Peritumoral edema and karyometric variables in astrocytoma of the brain.

Peritumoral edema and karyometric variables in astrocytoma of the brain.
J BUON. 2007 Apr-Jun

Kostic A, Mihailovic D, Veselinovic S, Tasic G, Radulovic D, Stefanovic I.
Clinic of Neurosurgery, Clinical Centre Nis, Nis, Serbia.

PURPOSE: The aim of this study was to evaluate karyometry as a quantitative and objective histological method by showing correlation of some karyometric variables with the severity of peritumoral edema in patients with brain astrocytoma.

PATIENTS AND METHODS: 63 patients of different ages and both genders were enrolled. The patients were diagnosed with astrocytoma of the brain, histologically confi rmed on the surgically removed material. Maximal tumor excision was performed in all patients, who were postoperatively treated according to current oncologic therapeutic protocols. The intensity of perifocal edema (preoperative CT scan) was correlated to the duration of survival and the values of 9 karyometric tumor variables: area, density, maximal axis, mean axis, circumference, roundness, integrated optical density and number of nuclei.

RESULTS: There were 17 cases with small perifocal edema, 19 with medium-sized and 27 with large perifocal edema, and their respective survival was around 149, 62 and 48 weeks. Those with small edema had statistically signifi cant prolonged survival compared to those with medium and large perifocal edema (log-rank test, p=0.045). Six out of 9 karyometric variables examined were signifi cantly related (p<0.05)>

CONCLUSION: Patients with larger peritumoral edema have shorter survival. Correlation of karyometric variables with CT fi ndings revealed that higher degrees of tumor cellularity and nuclear wrinkling with increased integrated optical density is associated with larger peritumoral edema.

PMID: 17600879 [PubMed - in process]

Treatment of High Altitude Pulmonary Edema at 4240 m in Nepal

Treatment of High Altitude Pulmonary Edema at 4240 m in Nepal
High Alt Med Biol. 2007 Summer

Fagenholz PJ, Gutman JA, Murray AF, Harris NS.
Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts., Himalayan Rescue Association, Pheriche Clinic, Spring Season, 2006.

Fagenholz, Peter J., Jonathan A. Gutman, Alice F. Murray, and N. Stuart Harris.

Key Words: altitude sickness; pulmonary edema; altitude, mountaineering; rural populations

High altitude pulmonary edema (HAPE) is the leading cause of death from altitude illness and rapid descent is often considered a life-saving foundation of therapy. Nevertheless, in the remote settings where HAPE often occurs, immediate descent sometimes places the victim and rescuers at risk. We treated 11 patients (7 Nepalese, 4 foreigners) for HAPE at the Himalayan Rescue Association clinic in Pheriche, Nepal (4240 m), from March 3 to May 14, 2006. Ten were admitted and primarily treated there. Seven of these (6 Nepalese, 1 foreigner) had serious to severe HAPE (Hultgren grades 3 or 4).

Bed rest, oxygen, nifedipine, and acetazolamide were used for all patients. Sildenafil and salmeterol were used in most, but not all patients. The duration of stay was 31 +/- 16 h (range 12 to 48 h). Oxygen saturation was improved at discharge (84% +/- 1.7%) compared with admission (59% +/- 11%), as was ultrasound comet-tail score (11 +/- 4 at discharge vs. 33 +/- 8.6 at admission), a measure of pulmonary edema for which admission and discharge values were obtained in 7 patients.

We conclude it is possible to treat even serious HAPE at 4240 m and discuss the significance of the predominance of Nepali patients seen in this series.

High Altitude Medicine & Biology

The use of intravitreal etanercept in diabetic macular edema.

The use of intravitreal etanercept in diabetic macular oedema.

Semin Ophthalmol. 2007 Apr-Jun

Tsilimbaris MK, Panagiotoglou TD, Charisis SK, Anastasakis A, Krikonis TS, Christodoulakis E.
Retina Service, Department of Ophthalmology, University Hospital of Heraklion. Crete.

The aim of this pilot study was to investigate the effect of intravitreal administration of etanercept in refractory diabetic macular edema. Seven patients diagnosed with diabetic macular edema, refractory to previous treatment, were enrolled. They all received 2 consecutive intravitreal injections of 2.5 mg (0, 1 ml) of Etanercept (Enbrel), with a two-week interval. In all patients visual acuity assessment, fundoscopy and fluorescein angiography were performed prior to the first injection, weekly for the first month, as well as 2 and 3 months following the first injection. No adverse reactions or adverse events were noticed in any patient.

Analysis of the data indicates a trend for improvement of visual acuity, a slight worsening of hard exudates and fluorescein leakage, while hemorrhages remained stable, 3 months after initiation of therapy. However, no statistical significance has been reached.

This small pilot study did not reveal any improvement in the clinical course of patients with refractory diabetic macular edema after the intravitreal injection of etanercept. Further research is warranted in order to obtain conclusive results concerning the role of anti-TNF therapy in diabetic macular edema.

PMID: 17564925 [PubMed - in process]

Interlamellar flap edema due to steroid-induced ocular hypertension after laser in situ keratomileusis.

Interlamellar flap edema due to steroid-induced ocular hypertension after laser in situ keratomileusis.

Jpn J Ophthalmol. 2007 May-Jun

Miyai T, Yonemura T, Nejima R, Otani S, Miyata K, Amano S.
Meiwakai Medical Foundation, Miyata Eye Hospital, Miyakonojo, Miyazaki, Japan.

(1)
Meiwakai Medical Foundation, Miyata Eye Hospital, Miyakonojo, Miyazaki, Japan
(2)
Department of Ophthalmology, The University of Tokyo School of Medicine, Tokyo, Japan
(3)
Department of Ophthalmology, The University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

Key words: interlamellar flap edema - laser-assisted in situ keratomileusis - ocular hypertension

BACKGROUND: Several recent studies have reported post-laser in situ keratomileusis (LASIK) complications related to a steroid-induced increase in intraocular pressure, including interface fluid and elevated intraocular pressure-induced interlamellar stromal keratitis. CASES: We examined two cases of interlamellar flap edema due to steroid-induced ocular hypertension after uneventful laser in situ keratomileusis.

OBSERVATIONS: Oral acetazolamide and discontinuance of topical steroids were effective for treating interlamellar stromal edema in both cases.

CONCLUSION: A rise in intraocular pressure should be considered a cause of interlamellar stromal edema after LASIK. Jpn J Ophthalmol 2007;51:228-230 (c) Japanese Ophthalmological Society 2007.

Springer Link

Vascular endothelial growth factors in pulmonary edema: an update

Vascular endothelial growth factors in pulmonary edema: an update.

J Thromb Thrombolysis. 2007 Jun 7

Kosmidou I, Karmpaliotis D, Kirtane AJ, Barron HV, Gibson CM.
Department of Medicine, Caritas St. Elizabeth’s Medical Center, Boston, MA, USA.

Pulmonary edema is a life-threatening complication of critical illness. Identification of the underlying mechanisms of pulmonary edema is a prerequisite for the development of adequate treatment. The initial description of fluid transportation across capillaries (Starling's law) while of critical importance, did not provide full insight into the underlying pathophysiology of vascular leakage.

Pulmonary edema can be differentiated into two distinct categories based on the Starling theory; the high-permeability type is attributed to inflammatory changes occurring in conditions such as the adult respiratory distress syndrome (ARDS) and the cardiogenic type is characterized by an imbalance in the Starling hydrostatic forces and occurs in acute or decompensated heart failure. However, it has long been recognized that there is significant overlap between the various types of pulmonary edema, raising important questions regarding the role of novel mechanisms that may contribute to the development of interstitial and alveolar leakage.

Recently, several studies on VEGF, an angiogenic growth factor which affects endothelial permeability, have identified this molecule as a potential regulator of vascular leakage and repair in pulmonary edema. We review here the underlying the mechanisms by which VEGF may do this and will discuss the still unanswered questions regarding vascular pharmacology in the setting of pulmonary edema.

PMID: 17554593 [PubMed - as supplied by publisher]

A rare cause of peripheral edema: exudative lymphocytic gastritis induced hypoprotidemia

A rare cause of peripheral edema: exudative lymphocytic gastritis induced hypoprotidemia

Nephrol Ther. 2007 Jun

Montagnac R, Blaison D, Ciupea A, Für A, Pradel J, Schillinger F.
Service de néphrologie–hémodialyse, centre hospitalier de Troyes, 10003 Troyes cedex, France.

Diagnosis of edema secondary to hypoprotidemia but without nutritional, renal, hepatic or cardiac cause, must consider exsudative digestive disease, of which the lymphocytic gastritis, as the authors report here a new observation diagnosed in a 73 year-old woman. Gastroscopy reveals varioliform gastritis and biopsy demonstrates diffuse infiltration of the gastric epithelium by lymphocytes, making of it a real histopathologic entity among the gastropathies.

Etiology and pathogeny remain still unknown but proton pump gastric inhibitors are an effective treatment.

PMID: 17540312 [PubMed - as supplied by publisher]

Edematous syndrome revealing an exudative lymphocytic gastritis: efficacy of omeprazole

[Article in French]
Cacoub P, Sbaï A, Costedoat-Chalumeau N, Bellanger J, Godeau P, Piette JC.Service de Médecine Interne, Hôpital de la Pitié-Salpêtrière, Paris. patrice.cacoub@psl.ap-hop-paris.fr

Lymphocytic gastritis is characterized by intense lymphocytic infiltration of gastric epithelium. Excessive gastric protein loss is uncommon. We describe the case of a 49-year-old white woman suffering from generalized edema and abdominal pain. She had severe serum hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. There was no renal, cardiac or hepatic origin of protein loss, and no protein-losing enteropathy. Endoscopic examination showed diffuse varioliform gastritis and histology confirmed lymphocytic gastritis with > 30% intraepithelial lymphocytes without Helicobacter pylori. The protein loss stopped within two weeks of the beginning of omeprazole and extensive edema disappeared. Four years later, the patient was still free from edema.

Inflammatory involvement of the gastric mucosa probably caused protein losing in this patient.

Recognition of this exsudative gastropathy is important because long term remission is obtained with omeprazole.

Masson