Validity of scores from communication skills instruments for patients and their dental student-clinicians.

The development of appropriate communication skills by healthcare providers is central to providing quality patient-centred care. Patients can provide valuable feedback to practitioners about their clinical communication. However, in oral health care, their involvement is uncommon and instruments specific for communication in oral health care have not been available. Recently, two complementary instruments have been developed by the Faculty of Dentistry, University of Manitoba for evaluating student-clinicians' clinical communication: one for patient evaluation and one for student self-evaluation. The aim of the current study was to provide validity evidence for the scores related to the internal structure of the revised 2007 versions of these instruments in two dental clinical/education contexts, namely the Universities of Manitoba, Canada (UM) and Adelaide, Australia (UA). The proposed factor structure and loadings, and their stability across contexts were assessed using confirmatory factor analysis, and the adequacy of the internal consistency reliability of the scores was analysed using Cronbach's alpha. The factor structure of the current 2007 versions of the patient and student instruments, derived from the previously developed longer versions of these instruments, was confirmed and was consistent across the two clinical/educational contexts. A model of partial invariance provided the best fit for these data due to variations in the magnitude of the factor loadings between sites. The internal consistency reliability of scores was high with a range of 0.88-0.97. In conclusion, the current study provides preliminary evidence regarding the validity of the scores of the current 2007 instruments, in terms of the internal structure, as measuring the five factors well. Replication of the factor structure of these instrument scores with more participants at both UA and other institutions is required.

Effects of individual and combined dietary weight loss and exercise interventions in postmenopausal women on adiponectin and leptin levels.

BACKGROUND: Excess body weight and a sedentary lifestyle are associated with the development of several diseases, including cardiovascular disease, diabetes and cancer in women. One proposed mechanism linking obesity to chronic diseases is an alteration in adipose-derived adiponectin and leptin levels. We investigated the effects of 12-month reduced calorie, weight loss and exercise interventions on adiponectin and leptin concentrations. METHODS: Overweight/obese postmenopausal women (n = 439) were randomized as follows: (i) a reduced calorie, weight-loss diet (diet; N = 118), (ii) moderate-to-vigorous intensity aerobic exercise (exercise; N = 117), (iii) a combination of a reduced calorie, weight-loss diet and moderate-to-vigorous intensity aerobic exercise (diet + exercise; N = 117), and (iv) control (N = 87). The reduced calorie diet had a 10% weight-loss goal. The exercise intervention consisted of 45 min of moderate-to-vigorous aerobic activity 5 days per week. Adiponectin and leptin levels were measured at baseline and after 12 months of intervention using a radioimmunoassay. RESULTS: Adiponectin increased by 9.5% in the diet group and 6.6% in the diet + exercise group (both P ≤ 0.0001 vs. control). Compared with controls, leptin decreased with all interventions (diet + exercise, -40.1%, P < 0.0001; diet, -27.1%, P < 0.0001; exercise, -12.7%, P = 0.005). The results were not influenced by the baseline body mass index (BMI). The degree of weight loss was inversely associated with concentrations of adiponectin (diet, P-trend = 0.0002; diet + exercise, P-trend = 0.0005) and directly associated with leptin (diet, P-trend < 0.0001; diet + exercise, P-trend < 0.0001). CONCLUSION: Weight loss through diet or diet + exercise increased adiponectin concentrations. Leptin concentrations decreased in all of the intervention groups, but the greatest reduction occurred with diet + exercise. Weight loss and exercise exerted some beneficial effects on chronic diseases via effects on adiponectin and leptin.

Autologous hematopoietic cell transplantation following high-dose immunosuppressive therapy for advanced multiple sclerosis: long-term results.

The purpose of the study was to determine the long-term safety and effectiveness of high-dose immunosuppressive therapy (HDIT) followed by autologous hematopoietic cell transplantation (AHCT) in advanced multiple sclerosis (MS). TBI, CY and antithymocyte globulin were followed by transplantation of autologous, CD34-selected PBSCs. Neurological examinations, brain magnetic resonance imaging and cerebrospinal fluid (CSF) for oligoclonal bands (OCB) were serially evaluated. Patients (n=26, mean Expanded Disability Status Scale (EDSS)=7.0, 17 secondary progressive, 8 primary progressive, 1 relapsing/remitting) were followed for a median of 48 months after HDIT followed by AHCT. The 72-month probability of worsening ≥1.0 EDSS point was 0.52 (95% confidence interval, 0.30-0.75). Five patients had an EDSS at baseline of ≤6.0; four of them had not failed treatment at last study visit. OCB in CSF persisted with minor changes in the banding pattern. Four new or enhancing lesions were seen on MRI, all within 13 months of treatment. In this population with high baseline EDSS, a significant proportion of patients with advanced MS remained stable for as long as 7 years after transplant. Non-inflammatory events may have contributed to neurological worsening after treatment. HDIT/AHCT may be more effective in patients with less advanced relapsing/remitting MS.

Markers of cartilage and bone matrix metabolism differ between the sera of macaque and squirrel monkeys.

BACKGROUND: Nonhuman primates develop the characteristic lesions of osteoarthritis, making them attractive biomedical models for the study of environmental factors, such as diet, which may influence the progress of the condition. METHODS AND MATERIALS: We used ELISA assays of potential markers of osteoarthritis which were developed for use in humans to see if we could determined the presence of immunoreactivity in two nonhuman primate genera - Macaca (macaque monkeys) and Saimiri (squirrel monkeys). RESULTS: Inter-generic differences were significant for most markers. Three markers (bone alkaline phosphatase, hyaluronin and YKL-40) were outside the human range and two markers (laminin and C2C) did not yield useful results because they were off-scale high. CONCLUSION: Our results indicate that most of the ELISA assays designed for use with human serum can be used in nonhuman primates. The highly significant differences we observed between the sera of Macaca and Saimiri, suggest that further examination is warranted.

Cell markers, cytokines, and immune parameters in cement mason apprentices.

OBJECTIVE: Cement masons are known to have significant silica exposure, and silica exposure and silicosis are thought to increase risk of autoimmune disease. Because the mechanisms remain obscure, with inconclusive reports of systemic immune effects following silica exposure, our goal was to identify potential early markers of silica-related immunologic and respiratory effects. METHODS: We conducted a cross-sectional study of cement mason apprentices and electrician (control) apprentices. Demographics, dust exposure history, symptoms, spirometry, exhaled nitric oxide, and blood (for immunoglobulins, cytokines, cell counts, and surface markers) were obtained from 11 cement mason apprentices and a comparison group of 21 electrician apprentices. RESULTS: Masons had significantly higher (P < 0.05) masonry dust exposure (42 versus 9 dust-hour-years), serum interleukin-1beta (IL-1beta; 12 versus 9 pg/ml), IL-2 (20 versus 8 pg/ml), IL-4 (193 versus 67 pg/ml), IL-10 (44 versus 21 pg/ml), and interferon-gamma (139 versus 65 pg/ml) compared with electricians. In contrast, masons had significantly lower percentages of CD25+ (12% versus 20%) and CD69+ (4% versus 9%) lymphocytes. CONCLUSION: Mason apprentices had higher levels of serum proinflammatory cytokines and lower percentages of CD25+ and CD69+ lymphocytes than did electrician apprentices. These preliminary findings suggest that mason apprentices may be at greater risk of a systemic proinflammatory state that is potentially linked to immune dysregulation. Although distinct limitations of this preliminary data are recognized, this is consistent with early biologic effects leading to increased incidence of autoimmune disease among silica-exposed workers. Prospective studies are needed to validate these initial findings and clarify the temporal sequence of observed relationships.

High-density SNP analysis of 642 Caucasian families with rheumatoid arthritis identifies two new linkage regions on 11p12 and 2q33.

We have completed a genome wide linkage scan using >5700 informative single-nucleotide polymorphism (SNP) markers (Illumina IV SNP linkage panel) in 642 Caucasian families containing affected sibling pairs with rheumatoid arthritis (RA), ascertained by the North American Rheumatoid Arthritis Consortium. The results show striking new evidence of linkage at chromosomes 2q33 and 11p12 with logarithm of odds (LOD) scores of 3.52 and 3.09, respectively. In addition to a strong and broad linkage interval surrounding the major histocompatibility complex (LOD>16), regions with LOD>2.5 were observed on chromosomes 5 and 10. Additional linkage evidence (LOD scores between 1.46 and 2.35) was also observed on chromosomes 4, 7, 12, 16 and 18. This new evidence for multiple regions of genetic linkage is partly explained by the significantly increased information content of the Illumina IV SNP linkage panel (75.6%) compared with a standard microsatellite linkage panel utilized previously (mean 52.6%). Stratified analyses according to whether or not the sibling pair members showed elevated anticyclic citrullinated peptide titers indicates significant variation in evidence for linkage among strata on chromosomes 4, 5, 6 and 7. Overall, these new linkage data should reinvigorate efforts to utilize positional information to identify susceptibility genes for RA.

Effect of tumour necrosis factor alpha antagonists on serum transaminases and viraemia in patients with rheumatoid arthritis and chronic hepatitis C infection.

BACKGROUND: Tumour necrosis factor alpha (TNF alpha) antagonists are effective for the treatment of rheumatoid arthritis (RA), but concerns remain about the safety of these agents in the presence of chronic infections, including hepatitis C virus (HCV) infection. OBJECTIVE: To examine the influence of treatment with TNF alpha antagonists on levels of HCV viraemia and serum transaminases in patients with RA and HCV. METHODS: In a retrospective survey the course of 16 HCV infected patients with RA who had received the TNF alpha antagonists etanercept or infliximab was analysed. Eight additional patients with RA and HCV were also enrolled into a three month prospective trial of etanercept. Serum concentrations of albumin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and HCV were followed. RESULTS: Viraemia was measured in 22 patients receiving a TNF alpha antagonist at the start of treatment and after 1-34 months (median 9 months follow up). Twenty four patients had serial tests of liver related enzymes and albumin. None of the differences between liver related tests at baseline and at follow up achieved significance (p>0.05). Similarly, the mean HCV measurement at 1-3, 4-6, 7-12, and 13-34 months did not differ significantly from baseline (p>0.05). CONCLUSION: In this study, liver related blood tests and HCV viral load measurements did not change substantially. These findings suggest that TNF alpha antagonists merit further study for the treatment of RA in HCV infected patients. Larger and longer term studies are still needed.

Cryoglobulinemic glomerulonephritis in thymic stromal lymphopoietin transgenic mice.

Mixed cryoglobulins are complexes of immunoglobulins that reversibly precipitate in the cold and lead to a systemic disease in humans. Renal involvement usually manifests as a membranoproliferative glomerulonephritis with marked monocyte infiltration and, at times, intracapillary thrombi. Thymic stromal lymphopoietin (TSLP) is a recently cloned cytokine that supports differentiation and long-term growth of B cells. Here we report that TSLP overexpression in mice results in the development of mixed cryoglobulins, with renal involvement closely resembling cryoglobulinemic glomerulonephritis as it occurs in humans. One hundred twenty-three mice were sacrificed at monthly intervals, with at least five TSLP transgenic mice and five controls in each group. Blood, kidneys, spleen, liver, lung, and ear were collected and studied by routine microscopy, immunofluorescence, immunohistochemistry, and electron microscopy. TSLP transgenic animals developed polyclonal mixed cryoglobulinemia (type III) and a systemic inflammatory disease involving the kidney, spleen, liver, lung, and ears. Renal involvement was of a membranoproliferative type demonstrating thickened capillary walls with cellular interposition and double contours of the basement membrane, expansion of the mesangium because of increased matrix and accumulation of immune-deposits, subendothelial immune-deposits, focal occlusion of capillary loops, and monocyte/macrophage influx. In contrast to the severe glomerular lesions, the tubulointerstitium was not involved in the disease process. The renal lesions and the disease course were more severe in females when compared to males. We describe a mouse strain in which a B-cell-promoting cytokine leads to formation of large amounts of mixed cryoglobulins and a systemic inflammatory injury that resembles important aspects of human cryoglobulinemia. This is the first reproducible mouse model of renal involvement in mixed cryoglobulinemia, which enables detailed studies of a membranoproliferative pattern of glomerular injury.

A genomewide screen in multiplex rheumatoid arthritis families suggests genetic overlap with other autoimmune diseases.

Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder with a complex genetic component. We report the first major genomewide screen of multiplex families with RA gathered in the United States. The North American Rheumatoid Arthritis Consortium, using well-defined clinical criteria, has collected 257 families containing 301 affected sibling pairs with RA. A genome screen for allele sharing was performed, using 379 microsatellite markers. A nonparametric analysis using SIBPAL confirmed linkage of the HLA locus to RA (P < .00005), with lambdaHLA = 1.79. However, the analysis also revealed a number of non-HLA loci on chromosomes 1 (D1S235), 4 (D4S1647), 12 (D12S373), 16 (D16S403), and 17 (D17S1301), with evidence for linkage at a significance level of P<.005. Analysis of X-linked markers using the MLOD method from ASPEX also suggests linkage to the telomeric marker DXS6807. Stratifying the families into white or seropositive subgroups revealed some additional markers that showed improvement in significance over the full data set. Several of the regions that showed evidence for nominal significance (P < .05) in our data set had previously been implicated in RA (D16S516 and D17S1301) or in other diseases of an autoimmune nature, including systemic lupus erythematosus (D1S235), inflammatory bowel disease (D4S1647, D5S1462, and D16S516), multiple sclerosis (D12S1052), and ankylosing spondylitis (D16S516). Therefore, genes in the HLA complex play a major role in RA susceptibility, but several other regions also contribute significantly to overall genetic risk.

Low-grade systemic inflammation in overweight children.

OBJECTIVE: Human adipose tissue expresses and releases the proinflammatory cytokine interleukin-6, potentially inducing low-grade systemic inflammation in persons with excess body fat. To limit potential confounding by inflammation-related diseases and subclinical cardiovascular disease, we tested the hypothesis that overweight is associated with low-grade systemic inflammation in children. DESIGN AND SETTING: The third National Health and Nutrition Examination Survey, 1988-1994, a representative sample of the US population. PARTICIPANTS: A total of 3512 children 8 to 16 years of age. OUTCOME MEASURES: Elevated serum C-reactive protein concentration (CRP; >/=.22 mg/dL) and white blood cell count (10(9) cells/L). RESULTS: Elevated CRP was present in 7.1% of the boys and 6.1% of the girls. Overweight children (defined as having a body mass index or a sum of 3 skinfolds (triceps, subscapula, and supra-iliac) above the gender-specific 85th percentile) were more likely to have elevated CRP than were their normal-weight counterparts. After adjustment for potential confounders, including smoking and health status, the odds ratio (OR) was 3.74 (95% confidence interval [CI]: 1.66-8.43) for overweight boys and the OR was 3.17 (95% CI: 1.60-6.28) for overweight girls, based on the body mass index. Based on the sum of 3 skinfolds, these ORs were 5.11 (95% CI: 2.36-11.06) and 2.89 (95% CI: 1.49-5.59) for boys and girls, respectively. Overweight was also associated with statistically significant higher white blood cell counts. The results were similar when restricted to healthy, nonsmoking, nonestrogen-using children. CONCLUSIONS: In children 8 to 16 years of age, overweight is associated with higher CRP concentrations and higher white blood cell counts. These findings suggest a state of low-grade systemic inflammation in overweight children. inflammation, obesity, children.

The influence of age, sex, and race on the upper reference limit of serum C-reactive protein concentration.

OBJECTIVE: The recommended reference range for serum C-reactive protein (CRP) concentrations is usually not adjusted for age and sex. We sought to determine if age, sex, and race or ethnicity influence the distribution of CRP values, and if upper reference limits of CRP should be adjusted by demographic factors. METHODS: Interviews, physical examinations, and blood draws were performed on > 22,000 individuals age > or = 4 yrs representative of the noninstitutionalized population of the United States, as part of the Third National Health and Nutrition Evaluation Survey (NHANES III). Serum CRP concentrations were measured by nephelometric immunoassay. RESULTS: The 95th percentile value of CRP in the overall population was 0.95 mg/dl for males and 1.39 mg/dl for females, and varied with age and race. For ages 25-70 yrs, the age adjusted approximate upper reference limit (mg/dl) was CRP = age/50 for males, and CRP = age/50 + 0.6 for females. The upper limits for Mexican-Americans and non-Hispanic whites were similar, whereas for non-Hispanic black adults the approximate upper limit was CRP = age/30 for males and CRP = age/50 + 1.0 for females. Even after accounting for identified inflammatory conditions, demographic factors influenced the reference limits of CRP. The 95th percentile values were uniformly lower in children than in older adults. CONCLUSION: Demographic factors, including age, sex, and race, should be used to adjust the upper reference limit for CRP. Clinicians should be aware of these factors when using CRP values to assess inflammatory diseases.

Antibodies to human myeloperoxidase in glomerular immune deposits of systemic lupus erythematosus.

Antibodies to human myeloperoxidase and cathepsin G have been detected in the serum of some patients with systemic lupus erythematosus. Therefore, the presence of antibodies to human myeloperoxidase and cathepsin G was examined in glomerular immune deposits. Glomerular basement membrane fragments were prepared from renal tissues obtained at autopsy from 19 patients with systemic lupus erythematosus. IgG was extracted from the glomerular basement membrane fragments and tested with sensitive immunoassays for antibodies to myeloperoxidase and cathepsin G. Antibodies to cathepsin G were not detected in the extracts but antibodies to human myeloperoxidase were found in extracts of one specimen. In the extract with 6M guanidine hydrochloride these antibodies were enriched 103-fold, compared to the initial supernatant of glomeruli, which served as a serum surrogate. The recovered antibodies to myeloperoxidase accounted for 12% of the recovered IgG. These findings add autoantibodies to human myeloperoxidase to the list of antibodies that have been shown to be present in glomerular immune deposits of patients with lupus glomerulonephritis.

SR proteins are autoantigens in patients with systemic lupus erythematosus. Importance of phosphoepitopes.

OBJECTIVE: To determine whether members of the highly phosphorylated SR protein family are autoantigens and, if so, to determine the frequency and molecular basis of antigen recognition. METHODS: Native human SR proteins were purified to homogeneity from HeLa cells, and an enzyme-linked immunosorbent assay (ELISA) was developed. Further studies employed immunoblotting of both phosphorylated and dephosphorylated SR proteins. RESULTS: Anti-SR protein reactivity was frequently detected in the sera of patients with systemic lupus erythematosus (SLE). Sera from 52% of the SLE patients in a group of patients with a variety of autoimmune and other disorders (n = 137) and from 50% of the SLE patients in a separate group (n = 102) were positive in an ELISA. In contrast, sera from patients with other disorders, such as rheumatoid arthritis and primary antiphospholipid syndrome, reacted infrequently. Reactivity with double-stranded DNA (dsDNA), used in the diagnosis of SLE, did not correlate with SR protein reactivity. Anti-SR autoantisera did not bind highly charged unphosphorylated peptides related to the SR domain, which is rich in arginine and phosphoserine residues. Surprisingly, many of the epitopes were influenced by the presence or absence of SR protein phosphorylation. In immunoblots, some patient sera lost reactivity upon SR protein dephosphorylation, while others significantly gained reactivity. CONCLUSION: We have identified a novel set of autoantigens in SLE, the SR protein family of non-small nuclear RNP pre-messenger RNA splicing factors. Anti-SR autoantibodies are distinct from those which bind dsDNA. The identification of this new set of autoantigens and the observation that the auto-epitope(s) involves posttranslational modification offer new possibilities for understanding autoimmunity and its development.

Elevated C-reactive protein levels in overweight and obese adults.

CONTEXT: Human adipose tissue expresses and releases the proinflammatory cytokine interleukin 6, potentially inducing low-grade systemic inflammation in persons with excess body fat. OBJECTIVE: To test whether overweight and obesity are associated with low-grade systemic inflammation as measured by serum C-reactive protein (CRP) level. DESIGN AND SETTING: The Third National Health and Nutrition Examination Survey, representative of the US population from 1988 to 1994. PARTICIPANTS: A total of 16616 men and nonpregnant women aged 17 years or older. MAIN OUTCOME MEASURES: Elevated CRP level of 0.22 mg/dL or more and a more stringent clinically raised CRP level of more than 1.00 mg/dL. RESULTS: Elevated CRP levels and clinically raised CRP levels were present in 27.6% and 6.7% of the population, respectively. Both overweight (body mass index [BMI], 25-29.9 kg/m2) and obese (BMI, > or =30 kg/m2) persons were more likely to have elevated CRP levels than their normal-weight counterparts (BMI, <25 kg/m2). After adjustment for potential confounders, including smoking and health status, the odds ratio (OR) for elevated CRP was 2.13 (95% confidence interval [CI], 1.56-2.91) for obese men and 6.21 (95% CI, 4.94-7.81) for obese women. In addition, BMI was associated with clinically raised CRP levels in women, with an OR of 4.76 (95% CI, 3.42-6.61) for obese women. Waist-to-hip ratio was positively associated with both elevated and clinically raised CRP levels, independent of BMI. Restricting the analyses to young adults (aged 17-39 years) and excluding smokers, persons with inflammatory disease, cardiovascular disease, or diabetes mellitus and estrogen users did not change the main findings. CONCLUSION: Higher BMI is associated with higher CRP concentrations, even among young adults aged 17 to 39 years. These findings suggest a state of low-grade systemic inflammation in overweight and obese persons.

Utility of laboratory testing in autoimmune inner ear disease.

OBJECTIVES: To assess the utility of various laboratory tests used to diagnose autoimmune inner ear disease. STUDY DESIGN: Retrospective study of 82 patients evaluated at the University of Washington Otology Clinic from 1996 through 1998 with review of clinical history, laboratory tests, audiograms, response to therapy, and final diagnoses. METHODS: Charts were reviewed for presenting history and initial workup including test results for erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Clq binding assay, anticardiolipin antibody (aCL), antineutrophil cytoplasmic antibody (ANCA), microhemagglutinin assay for Treponema pallidum (microhemagglutination assay), Lyme disease titers, and the Western blot for heat shock protein 70 (hsp 70). RESULTS: The Western blot for hsp 70 is the best test for predicting corticosteroid responsiveness. The sensitivity was low at 42%, although the specificity was 90%, and the positive predictive value of this test was excellent at 91%. The ESR was as good as the CRP in detecting acute-phase reactants. The other, more specific tests in the laboratory panel (aCL, ANCA, MHA, and Lyme disease titers) did not detect any new cases of autoimmune disease in addition to those which were already identified by an abnormal ESR. CONCLUSIONS: A diagnostic test panel for autoimmune inner ear disease should include an ESR and the Western blot for hsp70. More specific laboratory testing for systemic disease is warranted when the ESR is elevated. In patients with a positive Western blot, a trial of corticosteroid therapy can be given with good conviction because the test is quite specific. However, many people who are Western blot negative may also respond to corticosteroid therapy because the test lacks sensitivity.

Clinicopathologic correlations in lupus nephritis in Lima, Peru.

BACKGROUND: We assessed whether immunohistologic markers for glomerular or tubulointerstitial injury might provide better correlations with ongoing renal function and disease activity as compared with the WHO classification or the NIH activity and chronicity indices in lupus nephritis. METHODS: Thirty-three patients with clinically defined systemic lupus underwent renal biopsy over a 1-year period at Hospital Loayza in Lima, Peru. Biopsy specimens were evaluated for macrophages, proliferating cells, alpha-actin expression, and type IV collagen deposition in both glomeruli and the tubulointerstitium and the results compared with the current WHO and NIH classifications in relation to the clinical presentation. RESULTS: Patients with WHO class IV lupus nephritis were more likely to have lower serum complements, greater proteinuria and hematuria, and worse renal function. An elevated NIH activity index correlated with microhematuria, proteinuria, and impaired renal function, whereas an elevated chronicity index correlated with renal function, hypertension, and microhematuria, but not with proteinuria. The presence of glomerular macrophages correlated with both glomerular alpha-actin expression and type IV collagen deposition, but did not correlate with renal function or proteinuria. In contrast, interstitial macrophages correlated not only with interstitial collagen deposition and myofibroblast accumulation, but also correlated with both renal function and the presence of nephrotic syndrome. CONCLUSIONS: Both the WHO classification and the NIH activity/chronicity indices correlate with clinical manifestations of lupus nephritis. While glomerular macrophage accumulation correlates with mesangial cell activation (alpha-actin expression) and collagen deposition, and interstitial macrophage accumulation correlates with interstitial fibroblast activation and collagen deposition, only interstitial macrophages correlate with renal function. Of particular interest will be future studies to determine whether these markers correlate with the prognosis.

Destructive tophaceous calcium hydroxyapatite tumor of the infratemporal fossa. Case report and review of the literature.

Tophaceous pseudogout is one of the rarest forms of crystal deposition disease, typically presenting as a destructive and invasive mass involving the temporomandibular joint or the infratemporal fossa region in the absence of any other articular manifestations. Previous cases have been assumed to be caused by calcium pyrophosphate dihydrate (CPPD) crystal deposition, based on finding weakly birefringent crystals in the involved tissues. The authors present the unique case of a 65-year-old woman with a destructive and invasive facial mass extending to the middle cranial fossa with microscopic and clinical features consistent with tophaceous pseudogout. High-resolution x-ray crystallographic powder diffraction and Fourier transformed infrared spectroscopy subsequently revealed that the crystals were composed of calcium hydroxyapatite without CPPD. The patient was later found to have primary hyperparathyroidism and mild hypercalcemia. This case demonstrates that tissue deposits of calcium hydroxyapatite can cause a destructive and invasive mass containing weakly birefringent crystals and raises the question of whether previous cases attributed to tophaceous pseudogout resulting from CPPD actually were composed of birefringent calcium hydroxyapatite.

Teaching the microscopic examination of urine sediment to second year medical students using the Urinalysis-Tutor computer program.

The microscopic examination of urine sediment is a common diagnostic tool taught to medical students, medical technologists, and others. The urine microscopic exam is difficult to teach because supervised instruction and textbook-based teaching suffer from numerous drawbacks. Here, we describe Urinalysis-Tutor, a computer program that uses digitized microscope images and computer-based teaching techniques to systematically teach the urine microscopic exam. In addition, we report the results of a 2-year study that evaluated the effectiveness of the program in 314 second year medical students who were required to use the program. The program contained two, 20-question exams. In the first year of the study (1996), one of the exams was chosen as the pretest and the other as the posttest; the pretest had to be completed before the students viewed the contents of the program, and the posttest was taken after finishing the tutorial. In 1997, the order of the two exams was reversed. In 1996, 159 students completed the study. The mean pretest score was 34% (SD, 14%), the mean posttest score was 71% (SD, 13%), and the improvement was significant (P <0.001, paired t-test). In 1997, 155 students participated. The mean pretest score was 41% (SD, 11%), the mean posttest score was 71% (SD, 13%), and the improvement was significant (P <0.001, paired t-test). The study shows that Urinalysis-Tutor helps medical students learn to interpret the microscopic appearance of urine sediment and that it is feasible to implement this tutorial in a medical school class.

Histoplasmosis-like choroiditis in a nonendemic area: the northwest United States.

PURPOSE: Histoplasmosis is not endemic in the U.S. northwest, but a type of multifocal choroiditis resembling ocular histoplasmosis occurs there. This study was designed to find a group of affected patients and study their clinical characteristics and immunologic responses to Histoplasma antigens. METHOD: Ten patients were found in the authors' files whose geographic histories made it unlikely that they had ever been exposed to Histoplasma capsulatum and yet they had features of ocular histoplasmosis. They were recalled for examination and testing by lymphocyte-stimulation assay for previous exposure to histoplasmosis. RESULTS: The clinical features of these patients resembled those of patients with ocular histoplasmosis, but their histories and the results of the assay did not support H. capsulatum as the cause of the ocular disease. CONCLUSION: This study confirmed that there is a type of choroiditis that resembles ocular histoplasmosis but is due to another agent or agents.