[The dietary protein contribution and hepatic encephalopathy in cirrhosis].

Hepatic encephalopathy is a neuropsychiatric syndrome, which can occur in the clinical course of acute (fulminant) or chronic hepatic failure of various aetiology; reversible metabolic abnormalities without neuronal structural changes are frequently found in this condition. High blood ammonia levels, an imbalance between plasma concentrations of branched-chain and aromatic amino acids, false neurotransmitters and neurotransmitters receptor changes in CNS are the commonly recognized pathogenetic mechanism of this syndrome. Protein malnutrition is a frequent occurrence in liver cirrhosis, especially of alcoholic aetiology.

Ultrastructural alterations and virus-like particles in lymph nodes of drug addicts with lymphadenopathy syndrome (LAS).

Lymph node biopsies from 16 cases of intravenous drug addicts with lymphadenopathy syndrome (LAS) have been examined at the electron microscope. The main ultrastructural alterations observed in the lymphocytes, dendritic reticulum cells and endothelial cells were tubulo-reticular structures (TRS), test tube and ring shaped forms (TRF) and nuclear pockets (NP). Images suggesting virus budding from lymphocytes and virus-like particles have also been found in 9 out of the 16 cases.

AIDS-like immunologic alterations in clinically unaffected drug users.

Peripheral blood lymphocyte subpopulations (PBLS) and HLA-DR phenotype have been evaluated in 30 IV drug users who were not affected by acquired immune deficiency syndrome (AIDS). A strongly significant reduction in helper/suppressor ratio was found in these subjects as compared to the control population. When the group under study was subdivided according to the presence or absence of signs of lymphadenopathy syndrome (LAS), the apparently unaffected individuals still had significant modifications in PBLS when compared with controls.

Acquired factor VIII inhibitor in a non-haemophilic patient: successful treatment with plasma exchange associated with factor VIII concentrate and immunosuppressors.

We report the successful treatment of a 55-year-old man with an acquired factor VIII inhibitor, the appearance of which followed surgery for a carcinoma of the biliary tract. The patient, who had recurrent life-threatening bleeding episodes, was treated with intensive plasmapheresis, factor VIII concentrates, azathioprine and methylprednisolone. Disappearance of the inhibitor was observed after the second series of plasma exchanges.