Parental information needs in chronic renal failure and diabetes mellitus

The information needs of parents of children with end stage renal failure (ESRF) or with insulin dependent diabetes mellitus (IDDM) were assessed by questionnaires over a 2-year period. Questionnaires were posted on seven occasions at 4-monthly intervals and were sent to both mothers and fathers. Most information needs were reported to be for detailed test results, for new information about the condition and about the child's future social development. Questions responsible for the three highest scores were concerned with the future: the child's fertility; their social, career and marriage prospects; and the hope for a new improved treatment. For the IDDM mothers, scores were significantly different depending on age of the child (P = 0.02). Change in treatment mode had no significant effect on the information needs of parents of children with ESRF (P = 0.81). Occupation was significantly associated with the mean general information needs scores for parents, with occupations of a lower socioeconomic status associated with higher information needs scores. There were no significant differences between the reported mean general information needs scores of parents of children with ESRF and of parents of children with IDDM (P = 0.69) or between mothers and fathers mean general information needs scores (P = 0.58). CONCLUSION: Multidisciplinary team members need to tailor information to the needs of the individual families and be sensitive to socioeconomic factors and communication issues.

NADPH oxidase and heart failure

Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.

Mitochondrial superoxide anion radicals mediate induction of apoptosis in cardiac myoblasts exposed to chronic hypoxia

Both reactive oxygen species (ROS) and ATP depletion may be significant in hypoxia-induced damage and death, either collectively or independently, with high energy requiring, metabolically active cells being the most susceptible to damage. We investigated the kinetics and effects of ROS production in cardiac myoblasts, H9C2 cells, under 2%, 10% and 21% O2 in the presence or absence of apocynin, rotenone and carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone. H9C2 cells showed significant loss of viability within 30 min of culture at 2% oxygen which was not due to apoptosis, but was associated with an increase in protein oxidation. However, after 4 h, apoptosis induction was observed at 2% oxygen and also to a lesser extent at 10% oxygen; this was dependent on the levels of mitochondrial superoxide anion radicals determined using dihydroethidine. Hypoxia-induced ROS production and cell death could be rescued by the mitochondrial complex I inhibitor, rotenone, despite further depletion of ATP. In conclusion, a change to superoxide anion radical steady state level was not detectable after 30 min but was evident after 4 h of mild or severe hypoxia. Superoxide anion radicals from the mitochondrion and not ATP depletion is the major cause of apoptotic cell death in cardiac myoblasts under chronic, severe hypoxia.

Visual stress symptoms secondary to stroke alleviated with spectral filters and precision tinted ophthalmic lenses:a case report

Visual stress is a condition characterised by symptoms of eyestrain, headaches and distortions of visual perception when reading text. The symptoms are frequently alleviated with spectral filters and precision tinted ophthalmic lenses. Visual stress is thought to arise due to cortical hyperexcitability and is associated with a range of neurological conditions. Cortical hyperexcitability is known to occur following stroke. The case presented describes visual stress symptoms resulting from stroke, subsequently managed with spectral filters and precision tinted ophthalmic lenses. The case also highlights that the spectral properties of the tint may need to be modified if the disease course alters.

The prevalence and phenotype of activated microglia/macrophages within the spinal cord of the hyperostotic mouse (twy/twy) changes in response to chronic progressive spinalcord compression:implications for human cervical compressive myelopathy

Background:Cervical compressive myelopathy, e.g. due to spondylosis or ossification of the posterior longitudinal ligament is a common cause of spinal cord dysfunction. Although human pathological studies have reported neuronal loss and demyelination in the chronically compressed spinal cord, little is known about the mechanisms involved. In particular, the neuroinflammatory processes that are thought to underlie the condition are poorly understood. The present study assessed the localized prevalence of activated M1 and M2 microglia/macrophages in twy/twy mice that develop spontaneous cervical spinal cord compression, as a model of human disease.Methods:Inflammatory cells and cytokines were assessed in compressed lesions of the spinal cords in 12-, 18- and 24-weeks old twy/twy mice by immunohistochemical, immunoblot and flow cytometric analysis. Computed tomography and standard histology confirmed a progressive spinal cord compression through the spontaneously development of an impinging calcified mass.Results:The prevalence of CD11b-positive cells, in the compressed spinal cord increased over time with a concurrent decrease in neurons. The CD11b-positive cell population was initially formed of arginase-1- and CD206-positive M2 microglia/macrophages, which later shifted towards iNOS- and CD16/32-positive M1 microglia/macrophages. There was a transient increase in levels of T helper 2 (Th2) cytokines at 18 weeks, whereas levels of Th1 cytokines as well as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and macrophage antigen (Mac) -2 progressively increased.Conclusions:Spinal cord compression was associated with a temporal M2 microglia/macrophage response, which may act as a possible repair or neuroprotective mechanism. However, the persistence of the neural insult also associated with persistent expression of Th1 cytokines and increased prevalence of activated M1 microglia/macrophages, which may lead to neuronal loss and demyelination despite the presence of neurotrophic factors. This understanding of the aetiopathology of chronic spinal cord compression is of importance in the development of new treatment targets in human disease. © 2013 Hirai et al.

Photodynamic therapy:a treatment option in choroidal neovascularisation secondary to punctate inner choroidopathy

Punctate inner choroidopathy is an idiopathic inflammatory ocular disorder characteristically seen in young myopic women. Visual prognosis is generally good but sight threatening choroidal neovascularisation may develop in up to 40% patients.1 We discuss verteporfin photodynamic therapy in subfoveal choroidal neovascularisation secondary to punctate inner choroidopathy that failed to respond to oral corticosteroids and had poor results with submacular surgery in the contralateral eye.

Photodynamic therapy with verteporfin for juxtafoveal choroidal neovascularisation secondary to pathological myopia

The treatment of choroidal neovascularisation (CNV) secondary to pathological myopia has presented a number of problems to ophthalmologists over the years, but the advent of photodynamic therapy (PDT) with verteporfin has changed how we manage these patients. Until PDT became available, the use of laser photocoagulation for extra and juxtafoveal lesions had been shown to be effective in the short term in preventing loss of vision, although the risk of regrowth of CNV and undertreatment were well recognised. However, even in apparent successful cases of photocoagulation, laser scar enlargement and creepage into the fovea in the mid-to-long term often occurred with resulting loss of central vision.1 Other options for treatment were very limited with little evidence that other modalities such as transpupillary thermotherapy or submacular surgery and macular transplantation surgery would be successful in highly myopic eyes. The evidence for the role of PDT and verteporfin CNV secondary to pathological myopia comes from the verteporfin in photodynamic therapy (VIP) study that has shown how effective this treatment is in eyes with subfoveal CNV.2, 3 Now in this publication, Lam et al4 from Hong Kong have shown that PDT is also effective in juxtafoveal CNV, with high myopia. They performed a small prospective study of 11 patients of mean age 44.8 years, with 12 months of follow-up. They found that there was a mean improvement of 1.8 lines of LogMAR best-corrected visual acuity (BCVA) at 12 months, with a mean number of 2.3 PDT treatments. The most rapid improvement occurred within the first 3 months of treatment and by 12 months none of the patients had suffered a deterioration in BCVA from baseline. There were no cases of adverse effects from the infusion or laser treatment. For ophthalmologists dealing with patients with CNV secondary to causes other than AMD, this is further evidence of the effectiveness of PDT with verteporfin in maintaining vision. These patients are likely to be younger than those with AMD and are likely to be in active employment and supporting families, and clearly the preservation of best vision possible is imperative in this group. It is therefore encouraging for ophthalmologists in the United Kingdom that the verteporfin in PDT Cohort Study (VPDT Study) includes the ability to treat patients with subfoveal CNV secondary to high myopia if they fulfill National Institute of Clinical Excellence guidelines, and will allow representations to be made on an individual basis for treatment of juxtafoveal lesions.5 For those ophthalmologists used to juggling increased patient expectations with scarce NHS resources, this is promising news and will allow us to offer a better standard of care to our patients.

Should topical opioid analgesics be regarded as effective and safe when applied to chronic cutaneous lesions?

Objectives: The induction of analgesia for many chronic cutaneous lesions requires treatment with an opioid analgesic. In many patients suffering with these wounds such drugs are either contraindicated or shunned because of their association with death. There are now case reports involving over 100 patients with many different types of chronic superficial wounds, which suggest that the topical application of an opioid in a suitable gel leads to a significant reduction in the level of perceived pain. Key findings: Some work has been undertaken to elucidate the mechanisms by which such a reduction is achieved. To date there have been no proven deleterious effects of such an analgesic system upon wound healing. Although morphine is not absorbed through the intact epidermis, an open wound provides no such barrier and for large wounds drug absorption can be problematic. However, for most chronic cutaneous lesions, where data has been gathered, the blood levels of the drug applied ranges from undetectable to below that required for a systemic effect. Summary If proven, the use of opioids in this way would provide adequate analgesia for a collection of wounds, which are difficult to treat in patients who are often vulnerable. Proof of this concept is now urgently required. © 2011 Royal Pharmaceutical Society.

Identifying the scope for savings at inpatient episode level:an illustration applying DEA to chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterized by a largely irreversible obstruction of the airways, and is one of the leading causes of chronic morbidity and mortality worldwide. This paper illustrates the use of Data Envelopment Analysis (DEA) to assess the potential for cost savings at COPD inpatient episode level. The analysis uses the length of stay of each episode as a surrogate for expenditure on that episode while allowing for the medical condition of the patient and the quality of care received. We find substantial possible reductions in length of stay which would translate to cost savings. The paper also explores differences both between hospitals and between care teams within hospitals so that cost efficient protocols of treatment can be identified and disseminated.