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Background: Acne is a dermatosis characterized by a chronic folliculitus caused by Propionibacterium acnes associated to keratinization disturbance of corneal layer with comedons formation and fat overproduction named seborrhea. Is a skin illness that affects pilosebaceous follicles. Provokes inflammatory and non inflammatory lesions in skin zones with more sebaceous glands as face, chest ant the upper back. Affects approximately 80% of humans between 11 and 30 years old. Objective: To quantify the production of IL-1β, IL-8 and TNF-α directly to inflammatory acne lesions that showed delayed hypersensitivity response in patients by ELISA technique. Patients and methods: To 40 patients from Centro Dermatologico Ladislao de la Pascua with inflammatory acne was cleaned at the sample zone and by punction with a sterile lancet. The sample was recovered in a filter paper directly. Before to develop the ELISA technique the paper filter was impregned with 300 µL of sterile saline solution. The cytokines were quantified by commercial kits Quantikine R&D systems IL-1β (DBL 50), IL-8 (D800c) and TNF-α (DTA00C). Results: 26 of 40 patients showed at least one of the interleukins elevated and represent 65% of population. The rest of patients (14) had normal values (35%). The cytokine that showed the highest concentration in the majority of patients was IL-8 (16), IL-1β (13) and TNF-α (11) respectively. Discussion: Our results demonstrate clearly that 65% of the patients have high concentrations al least of one interleukin derived from inflammatory cells that were attracted and activated by inflammatory process induced by P. acnes in skin. Those patients with treatment compared against control patients without treatment present similar values in IL-8 and TNF-α; however, the IL-8 was present in high concentration in larger patients (40%), TNF-α in 27% and IL-1β was reduced in patients with treatment (5%) comparatively to patients without treatment (27%). With these results we think that anti-inflammatory drugs used in these treatments inhibit the production of IL-1β that is an important molecule in inflammatory response. Conclusion: In 65% of the patients with inflammatory acne it was demonstrated that cells present in lesions were activated because the levels of cytokines IL-8, IL-1β y TNF-α are elevated in this order in these samples. [ABSTRACT FROM AUTHOR]

Introduction. Acute Hepatitis as a clinical entity caused mainly by viruses or chemical agents. Its prognostic is generally fatal, reaching up to 70-90% mortality. It is well known that in this pathology, the oxidative stress and proinflamatory cytokines (TNF α, IL-1 and IL-6) are very important factors that contribute to the negative prognostic of the disease. On the other hand, besides the haemorrhogical effects of pentoxyphillin, it also shows anti-oxidant activity and is a strong inhibitor of the proinflamatory cytokines secretion. This paper reports two paediatric cases of subacute hepatitis, caused by the hepatitis virus type A. Clinic Cases. Hepatitis virus A, diagnosed according to the criteria of the British King's College. Both cases were submitted for medical treatment with anti-ammonium measures with 1.5 gr of Ornitate-L-L-Aspartate by nasogastric tube, vitamin K 2 mg/12 h iv, mannitol 0.4 mg/kg/12 h iv sodium diphenylhydantoinate 3 mg/kg/8 h iv omeprazole 10 mg/12 h iv, metronidazole 210 mg, fresh plasma, parenteral solutions with glucose at 10%, O2 3 litres/minute and hypercaloric diet based on vegetal fiber by nasogastric tube. Based on the foregoing, pentoxyphillin was added at of 70 mg iv/8 h. Both cases responded successfully to that and after 15 days of treatment, the patients were sent home safely. Commentaries: Although this report is not definitive, results show the potential of pentoxyphillin to encourage its use in a future study for the treatment of acute hepatitis. [ABSTRACT FROM AUTHOR]

Few spaces exist in critical medicine that have woken up so much interest, investigation and frustration as sepsis. In spite of the advances in diagnostic and therapeutic methods, the morbidity and mortality keep on being unacceptably elevated. Sepsis is the systemic reaction exaggerated of the guest to the infection that alters the homeostasis through a waterfall gone out of control of inflammation, immunosuppression, upsets in the coagulation and the fibrinolysis' alteration. Damage provokes hipoxia to microcirculation and direct damage to the tissues that usually leads patients to shock, multiple organic dysfunction and death. This paper includes the main physiopathological mechanisms of host response to pathogen microorganisms invasion, including proinflammatory cytokines release, immunosuppression, coagulation cascade affection and the importance of genetic susceptibility to sepsis. [ABSTRACT FROM AUTHOR]

The role of reactive oxygen species (ROS) in the pathogenesis of Alzheimer's disease derives from a prolonged pro-oxidant state that induces the synthesis by immunocompetent mononuclear cells of soluble mediators in the brain of patients. The present paper focuses on determining the levels of oxidative metabolism indicators and pro-inflammatory cytokines in brain tissues of cognitive-deficient elderly rats, to evaluate the probable interaction among these variables and their implication in the neuropathology of this disease. Behavioral studies were carried out in animals to demonstrate cognitive deterioration, the biochemical and immunological indicators quantified by spectrophotometric and immunoenzymatic methods. Changes were observed in aging-associated oxidative metabolism indicators. The oxidative stress showed a changing pattern of antioxidant enzymes in the brain, where the superoxide dismutase was over-activated in all the regions studied and catalase were only over-activated in those regions where the neurodegenerative process was prominent (hipocampus and striata). The concentrations of malondialdehyde, phospholipase A2 and Tumor necrosis factor a changed with aging, confirming ROS as cellular messengers and not only as deleterious agents. This study evidences a strong relationship between oxidative metabolism and agingassociated cognitive processes. [ABSTRACT FROM AUTHOR]