[Viral hypothesis in Behçet's disease].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Schattner.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A 31-year-old woman with untreated chronic schizophrenia developed extreme polydipsia which rapidly led to coma and death due to cerebral edema. Hyponatremia (120 mEq/liter) and serum hypo-osmolality (260 mOsm/kg) were associated with marked polyuria (up to 1850 ml/hour) and appropriately low urinary osmolality (90 mOsm/kg) which responded to treatment. This case and few qualifying previous reports which are reviewed support the possibility that pure self-induced water intoxication with no major contribution of inadequate release of antidiuretic hormone may occur, and that extreme polydipsia can sometimes overwhelm normal renal diluting capacity in psychotic patients.
Fourteen patients with anorexia nervosa (AN) were studied for the production of tumour necrosis factor (TNF), the activation of the interferon (IFN) system and cell-mediated cytotoxicity (CMC) and the results were compared with 16 age-matched healthy women. AN patients had significantly increased spontaneous TNF production by peripheral blood mononuclear cells (PBMC) in vitro (16 +/- 5 U/ml versus 4 +/- 3 U/ml in the control group; P less than 0.05), although no TNF was detectable in the plasma from either group. TNF production in vitro, following stimulation of PBMC by phytohaemagglutinin (PHA) or tumour cells, was similar in AN patients and controls; however, lipopolysaccharide (LPS) induced TNF production was found to be lower in AN (P less than 0.1). CMC was significantly lower in AN patients (4 +/- 2 versus 10 +/- 3 in controls, expressed as lytic units/10(6) cells; P less than 0.05), but no difference could be found between AN and controls in IFN activity as reflected by the level of the IFN-induced enzyme 2'-5' oligoadenylate synthetase (2-5A) in PBMC. Beta-endorphins in the plasma were higher in the AN group (P less than 0.05) but these levels could not be correlated to those of IFN, CMC or TNF. Defective CMC and increased TNF production by PBMC in patients with anorexia nervosa may possibly result from the nutritional deficiencies and neuroendocrine abnormalities associated with the disease, and may contribute to the pathophysiology of AN.
A previously healthy woman developed acute anicteric hepatitis which slowly resolved, though bilateral anterior uveitis then appeared. No other cause than an occupational exposure to trichloroethylene was found, and rechallenge by resuming work has led to a transient increase in serum alkaline phosphatase. Both manifestations may constitute a rare systemic reaction to trichloroethylene.
The autoimmune response in myasthenia gravis is well characterized, but little is known about the mechanisms initiating it. We have studied the interferon system and natural killer cell activity in 25 patients with myasthenia gravis and compared them to 68 healthy subjects and 96 patients with acute viral infections. Forty-four per cent of patients had circulating interferon (greater than 16 mu/ml), and in a similar proportion their peripheral blood mononuclear cells were in an antiviral state, i.e., showed low levels of viral replication when infected by vesicular stomatitis virus. Spontaneous in vitro interferon production by patients' peripheral blood mononuclear cells was also common (greater than 10 mu/ml, 32 per cent), while the response to the alpha-interferon inducer poly I:C was lower than expected, possibly reflecting the already high state of activation of the interferon system. These results were essentially similar to those obtained in patients with viral illnesses and differed significantly from healthy controls. In many myasthenia gravis patients (16 of 22, 73 per cent), a markedly deficient natural killer cell activity was found, with a median cytotoxicity of 6.5 per cent compared to 29 per cent in healthy subjects (p less than 0.005). Thus, many patients with myasthenia gravis have evidence of an activated interferon system and defective natural killer cell activity, suggesting an occult viral infection or reflecting nonspecific stimulation which may nevertheless contribute to the pathogenesis of the autoimmune response.
"Natural" cell-mediated cytotoxicity (CMC), spontaneous release of tumor necrosis factor-alpha (TNF-alpha) by mononuclear cells in vitro and PHA-induced interferon-gamma (IFN-gamma) production were examined by standard methods (confirmed by neutralization with monoclonal antibodies) in 14 female patients with marked weight loss due to anorexia nervosa (AN) and 16 matched healthy controls. We found a significant increase in TNF production in AN, as well as a depressed CMC and IFN-gamma production. Following successful refeeding and nutritional rehabilitation of the AN patients, all results normalized to levels similar to those of controls. Thus, undernutrition in AN is accompanied by changes in cytokines and defective "natural" cytotoxicity. The implications in vivo are unclear but our findings may reflect nutritional-related immunodeficiency in AN and moreover, the increased TNF-release may further suppress food intake and enhance tissue catabolism in anorexia nervosa.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In an attempt to assess the role of immune cytotoxic activity in the sequence of events leading to the acquired immunodeficiency syndrome (AIDS), natural cytotoxic activity was studied in 17 asymptomatic homosexual males, seropositive for anti-human immunodeficiency virus (HIV) antibodies, as compared to 16 of their seronegative counterparts and to 14 control healthy heterosexual individuals. Cell (contact)-mediated cytotoxicity (CMC) as well as cytotoxin (CTX) production by lipopolysaccharide (LPS)-stimulated, phytohemagglutinin (PHA)-stimulated, HeLa tumor cell-stimulated, and unstimulated peripheral blood mononuclear cells (PBMC) were determined using HeLa cell monolayer cultures, sensitized with cycloheximide, as targets. The CMC was markedly enhanced in the seropositive group (28 +/- 21 (mean +/- SD) lytic units/10(6) PBMC) as compared to the seronegative group (17 +/- 7; P less than 0.005) and to the heterosexual group (13 +/- 6; P less than 0.05). Likewise, CTX production by unstimulated PBMC from seropositive homosexuals (19 +/- 26 units/ml) was higher than that observed in the other groups (both 4 +/- 4 units/ml; P less than 0.05). CTX production by PHA-stimulated, LPS-stimulated, and HeLa cell-stimulated PBMC was significantly enhanced in both the seropositive and seronegative groups in comparison to the normal heterosexual controls. These results suggest that increased cytotoxic activity may be present in homosexuals prior to their exposure to HIV, and may be further enhanced after HIV infection.
Explore the source record for details and available documents.
A previously healthy 70-year-old woman was hospitalized for acute pain and edema of her right leg. Deep vein thrombosis was suspected, and she was put on anticoagulant therapy. Ten hours later, she developed a massive swelling of the leg with a well-demarcated violaceous discoloration of the skin and hemorrhagic bullae. She was in deep shock with signs of disseminated intravascular coagulation and adult respiratory distress syndrome. Gram stain of an aspirate from the bullae revealed short chains of Gram-positive cocci, and multiple blood cultures showed abundant growth of Streptococcus pyogenes. Despite intensive treatment, the patient died within hours. Autopsy findings showed extensive pyomyonecrosis of the leg muscles and changes secondary to septicemia. The misleading initial clinical picture and the rarity of this disease entity in temperate climates delayed the correct diagnosis and resulted in a fatal outcome.
A case of fatal torsade de pointes in a 53 year old patient treated with disopyramide is described. The arrhythmia followed the development of acute hepatocellular dysfunction and may have been due to failure of the liver to efficiently degrade the drug to its metabolites.
Explore the source record for details and available documents.