Innovative strategies to improve diabetes outcomes in disadvantaged populations.

Diabetes disproportionately affects disadvantaged populations. Eighty percent of deaths directly caused by diabetes occurred in low- and middle-income countries. In high-income countries, there are marked disparities in diabetes control among racial/ethnic minorities and those with low socio-economic status. Innovative, effective and cost-effective strategies are needed to improve diabetes outcomes in these populations. Technological advances, peer educators and community health workers have expanded methodologies to reach, educate and monitor individuals with diabetes. In the present manuscript we review the outcomes of these strategies, and describe the barriers to and facilitators of these approaches for improving diabetes outcomes.

Successful self-management among non-insulin-treated adults with Type 2 diabetes: a self-regulation perspective.

AIMS: To clarify the role of self-monitoring of blood glucose (SMBG) in the self-management of Type 2 diabetes from the patient's perspective, using in-depth interviews with non-insulin-treated adults to investigate how they learned to manage their diabetes effectively and whether SMBG played a significant role in this process. METHODS: Individual interviews were conducted with 14 non-insulin-treated adults with Type 2 diabetes who had significantly improved their glycaemic control [64% women; 50% black; 21% Hispanic; mean age 60 years; mean HbA(1c) concentration 43 mmol/mol (6.1%)]. Interviews were transcribed and analysed by a coding team, applying the concept of illness coherence from the Common Sense Model of Self-Regulation. RESULTS: The majority of participants relied on SMBG to evaluate their self-management efforts. Key themes included: adopting an experimental approach; experiencing 'a-ha' moments; provider-assisted problem-solving; using SMBG and other feedback to evaluate when their efforts were working; and normalizing diabetes-specific behaviour changes as being healthy for everyone. CONCLUSIONS: Our qualitative data are consistent with the argument that SMBG, if implemented appropriately with enough education and provider access, can be a powerful tool for non-insulin-treated adults with Type 2 diabetes to monitor their self-management. Establishing sufficient conditions for illness coherence to develop while individuals are learning to use SMBG could increase their sense of personal control in managing a complex and demanding illness.

Osteoarthritis year 2013 in review: imaging.

PURPOSE: To review recent original research publications related to imaging of osteoarthritis (OA) and identify emerging trends and significant advances. METHODS: Relevant articles were identified through a search of the PubMed database using the query terms "OA" in combination with "imaging", "radiography", "MRI", "ultrasound", "computed tomography", and "nuclear medicine"; either published or in press between March 2012 and March 2013. Abstracts were reviewed to exclude review articles, case reports, and studies not focused on imaging using routine clinical imaging measures. RESULTS: Initial query yielded 932 references, which were reduced to 328 citations following the initial review. MRI (118 references) and radiography (129 refs) remain the primary imaging modalities in OA studies, with fewer reports using computed tomography (CT) (35 refs) and ultrasound (23 refs). MRI parametric mapping techniques remain an active research area (33 refs) with growth in T2*- and T1-rho mapping publications compared to prior years. Although the knee is the major joint studied (210 refs) there is interest in the hip (106 refs) and hand (29 refs). Imaging continues to focus on evaluation of cartilage (173 refs) and bone (119 refs). CONCLUSION: Imaging plays a major role in OA research with publications continuing along traditional lines of investigation. Translational and clinical research application of compositional MRI techniques is becoming more common driven in part by the availability of T2 mapping data from the Osteoarthritis Initiative (OAI). New imaging techniques continue to be developed with a goal of identifying methods with greater specificity and responsiveness to changes in the joint, and novel functional neuroimaging techniques to study central pain. Publications related to imaging of OA continue to be heavily focused on quantitative and semiquantitative MRI evaluation of the knee with increasing application of compositional MRI techniques in the hip.

Measurements of medication adherence in diabetic patients with poorly controlled HbA(1c).

AIMS: To assess pharmacy claims and self-report data as measures of medication adherence and to describe baseline characteristics of subjects in the Improving Diabetes Outcomes Study. METHODS: Multi-ethnic, lower-income, insured adults (n = 526) in New York City with Type 2 diabetes were enrolled in a randomized, controlled, behavioural intervention study delivered by telephone. Baseline data were examined, including glycated haemoglobin (HbA(1c)), objective measures of diabetes medication adherence [claims data medication possession ratio (MPR)], and two self-report measures [Morisky Medication-taking Scale and the medication-taking item of the Summary of Diabetes Self-Care Activities (SDSCA)]. Associations of highest tertile HbA(1c) (>or= 9.3%) with lowest tertile MPR (< 42%) were assessed with logistic regression models adjusting for potential confounders. Subset analyses were performed based on assessment of potential interaction. RESULTS: Participants (mean +/- sd age 56 +/- 7 years) had median (interquartile range) HbA(1c) 8.6% (8.0-10.0). Correlations of baseline MPR with Morisky score and SDSCA medication-taking item were strongly significant (both rho = 0.21, P < 0.001). Lowest MPR was significantly (P = 0.008) associated with highest HbA(1c) in the group as a whole and among the subset taking two or more oral glucose-lowering agents (OGLA) (P = 0.002), but not among the subset taking only one (P = 0.83). Self-report adherence measures were not significantly associated with HbA(1c) in either the whole group or either subset. CONCLUSIONS: These results support the validity of MPR as an adherence measure for OGLA among insured diabetes patients with poorly controlled HbA(1c), especially those taking two or more OGLA.

Elevated cerebrospinal fluid (CSF) leptin in idiopathic intracranial hypertension (IIH): evidence for hypothalamic leptin resistance?

OBJECTIVE: The aetiology of idiopathic intracranial hypertension (IIH) is not known, but its association with obesity is well-recognized. Recent studies have linked obesity with abnormalities in circulating inflammatory and adiposity related cytokines. The aim of this study was to characterize adipokine and inflammatory cytokine profiles in IIH. DESIGN: Paired serum and cerebrospinal fluid (CSF) specimens were collected from 26 patients with IIH and compared to 62 control subjects. Samples were analysed for leptin, resistin, adiponectin, insulin, IL-1beta, IL-6, IL-8 (CXCL8), TNFalpha, MCP-1 (CCL2), hepatocyte growth factor, nerve growth factor and PAI-1 using multiplex bead immunoassays. RESULTS: CSF leptin was significantly higher in patients with IIH (P = 0.001) compared to controls after correction for age, gender and body mass index (BMI). In the control population, BMI correlated with serum leptin (r = 0.34; P = 0.007) and CSF leptin (r = 0.51; P < 0.0001), but this was not the case for the IIH population. Profiles of other inflammatory cytokines and adipokines did not differ between IIH patients and controls once anthropometric factors had been accounted for. CONCLUSIONS: IIH was characterized by significantly elevated CSF leptin levels which did not correlate with BMI. We suggest that CSF leptin may be important in the pathophysiology of IIH and that obesity in IIH may occur as a result of hypothalamic leptin resistance.

The corticosteroid metabolic profile of the mouse.

Data are presented on the urinary corticosteroid metabolic profile of the mouse strain 129/svJ. Through the use of GC/MS we have characterized, or tentatively identified corticosterone (Kendall's compound B) metabolites of both the 11beta-hydroxy and 11-carbonyl (compound A) series in urine. Full mass spectra of the methyloxime-trimethylether derivatives of 15 metabolites are included in the paper as an aid to other researchers in the field. Metabolites ranged in polarity from tetrahydrocorticosterone (THB) to dihydroxy-corticosterone with dominance of highly polar steroids. We found that prior to excretion corticosterone can undergo oxidation at position 11beta, reduction at position 20 and A-ring reduction. Metabolites retaining the 3-oxo-4-ene structure can be hydroxylated at position 6beta- as well as at an unidentified position, probably 16alpha-. Saturated steroids can be hydroxylated at positions 1beta-, 6alpha-, 15alpha- and 16alpha. A pair of hydroxy-20-dihydro-corticosterone metabolites (OH-DHB) were the most important excretory products accounting for about 40% of the total. One metabolite of this type was identified as 6beta-hydroxy-DHB; the other, of similar quantitative importance was probably 16alpha-hydroxy-DHB. The ratio of metabolites of corticosterone (B) to those of 11-dehydro-corticosterone (A) was greater than 9:1, considerably higher than that for the equivalent "human" ratio of 1:1 for cortisol to cortisone metabolites. Results from this study allowed the evaluation of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) activity in mice with deleted glucose-6-phosphate transporter (G6PT). These mice had attenuated back-conversion of A to B resulting in an increased ratio of A-metabolites to B-metabolites [Walker EA, Ahmed A, Lavery GG, Tomlinson JW, Kim SY, Cooper MS, Stewart PM, 11beta-Hydroxysteroid dehydrogenase type 1 regulation by intracellular glucose-6-phosphate, provides evidence for a novel link between glucose metabolism and HPA axis function. J Biol Chem 2007;282:27030-6]. We believe this study is currently the most comprehensive on the urinary steroid metabolic profile of the mouse. Quantitatively less steroid is excreted in urine than in feces by this species but urine analysis is more straightforward and the hepatic metabolites are less subject to microbial degradation than if feces was analyzed.

Corticosteroids, 11beta-hydroxysteroid dehydrogenase isozymes and the rabbit choroid plexus.

The epithelial cells of the choroid plexus (CP) are responsible for cerebrospinal fluid (CSF) secretion into the ventricles of the brain. The balance between CSF production and drainage, in part, facilitates a normal intracranial pressure. The secretion of Na(+) and anions by the CP creates an osmotic gradient driving water into the ventricles. This is opposite to classical Na(+) transporting tissues, such as the kidney, where Na(+) and water reabsorption is mediated by 11beta-hydroxysteroid dehydrogenase type 2 that protects the mineralocorticoid receptor by abrogating active cortisol to inactive cortisone. In the human ocular ciliary epithelium, Na(+) and water secretion is dependent on a novel mediator of ciliary epithelial Na(+) transport, 11beta-HSD type 1 (11beta-HSD1), that generates intraocular cortisol. In a mechanism analogous to that of the embryologically related ocular ciliary epithelium, we propose that autocrine regulation of intracranial cortisol is dependent on 11beta-HSD1 expression in the CP epithelial cells. By conducting immunolocalisation studies on brains from New Zealand White Albino rabbits, we defined the expression of 11beta-HSD1 in the secretory CP epithelial cells. Enzyme assays performed on intact rabbit CP whole tissue explants confirmed predominant 11beta-HSD1 activity, generating cortisol that was inhibited by glycyrrhetinic acid (an 11beta-HSD inhibitor). Using the real time-polymerase chain reaction, rabbit CP tissue was found to express levels of 11beta-HSD1, glucocorticoid receptor alpha and serum and glucocorticoid-regulated kinase 1 mRNA comparable to that expressed in rabbit ocular ciliary body, thereby highlighting the similarity between these two tissues. Furthermore, an enzyme-linked immunosorbent assay of rabbit CSF revealed a median cortisol concentration of 1.7 nmol/l (range 1.4-4.3 nmol/l, n = 9). Our data have identified a functional 11beta-HSD1 within the CP, mediating intracranial cortisol bioavailability. Expression of 11beta-HSD1 may be fundamental in the regulation of CSF secretion and the local generation of cortisol may represent a pathophysiological mechanism underlying cortisol-dependent neuroendocrine diseases.

In vivo pharmacological resultant analysis reveals noncompetitive interactions between opioid antagonists in the rat tail-withdrawal assay.

BACKGROUND AND PURPOSE: Pharmacological resultant analysis is a technique that can detect secondary effects of competitive antagonists in vitro. The utility of pharmacological resultant analysis as a potential tool for the investigation of antagonist interactions in vivo was examined in the present study using two opioid antagonists, naltrexone and CTAP. EXPERIMENTAL APPROACH: Using the experimental design of pharmacological resultant analysis, the well-characterized opioid antagonist naltrexone was examined in the presence of multiple doses of CTAP to block the antinociceptive effects of morphine in the rat warm-water (55(o)C), tail-withdrawal assay. KEY RESULTS: Alone, all doses of naltrexone, CTAP, and CTOP examined blocked the antinociceptive effects of morphine. In the presence of fixed doses of 1 or 10 microg CTAP, increasing doses of naltrexone produced dose-dependent shifts to the right in the morphine dose-response curve. However, a lower dose of naltrexone in combination with 1 or 10 mug CTAP failed to alter the morphine dose-response curve. In the presence of a fixed dose of 0.1 mg kg(-1) naltrexone, CTAP doses produced irregular shifts to the right in the morphine dose-response curves. CONCLUSIONS AND IMPLICATIONS: Resultant analysis was applied and an apparent pK(C) value for CTAP was found to be one log unit higher than the apparent pA(2) value for CTAP, evidence that CTAP may have secondary actions or that a signal transducer function may be altered by the combinations of these antagonists. Taken together, these data suggest pharmacological resultant analysis can reveal novel interactions between antagonists in vivo.

Intake of volatile nitrosamines from consumption of alcohols.

Volatile nitrosamines were determined in alcoholic drinks during epidemiologic studies on the relationship between esophageal cancer incidence and alcohol consumption in Normandy, France. Nitrosodimethylamine (NDMA) was found commonly in most alcoholic drinks tested, with the exception of wine. The average level, about 2 micrograms/liter in beers, was higher than that for other drinks; the range was 0.2--8.6 micrograms/liter. Traces of nitrosodiethylamine (NDEA) were also detected in spirits and ciders. No significant increases in levels were found after nitrosation. Calculation of daily intake in the study region showed that the main intake of volatile nitrosamine is from NDMA in beer. The intake of NDEA through consumption of cider is about one-third that of NDMA from all sources.

Costs of health care use by women HMO members with a history of childhood abuse and neglect.

BACKGROUND: Early childhood maltreatment has been associated with adverse adult health outcomes, but little is known about the magnitude of adult health care use and costs that accompany maltreatment. We examined differences in annual health care use and costs in women with and without histories of childhood sexual, emotional, or physical abuse or neglect. METHODS: A random sample of 1225 women members of a health maintenance organization completed a 22-page questionnaire inquiring into childhood maltreatment experiences as measured by the Childhood Trauma Questionnaire. Health care costs and use data were obtained from the automated cost-accounting system of the health maintenance organization, including total costs, outpatient and primary care costs, and emergency department visits. RESULTS: Women who reported any abuse or neglect had median annual health care costs that were $97 (95% confidence interval, $0.47-$188.26) greater than women who did not report maltreatment. Women who reported sexual abuse had median annual health care costs that were $245 (95% confidence interval, $132.32-$381.93) greater than costs among women who did not report abuse. Women with sexual abuse histories had significantly higher primary care and outpatient costs and more frequent emergency department visits than women without these histories. CONCLUSION: Although the absolute cost differences per year per woman were relatively modest, the large number of women in the population with these experiences suggests that the total costs to society are substantial.

Quality assurance for blood glucose monitoring in health-care facilities.

OBJECTIVE: To describe the practice of quality assurance (QA) for capillary blood glucose monitoring (CBGM) in health-care facilities. RESEARCH DESIGN AND METHODS: Descriptive survey data were collected from a purposive sample of 378 health-care providers, who use CBGM and direct CBGM QA programs, from acute- and chronic-care facilities in 47 states. Subjects completed a 36-item multiple-choice survey about QA practices for CBGM by providers. RESULTS: Only 53.4% of respondents reported a multidisciplinary advisory group to assist in decision making for the CBGM program. Almost one-third reported no clinical laboratory involvement in their QA program. Over 70% of respondents reported inclusion of all clinical areas in the CBGM program. Comparison of results of the same patient sample by laboratory reference method and CBGM system was done routinely by only 43.6% of respondents. Scheduled proficiency testing was reported by 33.4%. Only 5.8% of respondents reported the coexistence of a CBGM advisory group, full participation of the laboratory, and quarterly proficiency testing. Over 50% of respondents reported a patient charge for CBGM. CONCLUSIONS: When survey results are compared with regulatory and accreditation standards, it is evident that a wide gap exists. Resources to bridge this gap may be scarce in many facilities. Further research is needed to determine minimal QA standards for CBGM that provide for optimal patient outcomes.

Modulation of 11beta-hydroxysteroid dehydrogenase isozymes by proinflammatory cytokines in osteoblasts: an autocrine switch from glucocorticoid inactivation to activation.

Tissue damage by proinflammatory cytokines is attenuated at both systemic and cellular levels by counter anti-inflammatory factors such as corticosteroids. Target cell responses to corticosteroids are dependent on several factors including prereceptor regulation via local steroidogenic enzymes. In particular, two isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD), by interconverting hormonally active cortisol (F) to inactive cortisone (E), regulate the peripheral action of corticosteroids 11beta-HSD1 by converting E to F and 11beta-HSD2 by inactivating F to E. In different in vitro and in vivo systems both 11beta-HSD isozymes have been shown to be expressed in osteoblasts (OBs). Using the MG-63 human osteosarcoma cell-line and primary cultures of human OBs, we have studied the regulation of osteoblastic 11beta-HSD isozyme expression and activity by cytokines and hormones with established roles in bone physiology. In MG-63 cells, interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) potently inhibited 11beta-HSD2 activity (cortisol-cortisone conversion) and messenger RNA (mRNA) levels in a dose-dependent manner while stimulating reciprocal expression of 11beta-HSD1 mRNA and activity (cortisone-cortisol conversion). A similar rise in 11beta-HSD1 reductase activity also was observed in primary cultures of OBs treated with 10 ng/ml TNF-alpha. Pretreatment of MG-63 cells with 0.1 ng/ml IL-1beta resulted in increased cellular sensitivity to physiological glucocorticoids as shown by induction of serum and glucocorticoid-inducible kinase (SGK; relative increase with 50 nM F but no IL-1beta pretreatment 1.12 +/- 0.34; with pretreatment 2.63 +/- 0.50; p < 0.01). These results highlight a novel mechanism within bone cells whereby inflammatory cytokines cause an autocrine switch in intracellular corticosteroid metabolism by disabling glucocorticoid inactivation (11beta-HSD2) while inducing glucocorticoid activation (11beta-HSD1). Therefore, it can be postulated that some of the effects of proinflammatory cytokines within bone (e.g., periarticular erosions in inflammatory arthritis) are mediated by this mechanism.

Constitutive expression of 25-hydroxyvitamin D3-1alpha-hydroxylase in a transformed human proximal tubule cell line: evidence for direct regulation of vitamin D metabolism by calcium.

Circulating levels of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) are dependent on activity of the renal mitochondrial cytochrome P450 enzyme, 25-hydroxyvitamin D3-1alpha-hydroxylase (1alpha-hydroxylase). Production of 1,25-(OH)2D3 occurs predominantly in the renal proximal tubule, with 1alpha-hydroxylase activity being impaired in renal insufficiency and renal disease. The expression and activity of 1alpha-hydroxylase are tightly regulated in response to serum levels of PTH, calcium, phosphate, and 1,25-(OH)2D3 itself. As a consequence of this, the characterization of 1alpha-hydroxylase in human renal tissue has proved difficult. In this study we have characterized constitutive 1alpha-hydroxylase expression in a simian virus 40-transformed human proximal tubule cell line, HKC-8. Initial analyses of [3H]25-hydroxyvitamin D3 (25OHD3) metabolism in these cells using straight and reverse phase HPLC revealed product peaks that coincided with authentic 1,25-(OH)2D3 as well as 24,25-dihydroxyvitamin D3 (24,25-(OH)2D3). Enzyme kinetic studies indicated that the Km for synthesis of 1,25-(OH)2D3 in HKC-8 cells was 120 nmol/liter 25OHD3, with a maximum velocity of 21 pmol/h/mg protein. This activity was inhibited by treatment with ketoconazole, but not diphenyl phenylenediamine. RT-PCR analysis of RNA from HKC-8 cells revealed a transcript similar in size to that observed in keratinocytes and primary cultures of human proximal tubule cells, and protein was detected by Western blot analysis. Synthesis of 1,25-(OH)2D3 was up regulated by treatment with forskolin (10 micromol/liter, 24 h) and was down-regulated by 1,25-(OH)2D3 (10 nmol/liter, 24 h). 1Alpha-hydroxylase activity in HKC-8 cells was also sensitive to the concentration of calcium. Cells grown in low calcium (0.5 mmol/liter) showed a 4.8-fold induction of 1alpha-hydroxylase, whereas treatment with medium containing high levels of calcium (2 mmol/liter) significantly inhibited 1,25-(OH)2D3 production. These data suggest that direct effects of calcium on proximal tubule cells may be an important feature of the regulation of renal 1,25-(OH)2D3 production.

Association studies between microsatellite markers within the gene encoding human 11beta-hydroxysteroid dehydrogenase type 1 and body mass index, waist to hip ratio, and glucocorticoid metabolism.

Two isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) interconvert active cortisol (F) and inactive cortisone (E). 11beta-HSD1 is an oxo-reductase (E to F) expressed in several glucocorticoid target tissues, including liver and adipose tissue, where it facilitates glucocorticoid-induced gluconeogenesis and adipocyte differentiation, respectively. We have isolated a full-length HSD11B1 genomic clone; the gene is more than 30 kb in length, not 9 kb in length as previously reported, principally due to a large intron 4. Two polymorphic (CA)(n) repeats have been characterized within intron 4: a CA(19) repeat 2.7 kb 3' of exon 4 and a CA(15) repeat 3 kb 5' of exon 5. The microsatellites, CA(19) and CA(15), were PCR amplified using fluorescent primers and were genotyped on an ABI 377 DNA sequencer from DNA of 413 normal individuals enrolled in the MONICA study of cardiovascular risk factors and 557 Danish men (ADIGEN study), of whom 234 were obese [body mass index (BMI), >/=31 kg/m(2) ] at draft board examination and 323 were randomly selected controls from the draftee population with BMI below 31 kg/m(2) (mean +/- SE, 21.7 +/- 0.41). Genotypic data from the normal MONICA cohort was compared with gender, 5beta-tetrahydrocortisol+5alpha-tetrahydrocortisol/tetrahydrocortisone ratio, and waist to hip (W:H) ratio. When analyzed by allele length (0, 1, or 2 short alleles) for the CA(19) marker, there was a trend toward a higher 5beta-tetrahydrocortisol+5alpha-tetrahydrocortisol/tetrahydrocortisone ratio (P = 0.058) and an increased W:H ratio (2 vs. 0.1 short; P(c) = 0.10) with overrepresentation of short alleles. The opposite was true for the CA(15) locus, with longer alleles at this locus predicting increased 11beta-HSD1 activity, particularly in females. Genotypic data from the ADIGEN case-control population was compared with clinical markers of obesity such as BMI and W:H ratio. There was no significant difference in the distribution of either microsatellite marker between lean and obese groups. Allele distributions were binomial, as seen for the MONICA cohort, and the data were split accordingly (zero, one, or two short alleles). No significant association was seen between grouped alleles and the clinical parameters. No association was observed between HSD11B1 genotype and BMI in either population. These data suggest that 11beta-HSD1 is not a major factor in explaining genetic susceptibility to obesity per se. However, weak associations between HSD11B1 genotype, increased 11beta-HSD1 activity, and W:H ratio suggest that polymorphic variability at the HSD11B1 locus may influence susceptibility to central obesity through enhanced 11beta-HSD1 activity (E to F conversion) in visceral adipose tissue.

Irritable bowel syndrome and psychiatric illness.

Psychiatric illnesses such as mood, anxiety, and somatization disorders share many common features with irritable bowel syndrome. The authors review recent developments in the definition of irritable bowel syndrome and its relationship to psychiatric illness, discuss the diagnostic validity of irritable bowel syndrome from several perspectives, and offer a pathophysiological model of irritable bowel syndrome that integrates many of the biological and psychosocial findings of earlier studies. Psychiatric evaluation appears to be an important factor in the diagnosis and treatment of patients with irritable bowel syndrome.

Histories of sexual victimization in patients with irritable bowel syndrome or inflammatory bowel disease.

OBJECTIVE: Two reports have suggested a possible association between a history of sexual trauma and irritable bowel syndrome, but several factors in their study designs limited their generalizability. The authors used a more rigorous methodology to confirm this association. METHOD: They administered structured psychiatric and sexual trauma interviews to 28 patients with irritable bowel syndrome and 19 patients with inflammatory bowel disease and compared prevalence rates of sexual victimization in the two groups. RESULTS: Compared with patients diagnosed as having inflammatory bowel disease, patients with irritable bowel syndrome had a significantly higher rate of severe lifetime sexual trauma (32% versus 0%), severe childhood sexual abuse (11% versus 0%), and any lifetime sexual victimization (54% versus 5%). The nine patients who had experienced severe lifetime victimization had significantly higher odds ratios for lifetime depression, panic disorder, phobia, somatization disorder, alcohol abuse, functional dyspareunia, and inhibited sexual desire than the 38 patients who had experienced less severe sexual trauma or no trauma. A logistic regression analysis showed that gender, the number of medically unexplained physical symptoms, and self-reported anxiety and hostility accounted for all of the variance in the victimized group. CONCLUSIONS: These preliminary results suggest that sexual victimization may be an important factor in the development of irritable bowel syndrome in some patients. Future studies attempting to categorize subgroups of patients with irritable bowel syndrome should inquire into past histories of sexual victimization.

PIP: This study confirms the previously studied findings by using a more rigorous methodology concerning the association of sexual victimization history and irritable bowel syndrome or inflammatory bowel disease. Structured psychiatric and sexual trauma interviews were given to 28 patients with irritable bowel syndrome and 19 inflammatory bowel disease, and the prevalence rates of sexual victimization in the 2 groups were compared. A logistic regression analysis was performed to summarize the differences between patients who had severe trauma and those who had none, and to account for intercorrelations among the study variables. Results showed that patients with irritable bowel syndrome were more likely to have a history of previous sexual victimization. The odd ratios for current and lifetime psychiatric disorders in the 9 patients who had experienced severe forms of victimization showed that they were at significantly greater risk for affective, anxiety, and somatoform disorders as well as substance abuse and sexual dysfunction. It was also demonstrated that the best predictors of having experienced severe forms of victimization were gender, the number of medically unexplained physical symptoms, and self-reported anxiety and hostility. This study suggests that irritable bowel syndrome may be part of a chronic adjustment to previous sexual victimization in some patients.

Dissociation in women with chronic pelvic pain.

OBJECTIVE: The authors' goal was to determine if women with chronic pelvic pain are significantly more likely to use dissociation as a coping mechanism than women without pain. METHOD: The subjects were recruited from women who attended a university women's clinic during a 1-month period. Twenty-two women who reported that they had at any time in their lives experienced pelvic pain nearly every day for a period of at least 6 months were included in the study, along with 21 randomly selected women without a history of chronic pelvic pain. The 43 women were given structured sexual assault interviews and completed psychological self-report measures. RESULTS: The women with chronic pain were significantly more likely to use dissociation as a coping mechanism, to show current psychological distress, to see themselves as medically disabled, to experience vocational and social decrements in function, and to amplify physical symptoms. They were also significantly more likely to have experienced severe childhood sexual abuse. In the total study group, women with a childhood history of sexual abuse had significantly higher scores on measures of psychological distress, somatization, and dissociation and viewed their physical health and functioning as more impaired. CONCLUSIONS: The authors discuss a model for the development of somatization, dissociation, and pain symptoms in victims of early sexual abuse.

Psychiatric illness and irritable bowel syndrome: a comparison with inflammatory bowel disease.

Structured psychiatric interviews and psychological self-report measures were administered to 28 patients with irritable bowel syndrome and 19 patients with inflammatory bowel disease. Significantly more of the patients with irritable bowel syndrome had lifetime diagnoses of major depression, somatization disorder, generalized anxiety disorder, panic disorder, and phobic disorder. They had significantly more medically unexplained somatic symptoms, and most had suffered from psychiatric disorders, particularly anxiety disorders, before the onset of their irritable bowel symptoms.

The patient-provider relationship: attachment theory and adherence to treatment in diabetes.

OBJECTIVE: Lack of adherence to diabetic self-management regimens is associated with a high risk of diabetes complications. Previous research has shown that the quality of the patient-provider relationship is associated with adherence to diabetes treatment. This study attempts to improve understanding of both patient and provider factors involved in lack of adherence to treatment in diabetic patients by using the conceptual model of attachment theory. METHOD: Instruments that assessed attachment, treatment adherence, depression, diabetes severity, patient-provider communication, and demographic data were administered to 367 patients with type 1 and 2 diabetes in a health maintenance organization primary care setting. Glucose control, medical comorbidity, and adherence to medications and clinic appointments were determined from automated data. Analyses of covariance were used to determine if attachment style and quality of patient-provider communication were associated with adherence to treatment. RESULTS: Patients who exhibited dismissing attachment had significantly worse glucose control than patients with preoccupied or secure attachment. An interaction between attachment and communication quality was significantly associated with glycosylated hemoglobin (Hb A(1c)) levels. Among the patients with a dismissing attachment style, there was a significant difference in glycosylated hemoglobin levels between those who rated their patient-provider communication as poor (mean=8.50%, SD=1.55%) and those who rated this communication as good (mean=7.49%, SD=1. 33%). Among all patients who were taking oral hypoglycemics, adherence to medications and glucose monitoring was significantly worse in patients who exhibited dismissing attachment and rated their patient-provider communication as poor. CONCLUSIONS: Dismissing attachment in the setting of poor patient-provider communication is associated with poorer treatment adherence in patients with diabetes.