The use of 0.25% zinc pyrithione spray does not enhance the efficacy of clobetasol propionate 0.05% foam in the treatment of psoriasis

BACKGROUND: It was discovered that Skin Cap (Cheminova Internacional S.A., Madrid, Spain), an over-the-counter psoriasis therapy with zinc pyrithione, contained clobetasol propionate and it was withdrawn from the market by the US Food and Drug Administration review. Some suggested that there might be a synergistic effect of zinc pyrithione with clobetasol propionate. OBJECTIVE: We sought to evaluate the efficacy of clobetasol propionate 0.05% foam with and without the coadministration of a topical 0.25% zinc pyrithione spray in treating psoriasis involving sites other than the scalp. METHODS: We conducted a randomized, double-blind, right/left study of patients with mild to moderate, generally symmetric, plaque-type psoriasis. Patients were assigned to treatment with clobetasol propionate foam on all psoriatic lesions and then randomly assigned to use zinc pyrithione spray to either the right or left side of their body (vehicle spray to be applied to the opposite side). There was a 2-week treatment phase (visits at baseline, week 1, and week 2) and a follow-up phase (visit at week 4), and all treatments were administered twice daily for 2 weeks. The primary outcome measure was the change from baseline to week 2 in the composite score of the signs of psoriasis (erythema, scaling, plaque thickness) for symmetric target lesions. RESULTS: A total of 25 patients were enrolled; 24 completed the trial and 1 was lost to follow up. Of those who completed the study, 63% (15 of 24) were men, and the mean age (+/-SD) was 50 years (+/-12.2). After 2 weeks of therapy, the average decline in the composite score was 3.5 (+/-1.8) for monotherapy (clobetasol propionate foam and vehicle) and, similarly, 3.3 (+/-1.8) for clobetasol propionate foam plus zinc pyrithione spray (P =.5). DISCUSSION: Zinc pyrithione spray does not appear to enhance the efficacy of clobetasol propionate foam after 2 weeks of therapy.     

Inpatient care for persons with Alzheimer's disease

In the United States, 4.9 million people aged 65 years and older have Alzheimer's disease (AD). Medicare costs for patients with heart disease, diabetes, congestive heart failure, or chronic obstructive pulmonary disease and dementia are higher than for those without dementia. Although one principle of care for persons with AD is "do not hospitalize," comorbidities may require inpatient care. This article presents a definition, the diagnostic criteria for AD, and information about differential diagnosis, risk factors, pathology, progression, evidence base for practice, assessment, pharmacologic management, guidelines for general inpatient care, discharge planning, and interventions related to communications, environment, spirituality, special tasks (eating, protecting tubes and dressings, bathing), stages of AD, and special problems (wandering, pain, incontinence, hallucinations, aggression).     

PVN electrical stimulation prolongs withdrawal latencies and releases oxytocin in cerebrospinal fluid, plasma, and spinal cord tissue in intact and neuropathic rats

We are studying an endogenous, oxytocinergic analgesia system to obtain more information about normal and pathological pain processes. In the recent years, this oxytocinergic system has been shown to be involved in normal and pathological pain suppression. The paraventricular nucleus (PVN) of the hypothalamus is an important source of brain oxytocin (OT). A descending pathway reaching the dorsal horn in the spinal cord was postulated to mediate analgesic effects at the spinal cord level. However, the oxytocin concentration during pain conditions and during PVN electrical stimulation needs to be determined. We designed experiments to measure the OT concentration in cerebrospinal fluid (CSF), plasma, and OT protein in lumbar spinal cord tissue in control and neuropathic rats. Sciatic loose ligature was used as the experimental method to produce neuropathic pain. The main findings were (1) Chronic pain experiments in animals showed that the stimulation of the anterior part of the PVN increased OT concentration and produced analgesia states, as measured by von Frey, cold, and heat plantar tests. (2) Differential effects were produced by electrical stimulation of the anterior or posterior regions of the PVN; electrical stimulation of the anterior part of the PVN enhanced the OT concentration in CSF and plasma, and it also increased OT protein concentrations in the spinal cord tissue; in contrast, the stimulation of the posterior part of the PVN only increased OT concentrations in CSF. These results suggest the participation of an endogenous analgesia system mediated by OT.     

Serum levels of brain-derived neurotrophic factor in schizophrenia on a hypocaloric diet

Dietary factors influence BDNF in animal studies, but there is no comparable data in clinical populations. We examined the effect of a dietary intervention on BDNF serum levels in 67 DSM-IV schizophrenic outpatients (51 males and 16 females). Two groups were assessed in a cross-sectional study: one on a hypocaloric diet (HD) and the other not on a hypocaloric diet. Weight, height and BMI data were collected concurrently with 5-ml blood sampling of each subject. BDNF levels were measured with a sandwich-ELISA. The blood sample was obtained a minimum of one month after the exposure to dietary intervention. Serum BDNF levels were significantly higher in patients on the HD (p=0.023). Additional research examining the interaction among patterns of nutritional food behavior and underlying physiopathology may result in insights upon which evidence-based decisions regarding dietary interventions can be made in people identified with major psychiatric disorders, such as schizophrenia.     

Transient 5-(4-phenylbutoxy)psoralen (PAP-1) treatment dissociates developing pathologies in autoimmune optic neuritis into two distinct pathology profiles

Discovery of treatments to protect axonal function of neurons and prevent permanent disability associated with progressive multiple sclerosis (MS) has faced the uphill challenge of assessing relatively small changes in accumulated axon damage within a background environment that is disorganized by CNS inflammation. We hypothesized that transient immunosuppression after initiation of MS-like autoimmune mechanisms would disassociate development of MS-like myelinated axon pathology from development of CNS inflammation in a rat model of autoimmune optic neuritis (AON). A rat model of myelin oligodendrocyte glycoprotein peptide-induced AON was transiently treated (on days 3-7 after antigen exposure) with 5-(4-phenylbutoxy)psoralen (PAP-1), an immunomodulatory drug previously shown specifically to suppress proliferation of effector memory T-cells and immunoglobulin class-switched B-cells. Thirteen days after antigen exposure, optic nerves were harvested for quantitative assessment of 12 MS-associated pathologies using microfluorimetry. With one exception, the immunoreactivities (-ir) for eight markers of MS-like neuroinflammation and immune infiltration were significantly reduced (P < 0.05) by transient PAP-1 treatment, often to levels significantly below those detected in normal control rat optic nerves. With one exception, four immunoreactive markers of MS-like myelinated axon pathology were detected at levels indicating increased axon/myelin pathology compared with vehicle-treated rats with AON (P < 0.05). These data suggest the conclusion that early causative mechanisms in CNS autoimmunity initiate signaling mechanisms that diverge into two separate pathways, one that is strongly associated with inflammatory responses and one that is associated predominantly with disturbed axon-myelin interactions and impaired fast axonal transport.