Adenosin deaminasa como molécula coestimuladora y marcador de inmunidad celular / Adenosine deaminase as costimulatory molecule and marker of cellular immunity

La adenosin deaminasa (ADA), es una enzima del metabolismo de las purinas que ha sido objeto de mucho interés debido a que el defecto congénito de esta enzima causa el síndrome de inmunodeficiencia combinada severa. Una de las tres isoformas de la enzima (ecto-ADA) es capaz de unirse a la glicoproteína CD26 y a los receptores de adenosina A1 y A2B. La interacción ADA-CD26 produce una señal coestimuladora en los eventos de activación de las células T y en la secreción de IFN-g, TNF-a e IL-6. Durante dicha activación la actividad de la enzima está regulada de manera positiva por IL-2 e IL-12 y negativamente por IL-4, basado en un mecanismo de translocación. Diversos estudios señalan que los niveles séricos y plasmáticos de ADA se elevan en algunas enfermedades causadas por microorganismos que infectan principalmente a los macrófagos; así como en trastornos hipertensivos, lo cual podría representar un mecanismo compensatorio como consecuencia de la elevación de los niveles de adenosina y la liberación de mediadores hormonales e inflamatorios estimulados por la hipoxia.

Adenosine deaminase (ADA) is an enzyme of purine metabolism which has been the subject of much interest because the congenital defect of this enzyme causes severe combined immunodeficiency syndrome. One of the three isoforms of the enzyme (ecto-ADA) is capable of binding to the glycoprotein CD26 and adenosine receptors A1 and A2B. ADA-CD26 interaction produces a costimulatory signal in the events of T cell activation and secretion of IFN-g, TNF-a and IL-6. During this activation, the enzyme activity is regulated positively by IL-2 and IL-12 and negatively by IL-4, based on the mechanism of translocation. Diverse studies suggest that seric and plasmatic levels of ADA rise in some diseases caused by microorganisms infecting mainly the macrophages and in hypertensive disorders, which may represent a compensatory mechanism resulting from increased adenosine levels and the release of hormones and inflammatory mediators estimulated by hipoxia.

Serum paraoxonase 1 activity status in patients with liver disorders

Paraoxonase 1 [PON1] is an esterase, exclusively synthesized by liver. The present study has two objectives: to determine the PON1 activity status in various disorders associated with hepatocellular damage and to correlate the changes of PON1 activity with the standard liver function and fasting lipid profile tests in these disorders. The study groups consisted of 95 patients with liver diseases including acute viral hepatitis [14], cirrhosis with portal hypertension [33], leptospirosis [14], sepsis and multi organ failure [15], left ventricular failure [9], and falciparum malaria [10]; and 53 healthy controls. Serum PON1 activity was measured manually using spectrophotometer. Liver function test parameters and fasting lipid profile were performed in clinical chemistry auto analyzer [HITACHI 912]. The serum PON1 activity in patients with acute viral hepatitis and sepsis decreased significantly [P<0.001] and moderately in falciparum malaria [P<0.05]. However, in patients with cirrhosis, leptospirosis and left ventricular patients, its activity did not change significantly. On applying Pearson correlation, serum PON1 activity correlated positively with high-density lipoprotein-cholesterol [HDL-C] in patients with sepsis [r=0.633, P<0.05], left ventricular failure patients [r=0.814, P<0.05] and negatively with acute viral hepatitis patients [r=-0.528, P<0.05]. PON1 activity has decreased significantly in acute viral hepatitis, sepsis with multi organ failure and falciparum malaria patients. Determination of PON1 activity may serve as a useful additional test in assessing these conditions

Acute hepatitis due to dengue virus in a chronic hepatitis patient

We present a case of acute hepatitis caused by dengue virus, with a significant increase in aspartate transferase and alanine transferase levels in a chronic hepatitis patient attended at the Cane Sugar Planters Hospital of Campos dos Goytacazes, RJ.

[Diagnosis of hyper transaminasemia in childhood]

Elevated serum levels of transaminases must always be considered as an abnormal finding in children. Drugs and toxins must be eliminated first as possible hepatotoxic agents or co-factors. Antiviral hepatitis A immunoglobulin M serology is the first test to perform. However, others viruses with spontaneous benign courses are the most frequent cause. Only if initial presentation is severe or if liver tests remain abnormal after several weeks, other rare diseases can be sought. Aetiologies of persistent cytolysis associated to cholestasis are different in infancy and childhood. Metabolic, auto immune, genetic, muscular, endocrine disorders and obesity may cause isolated persistent hyper transaminasemia. Early diagnosis and management is essential, Isolated elevation of serum amino transferases in healthy looking children with negative investigations is mostly a benign condition that usually resolves within a year. Liver biopsy does not contribute much to diagnosis and is probably unnecessary

Re-evaluation of serum enzymes in diagnosis of acute viral hepatitis

The present study re-evaluates AST/ALT [D[e]R[i]tis ratio] and ALP/ALT ratios in 65 icteric and 24 anicteric cases of viral hepatitis. The icteric cases were hospitalized and followed up to 5th week of jaundice when most of the patients [80%] recovered clinicobiochemically. AST/ALT ratio showed significance only in early diagnosis of icitric cases of acute viral hepatitis, but the relevant history with other biochemical testes eclipsed its value. Further, 16% of cases had reverse ratio. The ALP/ALT ratio provided a remarkable help in the diagnosis of both anicteric and icteric cases and proved to be preferable, as compared to AST/ALT ratio even in cases of cholestasis