Prophylactic use of platelet-rich plasma for post-spinal low back pain following gynecological surgery: a randomized clinical trial.

BACKGROUND: Post-spinal back pain is suggested to occur as a result of a localized inflammatory response that is often associated with some degree of muscle spasm. We aimed to evaluate the effect of platelet-rich plasma (PRP) in reducing the incidence of post-spinal back pain. METHODS: One hundred patients were randomly enrolled and scheduled for elective gynecological surgery under spinal anesthesia. After the subarachnoid block, group A (placebo) received 2 mL of sodium chloride 0.9% injected into the track of spinal needle during its withdrawal (2 mm after outward withdrawal in muscles and subcutaneous tissues). While patients in group B (PRP); received 2 ml of PRP injected into the track of the spinal needle during its withdrawal. The primary outcome was the number of patients who developed post-spinal low back pain within the first week following the subarachnoid block. Secondary outcomes included the time of the first analgesic request and total meperidine consumption during the first 24 h postoperatively. RESULTS: Fifteen patients in the PRP group developed low back pain during the first week following subarachnoid block compared to 26 patients in the placebo group (p = 0.037). There was a significant decrease in the mean meperidine consumption during first 24 h postoperatively in PRP group (174 ±â€¯14 mg) compared to placebo group (210 ±â€¯22 mg) (p < 0.0001). Also, the first analgesic request was significantly delayed in PRP group (243 ±â€¯21 min.) compared to placebo group (185 ±â€¯31 min.) (p < 0.0001). CONCLUSION: This study demonstrated the positive effects of platelet-rich plasma on the prevention of post-spinal backache.

A Possible Role for TNF-α in Coordinating Inflammation and Angiogenesis in Chronic Liver Disease and Hepatocellular Carcinoma.

BACKGROUND: Increasing evidence supports the hypothesis that chronic and persistent inflammation contributes to cancer development. However, the molecular mechanisms that lead to cancer in chronic inflammation and the role of angiogenesis in inflammation-associated cancer remain poorly understood. METHODS: NINETY PATIENTS WERE ENROLLED: 30 cases of CHC without cirrhosis, 28 cases of CHC with liver cirrhosis, and 32 cases of HCC and hepatitis C virus infection. Ten wedge liver biopsies, taken during laparoscopic cholecystectomy, served as normal controls. Serum TNF-α levels were measured using the ELISA technique; in situ hybridization and immunohistochemical studies were used to detect hepatic levels of messenger RNA (mRNA) transcripts and mature protein, respectively, for both TNF-α and VEGF. RESULTS: The highest hepatic expression of TNF-α was noticed in liver cirrhosis specimens compared to noncirrhotic CHC and HCC. Hepatic expression of VEGF and serum level of TNF-α revealed significant increases in the progression of the disease. Moreover, cases with higher grades of inflammation or stages of fibrosis showed significant increases in serum TNF-α and expression of TNF-α and VEGF. Expression of mRNA of both TNF-α and VEGF shows increasing expression with positive correlation to progression of viral hepatitis to cirrhosis with more positivity in cases developed HCC. CONCLUSIONS: VEGF signaling could be one of the molecular signaling pathways involved in TNF-α induced angiogenesis which might pose an important link between inflammation and fibrosis in CHC and HCC development and progression. Moreover, serum inflammatory biomarkers can be used to monitor the disease progression.

Neutrophil apoptosis: impact of granulocyte macrophage colony stimulating factor on cell survival and viability in chronic kidney disease and hemodialysis patients.

INTRODUCTION: Altered neutrophil apoptosis might be responsible for recurrent bacterial infections encountered in hemodialysis (HD) and chronic kidney disease (CKD) patients. This work was designed to assess the neutrophil apoptotic activity and the impact of implementation of granulocyte macrophage colony stimulating factor (GM-CSF), as a survival factor, on neutrophil apoptosis among these patients. MATERIAL AND METHODS: Twenty-five patients on regular HD along with 34 CKD patients on conservative treatment, as well as 15 healthy controls, were investigated for apoptotic rate via assessment of neutrophil expression of Annexin-V by flow cytometry, before and after 20 h culture in absence and presence of GM-CSF. Neutrophil viability was determined using light microscopy. The preservation of neutrophil activation in these patients was analyzed by flow cytometric CD18 neutrophil expression. Chronic inflammatory state was evaluated by estimating C-reactive protein (CRP) and soluble intercellular adhesion molecule-1 (sICAM-1). Obtained data were statistically analyzed. RESULTS: Compared to controls, both HD and CKD groups had a significant increase of Annexin-V and CD18 expression and significant decrease in neutrophil viability. Culture of their neutrophils with GM-CSF showed significant decrease of apoptosis accompanied by improvement of neutrophil viability compared to their cultured cells without GM-CSF. These patients also showed significant elevation of CRP and sICAM-1. CONCLUSIONS: Granulocyte macrophage colony stimulating factor demonstrated an evident impact on improving in vitro neutrophil survival and viability in HD and CKD patients. Therefore, this may represent promising preventive and/or therapeutic strategies against infection frequently observed in these patients and causing morbidity and mortality.

Hepatopulmonary syndrome: prevalence and predictors in Egyptian cirrhotic patients.

BACKGROUND: The reported prevalence of hepatopulmonary syndrome (HPS) in cirrhotic patients is heterogeneous. Although the prevalence of chronic liver diseases is high in Egypt, however, scanty data is available about HPS. AIM: To assess the frequency of HPS and factors predictive of diagnosis of HPS in Egyptian patients with liver cirrhosis. METHODS: Fifty cirrhotic patients were evaluated for the presence of HPS. Orthodeoxia was measured by arterial blood gas test. The patients positive for diagnostic criteria of HPS (the presence of A-a O2 > or = 15 mmHg and pulmonary vascular dilatation assessed by contrast enhanced echocardiography) were defined as clinical HPS cases and those manifesting with intrapulmonary arterial dilation but no other criteria were defined as subclinical HPS cases. RESULTS: Subclinical HPS and clinical HPS was observed in 10 (20%) and 17 (34%) of the patients, respectively. The presence of HPS was significantly associated with severity of liver disease assessed by the Child-Pugh score (CP) or MELD score. Portal vein diameter (mm) (OR 3.3; 95% C.I 1.3-8.2; p=0.01) was the only independent predictor for HPS; the specificity of orthodeoxia for diagnosis of HPS was 100%. CONCLUSIONS: HPS and intrapulmonary vein dilation are relatively frequent in patients with liver cirrhosis and occur in 34% and 20% of cirrhosis patients, respectively. They are associated with disease severity according to the MELD and CP score. Alveolar arterial oxygen gradient is the most valuable negative and positive diagnostic predictor for presence of HPS in cirrhotic patients.