Lactation breast abscess treated with Gualou Xiaoyong decoction and painless lactation manipulation: A case report and review of literature.

BACKGROUND: Breast abscess during lactation is a severe complication of acute mastitis, which can lead to discomfort, high fever, breast fistula, sepsis, septic shock, breast damage, disease persistence and frequent hospitalization. Breast abscesses may also lead the mother to discontinue breastfeeding, thereby harming the infant's health. The predominant pathogenic bacteria are Staphylococcus aureus, Staphylococcus epidermidis and Streptococcus. The incidence of breastfeeding abscesses in breastfeeding women ranges between 4.0% and 11.0%. In cases of breast abscess, the rate of cessation of lactation is 41.0%. In instances of breast fistula, the rate of cessation of lactation is very high (66.7%). Furthermore, 50.0% of women with breast abscesses must be hospitalized and treated with intravenous antibiotics. Treatment includes antibiotics, abscess puncture and surgical incision and drainage. The patients suffer from stress, pain and easily induced breast scarring; the disease's progression is prolonged and recurrent, interfering with infant feeding. Consequently, it is crucial to discover an adequate cure. CASE SUMMARY: A 28-year-old woman with a breast abscess was treated with Gualou Xiaoyong decoction and painless breast opening manipulation 24 d after cesarean delivery. On the 2nd d of treatment, the patient's breast mass was significantly reduced, the pain was significantly reduced, and the general asthenia was improved. All conscious symptoms disappeared after 3 d, breast abscesses faded after 12 d of treatment, inflammation images disappeared after 27 d, and normal lactation images were restored. CONCLUSION: In treating breast abscesses during breastfeeding, the combination of Gualou Xiaoyong decoction and painless lactation provides a positive therapeutic impact. This disease's treatment offers the advantages of a short course of treatment, no need to discontinue breastfeeding and the ability to rapidly mitigate symptoms, which can be used as a reference in clinical practice.

Efficacy and safety of coenzyme A versus fenofibrate in patients with hyperlipidemia: a multicenter, double-blind, double-mimic, randomized clinical trial.

Background: We investigated the lipid-lowering efficacy and safety of coenzyme A (CoA) versus fenofibrate in Chinese patients with moderate dyslipidemia.Methods: A total of 417 subjects (aged 18-75 years) diagnosed with moderate dyslipidemia (triglyceride 2.3-6.5 mmol/L) from 13 large cardiovascular centers in China were recruited and randomly divided into a fenofibrate group (n = 207), which received 200 mg of fenofibrate orally once daily, and a CoA group (n = 210), which received 400 mg of CoA orally once a day. Blood lipoproteins, liver and renal function, creatine kinase, and blood glucose were measured at baseline, and after 4 and 8 weeks of treatment.Results: The baseline triglyceride (TG) level in the fenofibrate group and the CoA group was 3.39 ± 0.99 mmol/L and 3.60 ± 1.11 mmol/L, respectively. After treatment for 4 and 8 weeks with fenofibrate, TG was reduced by 31.62% and 33.13%. In the CoA group, TG was reduced by 17.29% and 23.80%. Compared with baseline, total cholesterol (TC) was significantly decreased in both groups after either 4 or 8 weeks of treatment (p < .05). CoA increased high-density lipoprotein cholesterol (HDL-C) after 4 weeks of treatment, whereas it had no significant effect on HDL-C after 8 weeks of treatment. Low-density lipoprotein cholesterol (LDL-C) was not modified in either group. The incidence of side effects was significantly lower in the CoA group compared with the fenofibrate group (p < .05).Conclusions: Compared with fenofibrate, CoA has less effect on reducing plasma TG levels in subjects with moderate dyslipidemia. However, it has fewer adverse effects.

[Relationship between factors of labour pain and delivery outcomes].

OBJECTIVE: To evaluate factors associated with labor pain and delivery outcomes. METHODS: From Jul. to Dec. 2009, 111 normal singleton cephalic presentation pregnancies (including 5 elderly parturient) who delivered at the Department of Obstetrics and Gynecology, Second Affiliated Hospital, Zhejiang Chinese Medical University were enrolled in this study to evaluate the relationship between factors of labor pain and delivery outcomes. The labor pain of latent phase and active phase were scored by the visual analogue scale (VAS). Factors associated with pain included the age of parturient, the number of gravidity and parity, occupation, education profile, dwell location, etc. The questionnaire was designed by ourselves. Childbirth awareness, psychological preparation of delivery, emotional controllability, couple relationship, the relationship of parturient and mother-in-law, the relationship of parturient and parents, family economic status, use of sedative during the labor process and delivery outcomes were collected and analyzed. RESULTS: (1) Factors associated with pain: in the latent phase, the rate of moderate labour pain of 1/5 in women with more than 35 years old was statistically lower than 76.4% (81/106) in suitable age group (P < 0.05). The women with a good understanding about delivery had a statistically lower rate of moderate pain of 64.7% (44/68) than 88.4% (38/43) of those having a poor understanding (P < 0.05). The women who had a better couple relationship had a significantly higher rate of moderate pain of 77.2% (78/101) than 4/10 of those who had a general couple relationship (P < 0.05). There was significant difference in rate of moderate pain between pluripara group (50.0%, 11/22) and primipara group (79.8%, 71/89; P < 0.01). In the active phase, women with tense, scared or a poor emotion control expressed significantly severe labour pain (59.0%, 36/61) than 35.6% (16/45) in well-prepared group. The rate of severe labour pain in good control of emotion group of 44.8% (43/96) was a statistically lower than 9/10 in poor control group. There was a statistically lower severe labour pain in women given by sedatives (29.2%, 7/24) than 54.9% (45/82) in women without sedatives treatment (P < 0.05). (2) Delivery outcomes: in latent phase, the rates of fetal distress and cesarean section were 36.6% (30/82) and 39.0% (32/82) in moderate pain group, which were significantly higher than 13.8% (4/29) and 17.2% (5/29) in mild pain group. In active phase, the rate of fetal distress, cesarean section and postpartum hemorrhage were 36.5% (19/52), 40.4% (21/52) and 13.5% (7/52) in severe pain group, which were significantly higher than [18.5% (10/54); 20.4% (11/54); 0] in moderate pain group (P < 0.05). CONCLUSIONS: Women with poor understanding of delivery, tense, scared, poor emotion control, young age and uniparous have severe labour pain. Sedative use could alleviate pain in active phase. Women with mild labour pain have good delivery outcomes.

Pioglitazone reduces tumor necrosis factor-alpha serum concentration and mRNA expression of adipose tissue in hypercholesterolemic rabbits.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory cytokine involved in atherogenesis. Adipose tissue is an important source of endogenous TNF-alpha production. Pioglitazone, a member of the thiazolidinediones (TZDs), has anti-inflammatory and anti-atherogenic properties, while underlying mechanism has not been fully elucidated. The aim of this study was to evaluate the effect of pioglitazone on TNF-alpha serum concentration and mRNA expressions of subcutaneous adipose tissue in hypercholesterolemic rabbits. METHODS: Ten rabbits fed with high-cholesterol diet for 8 weeks were randomly divided into two groups: (1) high cholesterol group (n=5): maintained high cholesterol diet for 4 weeks; (2) pioglitazone group (n=5): the same cholesterol diet plus pioglitazone (3 mg/kg/day) for 4 weeks. Control group (n=5) was fed with normal diet for 12 weeks. Subcutaneous adipose tissue was collected for RNA analysis. The direct effect of pioglitazone on TNF-alpha release was assayed in primary rabbit adipocytes. TNF-alpha levels in serum and adipocytes culture supernatant were measured by ELISA. RT-PCR was used to evaluate TNF-alpha mRNA expressions in adipose tissue and adipocytes. RESULTS: Compared with control group, rabbits fed with high cholesterol diet showed significantly higher levels of serum total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and TNF-alpha. Though having no effect on serum glucose level and lipid profile, pioglitazone administration significantly reduced circulating TNF-alpha concentrations, which were positively correlated with TNF-alpha mRNA expressions of adipose tissue (r=0.53, P<0.01). Pioglitazone dose-dependently inhibited lipopolysaccharide (LPS)-induced TNF-alpha secretion and mRNA expression in cultured adipocytes. CONCLUSION: Pioglitazone significantly reduced serum TNF-alpha level in hypercholesterolemic rabbits independent of its metabolic actions, which may at least partly be due to its direct inhibition of TNF-alpha expression and secretion of adipocytes. This may help to explain the mechanism by which pioglitazone exert anti-atherosclerotic effects.

[Clinical significance of rapid increase of heart rate at onset of treadmill exercise test].

OBJECTIVE: To analyze the correlation between rapid increase of heart rate at onset of electrocardiogram treadmill exercise test and coronary artery lesion. METHODS: We selected 245 patients who underwent electrocardiogram treadmill exercise and coronary angiography. The patients were divided into a coronary heart disease (CHD) group and a non-CHD group according to the Results of coronary angiography. The patients of the CHD group were divided into a single-vessel disease group, a double-vessel disease group, and a triplet-vessel disease group. The increased heart rate during the first minute (DeltaHR 1minute) of treadmill exercise test and the extent of coronary artery lesion were analyzed. RESULTS: DeltaHR 1minute in the CHD group was significantly higher than that in the non-CHD group(P<0.01). DeltaHR 1minute had an increasing trend with the severity of coronary artery lesion. DeltaHR 1minute was positively correlated to the depression of ST segment and the severity of coronary artery lesion(r=0.252,0.470, P<0.01). CONCLUSION: Patients with CHD have an increased DeltaHR 1minute. DeltaHR 1minute can be one of the indexes to estimate the extent of myocardial ischemia and coronary artery lesion.

[Diagnostic value of chronotropic incompetence in coronary heart disease].

OBJECTIVE: To determine the diagnostic value of chronotropic incompetence (CI) in coronary heart disease (CHD). METHODS: Two hundred thirty three patients who underwent the electrocardiogram treadmill exercise test (TET) and coronary angiography (CAG) were included in this study. CAG was used as the standard of diagnosing CHD. The sensitivity, specificity, and accuracy of CI were compared with the traditional index of TET. RESULTS: There was no significant difference between the sensitivity, specificity and accuracy of CI (81.7%, 64.3%, and 71.2% respectively) and those of the traditional index (73.1%, 69.3%, and 70.8% respectively, P> 0.05), while the specificity (87.9%) and accuracy (79.4%) were significantly higher after combining CI and the traditional index than that of the traditional index alone (P<0.05). There was no significant difference in the sensitivity (P> 0.05). CONCLUSION: CI was a usefull index in diagnosing CHD. CI combined with the traditional index of TET can significantly improve the specificity and accuracy of TET for CHD.

Xuezhikang, an extract of cholestin, reduces cardiovascular events in type 2 diabetes patients with coronary heart disease: subgroup analysis of patients with type 2 diabetes from China coronary secondary prevention study (CCSPS).

Lipid-lowering therapy has been proven to reduce macrovascular complications of type 2 diabetes. Xuezhikang is an extract of cholestin and has a markedly modulating effect on lipids, but the effect of xuezhikang on reducing coronary events in diabetic patients with coronary heart disease (CHD) is less clear. A total of 591 diabetic patients with CHD were randomized to the xuezhikang group (n=306) and the placebo group (n=285). During the average 4 years of follow-up, there were 28 cases of CHD events (9.2%) in the xuezhikang group and 53 cases (18.6%) in the placebo group. Risk reduction for CHD events was 50.8% (P<0.001) by xuezhikang treatment. Xuezhikang decreased the risk of non-fatal MI by 63.8%, fatal MI by 58.5%, CHD sudden death by 26.9%, and other CHD death by 53.4%. CHD death totaled to 21 cases in the xuezhikang group (6.9%) and 35 cases in the placebo group (12.3%), indicating that xuezhikang significantly decreased the risk of CHD death by 44.1% (P<0.05). Seventy-two patients died from various causes, among which there were 27 patients in the xuezhikang group and 45 patients in the placebo group. The risk for all-cause death was 44.1% lower in the xuezhikang group than in the placebo group (P<0.01). This investigation demonstrates that xuezhikang therapy can be effective on reduction of cardiovascular events in diabetic patients with CHD with a reliable safety.

The beneficial effects of high-density lipoprotein on adipocytes may relate to its anti-atherogenic properties.

High-density lipoprotein (HDL) has significant anti-atherogenic properties, whereas the underlying mechanisms are complex and have not been completely elucidated. Adipocytes produce a variety of adipokines with cardiovascular effects. The dysregulated secretion of adipokines by adipocytes may contribute to the increased risk of atherosclerosis associated with obesity. Clinical evidences indicate that higher plasma HDL-C levels are associated with a favourable adipokines secretion profile, suggesting that HDL might improve the dysregulated adipokines secretion. HDL may diminish lipid accumulation in adipocytes through phosphorylation of PPARgamma and inhibition of aP2 expression, which possibly account for the favourable effects of HDL on adipokines secretion. Therefore, we hypothesize that HDL might exert several beneficial effects on adipocytes, which may relate to its anti-atherogenic properties.

Effect of atorvastatin on SR-BI expression and HDL-induced cholesterol efflux in adipocytes of hypercholesterolemic rabbits.

BACKGROUND: Adipose tissue contains a large amount of cholesterol and performs a buffer function for circulating cholesterol. Scavenger receptor class B type I (SR-BI) might play a significant role in adipocytes cholesterol metabolism through mediation of cholesterol efflux. We evaluated the effect of atorvastatin on SR-BI expression and HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits. METHODS: Sixteen rabbits fed with high-cholesterol diet for 8 weeks were randomly divided into 2 groups: (1) maintained on a high cholesterol diet for 6 weeks (n=8); (2) the same cholesterol diet plus atorvastatin (2.5 mg/kg/day) for 6 weeks (n=8). Control group (n=5) was fed with normal diet for 14 weeks. Subcutaneous adipose was collected for adipocyte culture. Reverse transcription polymerase chain reaction (RT-PCR) was used to evaluate adipocytes SR-BI mRNA expression. Cholesterol efflux rate was determined through measuring release of radioactivity from (3)H-cholesterol prelabeled cells into medium containing high-density lipoprotein (HDL). The direct effect of atorvastatin on SR-BI mRNA expression in primary rabbit adipocytes was assayed. RESULTS: High-cholesterol diet decreased SR-BI mRNA expression and reduced HDL-induced cholesterol efflux rate in adipocytes. Six weeks of atorvastatin treatment significantly enhanced the cholesterol efflux from adipocytes, which was related to the increased mRNA expression of SR-BI (r=0.58, P<0.05). Adipocytes SR-BI mRNA expression were negatively correlated with the serum total cholesterol levels at the end of the study (r=-0.46, P<0.05). Atorvastatin dose-dependently stimulated SR-BI mRNA expression in cultured adipocytes. CONCLUSION: Atorvastatin can up-regulate SR-BI mRNA expression and promote the HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits possibly through lowering serum cholesterol levels and directly stimulating SR-BI mRNA expression.

Anti-atherogenic properties of fibrates may be largely due to their anti-inflammatory effects.

Current understanding of the pathophysiology of atherosclerosis has undergone a remarkable evolution. Compelling evidence has evolved at both the basic science and clinical level for the importance of inflammation in the pathogenesis of atherosclerosis and its complications. Recent research has shown that both systemic and local inflammation plays a central role in all phases of the atherosclerotic process. Inflammatory cells dominate early atherosclerotic lesions, inflammatory cytokines accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. Robust clinical studies have affirmed that fibrates are anti-atherogenic and can improve the cardiovascular risk profile. Fibrates not only modulate the serum concentrations of triglyceride and cholesterol, but also inhibit systemic inflammatory statue and inflammatory response in vascular cells. Fibrates act anti-inflammatory effects in monocyte/macrophage, T lymphocyte, endothelial cells, vascular smooth muscle cells and adipocytes. Since atherosclerosis is now regarded as an inflammatory disease and those inflammatory cells play critical important roles in the initiation and development of atherosclerosis, we hypothesize that anti-atherogenic properties of fibrates may be largely due to their anti-inflammatory effects.

Fenofibrate enhances CD36 mediated endocytic uptake and degradation of oxidized low density lipoprotein in adipocytes from hypercholesterolemia rabbit.

BACKGROUND: CD36 as a fatty acid transporter is predominantly expressed in adipocytes. We studied whether adipocytes could uptake and degrade OxLDL through CD36 and explored the effect of fenofibrate on OxLDL uptake in adipocytes from hypercholesterolemia rabbits. METHODS: Subcutaneous adipose tissues were collected from normal, high-cholesterol and high-cholesterol plus fenofibrate treatment rabbits for adipocytes culture. CD36 and peroxisome proliferator-activated receptor gamma (PPARgamma) mRNA expression were evaluated by RT-PCR. RESULTS: Cellular expression of CD36 was confirmed during differentiation of adipose cell by RT-PCR. Upon incubation at 37 degrees C, (125)I-OxLDL was endocytosed in a dose-dependent fashion and underwent lysosomal degradation by adipocytes. In binding experiments at 4 degrees C, (125)I-OxLDL exhibited specific and saturable binding to adipocytes (K(D) = 4.2 microg/mL). The endocytic uptake and degradation of (125)I-OxLDL by adipocytes were inhibited by 56 and 54% with anti-CD36 antibody. Fenofibrate treatment enhanced the (125)I-OxLDL uptake and degradation and up-regulated CD36 mRNA expression in adipocytes and suppressed PPARgamma mRNA expression in adipose tissue from hypercholesterolemia rabbits. CONCLUSION: CD36 plays a novel role in adipose tissues and adipocytes possibly involve in clearance of OxLDL in blood. Fenofibrate treatment improved the OxLDL uptake and degradation in adipocytes from hypercholesterolemia rabbits.

Gemfibrozil reduces release of tumor necrosis factor-alpha in peripheral blood mononuclear cells from healthy subjects and patients with coronary heart disease.

BACKGROUND: Inflammatory process plays an important role in the pathogenesis of coronary heart disease (CHD). With the growing use of gemfibrozil and other fibrates, their anti-inflammatory effects have been noted. But little is known about the effect of gemfibrozil on tumor necrosis factor (TNF)-alpha secretion in peripheral blood mononuclear cells (PBMC) from patients with coronary heart disease. METHODS: PBMC were obtained from CHD patients (n=16) and healthy controls (n=13). PBMC (2x10(6) cells/ml) were cultured in 24-well plates with or without Ang II (10(-8), 10(-7), 10(-6) mol/l), or Ang II (10(-6) mol/l) plus gemfibrozil (10(-6), 10(-5), 10(-4) mol/l). After 24-h incubation, the supernatants were separated, and TNF-alpha was measured by an enzyme-linked immunosorbent assay (ELISA). RESULTS: Spontaneous release of TNF-alpha was 299.2+/-110.7 pg/ml in PBMC from CHD patients and 179.3+/-78.2 pg/ml in PBMC from control subjects (P<0.05). Incubated with Ang II (10(-8), 10(-7), 10(-6) mol/l), TNF-alpha secretion was 307.7+/-141.8, 318.9+/-135.6, 328.6+/-123.9 pg/ml in PBMC from CHD patients, and 225.3+/-135.4, 224.1+/-141.0,218.7+/-134.8 pg/ml in PBMC from control subjects, respectively. Ang II did not significantly trigger TNF-alpha secretion in both groups. Compared with that incubated with Ang II (10(-6) mol/l) alone, release of TNF-alpha intervened by gemfibrozil (10(-6),10(-5),10(-4) mol/l) decreased to 279.4+/-132.2, 268.0+/-132.7, 226.6+/-102.7 pg/ml in PBMC from CHD patients, and 177.6+/-94.4, 156.1+/-69.4, 105.3+/-52.7 pg/ml in the control group, respectively. Gemfibrozil (10(-5),10(-4) mol/l) significantly inhibited TNF-alpha secretion in both groups (P<0.05). CONCLUSIONS: Our data demonstrated that gemfibrozil reduced release of TNF-alpha in PBMC both from CHD patients and controls. This effect may partially be relevant to the clinical benefits of gemfibrozil in the treatment of dyslipidemia and atherosclerosis.