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PubMed2005

Role of fibrillar Abeta25-35 in the inflammation induced rat model with respect to oxidative vulnerability.

The major pathological ramification of Alzheimer's disease (AD) is accumulation of beta-Amyloid (Abeta) peptides in the brain. An emerging therapeutic approach for AD is elimination of excessive Ass peptides and preventing its re-accumulation. Immunization is the most effective strategy in removing preexisting cerebral Abetas and improving the cognitive capacity as shown in transgenic mice model of AD. However, active immunization is associated with adverse effect such as encephalitis with perivascular inflammation and hemorrhage. Details about the mechanistic aspects of propagation of these toxic effects are matter of intense enquiry as this knowledge is essential for the understanding of the AD pathophysiology. The present work aimed to study the oxidative vulnerability in the plasma, liver and brain of the inflammation-induced rats subjected to Ass immunization. Induction of inflammation was performed by subcutaneous injection of 0.5?ml of 2% silver nitrate. Our present result shows that the proinflammatory cytokines such as IL1alpha and TNFalpha are increased significantly in the inflammation-induced, Abeta1-42, Abeta25-35 treated groups and inflammation with Abeta25-35 treated group when compared to control, complete Freund's adjuvant and Abeta35-25 treated groups. These increased proinflammatory cytokines concurrently releases significant amount of free radicals in the astrocytes of respected groups. The present result shows that nitric oxide (NO) level was significantly higher (P<0.001) in plasma, liver and brain of the rat subjected to inflammation, Abeta1-42, Abeta25-35 and inflammation with Abeta25-35 injected groups when compared to control. The increased level of lipid peroxides (LPO) (P<0.001) and decreased antioxidant status (P<0.05) were observed in the plasma, liver and brain of inflammation-induced group when compared to control. Our result shows that significant oxidative vulnerability was observed in the inflammation with Ass treated rats when compared to other groups. Based on our results, we suggest that immunization of AD patients with Ass should be done with caution as the increase in Ass could trigger the brain inflammation in uncontrollable level.

Alzheimer Disease↗
PubMed2004

Daily iron alone but not in combination with multimicronutrients increases plasma ferritin concentrations in indonesian infants with inflammation.

Iron deficiency is a public health problem in infancy. We assessed the efficacy of iron supplements in infants with inflammation on iron status and subsequent inflammation. This was a prospective, nested, case-control study of 6- to 12-mo-old infants participating in the International Research on Infant Supplementation study, Indonesia. Cases (n = 46) were selected on the basis of their inflammation status at baseline, C-reactive protein (>5 mg/L) or alpha-1 acid glycoprotein (>1 g/L); there were 44 controls without inflammation. Infants received 10 mg/d of elemental iron alone or in combination with multimicronutrients, or placebo. Blood samples were collected at baseline and at 6 mo for determinations of plasma ferritin, zinc, copper, retinol, beta-carotene, alpha-tocopherol, and inflammation status. Data on breast-feeding and acute respiratory infections (ARI) were collected daily. At baseline, 33% of infants had iron deficiency, and those with inflammation had lower retinol, beta-carotene, higher concentrations of copper and higher rates of ARI compared with controls. After 6 mo, compared with infants given placebo, ferritin concentration increased significantly in infants administered iron alone independently of inflammation status at baseline or at the end of the study. In those given multimicronutrients with iron, ferritin increased significantly in infants who did not have inflammation at baseline or at the end of the study compared with those given placebo. Consequently, iron alone resolved iron deficiency, whereas multimicronutrients reduced the deterioration of iron stores compared with placebo (chi(2), P < 0.05), without enhancing inflammation. Iron alone is recommended in populations in which iron deficiency is a public health problem despite the presence of inflammation in infants who are still breast-feeding.

Acute-Phase Proteins↗
PubMedDate not supplied

Leukocyte CD11b and CD62l expression in response to interstitial inflammation in CAPD patients.

OBJECTIVE: Very little is known about the kinetics of leukocyte recruitment and the modulation of adhesion molecules on leukocytes in the interstitium at the site of inflammation outside the peritoneal cavity in patients on peritoneal dialysis. These issues were addressed in the present study. PATIENTS AND METHODS: Two skin blisters were raised in 10 patients on peritoneal dialysis and in 19 healthy subjects. After 12 hours, blister exudates were collected and the blisters were thereafter challenged with buffer or autologous serum in order to establish an intermediate and an intense cutaneous inflammation. Leukocyte count, leukocyte CD11b/CD62L expression, monocyte chemotactic protein-1 (MCP-1), and interleukin-8 (IL-8) were determined in blood and at the three sites of interstitial inflammation by immunostaining, flow cytometry, and ELISA. RESULTS: In monocytes and granulocytes, expression of CD11b increased and CD62L decreased significantly during the transmigration process from the peripheral blood into the three sites of interstitial inflammation. In the nonstimulated blister, expression of CD11b on both monocytes and granulocytes was similar in patients and healthy subjects. At the site of intermediate inflammation, expression of CD11b on both monocytes and granulocytes was significantly higher in healthy subjects compared to patients (p < 0.05 and p < 0.001 respectively). At the site of intense inflammation, expression of CD11b on granulocytes was significantly lower (p < 0.001), and CD62L significantly higher (p < 0.001) in patients. Interstitial concentrations of MCP-1 and IL-8 at the sites of intermediate inflammation were significantly higher in healthy subjects compared to patients (p < 0.05 and p < 0.05 respectively). However, at the site of intense inflammation, similar concentrations of MCP-1 and IL-8 were observed. Furthermore, there were no significant correlations between concentrations of MCP-1 and IL-8 in blister exudates and expression of CD11b on monocytes and granulocytes at the sites of interstitial inflammation. CONCLUSION: The ability of monocytes and granulocytes to modulate the expression of adhesion molecule in response to interstitial inflammation was significantly impaired in patients on peritoneal dialysis. Furthermore, these data suggest that the expression of CD11b on leukocytes is not dependent on concentrations of IL-8 and MCP-1 in interstitium in this patient group.

Aged↗
PubMed2005

Chronic pelvic pain associated with autoimmunity and systemic and peritoneal inflammation and treatment with immune modification.

OBJECTIVE: To determine the prevalence of chronic inflammation of the pelvic peritoneum, systemic inflammation and autoimmunity in chronic pelvic pain and to explore the significance of these findings and assess the response to treatment with immune modification. STUDY DESIGN: Prospective, observational clinical studies from 2 centers were performed on 3,238 women presenting with pelvic pain to determine the prevalence of chronic inflammation by biopsy when endometriosis was absent. A second study included 40 women with chronic pelvic pain not resulting from endometriosis; immunologic investigations were carried out and therapy instituted. RESULTS: Chronic inflammation of the peritoneum, while not evident in the absence of pelvic pain, was present in 15.7% of women with chronic pelvic pain. In the second group, 10% had histologic evidence of chronic inflammation, 55% demonstrated evidence of systemic inflammation, and 37.5% were found to have autoimmune disorders. Chronic inflammation of the vagina was found in 42.5% and polycystic ovary syndrome in 22% of those with systemic inflammation. Twelve of the 40 were subsequently treated, with considerable success, with immune-modifying drugs, hydroxychloroquine and methotrexate. CONCLUSION: Chronic pelvic pain is frequently associated with systemic inflammation, including autoimmune diseases. Peritoneal chronic inflammation is sometimes also associated. It is often successfully treated with immune-modifying drugs.

Adolescent↗
PubMed1988

[The interrelation of the "local" and the "general" in inflammation].

The relationships between the local and the general in inflammation are analysed basing on the literature and original data. Local chemoattraction is postulated to be an underlying factor initiating primary local cooperation of cells relevant to inflammation. Being essential in this cooperation, macrophage seems to warrant both the local developments and triggering of general mechanisms of regulation which are relevant to control over subsequent secondary cell cooperation. The latter is biologically aimed at localization of the inflammation focus and separation of its pathogenic factors from intact internal medium. General mechanisms of inflammation control are provided by neuroendocrine, immune, vascular, coagulative, fibrinolytic and other systems, and operate through the products of the acute phase, by immune defence factors and rearrangement of nervous regulation of homeostasis in intact organs and tissues. The result of the regulation manifests with sequential presentation of the inflammation stages in time, correlation of local and general responses intensity. Eventually, local inflammation and lesion involve stress and intoxication which are not considered direct attributes of inflammation, nevertheless can influence general regulatory systems concerned with the course of local inflammation. It is concluded that inflammation implies dialectic unity of local and systemic responses of the body outlined to resolve inflammation and restore homeostasis.

Animals↗
PubMed1995

Air enema radiology compared with leukocyte scintigraphy for imaging inflammation in active ulcerative colitis.

OBJECTIVE: To compare air enema radiology with a leukocyte scintigraphy technique using technetium-99m-hexamethyl propylene amine oxime-labelled leukocytes for imaging colonic inflammation in ulcerative colitis. DESIGN: Prospective study in a University hospital. One radiologist and one nuclear physician independently graded the degree of inflammation in six colon segments per patient using radiographs and leukocyte scans. PATIENTS: Twenty consecutive patients with symptoms of active ulcerative colitis requiring corticosteroids, inflammation on rigid sigmoidoscopy and a positive leukocyte scan above the rectum. RESULTS: Using air enema radiology, inflammation above the rectum was observed in 17 of the 20 patients. Eleven patients had the same extent of disease with both imaging techniques (total n = 5; extensive n = 3; distal n = 3). Seven patients had more widespread colitis using leukocyte scintigraphy. In the remaining two patients with extensive inflammation at scintigraphy, air enema films showed total colitis. When the colon was subdivided into six different segments, prediction of the presence of inflammation in individual segments was 0.88 for air enema radiology compared with leukocyte scintigraphy and 0.60 for the prediction of absence of inflammation. All segments with an irregular mucosal contour or ulceration on air enema films had intense inflammation at scintigraphy. CONCLUSIONS: In patients with active ulcerative colitis, air enema radiology underestimates the extent of inflammation because this investigation shows secondary patho-anatomical changes, while leukocyte scintigraphy visualizes the acute cellular infiltrate. In patients with more severe inflammation, there is excellent agreement between the two methods.

Adolescent↗
PubMedDate not supplied

[The effect of phenobarbital and cimetidine on the elimination kinetics and distribution in the heart and liver of propranolol in rats with acute and chronic inflammations].

Intravenous administration of propranolol (10 mg/kg) to rats with turpentine-induced inflammation and adjuvant-induced arthritis results in the reduction of the systemic clearance (Cltot.p), volume distribution (Vd,ss) and free fraction (fu). At the same time the area under the pharmacokinetic curve (AUC) increases and the half-life period (t1/2 beta) remains the same. In the phenobarbital-treated rats with acute inflammation Cltot.p increases, AUC and t1/2 beta decreased. Administration of cimetidine resulted in the opposite effect. In rats with adjuvant arthritis phenobarbital and cimetidine administration did not affect the propranolol elimination kinetics. In the phenobarbital-treated rats with inflammation Vd,ss significantly decreased and virtually did not change in cimetidine treated rats. The fu of propranolol increased markedly after the cimetidine treatment in all rats with inflammation, whereas phenobarbital treatment appeared effective only in rats with acute inflammation. The tissue-to plasma concentration ratio (Kp) of propranolol decreased in the liver of rats both with acute and chronic inflammation, whereas in the heart the effect was observed only in rats with chronic inflammation. The tissue to plasma concentration ratio of unbound propranolol (Kpu) decreased only in the liver of rats with acute inflammation. In the phenobarbital-treated rats with adjuvant arthritis Kp of propranolol in the liver increased and in the heart decreased, whereas cimetidine-treatment did not change Kp of propranolol in heart and decreased it in the liver. The Kpu of propranolol decreased only in the heart of rats with acute inflammation after phenobarbital treatment, whereas after cimetidine administration this parameter decreased in the heart and in the liver of rats regardless of the character of inflammation.

Acute Disease↗
PubMedDate not supplied

Clinical significance of increasing histologic severity of acute inflammation in the fetal membranes and umbilical cord.

The purpose of this study was to determine the importance of varying histologic stages of inflammation in the placental membranes and cord. Acute inflammation was histologically staged in fetal membranes and umbilical cord sections from 2899 placentas received from consecutive singleton deliveries. Then clinical data were collected for a subset of randomly selected placentas with stage 1 through stage 4 membrane inflammation (n = 212) and without significant inflammation (stage 0, n = 216). Statistical analyses revealed that increasing stage of membrane inflammation was associated with an increasing rate of funisitis, perinatal death, and preterm birth (P < .05). Inflammation permeating the entire trophoblastic layer of the chorion (stage 1) was associated with clinical symptoms of intrauterine infection and thus was an important pathologic finding. Acute necrotizing chorioamnionitis was very strongly associated with perinatal death and preterm birth. Acute funisitis was a more specific but less sensitive marker for perinatal complications than inflammation in the membranes. With increasing stage of funisitis, there was an increased incidence of clinical symptoms of intrauterine infection, preterm birth, and perinatal death. Almost three-fourths of the cases with histologic evidence of membrane inflammation were clinically silent. In conclusion, increasing histologic stages of inflammation of the membranes and cord are associated with an increased rate of perinatal morbidity and mortality. Stage I membrane inflammation provides a clinically acceptable minimum threshold for the reporting of pathologic changes.

Biomarkers↗
PubMed1996

Calcitonin gene-related peptide is involved in the spinal processing of mechanosensory input from the rat's knee joint and in the generation and maintenance of hyperexcitability of dorsal horn-neurons during development of acute inflammation.

In an electrophysiological study in anaesthetized rats, the involvement of calcitonin gene-related peptide in the spinal processing of mechanosensory information from the normal and inflamed knee joint was investigated. Calcitonin gene-related peptide(8-37), a specific antagonist at calcitonin gene-related peptide 1 receptors was administered ionophoretically close to nociceptive neurons with input from the knee joint before, during, and after development of acute inflammation in the knee induced by the intra-articular injections of kaolin and carrageenan. Calcitonin gene-related peptide (8-37) selectively antagonized the effects of ionophoretically applied calcitonin gene-related peptide but not those of ionophoretically applied substance P, neurokinin A, and (R,S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid. Before inflammation, calcitonin gene-related peptide (8-37) reduced the responses to noxious pressure applied to the knee in 22 of 23 neurons; in 14 of 22 neurons, the responses to innocuous pressure were also reduced. In eight neurons calcitonin gene-related peptide (8-37) was administered during induction and in three periods within the first 90 min of inflammation. In these neurons the developing inflammation evoked a significantly smaller increase of the responses to innocuous and noxious pressure applied to the injected knee than in 13 control neurons which were not treated by the antagonist during induction of inflammation. In 16 of 16 neurons, calcitonin gene-related peptide (8-37) reduced the responses to innocuous and noxious pressure once inflammation and hyperexcitability of the spinal cord neurons were established. These data show that calcitonin gene-related peptide is involved in the spinal processing of mechanosensory input from the normal joint. Furthermore, this peptide and its spinal receptors significantly contribute to the generation and expression of inflammation-evoked hyperexcitability of spinal cord neurons during the development of inflammation. Finally, calcitonin gene-related peptide is involved in the maintenance of inflammation-evoked hyperexcitability. By these effects calcitonin gene-related peptide receptors may significantly contribute to the neuronal basis of hyperalgesia and allodynia associated with inflammation.

Animals↗
PubMed2004

Clinical significance of intra-amniotic inflammation in patients with preterm premature rupture of membranes.

OBJECTIVE: This study was conducted to determine the frequency and clinical significance of intra-amniotic inflammation in patients with preterm premature rupture of the membranes. STUDY DESIGN: Amniotic fluid was retrieved from 219 patients with preterm premature rupture of the membranes; the fluid was cultured for aerobic and anaerobic bacteria and mycoplasmas and assayed for neutrophil collagenase, which is also known as matrix metalloproteinase-8. Matrix metalloproteinase-8 was used because previous studies indicated that this was a sensitive and specific index of inflammation and that is correlated with the amniotic fluid white blood cell count. Intra-amniotic inflammation was defined as an elevated amniotic fluid matrix metalloproteinase-8 concentration (>23 ng/mL). Nonparametric and survival techniques were used for statistical analysis. RESULTS: The overall rate of intra-amniotic inflammation was 42% (93/219 samples); proven intra-amniotic infection was detected only in 23% (50/219 samples). Intra-amniotic inflammation with a negative amniotic fluid culture for micro-organisms was found in 23% (51/219 samples) and was as common as proven intra-amniotic infection. Pregnancy outcome was worse in patients with intra-amniotic inflammation and a negative culture than in those patients with a negative culture and without inflammation. There were no differences in the interval-to-delivery or rate of complications between patients with intra-amniotic inflammation and a negative culture and patients with proven amniotic fluid infection. CONCLUSION: We conclude that intra-amniotic inflammation, regardless of culture result, is present in 42% of patients with preterm premature rupture of the membranes and that it is a risk factor for impending preterm delivery and adverse outcome. We propose that intra-amniotic inflammation, rather than infection, be used to classify and treat patients with preterm premature rupture of the membranes.

Adult↗
PubMed2006

Spinal manipulation reduces pain and hyperalgesia after lumbar intervertebral foramen inflammation in the rat.

OBJECTIVE: To document potential mediating effects of the Activator-assisted spinal manipulative therapy (ASMT) on pain and hyperalgesia after acute intervertebral foramen (IVF) inflammation. METHODS: The IVF inflammation was mimicked by in vivo delivery of inflammatory soup directly into the L5 IVF in adult male Sprague-Dawley rats. Thermal hyperalgesia and mechanical allodynia were determined by the shortened latency of foot withdrawal to radiant heat and von Frey filament stimulation to the hind paw, respectively. Intracellular recordings were obtained in vitro from L5 dorsal root ganglion (DRG) somata. DRG inflammation was examined by observation of the appearance and hematoxylin and eosin staining. ASMT was applied to the spinous process of L4, L5, and L6. A series of 10 adjustments were initiated 24 hours after surgery and subsequently applied daily for 7 consecutive days and every other day during the second week. RESULTS: (1) ASMT applied on L5, L6, or L5 and L6 spinous process significantly reduced the severity and duration of thermal and mechanical hyperalgesia produced by the IVF inflammation. However, ASMT applied on L4 did not affect the response in rats with IVF inflammation or the controls; (2) electrophysiological studies showed that hyperexcitability of the DRG neurons produced by IVF inflammation was significantly reduced by ASMT; (3) pathological studies showed that manifestations of the DRG inflammation, such as the increased vascularization and satellitosis, were significantly reduced 2 to 3 weeks after ASMT. CONCLUSIONS: These studies show that ASMT can significantly reduce the severity and shorten the duration of pain and hyperalgesia caused by lumbar IVF inflammation. This effect may result from ASMT-induced faster elimination of the inflammation and recovery of excitability of the inflamed DRG neurons by improving blood and nutrition supplement to the DRG within the affected IVF. Manipulation of a specific spinal segment may play an important role in optimizing recovery from lesions involving IVF inflammation.

Animals↗
PubMed1998

Quantification of synovistis by MRI: correlation between dynamic and static gadolinium-enhanced magnetic resonance imaging and microscopic and macroscopic signs of synovial inflammation.

Dynamic and static gadolinium-diethylenetriaminepentaacetic acid(Gd-DTPA)-enhanced magnetic resonance imaging (MRI) were evaluated as measures of joint inflammation in arthritis, by a comparison with macroscopic and microscopic signs of synovitis. Furthermore, the importance of the size of the evaluated synovial areas was investigated, as was the optimal time for enhancement measurements. Seventeen rheumatoid arthritis knees and 25 osteoarthritis knees, scheduled for arthroscopy or arthrotomy, were included. Macroscopic and microscopic synovial inflammation as well as nine histologic tissue characteristics were graded at four preselected biopsy sites. Preoperative T1-weighted dynamic fast low angle shot and static spin-echo Gd-enhanced MRI were performed. The dynamic enhancement rate and the static enhancement were measured in the entire synovial membrane of a preselected slice as well as at the four biopsy sites, and compared to synovial pathology. The rate of early enhancement of the total synovial membrane of the preselected slice, determined by dynamic MRI, was highly correlated with microscopic evidence of active inflammation (Spearman p = 0.73; p < 10(-7). Dynamic MRI could distinguish knees with and without synovial inflammation with a high predictive value (0.81-0.90). Moderate and severe inflammation could not be differentiated. The early enhancement rate was correlated with histologic features of active inflammation, particularly vessel proliferation and mononuclear leucocyte infiltration. Dynamic evaluation of small synovial sections at the biopsy sites and static spin-echo MRI resulted in considerably weaker correlations to histologic inflammation than dynamic evaluation of the total synovium. The optimal time for enhancement measurements was one-half to one minute after Gd injection, as the highest correlation coefficients to histologic inflammation were observed in this interval. Dynamic MRI can be used to determine synovial inflammation. Evaluation of large synovial areas one-half to one minute after Gd injection best reflects joint inflammation.

Adult↗
PubMed2000

Relation between colonic inflammation severity and total low-molecular-weight antioxidant profiles in experimental colitis.

Tissue antioxidant status is altered as a response to oxidative stress. This oxidative stress, caused by reactive oxygen species, is associated with inflammatory bowel disease (IBD). Our aim was to examine the relationship between total tissue low-molecular-weight antioxidant (LMWA) profile and inflammation severity in dinitrobenzene sulfonic acid (DNBS) experimental colitis in the rat. Rats were treated with three doses of DNBS: 1, 10, and 20 mg. Inflammation severity was assessed by tissue colonic wet weight, macroscopic evaluation, and tissue myeloperoxidase (MPO) activity. The capacity of water-soluble LMWA was assessed by measuring the reducing power of the tissues with cyclic voltammetry (CV) and by measuring tissue levels of reduced glutathione. While typical markers of inflammation (MPO, macroscopic examination, and colonic wet weight) indicated DNBS dose dependency, such dependency could not be demonstrated for the tissue LMWA as measured by reduced glutathione levels and by the tissues' reducing power. Mild colonic inflammation (induced by ethanol or by 1 mg of DNBS) caused an increase in the overall capacity of water-soluble LMWA. However, severe inflammation (induced by 20 mg of DNBS) caused a reduction in the tissue LMWA capacity. An intermediate dose of DNBS (10 mg) caused moderate inflammation, but did not cause a significant change in the tissue LMWA compared with a saline control treatment. In conclusion, LMWA changed in a biphasic pattern reflective of the severity of mucosal colonic inflammation. It is suggested that: low dose of DNBS (1 mg) and topical alcohol (25% v/v) caused an adaptation effect to the mild oxidative stress associated with mild inflammation. This resulted in an increase in the LMWA. A higher dose of DNBS (20 mg) caused more severe inflammation with an overall reduction in LMWA. The increased efflux of reactive oxygen species, associated with severe inflammation, led to an overall consumption of the tissue LMWA, which masked the increase in LMWA caused by the mild oxidative stress.

Animals↗
PubMed2002

Intense inflammation in bladder carcinoma is associated with angiogenesis and indicates good prognosis.

The aim of this study was to investigate the prognostic influence of microvessel density using the hot spot method in 107 patients diagnosed with transitional cell carcinoma of the bladder. In each case, inflammation was found in the invasive carcinoma, therefore we classified the degree of inflammation as minimal, moderate or intense. Microvessel density was then reevaluated in each tumour in areas corresponding to these three categories. Median microvessel density irrespective of degree of inflammation was 71. Areas of minimal, moderate and intense inflammation were found in 48, 92 and 32 tumours. Microvessel density increased significantly with increasing degree of inflammation. Disease-specific survival was improved if areas of intense inflammation were present in the carcinoma (P=0.004). High microvessel density, irrespective of the degree of inflammation, was associated with a significantly better disease-specific survival (P=0.01). Multivariate analysis using death of disease as endpoint demonstrated an independent prognostic value of N-classification (N0, hazard ratio (HR)=1 vs N1, HR=2.89 (range, 1.52-5.52) vs N2, HR=3.61 (range, 1.84-7.08)), and intense inflammation, HR=0.48 (range, 0.24-0.96). Malignancy grade, T classification and microvessel density were not independent significant markers of poor outcome. In conclusion, inflammation was significantly correlated to microvessel density, and areas of intense inflammation were an independent marker of good prognosis.

Carcinoma, Transitional Cell↗
PubMed1999

Asymptomatic inflammation and/or infection in benign prostatic hyperplasia.

OBJECTIVE: To determine the extent, pattern and clinical significance of asymptomatic histological inflammation and latent infection (National Institute of Health Category IV prostatitis) in benign prostatic hyperplasia (BPH). PATIENTS AND METHODS: The study included 80 patients (from a cohort of 100 consecutive potentially eligible subjects) with a diagnosis of BPH, but no history or symptoms of prostatitis. Histological sections were obtained from specimens collected prospectively at transurethral resection of the prostate (TURP), immunostained for leukocyte common antigen and scanned using a computerized image-analysis system. Foci of inflammation were categorized as glandular, periglandular, stromal or peri-urethral, and the inflammatory cell density graded from 1 to 3. Relationships and correlations were calculated between the volume, degree and type of inflammation, presence and type of bacteria (culture of deep prostatic biopsies), the use of catheters and prostate specific antigen (PSA) levels. RESULTS: Inflammation was identified in all patients but the mean tissue surface area involved was only 1.1% of the total specimen, with periglandular inflammation being the predominant pattern (0.5%). Of the prostate specimens, 44% showed bacterial growth (in 67% of the catheterized patients and 28% of those uncatheterized; 42% of patients were catheterized before TURP). There was no significant difference between any combination of inflammation pattern, volume or grade of inflammation in those catheterized or not (P=0.15) or culture-positive (pathogenic or not) and culture-negative cases (P=0.06). Neither total PSA or PSA density was significantly correlated (P>0.05) with the amount, degree or distribution of inflammation. CONCLUSION: Prostatic inflammation is an extremely common histological finding in patients with symptoms of BPH who have no symptoms of prostatitis. There was no correlation between the degree and pattern of inflammation, catheterization, presence of bacteria, serum PSA or PSA density. The clinical significance of asymptomatic Category IV chronic prostatitis associated with BPH has yet to be determined.

Bacterial Infections↗
PubMed1996

Long-term evolution of gut inflammation in patients with spondyloarthropathy.

BACKGROUND & AIMS: Intestinal inflammation has been observed in patients with spondyloarthropathy (SpA). This prospective study reports the evolution of the intestinal inflammation observed in patients with SpA. METHODS: One hundred twenty-three patients with SpA who had undergone initial endoscopy were clinically reassessed. Intestinal evolution was evaluated by ileocolonoscopy and the histological study of biopsy specimens in 49 patients. RESULTS: Articular remission rates were independent of initial gut inflammation and associated with endoscopic and histological remission. Persistent gut inflammation was observed in active joint disease. Gut inflammation rarely disappeared, despite the persistence of articular complaints. Initial chronic gut inflammation implied a high risk of evolution to ankylosing spondylitis. Evolution to inflammatory bowel disease (IBD) was observed in 7% of patients. Mainly patients with initial chronic inflammation and mild complaints of diarrhea were at risk. Sulfasalazine was more frequently needed in the treatment of patients with gut inflammation with a beneficial effect on articular and intestinal evolution but did not prevent evolution to IBD. CONCLUSIONS: This study supports the etiopathogenetic role of the gut in SpA. Presence of chronic gut inflammation and mild complaints of diarrhea implies a high risk of evolution to ankylosing spondylitis and IBD. Sulfasalazine has a beneficial effect on articular activity by controlling gut inflammation, but it cannot prevent evolution to overt IBD.

Adolescent↗
PubMed2003

Subclinical intestinal inflammation and sacroiliac changes in relatives of patients with ankylosing spondylitis.

BACKGROUND & AIMS: It has been suggested that subclinical intestinal inflammation plays a pathogenic role in the spondylarthropathy of ankylosing spondylitis (AS). We assessed the possible presence and inheritance pattern of subclinical intestinal inflammation in first-degree relatives of patients with AS. The relationship between this inflammation and the subjects' HLA-B27 genotype as well as computerized tomographic sacroiliac abnormalities was also assessed. METHODS: A total of 124 of 213 (58%) available first-degree relatives of 47 patients with AS in Iceland underwent investigation for intestinal inflammation (fecal calprotectin concentration), HLA-B27 genotyping, and computerized tomography of the sacroiliac joints. RESULTS: A total of 41% of the first-degree relatives had subclinical intestinal inflammation, whereas 15 of 17 spouses were normal. Variance components analyses suggest that the inheritance pattern of this inflammation is affected by a major additive gene. Some sacroiliac changes, suggestive of early AS, differed significantly between subjects with and without subclinical intestinal inflammation (mean diameter of subchondral cysts [2.9 vs. 1.2 mm; P = 0.026] and blurring of joint margins [9 of 44 (20%) vs. 1 of 41 (2%); P = 0.02]). Intestinal inflammation and sacroiliac changes did not relate to the subjects' HLA-B27 status. CONCLUSIONS: Many first-degree relatives of patients with AS appear to have an inherited abnormality that leads to subclinical intestinal inflammation. The association between the presence of this inflammation and the sacroiliac changes suggests that it may play a pathogenic role in the spondylarthropathy of AS.

Adult↗
PubMed2003

Intra-articular corticosteroid preparations: different characteristics and their effect during inflammation induced by monosodium urate crystals in the rat subcutaneous air pouch.

OBJECTIVE: To examine the effects of three commonly used intra-articular depot corticosteroid preparations tested in a rat air pouch model and their effect against monosodium urate (MSU) crystal-induced inflammation. Rheumatologists use intra-articular corticosteroid preparations to relieve pain and inflammation of acute monoarthritis without really knowing their effects on the synovial fluid and membrane or the differences between distinct preparations. This work compares the effect of three commonly used corticosteroid preparations in vivo, showing that they behave differently. METHODS: A subcutaneous air pouch was formed in male Sprague-Dawley rats. A first group of 6-day-old air pouches were injected with 10 ml of 6 mg/ml normal saline solution, 6 mg/ml betamethasone containing both depot betamethasone acetate and soluble betamethasone phosphate (Celestone) in 9 ml of normal saline solution, 20 mg/ml of prednisolone tebutate (Hydeltra) in 9 ml of normal saline solution or 20 mg/ml of triamcinolone hexacetonide (Aristospan) in 9 ml of normal saline solution. A second group (group 2) of air pouches were injected with 15 mg of synthetic MSU crystals and 24 h later they were reinjected with 1 ml of the same three corticosteroid suspensions. For each condition four rats were killed at 6, 24, 48 h and 7 days. Pouch fluid and tissue were analysed. RESULTS: In the first 6 h after normal saline solution or corticosteroid injection into the air pouch there were mildly increased leucocyte counts in the air pouch fluid. Betamethasone-injected pouches showed no cells in the fluid after 6 h and no crystals after 24 h, triamcinolone-injected pouches still showed rare cells at 7 days. Both triamcinolone and prednisolone crystals persisted in higher numbers and lasted longer in the fluid than did betamethasone (P<0.05). In group 2 MSU crystal phagocytosis in the fluid was decreased in the betamethasone- (P<0.01), prednisolone- (P<0.003) and triamcinolone- (P<0.006) injected pouches when compared with the MSU crystal-injected pouches alone. Pouches injected with MSU crystals alone showed the most intense tissue inflammation at all times. After MSU, betamethasone-injected pouches had a rapid but mild decrease in the number of lining cells and inflammation. In contrast, triamcinolone- and prednisolone-injected pouches showed a very thin tissue with few or no vessels and almost no inflammation at 7 days. The pouches injected with MSU crystals and any of the corticoid preparations had three times more tophus-like structures and persistent crystals identified than the ones injected with MSU crystals alone. CONCLUSION: Each of the corticosteroid preparations by themselves produced very mild transient inflammation. The betamethasone preparation with a soluble steroid component had a quicker but milder anti-inflammatory effect on MSU crystal-induced inflammation. In contrast to the doses used, prednisolone tebutate and triamcinolone hexacetonide preparations dramatically suppressed urate crystal-induced inflammation at 7 days, but both produced atrophy and necrosis of the membrane, yielding a very thin membrane with almost no vessels. When used for MSU crystal-induced inflammation these corticosteroid preparations suppressed some aspects of inflammation but may actually promote the persistence of MSU crystals and the formation of tophi.

Animals↗