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PubMedDate not supplied

[Pharmacology of non-steroidal anti-inflammatory drugs and ENT pathology].

1. BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) belong to a variety of chemical classes with no common features except the absence of a steroid structure. Their primary effect is pain relief, but also with anti-pyretic and anti-inflammatory effects. Basically prescribed for symptomatic relief, they do not have a curative effect on chronic disease processes. 2. INFLAMMATORY EFFECTS OF PROSTANOIDS (THROMBOXANE A2 AND PROSTAGLANDINS): Inflammation basically results from the pro-algogenic and vascular effects of prostanoids. Their pro-algogenic effects are explained by sensitization of nociceptive nerve endings to the stimulating effect (algogenic) of kinins (bradykinin), serotonin and histamine. In addition, production of prostanoids in the brain has a thermoregulatory effect. 3. MODE OF ACTION: NSAID have a common effect, inhibiting the production of prostanoids via reduced activity of two cyclo-oxygenases (COX-1 and COX-2). COX-2 is an isoform predominantly expressed during the inflammatory process. Excepting two compounds recently marketed (celecoxib, rofecoxib) selective for COX-2, all other NSAID have few or no selective properties. COX-1 is implicated in the regulation of many physiological functions. Inhibition of COX-1 explains most of the classical side effects of non-selective NSAID. 4. COMPARISON: It is classical to emphasize the interindividual variable anti-inflammatory and antalgesic effects of the different NSAID without developing a coherent explanation. In addition, it is very difficult to make objective comparisons between different NSAID because of the different sizes of the study populations, indications and dosages. There is no evidence favoring a given NSAID on the basis of its anti-inflammatory or antalgesic effect in a given indication; no hierarchy in terms of efficacy can be established. For acute pain, it is preferable to use oral NSAID absorbed rapidly to achieve rapid relief. 5. PARACETAMOL: This antalgesic, antipyretic drug has no anti-inflammatory action. Its mechanism of action remains to be fully elucidated. It is not a member of the NSAID class and is a poor inhibitor of COX, particularly COX-2 (30% maximal inhibition). For identical dose (1-3 g/d), the antalgesic activity of paracetamol is comparable to that of aspirin for pain in general. There does not appear to be any difference in the anti-pyretic efficacy between NSAID and paracetamol. 6. OFFICIAL INDICATIONS: In general, NSAID are not indicated for anti-inflammatory action in the ENT conditions discussed here. It this light, the official indications in France published on November 14, 1988 concerning ENT disease in children and adults without risk factors is most noteworthy. It is stipulated that there is no need to institute NSAID treatment at an anti-inflammatory dose in combination with general antibiotic therapy, except when there is an important inflammatory component. This guideline does not concern NSAID at antalgesic and antipyretic doses used for ENT conditions with or without an infectious component. 7. SELECTIVE INHIBITORS OF COX-2: Selective inhibitors are only indicated in two chronic inflammatory diseases: osteoarthritis and rheumatoid arthritis. There is no indication for these inhibitors in ENT disease. The only beneficial effect that has been demonstrated to date for the use of selective inhibitors of COX-2 is better digestive tract tolerance. 8. ROLE OF PROSTANOIDS IN THE CLINICAL EXPRESSION OF ALLERGIC RHINITIS: It is insufficient to warrant use of NSAID in this disease, particularly due to the efficacy of anti-H1 and local corticosteroids. NSAID are not indicated in nasal polyposis and are even contraindicated in case of intolerance to NSAID, observed in about 15-20% of all patients with nasal polyposis. However, local application of lysine acetylsalicylate at progressive doses from 20 micrograms to 4 mg can reduce relapse by half after polypectomy. There is no proof of the efficacy of NSAID in chronic sinusitis and their efficacy has not been studied in laryngitis. Finally, there is no sufficient evidence, either from experimental data or clinical trials, to recommend NSAID for otitis, with the exception for an antalgesic and/or antipyretic effect. 9. CHOOSING AN ANTI-INFLAMMATORY OR ANTALGESIC NSAID: The choice is generally guided by the frequency and severity of undesirable effects. These undesirable effects often appear during the first weeks of treatment. 10. DIFFERENT ADVERSE EFFECTS: Digestive tract effects appear in 20 to 40% of the patients after a few weeks of treatment using anti-inflammatory doses. Symptomatic gastroduodenal ulcers, digestive bleeding, and perforations are the most serious adverse effects of NSAID. Nevertheless, the risk of such complications, compared with the number of prescriptions, is very low. At high dose (anti-inflammatory dose), age over 60 years and history of severe gastrointestinal complications are factors increasing the risk of severe gastrointestinal adverse effects of NSAID. Minor adverse effects, and more importantly severe adverse effects, are significantly reduced with selective COX-2 inhibitors compared with classical NSAID. It is important to note that these beneficial effects in terms of tolerance are not better than with NSAID treatments except for treatments at anti-inflammatory doses for more than one week. Selective COX-2 inhibitors would have the same adverse effect on the kidney as classical NSAID, as pointed out by the precautions for use published by the manufacturers. COX-2 is not expressed by platelets. Specific inhibitors do not inhibit platelet aggregation and do not lengthen bleeding time. Specific inhibitors, like classical NSAID, are not recommended for women desiring pregnancy, especially because the risk of a teratogenic effect has not been excluded. Conversely, for patients with asthma triggered by classical NSAID, selective COX-2 inhibitors do not trigger acute asthma. Finally, selective COX-2 inhibitors are not currently indicated for children and not for ENT disease.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2005

Is interferon-alpha therapy safe and effective for patients with chronic hepatitis C and inflammatory bowel disease? A case-control study.

BACKGROUND: Hepatitis C virus infection is more common in patients with inflammatory bowel disease than in general population. Limited data are available as to the safety and efficacy of alpha-interferon therapy for chronic active hepatitis C in patients with concomitant inflammatory bowel disease. AIM: To evaluate the efficacy and safety of alpha-interferon monotherapy in patients with chronic active hepatitis C and inactive or mildly active inflammatory bowel disease. METHODS: A total of 513 consecutive inflammatory bowel disease patients at a single centre were tested for antibodies to hepatitis C virus (anti-hepatitis C virus) between 1995 and 2000. Twenty-one patients had detectable anti-hepatitis C virus Ab and were hepatitis C virus-RNA positive with histologically proved chronic active hepatitis. Each of these patients, whose inflammatory bowel disease was in clinical remission or mildly active, was sex- and age-matched to three controls with similar histological grade and stage of chronic hepatitis C virus but without inflammatory bowel disease; and all were treated with human leucocyte alpha-interferon 6 million units given thrice weekly for 12 months. Responses to treatment were classified as follows: complete response--persistently normal alanine aminotransferase and viral clearance (hepatitis C virus-RNA-ve) at the end-of-treatment, incomplete response--alanine aminotransferase normalization without viral clearance (hepatitis C virus-RNA+ve), and sustained response--alanine aminotransferase normalization and hepatitis C virus clearance 12 months after the end-of-treatment. RESULTS: Twenty-one patients with chronic active hepatitis C and inflammatory bowel disease (10 with Crohn's disease and 11 with ulcerative colitis) and 63 sex- and age-matched controls with chronic hepatitis C virus alone received alpha-interferon monotherapy. Response rates to interferon were similar for inflammatory bowel disease patients compared with controls [CR 42% vs. 35% and SR 24% vs. 18% (P, not significant), respectively]. None of the 21 inflammatory bowel disease patients had severe adverse effects and the mild ones observed were comparable with those seen in the control group. No patients developed an inflammatory bowel disease relapse during the interferon treatment period or in the 12 months thereafter. CONCLUSIONS: The biochemical and virological response to a 12-month human leucocyte alpha-interferon treatment in patients with chronic active hepatitis C are similar to that observed in matched controls with chronic hepatitis C virus without inflammatory bowel disease. Adverse effects are similar in both groups of patients and unrelated to the underlying inflammatory bowel condition. This provides hepatologists with evidence that alpha-interferon can be safely administered to patients with chronic hepatitis C virus and inflammatory bowel disease provided that the inflammatory bowel condition is in clinical remission.

Adult↗

PubMed1998

Anti-inflammatory actions of glucocorticoids: molecular mechanisms.

1. Glucocorticoids are widely used for the suppression of inflammation in chronic inflammatory diseases such as asthma, rheumatoid arthritis, inflammatory bowel disease and autoimmune diseases, all of which are associated with increased expression of inflammatory genes. The molecular mechanisms involved in this anti-inflammatory action of glucocorticoids is discussed, particularly in asthma, which accounts for the highest clinical use of these agents. 2. Glucocorticoids bind to glucocorticoid receptors in the cytoplasm which then dimerize and translocate to the nucleus, where they bind to glucocorticoid response elements (GRE) on glucocorticoid-responsive genes, resulting in increased transcription. Glucocorticoids may increase the transcription of genes coding for anti-inflammatory proteins, including lipocortin-1, interleukin-10, interleukin-1 receptor antagonist and neutral endopeptidase, but this is unlikely to account for all of the widespread anti-inflammatory actions of glucocorticoids. 3. The most striking effect of glucocorticoids is to inhibit the expression of multiple inflammatory genes (cytokines, enzymes, receptors and adhesion molecules). This cannot be due to a direct interaction between glucocorticoid receptors and GRE, as these binding sites are absent from the promoter regions of most inflammatory genes. It is more likely to be due to a direct inhibitory interaction between activated glucocorticoid receptors and activated transcription factors, such as nuclear factor-kappa B and activator protein-1, which regulate the inflammatory gene expression. 4. It is increasingly recognized that glucocorticoids change the chromatin structure. Glucocorticoid receptors also interact with CREB-binding protein (CBP), which acts as a co-activator of transcription, binding several other transcription factors that compete for binding sites on this molecule. Increased transcription is associated with uncoiling of DNA wound around histone and this is secondary to acetylation of the histone residues by the enzymic action of CBP. Glucocorticoids may lead to deacetylation of histone, resulting in tighter coiling of DNA and reduced access of transcription factors to their binding sites, thereby suppressing gene expression. 5. Rarely patients with chronic inflammatory diseases fail to respond to glucocorticoids, although endocrine function of steroids is preserved. This may be due to excessive formation of activator protein-1 at the inflammatory site, which consumes activated glucocorticoid receptors so that they are not available for suppressing inflammatory genes. 6. This new understanding of glucocorticoid mechanisms may lead to the development of novel steroids with less risk of side effects (which are due to the endocrine and metabolic actions of steroids). 'Dissociated' steroids which are more active in transrepression (interaction with transcription factors) than transactivation (GRE binding) have now been developed. Some of the transcription factors that are inhibited by glucocorticoid, such as nuclear factor-kappa B, are also targets for novel anti-inflammatory therapies.

Anti-Inflammatory Agents↗

PubMedDate not supplied

Update on the genetics of inflammatory bowel disease.

There is a general consensus that interplay of genetic and environmental factors leads to an overactive mucosal immune response, which mediates the tissue damage in inflammatory bowel disease. Ethnic aggregation of inflammatory bowel disease (particularly, increased incidence and prevalence in the Ashkenazim), familial aggregation of inflammatory bowel disease, and greater concordance for inflammatory bowel disease in monozygotic twins than dizygotic twins are 3 lines of evidence for a central role of genetic factors in the pathogenesis. The genetics of inflammatory bowel disease cannot be explained by simple Mendelian genetics; it is characterized by incomplete penetrance, multiple susceptibility loci and genetic heterogeneity. Unraveling the complex genetics of inflammatory bowel disease is a daunting challenge, but the perseverance of inflammatory bowel disease gene hunters has produced commendable results in recent years. Since 1996, the field of inflammatory bowel disease genetics has progressed from publication of the first systematic genome searches for inflammatory bowel disease susceptibility loci to the identification of Crohn disease-associated genetic variants in CARD15/NOD2. Strategies for finding additional inflammatory bowel disease genes include taking advantage of the greater resolution and power of linkage disequilibrium mapping, mapping by admixture disequilibrium in African-American and Hispanic-American populations, stratifying genetic analyses by genotypes at known inflammatory bowel disease loci, and refining inflammatory bowel disease phenotypes to reduce genetic heterogeneity and simplify the search for additional inflammatory bowel disease genes.

Carrier Proteins↗

PubMed1975

The possible occurrence of endogenous anti-inflammatory substances in the blood of injured rats.

1 Using the carrageenin rat paw oedema test as an assay, an attempt has been made to confirm the presence of anti-inflammatory activity in the blood of rats with a chronic inflammatory lesion induced by a polyester sponge, and to relate such activity to the systemic anti-inflammatory effect exerted in situ by the lesion. In addition, plasma from rats given acetic acid intraperitoneally has been examined for anti-inflammatory properties. 2 The activity of serum obtained from sponge-bearing adrenalectomized Wistar rats did not differ significantly from that obtained from animals without implants. Furthermore, implanted sponges exerted no systemic anti-inflammatory effect. 3 Similar experiments were performed in sponge-bearing adrenalectomized Sprague-Dawley rats, plasma instead of serum being examined for anti-inflammatory activity. The plasma removed from such animals possessed no anti-inflammatory activity, whilst implanted sponges exerted a small, yet significant, systemic inhibitory effect. 4 When the irritancy of sponge implants was augmented with croton oil, more marked systemic anti-inflammatory effects were observed. However, the plasma obtained from rats injured in this manner exerted no anti-inflammatory effect. 5 No anti-inflammatory activity could be detected in plasma samples obtained from rats treated with doses of acetic acid capable of producing pronounced systemic anti-inflammatory effects. 6 It was concluded that the induction of these inflammatory lesions in rats does not appear to lead to a detectable release of endogenous anti-inflammatory substances into the circulation.

Acetates↗

PubMed2006

Characterization of the pro-inflammatory signaling induced by protein acetylation in microglia.

Protein acetylation regulates the extent of inflammatory responses and disturbances in protein acetylation have been proposed to play an important role in inflammatory and neurodegenerative diseases. We have recently observed that histone deacetylase inhibitors, such as trichostatin A (TSA) and SAHA, strongly potentiate the LPS induced inflammatory response in several rat and mouse inflammatory models. Our aim here was to characterise pro-inflammatory signaling mediated via increased protein acetylation and protein phosphorylation in microglial N9 cells. First we observed that TSA induced pro-inflammatory response was independent of the different Toll-like receptors activated, since LPS, flagellin and unmethylated CpG oligonucleotides, equally potentiated IL-6 secretion from N9 microglia. Next we compared the protein acetylation induced potentiation to that induced by okadaic acid, a well-known inducer of pro-inflammatory responses. The time scale of the IL-6 responses showed that the effects of okadaic acid were clearly early-response effects appearing as soon as 6h after exposure, whereas TSA evoked a significant inhibition in IL-6 secretion up to 12h but after that it induced an exponential increase in cytokine and nitric oxide production up to 24h. It seems that okadaic acid induces an early moderate response and TSA a late but exponential potentiation of microglial inflammatory responses. The pro-inflammatory responses of TSA and okadaic acid were both dependent on NF-kappaB signaling but independent on the DNA-binding capacity of nuclear NF-kappaB complexes. Interestingly, we observed that the transactivation of the NF-kappaB-Luc reporter gene was clearly activated during TSA induced pro-inflammatory potentiation. Our studies imply that the potentiation of the inflammatory response by increased acetylation is due to the enhancement of transactivation of NF-kappaB driven inflammatory genes. Our studies on signaling pathways revealed that PI3K inhibitors LY294002 and Wortmannin blocked the TSA induced pro-inflammatory response but surprisingly did not affect the okadaic acid induced response. Furthermore, LY294002 did not inhibit DNA-binding activity of NF-kappaB but still inhibited NF-kappaB-Luc reporter gene transactivation. These results indicate that PI 3-kinase regulates the transactivation efficiency of NF-kappaB-dependent transcription rather than transduction of NF-kappaB signaling.

Acetylation↗

PubMed1992

Inflammatory aortic aneurysms: characteristic appearance on magnetic resonance imaging.

Ten to 15% of all aortic aneurysms show inflammatory change. They are characteristically covered on their anterior and lateral sides with thick white fibrous tissue. Peri-aortic fibrosis may spread into the retroperitoneum to encase and obstruct adjacent organs making operative treatment more difficult and increasing the operative morbidity and mortality. Fifteen patients with inflammatory aneurysms and 46 patients with simple non-inflammatory aneurysms were studied prospectively. Each patient underwent magnetic resonance imaging (MRI) using a Picker Vista MR2055 scanner operating at 0.5 tesla. Each scan was reviewed by a radiologist (G.G.H.) preoperatively and a diagnosis of inflammatory or non-inflammatory aneurysm made. At operation, the diagnosis of aneurysm type was made on macroscopic features of inflammatory change, and confirmed histologically using previously published criteria. The radiological diagnosis was found to correspond to the surgical and pathological diagnosis in all cases. In cases of inflammatory aortic aneurysm the aneurysm wall appeared laminated on MRI scan, showing three or more bright, high-signal layers. These appearances of inflammatory change are characteristic, and were present in all 15 patients with such aneurysms. There were no false positives among those patients with simple aneurysms, and no false negatives. Operative specimens of aortic wall were taken from four patients with inflammatory aortic aneurysms and four patients with simple non-inflammatory aortic aneurysms, and subjected to MRI scanning. The characteristic banding appeared only in the inflammatory aneurysm wall samples. Magnetic resonance imaging is a highly sensitive investigative technique for the detection of inflammatory aneurysms, showing characteristic changes. These changes are also seen in in vitro scans of wall samples from inflammatory aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1997

Inflammatory aortic aneurysms. A clinical review with new perspectives in pathogenesis.

OBJECTIVE: The authors present a review of abdominal aortic aneurysms (AAAs) and to examine the literature on the diagnosis, operative management, and long-term survival of patients with inflammatory AAAs. Furthermore, to review current theories on the cause of inflammatory AAAs and present recent studies that provoke new thought on the cause of these aneurysms. BACKGROUND DATA: Inflammatory AAAs represent 3% to 10% of all AAAs and present the surgical team with a unique challenge. Progress has occurred in the technical approach to these aneurysms, and operative morbidity and mortality have been reduced. However, the pathogenesis remains an enigma. Recent studies raise questions regarding the influence of tobacco and genetic factors that accentuate an antigen-driven inflammatory response. METHODS: The authors conduct a review of the literature on both noninflammatory and inflammatory AAAs. RESULTS: Review of the literature of inflammatory AAAs reveals advancement in the definition, diagnosis, management, and long-term survival of patients with inflammatory AAAs. This review found an evolution in thought regarding the cause of inflammatory AAAs. In contrast to initial reports describing a distinct clinical entity, recent evidence suggests that inflammatory AAAs arise from the same causal stimulus responsible for noninflammatory AAAs. Finally, recent studies show an influence of tobacco and genetic factors on the pathogenesis. CONCLUSIONS: The literature supports the theory that inflammatory AAAs arise from the same or similar antigenic stimulus which is responsible for the noninflammatory AAA. Genetic and chemical factors such as tobacco use predispose certain persons to the development of noninflammatory AAAs and others to develop the extreme end of an inflammatory spectrum, the inflammatory AAA. Furthermore, inflammatory AAAs can be managed with the same operative morbidity, mortality, and long-term survival as noninflammatory AAAs.

Aortic Aneurysm, Abdominal↗

PubMed2000

Inflammatory cells, motor weakness, and straight leg raising in transligamentous disc herniations.

STUDY DESIGN: Possible statistically significant relationships between inflammatory cells and either motor weakness or straight leg raising were determined. OBJECTIVES: To look for any clinically relevant links between inflammatory cells in disc herniations and signs of radiculopathy. SUMMARY OF BACKGROUND DATA: Many studies have during recent years shown a presence of various types of inflammatory cells in disc herniations, but their clinical relevance has been questioned. To be clinically relevant, a presence of inflammatory cells should show a clear relationship to clinical evidence of nerve root involvement. Macrophages repeatedly demonstrated in a high proportion of disc herniations studied are of particular interest. Their major role may be in disc herniations tissue resorption and not in sciatica. METHODS: A total of 96 disc herniations, all transligamentous, were analyzed by immunohistochemistry for presence of macrophages, T or B lymphocytes, and activated T lymphocytes separately. From recorded patient data, motor weakness and straight leg raising data were compared with a presence or absence of abundant (+ = at least 20 cells in a group) inflammatory cells. When not abundant, inflammatory cells were classified as "only few cells" (+) and grouped together with "no cells" (-). Patients with or without motor weakness were compared. Straight leg raising was compared for a positive (at <70 degrees ) or a negative test, and separately using the median as cut-off value. Groups were compared by chi-square analysis with the level of statistical significance set at P<0.05. RESULTS: None of the four inflammatory cell types showed any significant association with motor weakness. Nor was any association observed when comparing positive and negative straight leg raising. With the median (straight leg raising = 47.5 degrees ) as cut-off, only activated T cells showed a weak (chi2 = 4.40, P<0.05) relationship with tighter straight leg raising, but none of the other cell types did. Even when straight leg raising was < 47.5 degrees, three times more disc herniations lacked (n = 34) inflammatory cells than showed (n = 13) inflammation. In a subgroup of only sequestrated discs, the findings were similar. However, in the patients with a bilaterally positive straight leg raising (n = 25), the prevalence of at least one inflammatory cell type was much higher in sequestrated discs (80%) than in extrusions (33%). This may suggest more subtle interrelationships between type of disc herniation, straight leg raising, and inflammatory cells. CONCLUSIONS: The results of this study do not support a clinically relevant role for disc herniation inflammatory cells in sciatica. For the cells to be clinically relevant, a strong relationship between a presence of inflammatory cells and either or both of motor weakness and a tight straight leg raising should have been observed. The authors conclude that macrophages, which have been demonstrated in a high proportion of disc herniations in previous studies, are probably more important for disc tissue resorption processes than for producing sciatica. Other types of inflammatory cells are more rarely observed and may have no clinical meaning at all. However, more subtle interrelationships, considering the various types of disc herniations, should be further explored.

Adolescent↗

PubMed2001

Comparison of the prevalence of inflammatory cells in subtypes of disc herniations and associations with straight leg raising.

STUDY DESIGN: The prevalence of inflammatory cells in 205 disc herniations (DHs) and nine macroscopically normal discs for comparison was studied immunohistochemically. Inflammatory cells were separately analyzed in subtypes of DH. Immunohistochemical data were related to clinical parameters, the straight leg raising test (SLR) in particular. OBJECTIVES: The objectives of the study were to compare the occurrence of inflammatory cells in various subtypes of DH and to determine the association between clinical data and inflammatory cell occurrence in a more extensive sample of DH, with separate analysis of DH subtypes. SUMMARY OF BACKGROUND DATA: Previous studies have suggested a common occurrence of inflammation and inflammatory cells, particularly macrophages, in DHs. No studies on any larger material comprising different subtypes of DH have been done. METHODS: For immunohistochemistry the alkaline phosphatase antialkaline phosphatase method was used. Monoclonal antibodies to T cells in general (CD2), activated T cells (CD25), B cells (CD22), and macrophages (CD68) were used. Obtained immunostaining results were then compared with clinical data, e.g., duration of pain, SLR, and type of DH (sequesters 86, extrusions 103, protrusions 16). Associations were studied by the chi2 test or Fisher's exact test, as applicable (level of significance P < 0.05). RESULTS: Abundant T cells were seen in 17% of the 205 DHs, activated T cells in 17%, B cells in 16%, and macrophages in 37%. All cell types were 2-3 times more prevalent in sequestrated discs than in extrusions. In protrusions macrophages were abundantly seen in 25% (4 of 16) and no other inflammatory cells. In patients with positive SLR and a sequestrated disc abundant lymphocytes were seen three times more often than in extrusions. When patients with bilaterally negative SLR were compared with those with tight SLR (< or =30 degrees ) with respect to inflammatory cell occurrence, some significant differences were noted (CD68, P < 0.025; CD25, P = 0.04). A comparison between SLR bilaterally positive and bilaterally negative also showed associations for all four inflammatory cell types (P = 0.016 to P = 0.029). There was no correlation between inflammatory cells and duration of pain. Abundant inflammatory cells were never seen in control discs. CONCLUSIONS: When SLR was positive and the DH type was sequestered, inflammatory cells were most commonly seen. Our results showed some statistically significant associations between inflammatory cells and SLR, most clearly when comparing bilaterally positive and negative SLR. Interestingly, a bilaterally positive SLR showed an association with all four inflammatory cell types analyzed. Tight SLR also showed an association, particularly with macrophages. In addition to tissue resorption, they may participate in sciatic pain. Even though lymphocytes were less prevalent, they may have some role in sequestered discs and bilaterally positive SLR.

Adolescent↗

PubMedDate not supplied

A clinicopathological study of inflammatory pseudotumors of the liver with special reference to vessels.

BACKGROUND/AIMS: Inflammatory pseudotumor of the liver is rare, and patients with inflammatory pseudotumor frequently undergo unnecessary surgical resection as a result of misdiagnosis of malignancy. In this study, we therefore investigated inflammatory pseudotumor clinicopathologically to clarify its characteristics. METHODOLOGY: Twenty patients including 3 with inflammatory pseudotumor and 17 with various malignant liver tumors were studied. We further investigated tumor vessels by means of immunohistochemistry using monoclonal antibodies against CD34, factor VIII-related antigen and alpha-smooth muscle actin. RESULTS: Although serum levels of alkaline phosphatase were significantly higher in inflammatory pseudotumor patients than in other patients, the laboratory data alone could not precisely distinguish inflammatory pseudotumor from other hepatic tumors. On imaging studies such as ultrasonography and computed tomography, significant changes in tumor size, especially size reduction, during relatively short follow-up periods were often observed in inflammatory pseudotumor but not in other liver tumors. An enhancement of the peripheral regions of inflammatory pseudotumor was frequently observed in the early phase of contrast-medium dynamic computed tomography. This might be due to abnormal vessels located in the peripheral regions of inflammatory pseudotumor which might result from obliteration of some pre-existing vessels in portal tracts within inflammatory pseudotumor. Immunohistochemical analysis further revealed that abnormal vessels in the peripheral regions of inflammatory pseudotumor were positively stained with CD34, factor VIII-related antigen and alpha-smooth muscle actin as were tumor sinusoids within hepatocellular carcinoma and tumor capillaries in other malignant liver tumors. CONCLUSIONS: Although inflammatory pseudotumor seems to have some features in imaging studies, a biopsy is needed for a correct diagnosis of inflammatory pseudotumor.

Actins↗

PubMed1988

Glucose metabolism of injured skeletal muscle: the contribution of inflammatory cells.

Wounded muscle which has increased glucose uptake is infiltrated with a large number of inflammatory cells. Macrophages which are the predominant inflammatory cells in wounded muscle can increase glucose oxidation by epididymal fat pads. Therefore, the possibility that inflammatory cells could also alter glucose metabolism in skeletal muscle was investigated. Peritoneal inflammatory cells (67% macrophages, 7% lymphocytes, 15% polymorphonuclear leukocytes, and 11% eosinophils) were elicited with a 1% sodium caseinate solution. Extensor digitorum longus muscles, were incubated alone, in the presence of inflammatory cells or in an inflammatory-cell-conditioned media. Similar incubations were performed using epididymal fat pads. In addition, inflammatory cells were incubated alone. The present studies confirmed the previous finding that inflammatory cells release a factor(s) that increases glucose oxidation in epididymal fat pads. The coincubation of inflammatory cells with skeletal muscle resulted in a 22% increase in glucose uptake and a 19% increase in the conversion of glucose to lactate compared to the sum of these processes for muscle or inflammatory cells incubated alone. In addition, this study showed that the incubation of skeletal muscle in inflammatory-cell-conditioned medium produced a 117.6% increase in glucose uptake and a 147% increase in the conversion of glucose to lactate. Therefore, inflammatory cells can increase glucose metabolism in skeletal muscle through the release of a soluble factor(s). This effect does not require a direct contact of the inflammatory cells with skeletal muscle.

Animals↗

PubMed1992

Pelvic inflammatory disease: trends in hospitalizations and office visits, 1979 through 1988.

OBJECTIVES: We attempted to assess trends in pelvic inflammatory disease occurrence and to describe current antibiotic treatment and use of surgical procedures for pelvic inflammatory disease in the United States. STUDY DESIGN: Analyses of hospitalizations according to the National Center for Health Statistics, National Hospital Discharge Survey for 1979 to 1988, and of office visits to private physicians from the National Disease and Therapeutic Index for 1979 to 1989 were done. RESULTS: From 1979 to 1988, a mean of 181,700 women aged 15 to 44 years were hospitalized each year for acute pelvic inflammatory disease (3.03/1000 women) and 94,400 for chronic pelvic inflammatory disease (0.90/1000), and nearly 400,000 first visits for pelvic inflammatory disease were made each year to private physicians' offices (7.2/1000 women). Mean visit and hospitalization rates for acute pelvic inflammatory disease were highest for women aged 20 to 24 years and for other-than-white women. By 1987 to 1988, however, pelvic inflammatory disease hospitalization rates were highest for teenagers. Surgery was performed during 42% of hospitalizations for acute pelvic inflammatory disease and 90% of hospitalizations for chronic pelvic inflammatory disease. Over this time period, hospitalization rates for acute pelvic inflammatory disease decreased by 36% while office visit rates remained unchanged. CONCLUSION: This decrease in hospitalizations for pelvic inflammatory disease may indicate a true decrease in its incidence, changes in physician hospitalization practices, or a shift in the spectrum of severity of pelvic inflammatory disease.

Adolescent↗

PubMed1992

Pelvic inflammatory disease: findings during inpatient treatment of clinically severe, laparoscopy-documented disease.

OBJECTIVES: We evaluated the relationship between clinically severe pelvic inflammatory disease and laparoscopic diagnosis and grading, comparative treatment with clindamycin plus cefamandole or doxycycline, and a management protocol for inpatient pelvic inflammatory disease treatment. STUDY DESIGN: Thirty-three patients who met our clinical criteria for severe pelvic inflammatory disease underwent diagnostic laparoscopy. Pelvic inflammatory disease patients were randomized to double-blind treatment with clindamycin plus cefamandole or doxycycline within our management protocol; postdischarge oral antibiotics were omitted. RESULTS: Laparoscopy confirmed pelvic inflammatory disease in 23 (70%) patients; 10 (44%) had mild pelvic inflammatory disease by laparoscopic grading. Laparoscopic grade alone predicted necessary duration of therapy to response: mild pelvic inflammatory disease, 2.3 +/- 0.5 days; moderate pelvic inflammatory disease, 2.7 +/- 1.5 days; and severe pelvic inflammatory disease, 3.9 +/- 1.5 days (p less than 0.05). Using the management plan presented, response rates for both antibiotic regimens were 100%. CONCLUSIONS: Clinical diagnosis and grading of severe pelvic inflammatory disease has poor specificity. Laparoscopic grading of severity of pelvic inflammatory disease seems accurate. Both clindamycin plus cefamandole and clindamycin plus doxycycline are equally effective regimens for treatment of pelvic inflammatory disease and did not require supplementation after discharge. Our management plan is objective and practical; daily bimanual examination is the most sensitive indicator of persistent disease.

Adult↗

PubMed2003

Inflammatory bowel disease after liver transplantation: the effect of different immunosuppressive regimens.

BACKGROUND: Seemingly conflicting results have been reported on the prevalence and severity of inflammatory bowel disease after liver transplantation. Regimens with different combinations of drugs can be used for immunosuppression after transplantation. AIM: To study retrospectively the prevalence of inflammatory bowel disease after liver transplantation, and the possible relationship with maintenance immunosuppressive regimens. METHODS: All 78 patients with end-stage primary sclerosing cholangitis (48 patients) or autoimmune cirrhosis (30 patients), transplanted between 1979 and July 2001, and with a follow-up of at least 1 year, were eligible for this study. In addition to patient and transplant characteristics, data on inflammatory bowel disease and immunosuppression before and after transplantation were collected. The Kaplan-Meier method was used for survival analysis. Possible risk factors for inflammatory bowel disease after transplantation were analysed by Cox univariate and multivariate regression. RESULTS: The median follow-up after transplantation was 7.2 years (range, 1.1-22.3 years). Nine of 25 patients with pre-transplant inflammatory bowel disease experienced flare-ups after transplantation. Six of 53 patients without pre-transplant inflammatory bowel disease developed de novo inflammatory bowel disease after transplantation. The cumulative risks (standard errors in parentheses) for inflammatory bowel disease were 6% (3%), 12% (4%) and 20% (5%) at 1, 3 and 5 years after transplantation, respectively. The inflammatory bowel disease-free survival was significantly higher in patients not receiving tacrolimus vs. those receiving tacrolimus, in patients receiving azathioprine vs. those not receiving azathioprine and in patients taking the regimen prednisolone-azathioprine-ciclosporin A vs. those taking tacrolimus-prednisolone. Pre-transplant inflammatory bowel disease and the use of tacrolimus were found to be independent predictors for inflammatory bowel disease after transplantation. CONCLUSIONS: The prevalence of inflammatory bowel disease after liver transplantation is affected by the immunosuppression used. Azathioprine seems to have a protective effect and tacrolimus a promoting effect.

Adolescent↗

PubMed2005

Efficacy and tolerability of oral iron therapy in inflammatory bowel disease: a prospective, comparative trial.

BACKGROUND: In patients with inflammatory bowel disease, oral iron is anecdotally reported to be less effective and less well tolerated than in those without inflammatory bowel disease, and to increase disease activity. AIM: To study prospectively the effects of oral iron in patients with and without inflammatory bowel disease. METHODS: Patients with ulcerative colitis, Crohn's disease and non-inflammatory bowel disease controls, all with iron deficiency anaemia, were assessed with symptom diaries, a quality of life questionnaire (Inflammatory Bowel Disease Questionnaire; inflammatory bowel disease patients only) and blood tests to measure iron repletion, disease activity and antioxidant capacity before and after starting 4 weeks of oral iron. In patients with ulcerative colitis, sigmoidoscopic scoring and rectal biopsies for reactive oxygen metabolite production were performed before and after iron therapy. RESULTS: All groups showed increases in haemoglobin and ferritin. Iron intolerance occurred in about a quarter of patients in each group. Two of 33 (6%) of inflammatory bowel disease patients had a relapse during treatment. Symptoms worsened in ulcerative colitis, but not in Crohn's disease or non-inflammatory bowel disease patients; Inflammatory Bowel Disease Questionnaire scores improved in ulcerative colitis. Laboratory markers of disease activity, sigmoidoscopic scores, histological scores, antioxidant capacity levels and reactive oxygen metabolite production did not change. CONCLUSIONS: Oral iron is equally efficacious and well tolerated in inflammatory bowel disease and non-inflammatory bowel disease patients. A tiny minority of inflammatory bowel disease patients relapse in association with use of oral iron therapy.

Administration, Oral↗

PubMed2001

Prothrombotic inherited abnormalities other than factor V Leiden mutation do not play a role in venous thrombosis in inflammatory bowel disease.

OBJECTIVES: Because the incidence of thromboembolism is increased in patients with inflammatory bowel disease, we attempted to assess the role of prothrombotic inherited coagulation abnormalities in the development of thrombosis. METHODS: Four populations were compared: 15 patients with inflammatory bowel disease and a previous venous thrombosis, 58 control patients with inflammatory bowel disease but without thrombosis, 110 patients without inflammatory bowel disease but with previous deep venous thrombosis, and 84 healthy subjects. Inherited and acquired risk factors of venous thrombosis, e.g., factor V Leiden and prothrombin 20210A mutations, C677T methylenetetrahydrofolate reductase polymorphism, a polymorphism located in exon 13 of factor V gene, inflammatory and hypercoagulability markers were studied in each population. RESULTS: In the study, 14.3% of thrombotic patients with inflammatory bowel disease had factor V Leiden mutation versus 0% of control patients with inflammatory bowel disease (p = 0.04), 15.5% of thrombotic patients without inflammatory bowel disease (NS) and 3.6% of the healthy controls. A total of 14% of thrombotic patients with inflammatory bowel disease and 11.8% of thrombotic patients without inflammatory bowel disease carried prothrombin 20210A mutation, compared to 1.7% of control patients with inflammatory bowel disease; however, the difference was just below significance. Other inherited coagulation abnormalities were not statistically significantly different among the four populations. CONCLUSIONS: Our study confirms that factor V Leiden mutation increases the risk for thrombotic events but is not more frequent in patients with inflammatory bowel disease. Our results do not support the role of other thrombotic risk factors.

Adult↗

PubMed1994

Macrophage inflammatory protein-1 alpha in term and preterm parturition: effect of microbial invasion of the amniotic cavity.

PROBLEM: This study was conducted to determine whether: (1) gestational age, parturition, and microbial invasion of the amniotic cavity (MIAC) are associated with changes in amniotic fluid concentrations of immunoreactive macrophage inflammatory protein-1 alpha; (2) amniotic fluid concentrations of macrophage inflammatory protein-1 alpha are correlated with the white blood cell count and the concentrations of interleukin-8 in amniotic fluid. METHOD: Amniotic fluid was retrieved by amniocentesis from 126 patients; 54 women with preterm labor and intact membranes (no MIAC-delivery at term, N = 21; no MIAC-preterm delivery, N = 16; MIAC-preterm delivery, N = 17); 62 patients at term (no labor, N = 19; labor-no MIAC, N = 20; labor-MIAC, N = 23); and 10 patients in the midtrimester of pregnancy. Amniotic fluid was cultured for aerobic, anaerobic and Mycoplasma species. Determinations of amniotic fluid macrophage inflammatory protein-1 alpha and interleukin-8 were performed with immunoassays validated for amniotic fluid (sensitivity: 14.2 pg/ml and 0.3 ng/ml, respectively). Kruskal-Wallis analysis of variance (ANOVA) for censored data, Mann-Whitney U test and Spearman's rank correlation were performed for analysis. RESULTS: 1) Amniotic fluid macrophage inflammatory protein-1 alpha was present in only 31.0% (9/29) of patients not in labor (midtrimester and term). 2) Patients with preterm labor and MIAC had higher amniotic fluid concentrations of macrophage inflammatory protein-1 alpha than those without MIAC (no MIAC-delivery at term: median 0.0 pg/ml, range 0.0-221.2; no MIAC-preterm delivery: median 37.4 pg/ml, range 0.0-494.6; MIAC-preterm delivery: median 7171.0 pg/ml, range 402.5-37994.0; P < 0.00001). 3) Among patients at term, MIAC was associated with higher concentrations of amniotic fluid macrophage inflammatory protein-1 alpha than patients without MIAC (no labor: median 0.0 pg/ml, range 0.0-25.6; labor-no MIAC: median 16.7 pg/ml, range 0.0-161.6; labor-MIAC: median 103.8 pg/ml, range 0.0-4349.0, P < 0.001). 4) Among patients in preterm labor, a strong correlation was found between amniotic fluid concentrations of macrophage inflammatory protein-1 alpha and interleukin-8 (r = 0.9, P < 0.00001) and between amniotic fluid macrophage inflammatory protein-1 alpha concentrations and amniotic fluid white blood cell count (r = 0.6, P < 0.0001). CONCLUSIONS: (1) Macrophage inflammatory protein-1 alpha is undetectable in most amniotic fluid samples from patients in the midtrimester of pregnancy and at term not in labor. (2) Microbial invasion of the amniotic cavity is associated with increased concentrations of immunoreactive amniotic fluid macrophage inflammatory protein-1 alpha in both term and preterm gestations. (3) Amniotic fluid macrophage inflammatory protein-1 alpha concentrations significantly correlate with interleukin-8 levels and white blood cell count in amniotic fluid. Our data strongly suggest a role for macrophage inflammatory protein-1 alpha in the mechanisms responsible for the recruitment of leukocytes into the amniotic cavity during the course of intrauterine infection.

Amnion↗