Nutrient displacement associated with walnut supplementation in men.

BACKGROUND: Dietary guidance issued by various global government agencies recommends nut consumption within the context of a healthy-eating pattern. Nuts are nutrient dense and may promote nutrient adequacy. As an energy-dense food, nuts must replace other foods in the diet to prevent an excess of calories. METHODS: We evaluated how recommending the inclusion of walnuts (75 g day(-1) ) in the diet affected energy and nutrient intake in men (45-75 years; mean body mass index = 27.6 kg m(-2) ; n = 19) at risk for developing prostate cancer. Guidance was provided about incorporating walnuts isocalorically in a healthy diet. Three-day food records and body weight were collected at baseline and after two 8-week diet periods (usual versus walnut supplement diets). RESULTS: Energy intake on the walnut supplement diet exceeded the usual diet, although body weight was maintained. Energy intake was lower on the actual walnut supplement diet than the calculated walnut diet [10,865 kJ (2595 kcal) versus 11,325 kJ (2705 kcal) per day, respectively] and contributed 23% less energy than 75 g of walnuts. Approximately, 86% and 85% of the total fat and saturated fatty acids from walnuts were not displaced, whereas the increase in fibre from the usual diet to the actual walnut supplement diet represented less than one-half (39%) of the fibre provided by 75 g of walnuts. Walnuts were substituted, in part, for other foods, and the nutrient profile of the diet was improved, however, the beneficial effect of walnuts on the diet quality was not optimized. CONCLUSIONS: Individuals do not optimally implement food-based guidance. Consequently, nutrition professionals play a key role in teaching the implementation of food-based recommendations.

Site differences in mild cognitive dysfunction (MCD) among patients with systemic lupus erythematosus (SLE).

BACKGROUND: Mild cognitive dysfunction (MCD) is common in patients with systemic lupus erythematosus (MCD-SLE) but few studies have investigated potential site differences. METHODS: SLE patients from Denver, CO, and New York, NY, were enrolled in two different cognition studies employing similar screening methods. Using the resulting neuropsychological scores, cognitive impairment was calculated using a cognitive impairment index (CII). RESULTS: The rate of MCD-SLE was 24% at the Denver, CO, site and 60% at the New York, NY, site. The mean CII was 2.6 ± 2.3 versus 4.4 ± 2.7, respectively (p = 0.005). The NY participants had a significantly longer disease duration (p = 0.13) and higher American College of Rheumatology SLE criteria scores (p > 0.001). NY participants had a higher frequency of impairment in semantic verbal fluency (p = 0.005), visuomotor speed (p = 0.013), and motor sequencing (p = 0.001). A correlation was found between cognitive impairment and SLE disease duration (p = 0.03). CONCLUSIONS: The rate of MCD-SLE was greater in SLE patients from New York, NY, compared to patients in the Denver, CO, area. The greater duration of disease and higher prevalence of medical complications in the NY group might contribute to this difference. Findings suggest that MCD-SLE may differ by site, but future studies that better evaluate site or selection bias are recommended.

Immune function and brain abnormalities in patients with systemic lupus erythematosus without overt neuropsychiatric manifestations.

OBJECTIVE: This study examined the relationship between immune, cognitive and neuroimaging assessments in subjects with systemic lupus erythematosus (SLE) without histories of overt neuropsychiatric (NP) disorders. METHODS: In total, 84 subjects with nonNPSLE and 37 healthy controls completed neuropsychological testing from the American College of Rheumatology SLE battery. Serum autoantibody and cytokine measures, volumetric magnetic resonance imaging, and magnetic resonance spectroscopy data were collected on a subset of subjects. RESULTS: NonNPSLE subjects had lower scores on measures of visual/complex attention, visuomotor speed and verbal memory compared with controls. No clinically significant differences between nonNPSLE patients and controls were found on serum measures of lupus anticoagulant, anticardiolipin antibodies, beta 2-glycoproteins, or pro-inflammatory cytokines (interleukin (IL)-1, IL-6, interferon alpha (IFN-alpha), and interferon gamma (IFN-gamma)). Higher scores on a global cognitive impairment index and a memory impairment index were correlated with lower IFN-alpha. Few associations between immune functions and neuroimaging parameters were found. CONCLUSIONS: Results indicated that nonNPSLE patients demonstrated cognitive impairment but not immune differences compared with controls. In these subjects, who were relatively young and with mild disease, no relationship between cognitive dysfunction, immune parameters, or previously documented neuroimaging abnormalities were noted. Immune measures acquired from cerebrospinal fluid instead of serum may yield stronger associations.

Memory impairment associated with neurometabolic abnormalities of the hippocampus in patients with non-neuropsychiatric systemic lupus erythematosus.

OBJECTIVE: Memory impairment is common in patients with systemic lupus erythematosus (SLE). This study examined hippocampal volumes and neurometabolic alterations in relation to memory function in SLE patients without a history of neuropsychiatric syndromes (nonNPSLE). METHODS: Subjects included 81 nonNPSLE patients and 34 healthy controls. Volumetric magnetic resonance imaging and magnetic resonance spectroscopy of the right and left hippocampal areas (RH, LH) were performed. Verbal and visual memory tests were administered and a memory impairment index (MII) was derived from standardized tests. RESULTS: Higher memory impairment (MII) was correlated with lower RH glutamate + glutamine/creatine (p = 0.009) and lower RH N-acetylaspartic acid/creatine (p = 0.012) in nonNPSLE patients. A trend for a negative correlation between RH and LH volumes and MII was evident for absolute hippocampal volumes. Lower RH glutamate + glutamine/creatine was also correlated with worse performance in a mean visual memory index (p = 0.017). CONCLUSIONS: An association between reduced memory and lower N-acetylaspartic acid/creatine in the RH suggests neuronal damage in nonNPSLE patients with very mild and early disease. Alterations in glutamate + glutamine/creatine further indicate early metabolic changes in nonNPSLE are related to memory impairment, a finding that might suggest that memory impairment relates to presynaptic glutamatergic dysfunction in the hippocampus.

Evidence for the effects of a superantigen in rheumatoid arthritis.

While studying the alpha beta T cell receptor repertoire in rheumatoid arthritis (RA) patients, we found that the frequency of V beta 14+ T cells was significantly higher in the synovial fluid of affected joints than in the peripheral blood. In fact, V beta 14+ T cells were virtually undetectable in the peripheral blood of a majority of these RA patients. beta-chain sequences indicated that one or a few clones dominated the V beta 14+ population in the synovial fluid of individual RA patients, whereas oligoclonality was less marked for other V beta's and for V beta 14 in other types of inflammatory arthritis. These results implicate V beta 14-bearing T cells in the pathology of RA. They also suggest that the etiology of RA may involve initial activation of V beta 14+ T cells by a V beta 14-specific superantigen with subsequent recruitment of a few activated autoreactive v beta 14+ T cell clones to the joints while the majority of other V beta 14+ T cells disappear.

Combination therapy in fibromyalgia.

Fibromyalgia is an enigmatic medical condition whose specific etiology remains undiscovered but currently plagues five million Americans. Research indicates that the origin of the disease is most likely multifactorial. Treatment should therefore be tailored accordingly. Thus, it is often necessary to combine different options in order to achieve the maximum benefit in patients suffering from fibromyalgia.

Whole genomewide linkage screen for neural tube defects reveals regions of interest on chromosomes 7 and 10.

Neural tube defects (NTDs) are the second most common birth defects (1 in 1000 live births) in the world. Periconceptional maternal folate supplementation reduces NTD risk by 50-70%; however, studies of folate related and other developmental genes in humans have failed to definitively identify a major causal gene for NTD. The aetiology of NTDs remains unknown and both genetic and environmental factors are implicated. We present findings from a microsatellite based screen of 44 multiplex pedigrees ascertained through the NTD Collaborative Group. For the linkage analysis, we defined our phenotype narrowly by considering individuals with a lumbosacral level myelomeningocele as affected, then we expanded the phenotype to include all types of NTDs. Two point parametric analyses were performed using VITESSE and HOMOG. Multipoint parametric and nonparametric analyses were performed using ALLEGRO. Initial results identified chromosomes 7 and 10, both with maximum parametric multipoint lod scores (Mlod) >2.0. Chromosome 7 produced the highest score in the 24 cM interval between D7S3056 and D7S3051 (parametric Mlod 2.45; nonparametric Mlod 1.89). Further investigation demonstrated that results on chromosome 7 were being primarily driven by a single large pedigree (parametric Mlod 2.40). When this family was removed from analysis, chromosome 10 was the most interesting region, with a peak Mlod of 2.25 at D10S1731. Based on mouse human synteny, two candidate genes (Meox2, Twist1) were identified on chromosome 7. A review of public databases revealed three biologically plausible candidates (FGFR2, GFRA1, Pax2) on chromosome 10. The results from this screen provide valuable positional data for prioritisation of candidate gene assessment in future studies of NTDs.

Stress responses to repeated exposure to a combined physical and social evaluative laboratory stressor in young healthy males.

Repeated exposure to homotypic laboratory psychosocial stressors typically instigates rapid habituation in hypothalamic-pituitary-adrenal (HPA) axis-mediated stress responses in humans. However, emerging evidence suggests the combination of physical stress and social evaluative threat may be sufficient to attenuate this response habituation. Neuroendocrine, cardiovascular and subjective stress responses following repeated exposure to a combined physical and social evaluative stress protocol were assessed to examine the habituation response dynamic in this context. The speech task of the Trier social stress test (TSST; Kirschbaum et al., 1993) and the socially evaluated cold pressor task (SECPT; Schwabe et al., 2008) were administered in a combined stressor protocol. Salivary cortisol, cardiovascular and subjective stress responses to a non-stress control and repeat stressor exposure separated by six weeks were examined in males (N=24) in a crossover manner. Stressor exposure resulted in significant elevations in all stress parameters. In contrast to the commonly reported habituation in cortisol response, a comparable post-stress response was demonstrated. Cortisol, heart rate and subjective stress responses were also characterised by a heightened response in anticipation to repeated stress exposure. Blood pressure responses were comparatively uniform across repeated exposures. Findings suggest a combined physical and social evaluative stressor is a potentially useful method for study designs that require repeated presentation of a homotypic stressor.

Antideoxyribonucleic acid antibodies in Graves' disease.

Antidouble stranded DNA (dsDNA) antibodies have been detected by a sensitive RIA in the sera of 28-100% of patients with Graves' disease, but it remains unclear whether these assays have detected authentic dsDNA antibodies. We have obtained sera from 42 patients with active Graves' disease and no known connective tissue disorders. All sera were tested for dsDNA antibodies by 2 quantitative RIAs (Farr assay and Millipore filter assay; normal, less than 20% for both assays) and by an enzyme-linked immunosorbant assay for antibodies to dsDNA and to single stranded DNA (ssDNA). All sera were negative for dsDNA antibodies by the Farr assay and by enzyme-linked immunosorbant assay, 2 of 42 had mildly elevated levels (33% and 23%) by the Millipore filter assay, and 7 of 42 were positive for ssDNA antibodies. The 2 positive sera for dsDNA antibodies were also tested using the Crithidia luciliae indirect immunofluorescence assay, and both were negative. Patients with Graves' disease have been reported to have an increased prevalence of antinuclear antibodies, but the more recent findings of dsDNA antibodies in these patients is of interest because dsDNA antibodies are considered to be specific for systemic lupus erythematosus. Our data suggest that true immunoglobulin G dsDNA antibodies are not elevated during active Graves' disease, and positive assay results may be due to measurement of ssDNA antibodies, immunoglobulin M dsDNA antibodies, or nonantibody DNA binding.

High stress responsivity predicts later blood pressure only in combination with positive family history and high life stress.

High cardiovascular responsivity to stressors has not consistently improved prediction of later blood pressure increases beyond the predictive effects of baseline pressure. Animal models suggest that genetic susceptibility to hypertension and frequent stress exposure are important modulating factors in stress-related hypertension. Thus in 103 men originally tested at age 18 to 22 years and reassessed 10 years later, interactive effects of genetic susceptibility (defined as 1 or more hypertensive parents) with high stress responsivity (defined as top 25% on the basis of blood pressure and cardiac responses during both reaction time and cold pressor tasks) were examined in relation to follow-up systolic and diastolic levels and to change in blood pressure status from normal (diastolic<80 mm Hg) to marginally elevated (diastolic 85 to 95 mm Hg). Men with the combination of high stress response and hypertensive parents demonstrated higher systolic (P<0.05) and diastolic levels (P<0.05) at follow-up, and they showed a 7-fold increase (7.5, 95% confidence intervals 2.3, 24.3; P<0.001) in relative risk of change in blood pressure status versus men with no family history and a 3-fold increase (3.8, confidence intervals 1.5, 9.6; P<0.004) versus less stress-responsive men who also had hypertensive parents. In 65 men who also provided ratings of daily stress, family historyxstress responsivityxdaily stress interactions were significant in predicting follow-up systolic and diastolic levels (P<0.006 and 0.03, respectively), with highest pressure levels seen when high life stress was reported by high stress responders and/or men with hypertensive parents. In conclusion, results suggest that stress responsivity as a long-term predictor is modulated by both genetic and environmental factors.

Neuropsychiatric lupus erythematosus: a 10-year prospective study on the value of diagnostic tests.

PURPOSE: To evaluate which serologic, cerebrospinal fluid (CSF), and neuroradiographic tests alone or in combination are most useful in the diagnosis of neuropsychiatric lupus erythematosus (NPLE). PATIENTS AND METHODS: Prospective study of patients with systemic lupus erythematosus (SLE) hospitalized with neuropsychiatric disease between January 1982 and December 1991. Special tests evaluated as part of this study included serum antinuclear antibodies, complement levels, serum and CSF antineuronal antibodies, CSF special protein studies (immunoglobulin G [IgG] index and oligoclonal bands), serum antiribosomal-P antibodies, serum antiphospholipid antibodies, and cranial magnetic resonance imaging (MRI). Diagnostic sensitivity, specificity, and positive predictive value (PPV) were determined for single tests and combinations of tests. RESULTS: Fifty-two NPLE patients were categorized by neuropsychiatric presentation (32 diffuse, 10 focal, and 10 complex presentations) and compared to 14 SLE control patients. Each NPLE patient with a diffuse or complex presentation had abnormal CSF IgG index/oligoclonal bands, elevated CSF antineuronal antibodies, and/or serum antiribosomal-P antibodies, yielding a sensitivity of 100%, specificity of 86%, and PPV of 95% for this combination of tests. Nine of 10 patients with focal presentations and all with complex disease had evidence of vasculitis/livedo reticularis, antiphospholipid antibodies, and/or a cranial MRI with multiple lesions, giving a sensitivity of 95%, specificity of 86%, and a PPV of 90% for this battery of tests. These combinations of tests correctly diagnosed all nine SLE patients whose initial diagnosis proved to be incorrect based on subsequent clinical course. Abnormal test results frequently normalized or improved with successful therapy. CONCLUSIONS: Specific tests for CSF antibodies are most useful diagnostically in diffuse NPLE, implicating autoantibodies in the pathogenesis of this NPLE presentation. In those patients with diffuse NPLE who present with primarily psychiatric disease, serum antiribosomal-P antibodies appear to be helpful. In contrast, focal NPLE appears to be mostly secondary to vascular occlusion, and the presence of dermal vasculitis/livedo reticularis, antiphospholipid antibodies, and/or an abnormal cranial MRI are most helpful diagnostically. Patients with complex presentations demonstrate abnormalities characteristic of both diffuse and focal NPLE. Abnormal tests can be followed serially and appear to correlate with clinical responses to therapy.

Covert hypothyroidism presenting as a cardiovascular event.

Hypothyroidism presenting with classic signs and symptoms is generally easily recognized. Less often, patients with hypothyroidism may present with symptoms and laboratory abnormalities suggestive of cardiovascular disease. In this article, we describe six such patients. Hypothyroidism was suspected when creatine phosphokinase (CPK) levels were persistently elevated. The diagnosis was confirmed by thyroid function tests, and thyroid hormone therapy resulted in resolution of symptoms and CPK elevations. Persistently elevated CPK levels associated with cardiovascular symptoms but without demonstrable myocardial damage should prompt consideration of covert hypothyroidism.

Association of psychiatric manifestations with antibodies to ribosomal P proteins in systemic lupus erythematosus.

PURPOSE: The goal of this study was to determine whether elevated serum levels of antibodies to ribosomal P proteins (anti-P antibodies) are associated with neuropsychiatric manifestations in patients with systemic lupus erythematosus (SLE). Additional experiments examined characteristics of these antibodies that might be associated with pathogenicity. PATIENTS AND METHODS: A large number of serum samples were collected from patients with SLE, control subjects with other rheumatic diseases, and normal individuals. At the time serum samples were obtained, patients with SLE were categorized according to the presence of psychosis, depression, and other manifestations of central nervous system (CNS) involvement. Serum anti-P antibody activity was quantitated by an enzyme-linked immunosorbent assay utilizing a synthetic peptide corresponding to the major P protein epitope. RESULTS: In a group of 79 normal individuals, mean (+/- SE) IgG anti-P activity was 0.01 +/- 0.003 and no individuals had values greater than 3 SD above the mean. Similar results were obtained measuring IgM anti-P activity. Normal levels were found in all sera from 21 patients with rheumatoid arthritis. Of 119 patients demonstrating various patterns of antinuclear and anticytoplasmic antibody activity, elevated anti-P levels were found only in patients with SLE. Overall, 19% of 269 patients with SLE demonstrated elevated levels of IgG or IgM anti-P antibodies, including 14% of 187 patients without and 29% of 82 patients with neuropsychiatric manifestations. The frequency of positive test results varied greatly depending on the nature of the CNS involvement. The frequency in patients with severe depression (n = 8) and psychosis (n = 29) was 88% and 45%, respectively, compared with only 9% in patients with nonpsychiatric neurologic disease (n = 45). For the entire SLE group, the odds ratio for the association of anti-P antibodies and severe psychiatric manifestations was 7.63 with a 95% confidence interval of 3.61 to 16.14. In a review of 187 patients with SLE originally classified as not having severe psychiatric disease, seven of 10 patients being treated with antidepressant medications had elevated levels of anti-P antibodies. In serial studies, the serum level of anti-P antibodies appeared to correlate with the activity of psychiatric disease and did not correlate with the activity of other manifestations of SLE. Anti-P antibodies in nearly all patients were IgG and directed primarily to the C-terminal 11 amino acids of the P protein. No difference in these characteristics was observed when patients with and without psychiatric manifestations were compared. Paired serum and cerebrospinal fluid (CSF) samples were also obtained from eight patients with active neuropsychiatric disease. Even when expressed as a fraction of the total IgG present, anti-P activity was markedly lower in CSF than in serum. CONCLUSIONS: Elevated levels of autoantibodies to the C-terminal region of ribosomal P proteins appear to be a specific marker for SLE, and are associated with both severe depression and psychosis in this disease. This assay is easily reproducible and may help distinguish SLE-induced psychiatric disease from that caused by other processes.

Hormone replacement improves hemodynamic profile and left ventricular geometry in hypertensive and normotensive postmenopausal women.

BACKGROUND: Postmenopausal estrogen replacement, with or without progestins, has been related to lower cardiovascular risks. OBJECTIVE: We investigated whether the actions of estrogen on vascular resistance contribute to this cardioprotective effect. DESIGN AND METHODS: In a 6-month double-blind study, pre- and post-treatment blood pressure, cardiac index, total vascular resistance index and plasma catecholamine responses during baseline and mental stressors were compared in 69 women (including 19 with mild hypertension but no history of heart disease). Women were randomized to receive either conjugated estrogens alone, estrogens plus medroxyprogesterone, or placebo. RESULTS: Both groups on active hormone replacement showed similar decreases in vascular resistance and modest blood pressure reductions, which differed from the unchanged responses of those on placebo (P< 0.05) after 3 and 6 months of treatment. Hypertensive women showed greater reductions in vascular resistance than normotensives (P< 0.05) and their blood pressure reductions tended to be larger. Women receiving hormone replacement showed increased stroke volume and cardiac index at 6 months, particularly among hypertensives and those receiving medroxyprogesterone (P < 0.05). Hormone replacement was also related to decreases in plasma norepinephrine. Finally, in 33 women receiving hormone replacement, significant 5 and 3% decreases in echocardiographic measures of left ventricular mass index and relative wall thickness were evident at 6 months (P < 0.05), while 20 placebo-treated women showed no reliable echocardiographic improvements (P= NS). CONCLUSIONS: These findings suggest that estrogen-mediated reductions in hemodynamic load on the heart may contribute to the reduced risk of cardiovascular events in relatively healthy postmenopausal women who use hormone replacement.

Postmenopausal smokers show reduced hemodynamic benefit from oral hormone replacement.

With use of a randomized, placebo-controlled trial, 62 healthy, postmenopausal smokers and nonsmokers were tested for resting and stress-induced hemodynamic variables before and after 6 months of treatment with either oral hormone replacement therapy or placebo. Smokers had significantly less reduction in both resting and stress-induced vascular resistance and blood pressure after treatment with oral hormone replacement therapy than nonsmokers.

Confirmation of linkage of hereditary partial lipodystrophy to chromosome 1q21-22.

Familial lipodystrophy is a genetically heterogeneous set of disorders characterized by a total or partial absence of subcutaneous fat, diabetes mellitus or impaired glucose tolerance, hyperlipidemia, and hypermetabolism [Senior and Gellis, 1964]. One subtype, familial partial lipodystrophy Dunnigan (FPLD), is a rare autosomal dominant trait that results in an gradual loss of subcutaneous fat in the lower trunk and limbs, Type V hyperlipoproteinemia, hypertriglyceridemia, and insulin-resistant diabetes. Previous reports of this condition have been limited to case reports or very small families. Recently, Peters et al. reported on linkage of five families of Western European descent to a 5.3 cM region on chromosome 1q21-22 between the flanking markers D1S305 and D1S1600 [Peters et al., 1998: Nat Genet 18:292-295]. We performed linkage and haplotype analysis using highly polymorphic, microsatellite markers on a large, multigeneration Caucasian kindred of German ancestry. The maximum two-point lod score achieved was 4.96 at theta(max) = 0 for marker D1S2721. Multipoint analysis gave an overall maximum lod score of 6.27 near marker D1S2721. The results of the haplotype analysis support the minimal candidate region as reported by Peters et al.

Sarcoidosis in autoimmune disease.

Sarcoidosis is a multisystem granulomatous disease of unknown etiology. Sarcoidosis coexisting with connective tissue diseases, once considered rare, complicates various such disorders, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjögren's syndrome, and the spondyloarthropathies. Symptoms common to sarcoidosis and autoimmune disease include keratoconjunctivitis sicca, weight loss, fever, lymphadenopathy, pulmonary complaints, and cutaneous lesions. Consequently, the diagnosis of sarcoidosis in association with connective tissue disease is often difficult and may require biopsy of the lung, liver, skin, lymph node, muscle, or bone marrow for pathological confirmation. Abnormalities of immune function as well as autoantibody production, including rheumatoid factor and antinuclear antibodies, are seen in sarcoidosis and in connective tissue diseases, suggesting a common immunopathogenic mechanism. The severity and course of sarcoidosis associated with autoimmune disease is variable. The incidence of sarcoidosis in association with rheumatic disease may be underestimated if new symptoms of sarcoidosis are attributed to the primary rheumatic disease and a secondary diagnosis is not pursued.

Comparison of bone scan, computed tomography, and magnetic resonance imaging in the diagnosis of active sacroiliitis.

Quantitative bone scan (QBS), computed tomography (CT), and magnetic resonance imaging (MRI) have each been used to confirm the diagnosis of active sacroiliitis (SI) in patients with low back pain (LBP). The authors prospectively evaluated 19 patients referred for symptoms of possible inflammatory LBP (group I), 26 seronegative spondyloarthropathy (SNSP) patients with LBP (group II, inflammatory or mechanical), and 5 SNSP patients without LBP (group III) to determine which radiological scan alone or in combination with other serological tests (Westergren erythrocyte sedimentation rate, C-reactive protein, HLA-B27, immunoglobulin A) was most useful in confirming a clinical diagnosis of active inflammatory SI. All patients were followed up for a minimum of 1 year to confirm the clinical diagnosis and evaluate response to therapy. Eight of 19 group I patients had active SI clinically or on plain radiographs on follow-up evaluation. Of these patients, 5 had abnormal QBS (71%), 3 had abnormal CT scans (38%), and 8 had abnormal MRI scans (100%, type I lesions). These type I MRI lesions were indicative of active inflammation manifested as subcortical bone marrow edema. The remaining 11 group I patients had negative scans for SI. Ten of 26 group II patients with LBP had SI diagnosed clinically and confirmed with positive QBS (60%), CT (100%), and MRI (100%, type I lesions). The remaining 16 group II patients had mechanical LBP without active SI clinically and had negative QBS (88%), CT (19%), and MRI (100%, normal or type II lesions). These type II MRI lesions represented old postinflammatory lesions with either fibrosis or fat replacement. All 5 group III patients had negative scans for active SI. Three patients (2 group I and group II) with inflammatory SI treated with sulfasalazine showed marked improvement on serial MRI scans. Westergren erythrocyte sedimentation rate, C-reactive protein, immunoglobulin A, and CT scan alone or in combination with other tests were not reliable predictors of active SI. Positive QBS and HLA-B27 tests were the best combination of screening tests with 82% predictability of inflammatory SI in whites, and QBS alone had an 80% predictability in black patients. However, MRI, which had 100% predictability, was the best single test for confirming active inflammatory SI.

Acute aerobic exercise reduces ambulatory blood pressure in borderline hypertensive men and women.

Ambulatory blood pressure (BP) monitoring was undertaken on two days in 31 men and women (11 with elevated resting and ambulatory BP and 20 who were normotensive), once following each of these treatment conditions: 20 min of moderate aerobic bicycle ergometry, and an equivalent control rest period. The two monitoring days were conducted within a 72 h period with the order of treatments counterbalanced across subjects. Mean BP and heart rate (HR) levels were calculated for each individual on an hourly basis and for work, home, and sleep periods, In the elevated BP group, the exercise day compared to the control day was associated with lower BP at work. Hour-by-hour analyses confirmed that the BP-lowering effect of exercise was significant for 5 h and diminished in magnitude between hours 6 and 9. These effects were not attributable to any marked differences in mood, total daily stress, posture, or activities between test days. Exercise was not associated with any appreciable differences in sleep BP or in the 24-h HR profile No differences in BP or HR as a function of exercise were seen in the normotensive group; however, the exercise-induced reduction in mean arterial BP (MAP) for hours 2 through 5 was significantly positively correlated with control day MAP levels at work in the total sample. Thus, moderate aerobic exercise, when engaged in prior to the stresses of daily living, seems to confer a protective reduction in ambulatory BP, particularly in individuals with elevated BP.

Methotrexate hepatotoxicity.

Hepatoxicity is a major adverse reaction that can occur during methotrexate treatment of the rheumatic diseases. The pathologic lesions are nonspecific and the pathogenesis is poorly understood. Early studies in psoriasis clearly established a relationship between hepatic injury and several risk factors, particularly alcohol use. Methotrexate hepatoxicity occurs less frequently in rheumatoid arthritis than previously reported in psoriasis patients. Consequently, the American College of Rheumatology guidelines for methotrexate monitoring do not recommend baseline and surveillance liver biopsies in low-risk patients. These guidelines seem to be useful and cost-effective.