Exploring the impact of patient views on ‘appropriate’ use of services and help seeking: a mixed method study

Background

There are commonly-held views relating to what constitutes appropriate and inappropriate use of finite NHS resources. However, very little is known about how and why such views have an impact on consultation patterns.

Aim

To quantify the prevalence of opinion on whether people use health services unnecessarily within primary care and accident and emergency (A&E) in order to examine the impact of these views on help-seeking behaviour.

Design of study

A mixed method study utilising cross-sectional questionnaire survey and semi-structured interviews.

Setting

A primary care practice in South West England, UK.

Method

Responders to the questionnaire survey were drawn from a random sample of individuals, stratified by sex, selected from one practice in the UK (n = 911). The qualitative sample (n = 22) were purposefully selected from the same general practice.

Results

The quantitative data suggest that the majority of people believe individuals utilise either GP or A&E services inappropriately (65.6%; 95% confidence interval [CI] = 62.4 to 68.7). However, strong views relating to this inappropriate healthcare use were not associated with reported seeking of immediate care (odds ratio [OR] = 0.98, 95% CI = 0.66 to 1.46 for ‘lump’ vignette). Responders tend to consider other people as time wasters, but not themselves. Individuals'' generally describe clear rationales for help seeking, even for seemingly trivial symptoms and anxiety level was strongly predictive of health-seeking behaviour (OR = 2.88; 95% CI = 1.98 to 4.19 for lump vignette).

Conclusion

Perceptions that individuals'' use health services inappropriately are unlikely to explain differences in help-seeking behaviours. The findings suggest that people do not take the decision to consult health services lightly and rationalise why their behaviour is not time wasting.     

Comparison of evoked arousability in breast and formula fed infants.

BACKGROUND: Currently, there is no consistent evidence that breast feeding reduces the risk for sudden infant death syndrome (SIDS). Arousal from sleep is believed to be an important survival mechanism that may be impaired in victims of SIDS. Previously it has been shown that arousability is impaired by the major risk factors for SIDS such as prone sleeping and maternal smoking. AIMS: To establish whether arousability was altered by method of feeding, and whether breast fed infants would have lower arousal thresholds. METHODS: Forty three healthy term infants were studied using daytime polysomnography on three occasions: 2-4 weeks post-term, 2-3 months post-term, and 5-6 months post-term. Multiple measurements of arousal threshold (cm H(2)O) in response to nasal air jet stimulation applied alternately to the nares were made in both active sleep (AS) and quiet sleep (QS) while infants slept supine. Arousal thresholds and sleep period lengths were compared between formula fed and breast fed infants at each age. RESULTS: Arousal thresholds were not different between breast fed and formula fed infants in QS. However, in AS breast fed infants were significantly more arousable than formula fed infants at 2-3 months of age. There was no difference between groups of infants when sleep period length was compared at any study. CONCLUSIONS: Breast fed infants are more easily aroused from AS at 2-3 months of age than formula fed infants. This age coincides with the peak incidence of SIDS.     

CHMP2B mutations are not a common cause of frontotemporal lobar degeneration

It was reported in 1995 that a large Danish family with familial frontotemporal dementia (FTD) was linked to the pericentromeric region of chromosome 3. It has since been claimed that a mutation in the splice acceptor site of exon 6 of CHMP2B is the pathogenic variant in this family. In order to determine whether CHMP2B mutations are a common cause of disease in patients with frontotemporal lobar degeneration (FTLD) we sequenced all exons and flanking regions of CHMP2B in 141 familial FTLD probands from the USA and UK. We failed to find a single pathogenic variant in any case. Polymorphisms were detected but were present in control samples. We conclude that mutations in CHMP2B are a rare cause of familial FTLD and may be specific to the Danish pedigree.     

Long-term preservation of cortically dependent visual function in RCS rats by transplantation.

Cell transplantation is one way of limiting the progress of retinal degeneration in animal models of blinding diseases such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD). Here we transplanted a human retinal pigment epithelial (RPE) cell line into the subretinal space of one such model, the Royal College of Surgeons (RCS) rat, and showed, using head tracking to moving stripes and pattern discrimination in conjunction with single-unit cortical physiology, that cortically mediated vision can be preserved with this treatment.     

Endobronchial adenosine monophosphate challenge causes tachykinin release in the human airway

BACKGROUND: Adenosine 5 monophosphate (AMP) has been shown to cause bronchoconstriction and a sensation of chest tightness when inhaled by asthmatic subjects. This response is attenuated after repeated inhalation of bradykinin, suggesting that AMP may act in part by the release of neuropeptides. OBJECTIVE: This study examined neuropeptide release in the human airway after endobronchial AMP challenge. METHODS: Endobronchial AMP challenge was performed in 20 subjects and tachykinin levels were measured after endobronchial AMP challenge and after placebo endobronchial challenge with saline. RESULTS: All subjects coughed immediately after adenosine challenge. There was a significant increase in neurokinin A and substance P levels (P < .01, P < .01 respectively) when post-saline and post-AMP levels were compared. There was, however, no significant change in calcitonin gene related peptide levels (P = .37). CONCLUSION: This study demonstrates that endobronchial AMP challenge causes tachykinin release in the human airway in vivo.     

Hydrosalpinges adversely affect markers of endometrial receptivity

While in-vitro fertilization (IVF) was initially developed in women with tubal factor infertility, recent clinical studies have suggested that the presence of hydrosalpinges lowers implantation and pregnancy rates. We postulated that these hydrosalpinges cause impaired endometrial receptivity. A total of 103 women with hydrosalpinges were prospectively evaluated, and compared with 55 infertile and 44 fertile controls. All women had endometrial biopsies during the window of implantation, analysed by conventional histological criteria, and also stained for three integrin markers of endometrial receptivity (alpha1beta1, alpha4beta1 and alpha vbeta3). Women with hydrosalpinges (cases) expressed significantly less of the alpha vbeta3 integrin compared with controls. There was no difference in expression of alpha1beta1 or alpha4beta1 among groups. A significantly greater number of cases had out of phase histology and missing alpha vbeta3 (type I defects) and absent integrin expression despite normal histological maturation (type II) defects, compared with controls. Of 20 women with impaired endometrial receptivity who were also biopsied after hydrosalpinx surgery, 70% demonstrated increased alpha vbeta3 expression. Seventy-seven percent of type I and 57% of type II defects were corrected postoperatively. Using markers of endometrial receptivity, this study demonstrates that inflammatory hydrosalpinges have an adverse effect on endometrial receptivity, which in some cases may be overcome by surgical treatment of the hydrosalpinx.      

bcl-2 transgene expression promotes survival and reduces proliferation of CD3-CD4-CD8- T cell progenitors

Proliferative expansion and apoptotic cell death play prominent roles in T cell development. The molecular control of cell cycle progression and apoptosis appear to be inter-connected since the Bcl-2 protein can inhibit apoptosis and slow cell cycle progression in cortical thymocytes and mature T cells, particularly during the transition from the quiescent state into the cell cycle. Here the impact of bcl-2 transgene expression on CD3-CD4-CD8- T cell progenitors was assessed. Bcl-2 enhanced the survival of these progenitors at all of the four major differentiation stages, CD25- CD44+ (pro-T1), CD25 + CD44+ (pro- T2), CD25 + CD44- (pro-T3) and CD25-CD44- (pro-T4). However, it reduced cell cycling and slowed turnover only in the pro-T4 subset. From an analysis of bcl-2 transgenic mice expressing a TCR transgene or bearing a mutation in the scid or rag-1 gene we conclude that Bcl-2 inhibits proliferation only of T cell progenitors that are activated via the pre- TCR, not those stimulated via c-Kit and the IL-7 receptor.      

Human papillomavirus is detectable in Barrett's esophagus and esophageal carcinoma but is unlikely to be of any etiologic significance

Barrett's esophagus (BE), a known precursor of esophageal adenocarcinoma has recently been associated with human papillomavirus (HPV). p16^INK4a expression is a recognized surrogate marker of HPV infection in the cervix.ObjectivesThis study has assessed the possible role of human papillomavirus (HPV) infection in BE and esophageal adenocarcinoma, in the North American population by screening esophageal tissues for HPV by a combination of assays.Study designFormalin-fixed, paraffin-embedded blocks from cases of Barrett's esophagus (n = 84), esophageal adenocarcinoma (n = 36) and normal gastro-esophageal junction (n = 29) were examined for HPV by PCR, chromogenic in situ hybridization, and p16^INK4a immunohistochemistry.ResultsHPV DNA was detected by PCR in 23 of 84 (27.4%) BE cases, 11 of 36 (31%) cases of adenocarcinoma and in 7 of 29 (24%) normal control cases (p = 0.82). p16^INK4a staining was positive in 10 (12%) cases of BE, 15 (42%) cases of adenocarcinoma and 6 (21%) cases of the control group. Positive p16^INK4a staining was not statistically different between the three groups whether positive or negative for HPV DNA (p = 0.91 and p = 0.91 respectively). Similarly, negative p16^INK4a staining did not show a difference between the three groups for whether positive or negative for HPV DNA (p = 0.50 and p = 0.28, respectively). HPV was not detected by CISH in the adenocarcinomas while in BE and control groups, CISH was non-contributory.ConclusionsThese data suggest that while HPV is detectable in a subset of esophageal lesions and tumors, the HPV detected is unlikely to be of etiologic significance or a factor accounting for the increase in BE and esophageal adenocarcinoma cases in the United States.     

Microduplication of Xp11.23p11.3 with effects on cognition,behavior, and craniofacial development

El‐Hattab AW, Bournat J, Eng PA, Wu JBS, Walker BA, Stankiewicz P, Cheung SW, Brown CW. Microduplication of Xp11.23p11.3 with effects on cognition, behavior, and craniofacial development. We report an ～1.3 Mb tandem duplication at Xp11.23p11.3 in an 11‐year‐old boy with pleasant personality, hyperactivity, learning and visual‐spatial difficulties, relative microcephaly, long face, stellate iris pattern, and periorbital fullness. This clinical presentation is milder and distinct from that of patients with partially overlapping Xp11.22p11.23 duplications which have been described in males and females with intellectual disability, language delay, autistic behaviors, and seizures. The duplicated region harbors three known X‐linked mental retardation genes: FTSJ1, ZNF81, and SYN1. Quantitative polymerase chain reaction from whole blood total RNA showed increased expression of three genes located in the duplicated region: EBP, WDR13, and ZNF81. Thus, over‐expression of genes in the interval may contribute to the observed phenotype. Many of the features seen in this patient are present in individuals with Williams‐Beuren syndrome (WBS). Interestingly, the SYN1 gene within the duplicated interval, as well as the STX1A gene, within the WBS critical region, co‐localize to presynaptic active zones, and play important roles in neurotransmitter release.     

A naturalistic study of the effects of pharmacotherapy on substance use disorders among ADHD adults

BACKGROUND: Studies of adults with attention deficit hyperactivity disorder (ADHD) show an elevated prevalence of substance use disorders (SUDs) and the substance abuse literature shows that ADHD is elevated in substance users. Some researchers postulate that stimulant treatment of ADHD increases the risk for SUD in ADHD patients but follow-up studies suggest treatment protects patients from subsequent SUDs. This report uses retrospective data to assess the impact of prior ADHD pharmacotherapy on SUDs in 206 ADHD adults (n=79 late-onset ADHD, n=127 full ADHD) grouped by lifetime history of ADHD treatment (no treatment, past treatment, current and past treatment). METHOD: Structured Clinical Interview for DSM-IV (SCID) data were used to establish abuse and dependence, and Drug Use Screening Inventory (DUSI) responses were used to establish prevalence of use, preference for cigarettes, alcohol and drugs of abuse, complications from use, and motivation for use (get high, change mood, sleep better). RESULTS: No differences were found in the prevalence of cigarette smoking, alcohol or drug abuse or dependence, as well as no significant differences in 1-month prevalence of any use or use more than 20 times. No differences were found in complications of drug or alcohol use across groups. Subjects with current treatment rated getting high as a motivating factor significantly more frequently than subjects in the past treatment group; this result lost significance when we included ADHD diagnostic category. CONCLUSIONS: Our results are consistent across substances and ADHD diagnoses, and support the hypothesis that pharmacotherapy does not cause subsequent SUDs.