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PubMed1994

Recovery from increased pressure or increased leakiness edema in perfused sheep lungs.

Two routes by which interstitial pulmonary edema liquid may leave the lung during recovery are reabsorption into the pulmonary circulation and clearance by lung lymphatics. We hypothesized that reabsorption of edema liquid of low protein concentration into the pulmonary circulation would be greater than reabsorption of edema liquid of high protein concentration because of the greater protein osmotic gradient in the former. On the basis of previous studies, lymph flow should contribute minimally to the recovery. In 22 in situ perfused sheep lungs with lymph fistulas, we produced approximately 100 g of osmotic or hydrostatic edema (low protein) or increased leakiness edema by calcium depletion (high protein). To induce reabsorption, we changed the perfusate from low- (1% albumin, osmotic pressure = 4 cmH2O) to high-protein (7% albumin, osmotic pressure = 22 cmH2O) solution in the osmotic group, decreased capillary pressure from 29 +/- 9 to 11 +/- 6 cmH2O in the hydrostatic group, or reversed leakiness by adding CaCl2 to the perfusate in the increased leakiness group. Reabsorption occurred only during recovery from osmotic (40 +/- 22% of filtered liquid) and hydrostatic (15 +/- 11%) edema. Total lung lymph flow during recovery from osmotic, hydrostatic, or increased leakiness edema was 4.9 +/- 3.4, 4.3 +/- 3.4, or 3.5 +/- 1.9 g, respectively. We conclude that during recovery from pulmonary edema interstitial liquid is reabsorbed into the circulation in inverse proportion to its protein concentration. We confirm that only a small fraction of the interstitial edema liquid is cleared by the lymphatics during recovery from any type of edema.

Animals↗
PubMed1994

Vascular permeability and epithelial transport effects on lung edema formation in ischemia and reperfusion.

To determine the role of various Na+ transport systems in the edema fluid accumulation after ischemia and reperfusion in the lung, we evaluated the effect of amiloride (a Na+ channel blocker), ouabain (a Na(+)-K(+)-adenosinetriphosphatase blocker), and phloridzin (a Na(+)-glucose cotransport blocker) in isolated rat lungs. Ischemia and reperfusion (I/R) significantly increased the edema accumulation, with the wet-to-dry weight ratios increasing to 10.14 +/- 0.58 from 6.03 +/- 0.05 in control lungs (P < 0.04). Amiloride significantly augmented the amount of edema fluid (wet-to-dry weight ratio 12.26 +/- 0.77), and ouabain further increased the amount of edema (wet-to-dry weight ratio 18.58 +/- 1.00). Phloridzin did not significantly affect edema formation associated with I/R. Isoproterenol decreased the amount of edema formation in the presence and absence of amiloride. This occurred because the endothelial permeability as assessed by filtration coefficient was restored to normal values and less edema formed. The present study indicates that Na+ channels and Na(+)-K(+)-adenosinetriphosphatase, components of the active Na+ absorption transport system, are very important in opposing edema fluid accumulation in rat lungs subjected to I/R injury and operate as an edema safety factor. However, if the endothelial damage associated with I/R is allowed to persist, then the transport processes, even if operative, are insufficient to prevent continuous edema accumulation.

Amiloride↗
PubMed1993

Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation.

Mechanical ventilation with high peak inspiratory pressure and large tidal volume (VT) produces permeability pulmonary edema. Whether it is mean or peak inspiratory pressure (i.e., mean or end-inspiratory volume) that is the major determinant of ventilation-induced lung injury is unsettled. Rats were ventilated with increasing tidal volumes starting from different degrees of FRC that were set by increasing end-expiratory pressure during positive-pressure ventilation. Pulmonary edema was assessed by the measurement of extravascular lung water content. The importance of permeability alterations was evaluated by measurement of dry lung weight and determination of albumin distribution space. Pulmonary edema with permeability alterations occurred regardless of the value of positive end-expiratory pressure (PEEP), provided the increase in VT was large enough. Similarly, edema occurred even during normal VT ventilation provided the increase in PEEP was large enough. Furthermore, moderate increases in VT or PEEP that were innocuous when applied alone, produced edema when combined. The effect of PEEP was not the consequence of raised airway pressure but of the increase in FRC since similar observations were made in animals ventilated with negative inspiratory pressure. However, although permeability alterations were similar, edema was less marked in animals ventilated with PEEP than in those ventilated with zero end-expiratory pressure (ZEEP) with the same end-inspiratory pressure. This "beneficial" effect of PEEP was probably the consequence of hemodynamic alterations. Indeed, infusion of dopamine to correct the drop in systemic arterial pressure that occurred during PEEP ventilation resulted in a significant increase in pulmonary edema. In conclusion, rather than VT or FRC value, the end-inspiratory volume is probably the main determinant of ventilation-induced edema. Hemodynamic status plays an important role in modulating the amount of edema during lung overinflation but does not fundamentally modify the characteristics of this edema which is consistently associated with major permeability alterations. These results may be relevant for ventilatory strategies during acute respiratory failure.

Albumins↗
PubMed2003

The LONFLIT4-VENORUTON study: a randomized trial prophylaxis of flight-edema in normal subjects.

This study evaluated the protective effects of Venoruton on the development of flight edema in normal subjects travelling in economy in long-haul flights (8-9 hours). Edema is a relevant aspect of long-haul flights affecting both venous patients and normal subjects. Edema and flight microangiopathy were studied in a group of 164 subjects randomized (after informed consent) into two groups to evaluate prophylaxis in 8- to 9-hour flights. The treatment group received Venoruton (hydroxyethyl rutosides) 1 g twice daily for 3 days (2 days before the flight and the day of the flight). The control group received comparable placebo. Edema was evaluated with a composite edema score based on the edema tester, on the measurements of ankle circumference, volume measurements, subjective swelling, and on a discomfort score. Items 1, 4, and 5 are based on an analogue scale line (1 to 10) directly defined by the subjects before and after the flights. Of the included subjects, 151 completed the study. Dropouts were due to poor compliance, travelling, or connection problems. Age and gender distribution were comparable in the two groups as were risk factor distributions. The level of edema at inclusion was comparable in the two groups of subjects. After the flight there was an average score of 6.7 (SD 1.7) in the control group, while in the Venoruton group the score was on average 3 (SD 1.1) (p < 0.05). In the control group 77% of the subjects had an evident increase in ankle circumference and volume, which was clearly visible at inspection and associated with discomfort. In the Venoruton group, edema was clearly present only in 8% of subjects (associated with discomfort rated between 3 and 6 on the analogue scale line) and it was mild, not associated with symptoms. Therefore the control of flight edema with Venoruton was clear both considering parametric data (circumference and volume) and non-parametric (analogue scale lines) measurements. The combined evaluation of the edema score is significantly favorable for subjects under prophylaxis with Venoruton.

Administration, Oral↗
PubMed1979

Enhancement of experimental cerebral edema after decompressive craniectomy: implications for the management of severe head injuries.

Decompressive craniectomy has been advocated as a treatment for the cerebral edema associated with massive head injury. Although craniectomy has been successful in lowering intracranial pressure after head injury, a comparison of computerized tomographic scans of comparable patients with traumatic brain edema treated by medical means or decompressive craniectomy showed that bony decompression resulted in apparent exacerbation of edema. To investigate the possibility of enhancement of brain edema by craniectomy, we produced standardized cold lesions in the brains of 10 dogs. Five animals served as controls. In the other 5 animals we performed large decompressive craniectomies after lesioning. Physiological parameters were comparable in both groups. The dogs were killed 8 hours after lesioning. After fixation, their brains were cut into 1-mm-thick slices. We used an image analysis facility built around a PDP 11/105 computer to measure the volume of edema as outlined by Evans blue staining. The mean volume of the brain edema in the control animals was 0.27 +/- 0.19 ml. Mean edema volume was over 7 times greater in craniectomized animals (1.96 +/- 1.89 ml). This difference is statistically significant (p less than 0.05). The driving force for the formation of edema fluid is the difference between intravascular and interstitial presssure. Decompression of the brain by bone removal probably results in a reduction of interstitial fluid pressure and edema enhancement. The clinical literature contains no evidence that craniectomy decreases the morbidity or mortality of human head injury. In view of our experimental findings, this is not surprising. Indeed, pathological evidence indicates that severe edema (such as that accentuated by craniectomy) may produce permanent changes in the neuropil.

Animals↗
PubMed1989

Pulmonary edema as a complication of interleukin-2 therapy.

Eight patients underwent IV bolus therapy with recombinant interleukin-2 (Cetus Corporation, Emeryville, CA) for treatment of metastatic melanoma or renal cell carcinoma. The patients were randomized to receive interleukin-2 alone or interleukin-2 in combination with lymphokine-activated killer cells. Radiographs showed pulmonary edema in five of the eight patients. The changes ranged from mild interstitial edema (two patients) to frank pulmonary edema (three patients). The edema generally resolved within 4 days after the termination of therapy (four patients), however, one patient developed edema and arrhythmias approximately 7 days after interleukin-2 therapy ended. Seven of the eight patients had either cardiac arrythmias or angina. The mechanisms that contribute to the pathogenesis of these cardiac complications with interleukin-2 therapy remain unclear. The development of pulmonary edema is thought to be caused by capillary leakage and cardiac pulmonary edema due to cardiac toxicity of the drug. The radiologic appearances of these types of pulmonary edema were indistinguishable from one another and from other causes of pulmonary edema. Our study shows that interleukin-2 can cause pulmonary edema, cardiac arrhythmias, and unstable angina. The severity of these conditions is unrelated to dose.

Adult↗
PubMed1992

Correlates of brain edema in uncontrolled IDDM.

Blood glucose, plasma sodium, bicarbonate (HCO3-), vasopressin, and hematocrit were monitored before and during treatment in patients with uncontrolled insulin-dependent diabetes mellitus (IDDM). These parameters were correlated with simultaneous serial cranial computed tomography readings of brain edema. Six of seven patients had positive computed tomography readings for brain edema on admission. Initial brain edema correlated directly with blood glucose (r = 0.79, P = 0.033) and inversely with HCO3- (r = -0.76, P = 0.047). At 6 h, brain edema still correlated with acidosis (HCO3-; r = -0.79, P = 0.033) but no longer with blood glucose. At that time, however, brain edema correlated with the rate of change in blood glucose (r = 0.915, P = 0.005). Results of interactive stepwise regression analysis suggest that the change in the calculated effective plasma osmolality plays a predominant role in the progression of brain edema during therapy (r = 0.995, P less than 0.001). Thus, although hyperglycemia and acidosis probably predispose to diabetic brain edema, osmotic factors may be major predictors of its evolution. No relationships were detected between brain edema and initiation of insulin therapy, plasma vasopressin, or changes in hematocrit. The factors responsible for initial brain edema and its progression, statistically identified in this study, require reassessment of common theories that attribute brain edema exclusively to therapy.

Adolescent↗
PubMed1983

Factors associated with edema of the mammary gland in primigravid dairy heifers.

The severity and anatomical extent of mammary edema (edema) of 73 primigravid Holstein heifers was scored, and certain hormones in peripheral blood plasma were quantified. The objective was to obtain by least-squares analysis of covariance independent estimates of the association of each hormone and other factors with edema scores around first calving. Mammary edema prepartum increased with age of heifer and gestation length, decreased as calf birthweight increased, but was unrelated to seasonal fluctuations in temperature and photoperiod. The increase in edema during the last week of pregnancy was accounted for by associations with prepartum concentrations of hormones in plasma. The independent estimates of hormonal relationships to edema score prepartum were positive for plasma estrone and estradiol-17 alpha and were negative for plasma estradiol-17 beta and progesterone. Plasma prolactin was not related to edema score. After parturition, estradiol-17 beta was the only independent variable associated (negatively) with edema. The results indicate a complicated interaction among the sex steroids of late pregnancy wherein some steroids may promote edema and other steroids may inhibit edema in heifers.

Age Factors↗
PubMed1982

Proton nuclear magnetic resonance studies on brain edema.

The water in normal and edematous brain tissues of rats was studied by the pulse nuclear magnetic resonance (NMR) technique, measuring the longitudinal relaxation time (T1) and the transverse relaxation time (T2). In the normal brain, T1 and T2 were single components, both shorter than in pure water. Prolongation and separation of T2 into two components, one fast and one slow, were the characteristic findings in brain edema induced by both cold injury and triethyl tin (TET), although some differences between the two types of edema existed in the content of the lesion and in the degree of changes in T1 and T2 values. Quantitative analysis of T1 and T2 values in their time course relating to water content demonstrated that prolongation of T1 referred to the volume of increased water in tissues examined, and that two phases of T2 reflected the distribution and the content of the edema fluid. From the analysis of the slow component of T2 versus water content during edema formation, it was demonstrated that the increase in edema fluid was steady, and its content was constant during formation of TET-induced edema. On the contrary, during the formation of cold-injury edema, water-rich edema fluid increased during the initial few hours, and protein-rich edema fluid increased thereafter. It was concluded that proton NMR relaxation time measurements may provide new understanding in the field of brain edema research.

Animals↗
PubMed2003

[The influence of spontaneous posterior vitreous detachment in resolution of diabetic macular edema in NIDDM].

PURPOSE: To establish the influence of posterior vitreous detachment on development and resolution of diabetic macular edema in NIDDM. To asses the posterior vitreous detachment role in argon laser treatment of diabetic macular edema. MATERIAL AND METHODS: Retrospective study. RESULTS: 68 eyes of 36 patients were involved into the study, 52 eyes (76.5%) with macular edema and 16 eyes (23.5%) without macular edema. Posterior vitreous detachment (PVD) was present in 62.5% of cases without macular edema, and only 30.77% of cases had macular edema. Laser treatment applied in accordance to general standards cased resolution of macular edema in all cases with posterior vitreous detachment. In group with no spontaneous posterior vitreous detachment, macular edema resolved only in 19.23% of cases. CONCLUSIONS: Diabetic macular edema is less common in eyes with spontaneous posterior vitreous detachment. This observation shows, that not only vascular factor but also vitreo-macular tractions are responsible for macular pathology in diabetic macular edema. The efficacy of standard argon laser treatment depends also on vitreo-macular relation--presence of PVD, and is more sufficient in eyes with posterior vitreous detachment.

Aged↗
PubMed2006

Hypertonic saline treatment in children with cerebral edema.

OBJECTIVE: To compare the efficacy and side effects of hypertronic saline and mannitol use in cerebral edema. DESIGN: Retrospective study. SETTING: Pediatric intensive care unit. SUBJECTS: 67 patients with cerebral edema. METHODS: Patients with cerebral edema treated with either mannitol or hypertronic saline (HS) (Group II: n = 25), and both mannitol and HS (Group III: n = 20) were evaluated retrospectively. Cerebral edema and increased intracranial pressure were based on the clinical and/or radiological (CT, MR) findings. When treating with both mannitol and HS (Group IIIA), if patients serum osmality was greater than 325 mosmol/L, mannitol was stopped and patients were treated with only HS (Group IIIB). All patients were closely monitored for fever, pulse, blood pressure, central venous pressure (CVP), oxygen saturation, volume of fluid intake and urine output. Mannitol was given at a dose of 0.25-0.5 g/kg while the hypertonic saline was given as 3% saline to maintain the serum-Na within the range of 155-165 mEq/L. RESULTS: There was no statistically significant difference in terms of Glasgow coma scale, age, gender, and etiologic distribution between the groups. And also distribution of the other treatments given for cerebral edema is not significiant. Mannitol was given for a total dose of 9.3 +/-5.0 (2-16) doses in Group I, and 6.5 +/-2.8 (2-10) doses in Group III. Hypertonic saline was infused for 4-25 times in Group II. Although there was no statistically significant difference in the highest serum Na and osmolarity levels of the groups, duration of comatose state and mortality rate were significantly lower in Group II and Group III A B. Patients who received only HS were subdivided according to their serum Na concentrations into 2 groups as those between 150-160 mEqL and those between 160-170 mEqL. The duration of comatose state and mortality was not different in patients with serum-Na of 150-160 mEqL and in patients with 160-170 mEqL in the hypertonic saline receiving patients. Four patients in the group II developed hyperchloremic metabolic acidosis and 2 patients in the group I had hypotension. As two patients in group II had diabetes insipidus and one patient had renal failure in group I, the treatment was terminated. The causes of death were septic shock, ventilator associated pneumonia with acute respiratory distress syndrome, progressive cerebral edema and cerebral edema with pulmonary edema. Multivariate analysis showed that age, gender, cause of cerebral edema, electrolyte imbalance, hyperglycemia and hyper-ventilation had no significant impact on outcome. CONCLUSION: Hypertonic saline seems to be more effective than mannitol in the cerebral edema.

Brain Edema↗
PubMed1990

Edema after femoropopliteal bypass surgery: lymphatic and venous theories of causation.

Edema of a lower extremity after femoropopliteal bypass surgery is a common problem. To study the causes of this phenomenon we evaluated 72 patients before and after surgery with noninvasive venous testing and venography. We also obtained postoperative lymphangiograms of a sample of 16 patients, eight with and eight without postoperative edema. Patients were sequentially assigned to one of four treatment groups: group A, a lymphatic-preserving inguinal dissection with conventional popliteal dissection; group B, a lymphatic-preserving popliteal dissection with conventional inguinal dissection; group C, lymphatic-preserving inguinal and popliteal dissections; group D, conventional inguinal and popliteal dissections. Twenty-nine (40%) of the 72 patients had postoperative edema. A similar proportion of patients with edema had deep venous thrombosis as patients without edema (3/29 [10%] vs 3/43 [7%], respectively). Patients in group D showed the highest incidence of edema, 17/20 or 85%, a rate significantly higher than the rates in the other three groups (p less than 0.001). Results of lymphangiograms were normal in six of the eight patients without edema (the other two had slight disruption), whereas they showed severe lymphatic disruption in all eight patients with edema. No association was found between edema and type of graft used or severity of preoperative symptoms. This study indicates that deep venous thrombosis is not an important cause of edema that occurs after bypass surgery and that intraoperative lymphatic disruption probably causes most cases of this complication.

Arterial Occlusive Diseases↗
PubMed1987

Delayed resolution of high-pressure pulmonary edema or capillary leak.

Both clinical and experimental evidence suggest that the time course of edema formation is different from that of edema resolution. To better describe and quantify this difference, we followed the accumulation of high-pressure pulmonary edema in live dogs with the thermal-green dye (TGD) double-indicator technique at steady-state levels of lung liquid. We raised left atrial pressure (PLa) in steps of 5 to 10 mm Hg as high as 25 mm Hg and followed edema to steady-state levels. Lung water was then measured as PLa was lowered to initial values. By plotting steady-state edema against PLa, pressure-volume relationships were constructed. There was little change in edema until PLa reached approximately 15 mm Hg, at which point further changes in PLa were associated with large increases in lung liquid. At PLa = 25 mm/kg, the average lung water had increased by 10 ml/kg. In each animal there was slow resolution of edema with decreases in PLa from its peak back to its initial value, but in no animal was edema fully reabsorbed even though PLa was maintained at about 5 mm Hg for as long as 10 hours. Several possible explanations account for these observations. Water could be trapped in alveolar and central interstitial spaces. In addition, vessel closure in edematous lung units could further influence water reabsorption. These observations raise the possibility that pulmonary edema in the presence of normal filling pressures may represent resolution of a transient high-pressure edema as opposed to a capillary leak syndrome.

Animals↗
PubMed1984

[Analysis of peritumoral edema--with special reference to the value of contrast-enhanced CT scan and dynamic CT scan].

Peritumoral edema, a common occurrence in patients with malignant gliomas and meningiomas, is a major cause of morbidity and mortality. However, the causative mechanism of peritumoral edema has yet to be clarified. In this study, seventy patients with brain tumors (34 glioblastomas, 21 meningiomas and 13 metastatic tumors) were examined by CT scan with and without contrast medium infusion and by postoperative histologic verification in all cases. Peritumoral hypodensity areas on CT scan have generally been interpreted as cerebral edema. Peritumoral edema as seen in CT scan was classified into four grades according to the ratio of the largest diameter of tumor and the size of the zone of edema. Grade 0: no peritumoral low density area is seen in CT scan. Grade I: a small amount of peritumoral low density area is seen in CT scan. Grade II: a moderate amount of peritumoral low density area is seen is CT scan. Grade III: a large amount of peritumoral low density area is seen in CT scan. Twenty-five out of 34 glioblastomas and all of 15 metastatic tumors demonstrated moderate or severe peritumoral edemas such as Grade II or III. However 16 out of 21 meningiomas demonstrated mild peritumoral edemas such as Grade 0 or I. The grade of peritumoral edema was closely related to the degree of malignancy of the brain tumors. 8 out of 9 glioblastomas which demonstrated slight peritumoral edema, Grade I, had large cystic formations which seemed to serve as buffer action to compression mechanism by brain tumors. The grade of peritumoral edema was also related to the location of the tumor and venous involvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

[Nuclear magnetic resonance studies of effects of glycerol on brain edema].

Effects of glycerol on the state of water in edematous brain tissues were studied by the pulse FT NMR technique. Brain edemas were induced experimentally by cold injury and triethyl tin (TET) intoxication in Wistar rats. Ten percent w/v glycerol (1 g/kg body weight) were injected intravenously at 30 minutes before decapitation for the NMR measurements. Transverse relaxation times (T2) in the cerebral gray and white matter were measured by Meiboom-Gill pulse sequence at the resonant frequency of 100 MHz. Water content was calculated from the difference between wet and dry weight after heating in an oven at 95-100 degrees C for 72 hours after the NMR measurements. In the normal brain T2 value was 76.4 msec and 75.4 msec in the gray and white matter respectively. In the edematous brain, T2 separated into two components, one slow and one fast, corresponding with the increase of water content. Values of the slow component (slow T2) were characteristic of both types of brain edema. In the cold injury edema, slow T2 values became 105 msec in the gray matter and 96 msec in the white matter, while in the TET induced edema, it became 450 msec in the white matter. After glycerol infusion, slow T2 became faster in these regions in both types of brain edema, showing 92.1 msec in the gray matter and 88.1 msec in the white matter of the cold injury edema, and 388 msec in the white matter of TET induced edema. The degree of the changes of slow T2 values per unit change of water content was greater in the cold injury edema than in the TET induced edema. Serum osmolality elevated 23.8 mOsmol greater than the control value after glycerol infusion in this experiment. It is concluded from these findings that glycerol retracts free mobile water molecules from the edema fluid by osmotic pressure gradient.

Animals↗
PubMed2003

Visual outcome in eyes with asymptomatic optic disc edema.

BACKGROUND: Asymptomatic optic disc edema may last for months before conversion to anterior ischemic optic neuropathy (AION). Alternatively, the optic disc edema may resolve with preservation of normal vision. The conversion rate of asymptomatic optic disc edema to AION has not been prospectively studied. We prospectively followed patients with asymptomatic disc edema to determine this conversion rate. METHODS: The cohort was followed from 1991 to 2000 at a single ophthalmology clinic in Israel. There were 23 patients aged 47-74 years with asymptomatic disc edema and no signs of optic nerve dysfunction in whom the disc edema had been incidentally discovered on routine fundus examination performed for diabetes, hypertension, or follow-up after AION in the fellow eye. RESULTS: In 9 (36%) eyes, optic disc edema progressed to overt AION with a mean latency of 16.8 weeks (range 2-80 weeks). In 16 (64%) eyes, optic disc edema resolved without loss of vision with a mean latency of 15.5 weeks (range 4-44 weeks). The conversion rate to AION was 40% in patients who had had AION in the fellow eye, 31% in patients with diabetes, 43% in patients with diabetic retinopathy, and 0% in four amiodarone-treated patients. CONCLUSION: Asymptomatic disc edema generally resolves with no visual loss, but one third of patients progress to full-blown AION. Diabetes mellitus is common in patients with asymptomatic optic disc edema. Perhaps patients diagnosed as having diabetic papillopathy actually have an impending AION that does not progress to overt disease.

Aged↗
PubMed2002

Anthrax edema toxin requires influx of calcium for inducing cyclic AMP toxicity in target cells.

The anthrax edema toxin comprises two proteins: protective antigen and edema factor. Anthrax protective antigen binds to the receptors on the surface of target cells and facilitates the entry of edema factor into these target cells. Edema factor (EF) is an adenylate cyclase that catalyzes the synthesis of cyclic AMP (cAMP) in the cytosol of the host cells. In this study, we examined the requirement of extracellular calcium for anthrax edema toxin-induced toxicity in host cells. The cAMP response generated by edema toxin was analyzed in a variety of cells, including CHO, macrophage-like RAW264.7, human neutrophils, and human lymphocytes. Our investigations reveal that after EF reaches the cell cytosol, a rapid influx of calcium is triggered in the host cell that has a pivotal role in determining the cAMP response of the affected cells. Although the cAMP response generated by edema toxin in different cell types varied in intensity and in the time of initiation, the influx of calcium invariably preceded cAMP accumulation. Agents that blocked the uptake of calcium also inhibited edema toxin-induced accumulation of cAMP in the host cells. This is the first report that demonstrates that edema toxin induces accumulation of cAMP in lymphocytes. By accumulating cAMP, a potent inhibitor of immune cell function, edema toxin may actually be poisoning the immune system and thus facilitating the survival of the bacteria in the host.

Adenylyl Cyclases↗
PubMedDate not supplied

Diabetic macular edema associated with glitazone use.

PURPOSE: To describe diabetic macular edema (DME) in patients who developed fluid retention as a consequence of glitazone use. METHODS: A chart review identified 30 patients who used pioglitazone or rosiglitazone and had both lower extremity edema and macular edema. Clinical reports, photographs, and fluorescein angiograms were reviewed. Patients followed for >3 months were analyzed separately. RESULTS: Seventeen patients took oral pioglitazone, 11 took rosiglitazone, and 2 took both drugs at different times. Eleven patients were observed for >3 months after cessation of glitazones. Mean weight gain during drug administration in this group was 30 lb, and mean weight loss after drug discontinuation was 19 lb. Rapid reduction in macular edema off drug occurred in only 4 of 11 patients, but 8 of 11 had reduced edema over 2 years. Mean visual acuity in this group at the initial visit was 20/60, and at the final visit, it was 20/85. Four eyes of three patients had resolution of diffuse macular edema with improved vision after cessation of glitazones without laser treatment. CONCLUSIONS: Fluid retention occurs in 5% to 15% of patients taking glitazones. In some of these patients, glitazone use appears to be a cause of macular edema, and drug cessation appears to result in rapid resolution of both peripheral and macular edema. Fluid retention associated with glitazone use should be considered when assessing treatment options for patients with DME, especially those with concomitant peripheral edema.

Administration, Oral↗