Evidence Of Inflammatory Process Research Articles

Patients with episodic migraine show increased T2 values of the trapezius muscles - an investigation by quantitative high-resolution magnetic resonance imaging.

BackgroundNeck pain is frequent in patients with migraine. Likewise, evidence for inflammatory processes in the trapezius muscles is accumulating. However, non-invasive and objectively assessable correlates are missing in vivo.MethodsTwenty-one subjects with episodic migraine (mean age: 24.6 ± 3.1 years, 18 females) and 22 controls (mean age: 23.0 ± 2.2 years, 17 females) without any history of headache prospectively underwent physical examination and quantitative magnetic resonance imaging of the trapezius muscles. A T2‐prepared turbo spin-echo sequence was acquired for manual segmentation of the trapezius muscles and extraction of mean T2 values.ResultsThere were no statistically significant differences regarding age, sex, body mass index, or number of myofascial trigger points (mTrPs) between groups. All patients with migraine presented with mTrPs in the trapezius muscles. T2 of the entire trapezius muscles was significantly higher in the migraine group when compared to controls (31.1 ± 0.8 ms vs. 30.1 ± 1.1 ms; p = 0.002).ConclusionsElevated T2 values of the trapezius muscles may indicate subtle inflammatory processes within musculature among patients with migraine because T2 increase is likely to stem from edematous changes. Future work may validate this finding in larger cohorts, but muscle T2 might have potential to develop into a viable in vivo biomarker for muscular affection in migraine.

Atypical course of Charcot-Marie-Tooth disease: what shall we be thinking of?

Charcot-Marie-Tooth disease (CMT) is an inherited polyneuropathy with a gradually progressive course. Atypical features such as acute or subacute deterioration and unusual electrophysiological findings should be alarming. A 54 year-old woman with medical history of hypothyroidism, was referred to our department for weakness of her 4 limbs with a subacute onset and rapid worsening. The family history was marked by feet deformities. The pedigree was suggestive of autosomal dominant inheritance. On examination the proband had steppage gait, with distal muscle weakness in four limbs, absent tendon reflexes, hummer toes and hollow feet. Nerve conduction studies showed homogeneous demyelination but with temporal dispersion in motor nerves. We noted slight increase in protein level in cerebrospinal fluid (CSF). The patient was diagnosed with autosomal dominant CMT type I based on family history, neurological examination of the proband and her relatives, and electrophysiological findings, associated with chronic inflammatory demyelinating polyneuropathy. The patient was treated with high-dose steroids and than moderately improved. Further reported features suggesting a co-existent hereditary and inflammatory process are: conduction blocks in motor nerve conduction studies, high protein levels in CSF, evidence of inflammatory process in nerve biopsy and nerve root enhancement in spinal imaging. Atypical course and unusaul biological, electrical and imaging features in CMT disease should be alarming about the co-existence of inflammatory neuropathy. Immunomodulatory treatment may substancially improve the outcome.

Synthesis and Biological Evaluation of an (18)Fluorine-Labeled COX Inhibitor--[(18)F]Fluorooctyl Fenbufen Amide--For Imaging of Brain Tumors.

Molecular imaging of brain tumors remains a great challenge, despite the advances made in imaging technology. An anti-inflammatory compound may be a useful tool for this purpose because there is evidence of inflammatory processes in brain tumor micro-environments. Fluorooctylfenbufen amide (FOFA) was prepared from 8-chlorooctanol via treatment with potassium phthalimide, tosylation with Ts2O, fluorination with KF under phase transfer catalyzed conditions, deprotection using aqueous hydrazine, and coupling with fenbufen. The corresponding radiofluoro product [18F]FOFA, had a final radiochemical yield of 2.81 mCi and was prepared from activated [18F]F− (212 mCi) via HPLC purification and concentration. The radiochemical purity was determined to be 99%, and the specific activity was shown to exceed 22 GBq/μmol (EOS) based on decay-corrected calculations. Ex-vivo analysis of [18F]FOFA in plasma using HPLC showed that the agent had a half-life of 15 min. PET scanning showed significant accumulation of [18F]FOFA over tumor loci with reasonable contrast in C6-glioma bearing rats. These results suggest that this molecule is a promising agent for the visualization of brain tumors. Further investigations should focus on tumor micro-environments.

Editorial Comments: Is multiple sclerosis a neurodegenerative or inflammatory disease?

The etiology of multiple sclerosis (MS) and its pathogenesis are unclear in spite of being the topic of much research for many years. Neuropathological examinations provide undisputable evidence of inflammatory processes in acute demyelinating lesions in MS. This by itself is not surprising, since even if these inflammatory processes are secondary to the initial lesion, they may still have unfavorable consequences. In fact, the beneficial effects of high-dose steroid administration in speeding up the recovery from acute MS relapses seem to support this view. The assumption that inflammation has a central role in the disease, rather than an epiphenomenon, has persisted for decades. This assumption that inflammation processes underlie the neurodegenerative process in MS was the basis for chronic therapy with steroids, which has been popular in the past. However, a more critical examination showed this to be an unrewarding treatment. Inflammation is a term used to describe many processes, sometime complementing and at other time opposing each other, some beneficial and others not. Therefore, a systematic study regarding the role of inflammation in MS should be made in a more focused way. The positive effects of b-interferons (which are anti-inflammatory) support a damaging role of inflammation in acute relapses. However, by the same token, their inefficacy during the secondary progenies phase argues against an inflammatory role in the chronic stage. The neurodegenerative component of MS may or may not be a consequence of inflammation. Neither corticosteroids nor specific anti-inflammatory agents like interferons are effective in the chronic progressive stage of MS. Whether other focused anti-inflammatory process modulation could be beneficial remains to be seen. However, the development of such drugs depends on a more refined definition of the inflammatory process components and discovery of specific targeted interventions. For the time being, the jury is still out: Is MS primarily an inflammatory disorder, where the neurodegeneration is a consequence, or is it primarily a neurodegenerative disorder, in which inflammatory responses are secondary, occurring at the beginning but later die out.

Panvascular Inflammation and Mechanisms of Injury in Perioperative CNS Outcomes

In this review, the evidence for inflammatory processes as being of fundamental importance in end-organ dysfunction- specifically stroke and neurocognitive impairment in patients undergoing cardiac surgery-will be reviewed. The risk of central nervous system (CNS) impairment following an off-pump cardiac surgery will be contrasted with that of patients undergoing percutaneous coronary intervention (PCI) or medical management, and the role of progression of underlying cerebrovascular disease and, in particular, panvascular inflammation as an accompaniment to unstable angina with attendant risk of stroke will be explored. In addition, the various roles of preoperative comorbidities, aortic atheroma, and the use of selective avoidance of aortic instrumentation as well as carotid endarterectomy as risk modification strategies will be evaluated. Finally, a summary of recommendations for strategies to decrease risk of perioperative CNS impairment will be presented.

Mat á járnbúskap með mælingu á transferrínviðtökum

The purpose of this study was to estimate the value of the transferrin receptor in serum (sTfR) for detecting iron deficiency and compare it with the value of some other blood tests for that purpose. All patients undergoing bone marrow aspiration in the FSA Hospital, Akureyri, Iceland, in the period 1999 to 2003 were eligible to participate in this prospective study. Included participants were 89. The sensitivity, specificity, efficiency, and Youden index of ferritin, MCV, CHr, sTfR, sTfR-Ferritin-index, the iron saturation of transferrin, and the Thomas-Plot method were calculated. The complete absence of stainable iron in bone marrow was used as the definitive marker of iron depletion. The best method to detect iron deficiency as estimated by the Youden index was the Thomas-Plot method. This method was very specific in cases without evidence of inflammatory processes (CRP <6 mg/L) and very sensitive in cases with elevated CRP (>6 mg/L). The sTfR-Ferritin-index came second and sTfR was the best single blood test to detect iron deficiency according to the Youden index. The Thomas-Plot method and the sTfR-Ferritin-index proved to be the most reliable blood tests to diagnose iron deficiency. These parameters can eliminate the need of using bone marrow aspirate to diagnose iron deficiency in some cases.

Ultrasonographic and Power Doppler Evaluation of the Patellar Tendon Ten Years after Harvesting Its Central Third for Reconstruction of the Anterior Cruciate Ligament

Background The long-term morphologic changes in the patellar tendon after harvesting its central third for the reconstruction of the anterior cruciate ligament have not been reported. Hypothesis Sonographic morphologic changes in the harvested patellar tendon are common 10 years after the harvesting procedure. Study Design Retrospective cohort study. Methods Thirty-one patients who had undergone an anterior cruciate ligament reconstruction using central-third bone-patellar tendon-bone autograft with a closure of the patellar tendon defect were included in this study. An ultrasonographic and Power Doppler examination was performed at a mean follow-up of 10 years. Results Ultrasonography of the harvested patellar tendon showed intratendinous calcification in 9 patients, hypoechoic lesion in 20 patients, hyperechoic lesion in 1 patient, and peritendinous changes in 1 patient. Only 3 (9.7%) of the 31 patients had no changes in the harvested patellar tendon. No abnormality was visible in the contralateral (normal) patellar tendons of the 31 patients. The harvested patellar tendon was significantly thicker than the contralateral patellar tendon (P < 0.05). Conclusions Sonographic morphologic changes of the patellar tendon were common 10 years after the harvesting procedure, although no evidence of inflammatory process, as could be seen in Power Doppler flow, was found inside of any patellar tendon.

Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin-1 system.

The evidence of inflammatory processes in the clinical manifestations and neuropathological sequelae of epilepsy have accumulated in the last decade. Administration of kainic acid, an analogue of the excitatory amino acid glutamate, induces a characteristic behavioural syndrome and a reproducible pattern of neurodegeneration in several brain areas, closely resembling human temporal lobe epilepsy. Results from studies using the kainic acid model indicate that manipulation of pro- and anti-inflammatory cytokines can modify the outcome with regard to the behavioural syndrome as well as the neuropathological consequences. Interleukin-1 is one of the most important cytokines and has several actions in the brain that are critical for the host defense against injury and infection, and it is involved in the initiation of early stages of inflammation. It is believed that interleukin-1 plays a pivotal role in the neuroinflammation associated with certain forms of neurodegeneration, including cerebral ischemia, trauma and excitotoxic brain injury. In this review, we have summarized the experimental data available with regard to the involvement of the interleukin-1 system in kainic acid-induced changes in the brain and emphasized the modulatory role of interleukin-1beta in this model of epilepsy

Increased serum IL‐6, TNF‐alpha and IL‐10 levels in patients with bullous pemphigoid: relationships with disease activity

AbstractAimThe present report analyzes the serum levels of three cytokines, interleukin‐6 (IL‐6), tumor necrosis factor‐alpha (TNF‐alpha) and interleukin‐10 (IL‐10) in 15 patients with bullous pemphigoid (BP) (compared with 20 healthy controls) to evaluate a possible involvement of these biological modulators in the clinical expression of this disease.BackgroundBP is a rare, bullous disease of autoimmune origin with evidence of inflammatory processes that cause skin lesions with local increase of various pro‐inflammatory mediators.MethodsDetermination of cytokine concentrations were obtained employing commercially available ELISA kits.ResultsThe sera of BP patients showed increased levels of these three cytokines (P &lt; 0.01). When the number of skin lesions (blisters and/or erosion) of each patient, employed as a marker of disease activity, was correlated with the serum levels of IL‐6 and TNF‐alpha, significant correlations were found (IL‐6: P &lt; 0.01 and TNF‐alpha: P &lt; 0.01, respectively), suggesting a possible role of these mediators in the development of BP blisters. The serum levels of IL‐6 also correlated (P= 0.01) with those of serum C reactive protein (CRP), an acute‐phase protein induced by IL‐6 in hepatocytes. In addition, serum TNF‐alpha and sE‐selectin (an adhesion molecule previously reported to be increased by this cytokine) levels were also correlated (P &lt; 0.05).ConclusionsOn the basis of these data, it may be indicated that at least IL‐6 and TNF‐alpha are associated with the clinical expression of BP and that the endothelial activation (possibly induced by the TNF‐alpha activity), seems to be an important phase of this dermatosis.

Increased serum IL-6, TNF-alpha and IL-10 levels in patients with bullous pemphigoid: relationships with disease activity

Aim The present report analyzes the serum levels of three cytokines, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) in 15 patients with bullous pemphigoid (BP) (compared with 20 healthy controls) to evaluate a possible involvement of these biological modulators in the clinical expression of this disease.Background BP is a rare, bullous disease of autoimmune origin with evidence of inflammatory processes that cause skin lesions with local increase of various pro-inflammatory mediators.Methods Determination of cytokine concentrations were obtained employing commercially available ELISA kits.Results The sera of BP patients showed increased levels of these three cytokines (P<0.01). When the number of skin lesions (blisters and/or erosion) of each patient, employed as a marker of disease activity, was correlated with the serum levels of IL-6 and TNF-alpha, significant correlations were found (IL-6: P<0.01 and TNF-alpha: P<0.01, respectively), suggesting a possible role of these mediators in the development of BP blisters. The serum levels of IL-6 also correlated (P=0.01) with those of serum C reactive protein (CRP), an acute-phase protein induced by IL-6 in hepatocytes. In addition, serum TNF-alpha and sE-selectin (an adhesion molecule previously reported to be increased by this cytokine) levels were also correlated (P<0.05).Conclusions On the basis of these data, it may be indicated that at least IL-6 and TNF-alpha are associated with the clinical expression of BP and that the endothelial activation (possibly induced by the TNF-alpha activity), seems to be an important phase of this dermatosis.

Dialysis Arthropathy: a Clinical, Biochemical, Radiological and Histological Study of 36 Patients

Out of a population of 97 haemodialysis patients, 36 patients with dialysis arthropathy were identified. Dialysis arthropathy is a chronic symmetrical polyarthritis which affected 97 per cent of the patients who had been undergoing cuprophane haemodialysis for more than 10 years. It commonly affected the shoulders, hips, hands, knees and wrists, worsening with time and extending to other joints. Fifty-eight per cent of the patients complained of morning stiffness and 47 per cent complained of exacerbation of shoulder pain during or after haemodialysis. Half of the patients also suffered from carpal tunnel syndrome, which recurred and was associated with a long-lasting disability. The most common radiological abnormality was periarticular bone cysts, followed by articular erosions and a destructive spondyloarthropathy, but clinical symptoms were more common than radiological signs. Patients with dialysis arthropathy had a higher C-reactive protein level than patients without arthropathy (18.6 mg/l versus 11.4 mg/l), indicative of an inflammatory process. Some of the clinical manifestations of the disease correlated with levels of C-reactive protein and ferritin. Serum ferritin levels correlated strongly with the units of blood transfused in the past five years (RS = 0.83), and the logarithm of ferritin level correlated weakly with C-reactive protein (r = 0.32). Haemarthroses were documented in 19 per cent of patients. Mean serum beta 2-microglobulin was elevated in the patients with (57.3 mg/l) and without arthropathy (50.7 mg/l), and there was no difference in the parathormone or aluminium levels between these groups. Articular tissue was obtained in 25 patients; beta 2-microglobulin amyloid was present in 24. Larger deposits were present in the capsular tissue, and these appeared to replace collagen bundles in eight cases. Amyloid deposits replaced the lining layer in six cases. It is likely therefore that amyloid disrupts normal joint function by replacing normal joint tissue. Mild chronic synovitis with haemosiderin deposition were found in approximately 60 per cent of cases. These findings suggest that amyloid derived from beta 2-microglobulin has a primary role in the pathogenesis of dialysis arthropathy, but there was also evidence of inflammatory processes. It is suggested that iron overload or haemarthroses might contribute to the inflammation, but other factors, such as dialysis-related bioincompatibility reactions, may also have a role.

The secretory activity of the seminal vesicles and its relationship to sperm motility: effects of infection in the male reproductive tract.

In 146 males aged between 20 years and 40 years attending an infertility service, the secretory activity of the seminal vesicles was assessed by measurement of corrected seminal fructose concentration. This value was related to the presence of a positive semen culture, other evidence of inflammatory processes in the reproductive tract and sperm motility. Only 48% of subjects with a positive semen culture showed evidence of inflammation in the reproductive tract, as assessed by the presence of more than 20 white blood cells per high power field, and greater than 10% spermagglutination in the ejaculate. There was a relationship between the inflammatory process, hypofunction of the seminal vesicles and poor sperm motility. When the semen culture was positive but there was no evidence of inflammation neither seminal vesicle function nor sperm motility was affected. When the semen culture was negative, i.e. no evidence of inflammation and the subjects were asthenozoospermic, the corrected fructose levels were normal. It is proposed that in these conditions the cause of asthenozoospermia may be factors other than accessory sex organ dysfunction. In conclusion, there was no close relationship between the bacteriological results and evidence of inflammation of the accessory glands. A positive semen culture was related to lower levels of corrected fructose (hypofunction of the seminal vesicles) when the positive sperm culture was associated with inflammation of the reproductive tract and asthenozoospermia.