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PubMed1996

MR characterization of post-irradiation soft tissue edema.

OBJECTIVE: Radiation therapy is often used to treat bone und soft tissue neoplasms, and commonly results in soft tissue edema in the radiation field. However, the time course, distribution and degree of this edema have not been well characterized. Our study was carried out to better define these features of the edema seen following neutron and photon radiation therapy. DESIGN AND PATIENTS: Two hundred and twenty-six patients underwent radiation therapy as part of combined modality management for musculoskeletal sarcomas between 1985 and 1993. Of these, 15 had surgical resection of their neoplasm, had no clinical evidence of recurrent disease, and had adequate MR follow-up that allowed sequential assessment of soft tissue following irradiation. Ten patients received photons with an average dose of 52.8 Gy. Five patients received neutrons with an average dose of 17.3 nGy. Sequential MR follow-up was available in these patients for an average of 22.8 months following radiation therapy. On each of the serial MR imaging studies, subcutaneous fat, muscle, and the intramuscular septa/fascial planes were graded subjectively as to size and signal intensity. RESULTS: In general, soft tissue signal intensity in the radiation field initially increased over time, peaking at about 6 months for neutron-treated patients and at about 12-18 months for photon-treated patients. Signal intensity then decreased slowly over time. However, at the end of the follow-up period, signal intensity remained elevated for most patients in both groups. Signal intensity in a particular tissue was greater and tended to persist longer on STIR sequences than on T2-weighted sequences. Survival analysis of signal intensity demonstrated much longer edema survival times for neutron-treated patients than for photon-treated patients. Signal intensity increase in the intramuscular septa persisted for much longer than for fat or muscle. A mild increase in size was noted in the subcutaneous fat and intramuscular septa. Muscle, on the other hand, showed a decrease in size following treatment. This was mild for the photon-treated group and more marked for the neutron-treated group. CONCLUSIONS: There is a relatively wide variation in the duration and degree of post-irradiation edema in soft tissues. This edema seems to persist longer in the intramuscular septa than in fat or muscle. Although the duration of follow-up was limited, our study suggests that this edema resolves in roughly half the photon-treated patients within 2-3 years post-treatment and in less than 20% of neutron-treated patients by 3-4 years post-treatment. Muscle atrophy was seen in both photon- and neutron-treated patients, but was more severe in the neutron-treated group.

Adipose Tissue↗
PubMedDate not supplied

Retroperitoneal edema: sonographic mimic of retroperitoneal fluid collection.

BACKGROUND: The sonographic finding of an anechoic retroperitoneal abnormality suggests a fluid collection (e.g., abscess, urinoma, hematoma). Our study was performed to evaluate cases in which this sonographic finding appeared to be a manifestation of systemic edema. SUBJECTS AND METHODS: Inpatient sonograms performed over a 40-month period were reviewed for the presence of anechoic areas suggestive of fluid collection in the retroperitoneum of the flank. Records of patients with such findings were reviewed for evidence of retroperitoneal abscess, urinoma, or hemorrhage, as well as for the presence and cause(s) of peripheral edema. RESULTS: Of the 29 patients identified with sonographic findings suspicious for retroperitoneal fluid collection, 13 (45%) had no cause for and no clinical evidence of focal retroperitoneal collection. All 13 patients had peripheral edema attributable to hypoalbuminemia, congestive heart failure, overhydration, cirrhosis, and/or the systemic inflammatory response (multiple organ failure) syndrome. Resolution of the retroperitoneal abnormality following therapy for congestive heart failure was documented in one case, and CT scan confirmed retroperitoneal edema in another. CONCLUSION: Anechoic regions that represent edema can be seen on sonograms of the retroperitoneum in patients with conditions that cause edema in other regions. The possibility of edema mimicking a fluid collection should be particularly considered prior to invasive procedures in the retroperitoneum.

Adult↗
PubMed2002

Peritumoral brain edema in intracranial meningiomas evaluated by dynamic perfusion-weighted MR imaging: a preliminary study.

Our objective was to semi-quantitatively evaluate the cerebral perfusion in the peritumoral brain edema of meningiomas using dynamic perfusion-weighted MR imaging. Six patients with intracranial meningiomas accompanied by peritumoral brain edema were prospectively examined by perfusion-weighted MR imaging. One patient was examined twice, once before and once 5 months after the surgical resection. The relative regional cerebral blood volume (rrCBV), the relative regional cerebral blood flow (rrCBF), and the relative regional mean transit time (rrMTT) were calculated for peritumoral brain edema and the contralateral white matter. These parameters were compared between peritumoral brain edema and the contralateral white matter. The time-concentration curve of the peritumoral brain edema was less prominent than that of the contralateral white matter, resulting in a significantly lower rrCBV (mean 46%) and rrCBF (mean 45%) in peritumoral brain edema than those of contralateral white matter. The serial perfusion-weighted MR imaging also demonstrated the recovery of these parameters after the removal of meningioma by means of surgical resection. Perfusion-weighted MR imaging can demonstrate significantly decreased rrCBV and rrCBF in peritumoral brain edema compared with those in normal white matter.

Aged↗
PubMed2006

Influence of an infrapatellar fat pad edema on patellofemoral biomechanics and knee kinematics: a possible relation to the anterior knee pain syndrome.

INTRODUCTION: An edema of the infrapatellar fat pad following knee arthroscopy or in case of chronic anterior knee pain syndrome is suspected to increase the patellofemoral pressure by a modification of the patellofemoral glide mechanism. The study was performed to evaluate this hypothesis. MATERIALS AND METHODS: Isokinetic knee extension from 120 degrees of flexion to full extension was simulated on 10 human knee cadaver specimens (six males, four females, average age at death 42 years) using a knee kinemator. Joint kinematics was evaluated by ultrasound sensors (CMS 100, Zebris, Isny, Germany), and retro-patellar contact pressure was measured using a thin-film resistive ink pressure system (K-Scan 4000, Tekscan, Boston). Infrapatellar tissue pressure was analyzed using a closed sensor cell which was implanted inside the fat pad (GISMA, Buggingen, Germany). An inflatable fluid cell was implanted by ultrasound control in the center of the infrapatellar fat pad and filled subsequently with water to simulate a fat pad edema. All parameters were recorded and analyzed from 0 to 5 ml volume of the fluid cell. RESULTS: Simulating a fat pad edema resulted in a significant (P < 0.01) increase of the infrapatellar fat pad pressure (247 mbar at 0 ml to 615 mbar at 5 ml volume). In knee extension and flexion the patella flexion (sagittal plane) was decreased while we did not find any other significant influence of the edema on knee kinematics. During the analysis of the patellofemoral biomechanics, a simulated fat pad edema resulted in a significant (P < 0.05) decrease of the patellofemoral force between 120 degrees of knee flexion and full extension. The contact area was reduced significantly near extension (0 degree-30 degrees) by an average of 10% while the contact pressure was reduced at the entire range of motion up to 20%. CONCLUSION: An edema of the infrapatellar fat pad does not cause an increase of the patellofemoral pressure or a significant alteration of the patellofemoral glide mechanism. Anterior knee pain in case of a fat pad edema may be related to a significant increase of the tissue pressure and possible histochemical reactions.

Adipose Tissue↗
PubMed1983

Clinical efficacy and safety of indapamide in the treatment of edema.

Whether edema is caused by "overflow" or "underfill," the excess retention of salt and water is common to virtually all forms. The use of natriuretic agents has been shown to be effective in most cases of edema. The present study compares the efficacy of a new long-acting indoline compound, indapamide, with that of hydrochlorothiazide, both given once daily, in the treatment of edema. This double-blind study was conducted in 17 centers. Edema was evaluated by weight change and pitting of the lower extremities. Indapamide was given in doses of 2.5, 5.0, and 10.0 mg and was compared with 100 mg of hydrochlorothiazide. Active treatment was continued up to 12 weeks. Weight change efficacy evaluation was done on 219 patients, and efficacy analysis for pitting edema was done on 214 patients. Of the 219 subjects, 90 were men and 129 were women. Mean age was 57.4 years, and mean body weight was 88.5 kg. By the end of 2 weeks of active treatment, the percentages of patients with no edema were 26%, 44%, and 31% for the indapamide groups (2.5, 5.0, and 10.0 mg), respectively, and 40% for the hydrochlorothiazide group (100 mg). Early response to treatment as measured by weight loss was demonstrated by all patients in the study regardless of treatment group. Hypokalemia was the most frequently reported adverse reaction. Other adverse reactions were infrequent, with no significant difference among the treatment groups. This study concluded that indapamide in once-daily oral doses of 2.5, 5.0, or 10.0 mg was as safe and effective as a once-daily 100 mg dose of hydrochlorothiazide for the treatment of 219 patients with edema from various causes.

Body Weight↗
PubMed1979

Abnormal regulation of antidiuretic hormone in idiopathic edema.

Idiopathic edema is characterized by impaired water excretion, particularly in the upright posture. Indirect evidence has shown that antidiuretic hormone is involved in this disease. For this reason, we measured urinary arginine vasopressin by radioimmunoassay before and during water loading (15 ml/kg) in 10 normal women and in 10 subjects with idiopathic edema in both the supine and upright postures. Daily sodium intake was 100 meq. Renin and aldosterone were concomitantly investigated, and abnormally high values were observed both in the recumbent and upright postures. Basal values for urinary arginine vasopressin were identical in control subjects and in patients with idiopathic edema. The water load significantly reduced urinary arginine vasopressin in normal women in both positions, but in those with idiopathic edema only in the supine position. In those with idiopathic edema, assumption of the upright posture was accompanied by a transient decrease in glomerular filtration, a major decrease in osmolar clearance and no decrease in urinary arginine vasopressin after water loading. Significant correlations were established between urinary arginine vasopressin and osmolar or volemic parameters in normal women, but these correlations were not found in those with idiopathic edema in either position. Arginine vasopressin regulation was abnormal in idiopathic edema, and this hormone was believed to play a part in the pathogenesis of this disease.

Adult↗
PubMed1984

Effect of primary capsulotomy with extracapsular surgery on the incidence of pseudophakic cystoid macular edema.

We performed a prospective randomized study of 288 patients to assess the effect of primary capsulotomy on the angiographic incidence of cystoid macular edema in patients undergoing extracapsular surgery with implantation of an intraocular lens. Patients either had a primary capsulotomy or the posterior capsule remained intact immediately following uneventful posterior chamber intraocular lens implantation. Of the 288 patients, 183 (63%) underwent fluorescein angiography. Angiographically confirmed cystoid macular edema occurred significantly more often in the primary capsulotomy group (20 of 93 patients) than in the intact capsule group (four of 71 patients), for an incidence of 21.5% vs 5.6% (P = .003). The cystoid macular edema appeared milder in the intact capsule group; all the patients with angiographically confirmed cystoid macular edema achieved visual acuities of 20/50 or better. The presence of cystoid macular edema made no difference on visual outcome in the intact capsule group. In contrast, the patients with angiographically confirmed cystoid macular edema in the primary capsulotomy group had significantly worse vision than those who did not have cystoid macular edema (P less than .02).

Aged↗
PubMed1984

Macular edema. A complication of diabetic retinopathy.

Diabetic macular edema is the leading cause of decreased vision from diabetic retinopathy. This decreased vision is caused by an increase in extracellular fluid within the retina distorting the retinal architecture and frequently taking on a pattern of cystoid macular edema. This fluid accumulates within the retina because of the breakdown of the barriers within the retinal blood vessels and possibly the pigment epithelium. Diabetic macular edema tends to be a chronic disorder. Although spontaneous recovery is not an uncommon occurrence, over one-half of diabetics with macular edema will lose two or more lines of visual acuity within two years. The most promising treatment for diabetic macular edema has been photocoagulation. It is recommended that in all patients with diabetic macular edema attempts be made to normalize elevated blood glucose, decrease elevated blood pressure, and improve cardiac or renal status. Reduction of serum lipids by diet or pharmacologic means is an unproven treatment at this time. The Early Treatment Diabetic Retinopathy Study hopefully will provide more definitive information as to whether photocoagulation is effective in various subgroups of patients with diabetic macular edema.

Blood Glucose↗
PubMed1984

A pharmacologic analysis of the action of platelet-activating factor in the induction of hindpaw edema in the rat.

Platelet-activating factor (PAF), a phospholipid product of neutrophils, alveolar macrophages, monocytes, and platelets and an important mediator of inflammatory reactions, was studied for its ability to evoke hindpaw edema in the rat. PAF caused edema, peaking at 1 hr and gradually declining over the next 2 hr. The H1 and H2 antihistamines, mepyramine and cimetidine, the serotonin/histamine antagonist, cyproheptadine, and the serotonin antagonist, methysergide, were ineffective in reducing PAF-induced paw edema. Indomethacin, acetylsalicylic acid, and dexamethasone did not inhibit the peak edematous response but significant reduction was noted with only dexamethasone at 3 hr. Prazosin and propranolol did not prevent PAF-induced edema, whereas, yohimbine, phentolamine, rauwolscine, verapamil and theophylline partially inhibited edema. Clonidine and guanfacine did not induce edema when injected into the rat hindpaw. These results suggest that PAF elicits edema at vascular sites of the rat hindpaw which are partially dependent on extracellular Ca2+ movement, are not due to alpha-1 or alpha-2-adrenoreceptor stimulation, histamine, serotonin, or prostaglandin activity, and demonstrates variable sensitivities to agents blocking Ca2+ entry. Inhibition of specific PAF-sensitive receptors await the discovery of specific PAF antagonists.

Animals↗
PubMed1995

Effects of prostaglandin antagonist phloretin derivatives on mouse ear edema induced with different skin irritants.

Edema was induced in one ear of male mice of the CFLP strain with solutions of different skin irritants (croton oil 10 microL/35 micrograms, dithranol 10 microL/30 micrograms, capsaicin 10 microL/40 micrograms or arachidonic acid to 10 microL/2 mg per ear). Edema, determined by the edema-disk gravimetric technique, was inhibited in a dose-dependent manner by the intraperitoneally administered prostaglandin antagonists polyphloretin phosphate (PPP) or di-4-phloretin phosphate (DPP). With croton oil-induced mouse ear edema, DPP 10 mg/kg caused a 38% inhibition, PPP 25 mg/kg a 33% inhibition. With dithranol-induced edema DPP 0.5 mg/kg caused a 57% inhibition, while PPP 25 mg/kg was needed to exert a similar effect. Doses of DPP and PPP needed to cause a > 40% inhibition of edema were 10 mg/kg and 25 mg/kg, respectively, for capsaicin, and 25 mg/kg and 100 mg/kg for arachidonic acid. The inhibition of the ear edema by the phloretin derivatives was: dithranol > croton oil > capsaicin > arachidonic acid. This probably reflects the different contributions of prostaglandins to the inflammation.

Animals↗
PubMed1986

Effects of dexamethasone on brain edema induced by kainic acid seizures.

The histopathological alterations developing in the hippocampus, piriform cortex and thalamus of the rat brain, the blood-brain barrier damage, and the effects of dexamethasone pretreatment on the brain edema were investigated 4 h following intraperitoneal kainic acid administration. The most pronounced Evans Blue extravasation accompanied by increases in the water and sodium contents and a decrease in the potassium content, were observed in the thalamus. Dexamethasone, injected in a dose of 5 mg/kg 2 h before kainic acid administration, reduced considerably the vasogenic edema and neuronal damage in the thalamus, but the cytotoxic edema of the hippocampus and piriform cortex remained unaltered. Kainic acid-induced seizures lead to the development of vasogenic brain edema mainly in the thalamus, as well as to cytotoxic edema in the hippocampus and piriform cortex. The vasogenic edema seems to contribute to the cell damage in the thalamus. Dexamethasone reduces the vasogenic edema and cell damage in the thalamus, possibly by inducing the synthesis of certain protein(s) with antiphospholipase A2 activity.

Animals↗
PubMed2006

Transient bone marrow edema syndrome of the knee: clinical and magnetic resonance imaging results at 5 years after core decompression.

PURPOSE: We report on 24 cases of transient bone marrow edema syndrome in 18 patients who underwent core decompression of the knee. METHODS: Diagnosis was made with the use of radiographs, magnetic resonance imaging (MRI), and core biopsy testing. Arthroscopic surgery and core decompression were carried out in all patients, and MRI was performed again, 5 years after surgery was performed. RESULTS: Medial and lateral femoral condyles were affected in 15 and 7 knees, respectively. In all, 6 patients presented with bilateral involvement of the knees (migrating transient bone marrow edema syndrome). Two of these patients had affections of the medial and lateral compartments within the same knee at different times, consistent with intra-articular regional bone marrow edema syndrome. Core biopsy specimens showed areas of bone marrow edema and vital trabeculae covered by osteoblasts and osteoid seams. Resolution of symptoms and normalization of MRI findings occurred in all patients within 12 weeks after surgery. CONCLUSIONS: Migrating bone marrow edema was found in a high percentage (33%) of patients at 5-year follow-up; however, all patients were clinically asymptomatic, and signal alterations on MRI had resolved completely. The high incidence of migrating bone marrow edema, the lack of osteonecrotic regions in our specimens, and the fact that none of these cases progressed to spontaneous osteonecrosis seem to further support the contention that bone marrow edema syndrome of the knee is a distinct entity. LEVEL OF EVIDENCE: Level II, diagnostic study; development of diagnostic criteria on the basis of consecutive patients and with universally applied reference gold standard.

Adult↗
PubMed2006

Leukotriene D4 induces brain edema and enhances CysLT2 receptor-mediated aquaporin 4 expression.

Cysteinyl leukotrienes (including LTC(4), LTD(4), and LTE(4)), potent inflammatory mediators, can induce brain-blood barrier (BBB) disruption and brain edema. These reactions are mediated by their receptors, CysLT(1) and CysLT(2) receptors. On the other hand, aquaporin 4 (AQP4) primarily modulates brain water homeostasis and edema after various injuries. Here, we aimed to determine whether AQP4 is involved in LTD(4)-induced brain edema. LTD(4) (1ng in 0.5mul PBS) microinjection into the cortex increased endogenous IgG exudation (BBB disruption) and water content (brain edema), and enhanced AQP4 expression in mouse brain. The selective CysLT(1) receptor antagonist pranlukast inhibited the IgG exudation, but not the increased water content and AQP4 expression induced by LTD(4). In the cultured rat astrocytes, LTD(4) (10(-9)-10(-7)M, for 24h) similarly enhanced AQP4 expression. The enhanced AQP4 expression was inhibited by Bay u9773, a non-selective CysLT(1)/CysLT(2) receptor antagonist, but not by pranlukast. LTD(4) (10(-9)-10(-7)M) also induced the mRNA expression of CysLT(2) (not CysLT(1)) receptor in astrocytes. These results indicate that LTD(4) modulates brain edema; CysLT(1) receptor mediates vasogenic edema while CysLT(2) receptor may mediate cytotoxic edema via up-regulating AQP4 expression.

Animals↗
PubMed2004

The role of endogenous versus exogenous tPA on edema formation in murine ICH.

To minimize the neurotoxic injury by clot-derived substances after intracerebral hemorrhage (ICH) on the surrounding brain tissue, minimally invasive neurosurgical protocols have evolved evacuating the hematoma by stereotaxic injection of a fibrinolytic agent such as recombinant tissue plasminogen activator (rtPA), followed by aspiration of the lysed clot. However, the possible contribution of the presence of exogenous tPA itself to the toxic effects of hematoma-derived factors complicates the rationale and efficacy of this therapeutic approach. To clarify the role of exogenous rtPA on edema development, we examined the extent of edema formation in a murine model of collagenase-induced ICH, which included tPA-deficient (tPA-/-) and wild-type (wt) mice. In 16 (7 tPA-/- and 9 wt mice) out of 32 mice, 1 mg/kg rtPA was injected into the hematoma 5 h after ICH induction followed by aspiration of the liquefied clot 20 min later. In the control group (8 tPA-/- and 8 wt mice), only collagenase was injected. The edema volume was quantified using SPOT software on Luxol Fast Blue and Cresyl violet-stained cross-sections 24 h, 3, and 7 days post surgery. Twenty-four hours after ICH induction, tPA-/- mice had a significantly smaller edema volume (P< 0.01), even when rtPA was administered. Between days 3 and 7 after ICH, exogenous rtPA exerts its edema-promoting effect irrespective of the underlying genotype and exhibits an extensive microglial activation adjacent to the clot. In conclusion, the role of the endogenous tPA appears to be limited to the early phase of edema formation, whereas exogenous rtPA is edema-promoting between days 3 and 7 after ICH.

Animals↗
PubMed2005

Free radicals as triggers of brain edema formation after stroke.

Brain edema is a leading cause of death after stroke. Cytotoxic edema, which is most severe in astrocytes, begins within a few minutes of adenosine triphosphate depletion and reflects the ultimate infarct size. Vasogenic edema is caused by uncontrolled fluid leakage from the blood to the brain parenchyma through a weakened blood-brain barrier (BBB) and contributes to an actual net volume increase of the brain, which often leads to death. Recent research on ischemia-induced injury mechanisms of the microvasculature has led to the disclosure of the mechanisms and cellular pathways leading to BBB breakdown. In addition, the introduction of magnetic resonance imaging to clinical practice has enabled the evaluation of edema severity in stroke patients and differentiation between cytotoxic and vasogenic edema. Free radicals exert their deleterious actions during both cytotoxic and vasogenic edema. They can contribute to BBB disruption directly and can also trigger molecular pathways related to the dysfunction of ion transporters in the cell membrane and those related to increased vascular permeability. The development of effective therapeutic strategies aimed at reducing brain edema based on targeting specific molecular pathways involved may reduce death and disability from stroke.

Blood-Brain Barrier↗
PubMed2005

Sequential evaluation of prostate edema after permanent seed prostate brachytherapy using CT-MRI fusion.

PURPOSE: To analyze the extent and time course of prostate edema and its effect on dosimetry after permanent seed prostate brachytherapy. METHODS AND MATERIALS: Twenty patients scheduled for permanent seed (125)I prostate brachytherapy agreed to a prospective study on postimplant edema. Implants were preplanned using transrectal ultrasonography. Postimplant dosimetry was calculated using computed tomography-magnetic resonance imaging (CT-MRI) fusion on the day of the implant (Day 1) and Days 8 and 30. The prostate was contoured on MRI, and the seeds were located on CT. Factors investigated for an influence on edema were the number of seeds and needles, preimplant prostate volume, transitional zone index (transition zone volume divided by prostate volume), age, and prostate-specific antigen level. Prostate dosimetry was evaluated by the percentage of the prostate volume receiving 100% of the prescribed dose (V(100)) and percentage of prescribed dose received by 90% of the prostate volume (D(90)). RESULTS: Prostate edema was maximal on Day 1, with the median prostate volume 31% greater than preimplant transrectal ultrasound volume (range, 0.93-1.72; p < 0.001) and decreased with time. It was 21% greater than baseline at Day 8 (p = 0.013) and 5% greater on Day 30 (p < 0.001). Three patients still had a prostate volume greater than baseline by Day 30. The extent of edema depended on the transition zone volume (p = 0.016) and the preplan prostate volume (p = 0.003). The median V(100) on Day 1 was 93.6% (range, 86.0-98.2%) and was 96.3% (range, 85.7-99.5%) on Day 30 (p = 0.079). Patients with a Day 1 V(100) >93% were less affected by edema resolution, showing a median increase in V(100) of 0.67% on Day 30 compared with 2.77% for patients with a V(100) <93 % on Day 1. CONCLUSION: Despite the extreme range of postimplant edema, the effect on dosimetry was less than expected. Dose coverage of the prostate was good for all patients during Days 1-30. Our data indicate that postimplant dosimetry on the day of implant is sufficient for patients with good dose coverage (Day 1 V(100) >93%).

Aged↗
PubMed2006

MRI of bone marrow edema-like signal in the pathogenesis of subchondral cysts.

OBJECTIVE: To determine if a relationship exists between bone marrow edema-like signal and subchondral cysts on magnetic resonance imaging (MRI). DESIGN: Retrospective cohort of 32 patients with two sequential knee MRI. Patients with acute trauma, infection, neoplasm, or osteonecrosis were excluded. The degree of osteoarthritis was assessed using an adaptation of the Baltimore Longitudinal Study of Aging (BLSA) scale. Initial and follow-up exams were reviewed for presence, location, size and changes of marrow edema-like signal, subarticular cysts and cartilage abnormality. All locations in the knee were aggregated for analysis with descriptive statistics. RESULTS: The mean time interval between exams was 17.52 months (range 2.1-40.1 months). There were 23 cysts: 11 (47.8%) new, 6 (26.1%) increased size, 1 (4.4%) decreased size, and 5 (21.7%) no change in pre-existing lesions. Cysts always arose from regions of marrow edema-like signal. There were 68 subarticular areas of marrow edema-like signal: 16 (23.5%) new, 23 (33.8%) increased size, 17 (25%) decreased size, 11 (16.2%) resolved and 1 (1.5%) no change in pre-existing lesion. Marrow edema-like signal size always changed with cyst development: increased in 6/11 (54.5%), decreased in 2/11 (18.1%) and resolved in 3/11 (27.2%). Change in cyst size was always accompanied by a change in edema-like signal size. An MRI visible cartilage abnormality was adjacent to 87% (20/23) of cysts. The mean BLSA score changed from 2.6 to 3.6 indicating an overall progression of osteoarthritis. CONCLUSION: Subchondral cysts develop in pre-existing regions of subchondral bone marrow edema-like signal.

Adult↗
PubMed2006

TIMP-1/MMP-9 imbalance in brain edema in rats with fulminant hepatic failure.

BACKGROUND: Fulminant hepatic failure (FHF) is a devastating disease. When coma sets in, brain edema develops, changing FHF into a lethal condition. Liver transplantation is the definitive treatment. However, a third of these patients die as the result of brain edema before a donor becomes available. Tissue inhibitor of matrix metalloproteinase (MMP), or TIMP, and MMP-9 are implicated in ischemic brain edema. We thus hypothesized that an imbalance in TIMP-1/MMP-9 relationship plays a role in the development of increased brain extravasation and edema in FHF. MATERIALS AND METHODS: FHF was induced with a single intraperitoneal injection of D-galactosamine (250 mg/kg). Control rats received saline. GM6001, a synthetic MMP inhibitor, was administered (30 mg/kg) every 12 h for 3 doses starting at 12 h after D-galactosamine injection. MMP-9 was assayed with standard gelatin zymography. Brain extravasation, a measurement of the blood-brain barrier permeability, was determined with Evans blue. Brain edema was determined using specific gravity method. RESULTS: The active MMP-9 in the systemic circulation was significantly increased in the comatose FHF as compared to the precoma FHF and control animals (6.5 +/- 0.7 versus 4.6 +/- 0.4 versus 2.6 +/- 0.5 pg/microg, respectively; P < 0.05). Conversely, TIMP-1 was steadily decreased in precoma and coma FHF rats by 35% and 45%, respectively. Blocking MMP-9 activity with GM6001 significantly attenuated brain extravasation and edema in rats with FHF. CONCLUSIONS: Our study strongly supports that the perturbation of decreased TIMP-1 and increased MMP-9 contributes to the pathogenesis of brain edema in FHF. Our findings present a potential therapeutic approach to effectively increase the window of opportunity for life-saving liver transplantation.

Animals↗