ABSTRACT
BACKGROUND: The hygiene hypothesis is often proposed to explain the high prevalence of atopy in the western world. Dysregulation of the immune system may result from inadequate exposure to micro-organisms such as mycobacteria. A small trial suggested that a killed extract of Mycobacterium vaccae ameliorates atopic dermatitis (AD). OBJECTIVES: To confirm in a large clinical trial whether killed M. vaccae ameliorates AD in 5-16-year-old children. METHODS: This was a randomized, placebo-controlled, double-blind, multi-centre study of the effect of intradermal injection of killed M. vaccae (0.1 or 1 mg) on patients, aged 5-16, with moderate-to-severe AD. Patients were followed up for 24 weeks. The primary end point was the change in severity of AD at 12 weeks, assessed using the six area, six-sign, atopic dermatitis (SASSAD) score. Secondary end points included changes in disease extent, patient's global assessment and children's dermatology life quality index. RESULTS: There were 166 patients randomized. The mean SASSAD score fell to a similar degree at week 12 in all treatment arms: from 33 to 24, (26%) in the high-dose group, from 30 to 23 (25%) in the low-dose group and from 36 to 27 (24%) in the placebo group (P>0.05). Secondary end points followed the same trend. Adverse events were generally those expected to occur in this population. Injection site reactions occurred in 32 patients at week 4. CONCLUSIONS: M. vaccae was no more effective than the placebo in ameliorating the severity of AD.
Subject(s)
Bacterial Vaccines/immunology , Dermatitis, Atopic/immunology , Mycobacterium/immunology , Adolescent , Bacterial Vaccines/administration & dosage , Bacterial Vaccines/adverse effects , Child , Child, Preschool , Dermatitis, Atopic/therapy , Double-Blind Method , Drug Administration Schedule , Eczema/drug therapy , Eczema/immunology , Female , Humans , Injections, Intradermal/adverse effects , Male , Severity of Illness Index , Treatment OutcomeABSTRACT
A patient with elevated levels of serum IgA developed purpuric lesions histologically resembling Henoch-Schönlein purpura brought on by consuming alcohol. Alcohol challenge with 5 units of alcohol reproduced the lesions, with a rapid rise of circulating CD4+ and CD8+ T cells followed by a fall of serum IgA and C3 concentration. The skin lesions and serum abnormalities resolved spontaneously within 6 weeks of the alcohol challenge.
Subject(s)
Ethanol/adverse effects , Immunoglobulin A/analysis , Skin Diseases, Vascular/chemically induced , Vasculitis/chemically induced , Adult , Humans , Leg Dermatoses/chemically induced , Leg Dermatoses/pathology , Male , Skin Diseases, Vascular/pathology , Vasculitis/pathologyABSTRACT
The uptake of L-[3H]arginine into synaptosomes prepared from rat cerebellum and cortex occurred by a high-affinity carrier-mediated process. The uptake of arginine appeared to be potentiated by removal of extracellular Na+, inhibited by high levels of extracellular K+, but not by depolarization with veratridine or 4-amino pyridine. The effect of Na+ removal or K+ elevation did not seem to be due to changes in intracellular Ca2+ or pH. In both brain regions, uptake was significantly inhibited by L-arginine, L-lysine, L-ornithine, and L-homoarginine, but not by D-arginine nor L-citrulline. Uptake was also inhibited by NG-monomethyl-L-arginine acetate, but not by NG-nitro-L-arginine methyl ester nor NG-nitro-L-arginine except in the cortex at a concentration of 1 mM. The results indicate that the carrier system operating in synaptosomes showed many of the characteristics of the ubiquitous y+ system seen in many other tissues, although its apparent sensitivity to variations in extracellular Na+ was unusual.
Subject(s)
Arginine/metabolism , Cerebellum/metabolism , Cerebral Cortex/metabolism , Synaptosomes/metabolism , Ammonium Chloride/pharmacology , Animals , Arginine/analogs & derivatives , Arginine/pharmacology , Biological Transport , Calcium/metabolism , Enzyme Inhibitors/pharmacology , Female , Hydrogen-Ion Concentration , Kinetics , Nitric Oxide Synthase/antagonists & inhibitors , Potassium/pharmacology , Rats , Rats, Wistar , Sodium/pharmacology , Sodium Acetate/pharmacology , TritiumABSTRACT
The dexamethasone suppression test (DST) was administered to 28 subjects who met DSM-III criteria for chronic schizophrenia and shared similar environments. Samples were assayed for both plasma cortisol and dexamethasone levels. After controlling for other factors, the mean postdexamethasone cortisol level (MPDC) was correlated with the patients' score on the Scale for the Assessment of Negative Symptoms (SANS). A significant relationship emerged between these 2 parameters, suggesting that the social deterioration seen in chronic schizophrenia is at least partly related to a biological disease process as reflected by the DST. The importance of quantifying the level of dexamethasone in the DST is discussed.
Subject(s)
Arousal/physiology , Dexamethasone , Hydrocortisone/blood , Schizophrenia/diagnosis , Schizophrenic Psychology , Adult , Female , Humans , Male , Middle Aged , Psychiatric Status Rating Scales , Schizophrenia/bloodABSTRACT
Twenty-six in-patients satisfying DSM-III criteria for major depressive episode were assessed using the Newcastle Diagnostic and ECT Predictor Scales and the dexamethasone suppression test (DST), prior to commencing a course of electroconvulsive therapy (ECT). The Newcastle ECT Predictor Scale was successful in predicting both immediate outcome and outcome over the 6 months following ECT; the DST was unsuccessful in predicting either immediate or 6-month outcome.
Subject(s)
Depressive Disorder/therapy , Electroconvulsive Therapy , Adult , Aged , Depressive Disorder/diagnosis , Dexamethasone , Female , Humans , Male , Middle Aged , Predictive Value of Tests , PrognosisABSTRACT
The non-suppression by dexamethasone of endogenous cortisol production has been held to be a specific and sensitive indicator of biological depression. Non-suppression has, however, been reported in a proportion of patients with severe dementia. In the present study failure of suppression was found in 10 out of 20 demented patients. The non-suppressors scored significantly higher on a scale of signs of depression. Following antidepressant treatment, 3 out of 8 non-suppressors reverted to normal suppression, but this was not associated with clinical improvements. The implications of these findings are discussed.
