Anti‑inflammatory effects of propofol during cardiopulmonary bypass: A pilot study.

Introduction: Propofol has been suggested as a useful adjunct to cardiopulmonary bypass (CPB) because of its potential protective effect on the heart mediated by a decrease in ischemia-reperfusion injury and inflammation at clinically relevant concentrations. In view of these potentially protective properties, which modulate many of the deleterious mechanism of inflammation attributable to reperfusion injury and CPB, we sought to determine whether starting a low dose of propofol infusion at the beginning of CPB would decrease inflammation as measured by pro-inflammatory markers. Materials and Methods: We enrolled 24 patients undergoing elective coronary artery bypass graft (CABG). The study group received propofol at rate of 120 mcg/kg/min immediately after starting CPB and was maintained throughout the surgery and for the following 6 hours in the intensive care unit (ICU). The control group received propofol dose of 30-50 mcg/kg/min which was started at the time of chest closure with wires and continued for the next 6 hours in the ICU. Interleukins (IL) -6, -8 and -10 and tumor necrosis factor alpha (TNFalpha) were assayed. Result: The most significant difference was in the level of IL-6 which had a P value of less than 0.06. Starting a low dose propofol early during the CPB was not associated with significant hemodynamic instability in comparison with the control group. Conclusion: Our study shows that propofol may be suitable as an anti-inflammatory adjunct for patients undergoing CABG.

Neuropathic pain in cancer patients: A brief review.

Neuropathic pain (NP) is initiated or caused by a primary lesion or dysfunction in the nervous system. The NP in cancer patients is typically due to a combination of inflammatory, neuropathic, ischemic, infiltrative, and compression mechanisms that involve one or more anatomic sites. These patients will often have various types of co‑existing pain syndromes and co‑morbidities. Thus, any treatment plan needs to be individualized. After a thorough clinical assessment and evaluation, a combination therapy including anticonvulsants, antidepressants, N‑methyl‑D‑aspartate antagonists, opiates, topical agents, and interventional procedures should be considered in these patients.

Cryptococcal liver abscess in HIV-negative individual.

Opportunistic fungal infections in immunocompromised patients are usually caused by candida, aspergillus, cryptococcus or zygomycetes. Rarely, fungal infections may occur in immunocompetent indivivals and are usually caused by cryptococcus or aspergillus. When infected by cryptococcus, the usual sites of infection include respiratory tract, central nervous system, or skin. Uncommon sites are liver, spleen, prostate, and bone marrow. When it involves liver, it can present with micro-abscesses, cholangitis, or hepatitis. Here we report a case of cryptococcal infection of liver in a HIV-negative patient presenting with micro-abscesses.

Serum zinc levels in hepatic encephalopathy.

BACKGROUND: Zinc is essential for various metabolic processes of the body. Since serum zinc levels are lowered in liver diseases, it has been postulated to be a precipitating factor for hepatic encephalopathy. METHODS: We prospectively studied serum zinc levels in consecutive patients with fulminant hepatic failure, subacute hepatic failure and chronic liver disease with encephalopathy. Serum zinc levels were correlated with various clinical and biochemical parameters and final outcome of patients. Serum zinc levels were estimated by atomic absorption spectrometry at admission and also 24 hours after recovery in survivors. RESULTS: Of the 55 patients (age 17-65 years, 35 men) studied, 30 had acute, 5 subacute and 20 chronic liver disease. Patients with hepatic encephalopathy had significantly lower serum zinc levels as compared to 20 age and sex matched controls. High serum bilirubin levels and prothrombin time showed inverse relationship with serum zinc levels. There was no relationship of serum zinc levels with age, sex, grade and duration of encephalopathy, liver size, ascites or splenomegaly. CONCLUSIONS: Hepatic encephalopathy is associated with low serum zinc levels. Recovery occurred in 17 patients despite persisting low serum zinc levels. Serum bilirubin > 23 mg/dL and prothrombin time prolongation > 12 seconds above control have inverse correlation with serum zinc level.