control group, the OSAHS group had significantly higher PWV [(1,720 +/- 247) cm/s vs (1,469 +/- 172) cm/s, P < 0.01] and CIMT [(1.10 +/- 0.34) mm vs (0.80 +/- 0.18) mm, P < 0.01], but significantly lower FMD [(5.8 +/- 1.7)% vs (8.9 +/- 1.4)%, P < 0.01]. When patients with hypertension from the two groups were compared, PWV [(1,850 +/- 244) cm/s vs (1,655 +/- 161) cm/s, P = 0.001] and CIMT [(1.24 +/- 0.35) mm vs (0.99 +/- 0.18) mm, P = 0.003] were significantly higher, and FMD [(5.2 +/- 1.7)% vs (7.5 +/- 1.1)%, P < 0.01] was significantly lower in the OSAHS group (n = 43) than in the control group (n = 21). In the OSAHS group, AHI was correlated positively with PWV and CIMT (r = 0.883, 0.698, all P < 0.01), but negatively with FMD (r = -0.711, P < 0.01). CONCLUSION: Vascular endothelial dysfunction and atherosclerosis are present in OSAHS patients, and related to the severity of OSAHS.