Increase of circulating endocan over sepsis follow-up is associated with progression into organ dysfunction.

How circulating inflammatory mediators change upon sepsis progression has not been studied. We studied the follow-up changes of circulating vasoactive peptides and cytokines until the improvement or the worsening of a patient and progression into specific organ dysfunctions. In a prospective study, concentrations of tumor necrosis factor-alpha (TNFα), interleukin (IL)-6, IL-8, IL-10, interferon-gamma (IFNγ), endocan and angiopoietin-2 (Ang-2) were measured in serum by an enzyme immunoassay in 175 patients at baseline; this was repeated within 24 h upon progression into new organ dysfunction (n = 141) or improvement (n = 34). Endocan and Ang-2 were the only parameters that were significantly increased among patients who worsened. Any increase of endocan was associated with worsening with odds ratio 16.65 (p < 0.0001). This increase was independently associated with progression into acute respiratory distress syndrome (ARDS) as shown after logistic regression analysis (odds ratio 2.91, p: 0.002). Changes of circulating cytokines do not mediate worsening of the critically ill patients. Instead endocan and Ang2 are increased and this may be interpreted as a key-playing role in the pathogenesis of ARDS and septic shock. Any increase of endocan is a surrogate of worsening of the clinical course.

Determination of venlafaxine in post-mortem whole blood by HS-SPME and GC-NPD.

Venlafaxine is a phenethylamine derivative widely prescribed for the treatment of depression which inhibits both serotonin and norepinephrine reuptake (SNRI). In treatment with antidepressants of patient with depression and other psychiatric disorders there is also increased risk of suicidal thought and behaviour. Several lethal intoxications involving venlafaxine usually among psychotic patients have been reported in the literature. Sample preparation is of the greatest significance for a successful toxicological analysis. The development of simple, effective and rapid extraction procedures of drugs from post-mortem biological samples is a challenge. Headspace-solid phase microextraction (HS-SPME) offers significant advantages such as simplicity, low cost, compatibility with analytical systems, automation and solvent-free extraction. The aim of our work was the optimization of a HS-SPME procedure for the determination of venlafaxine in post-mortem biological samples by gas chromatography (GC) with nitrogen-phosphorous detection (NPD). Venlafaxine was extracted on 100 µm Polydimethylsiloxone Coating-Red (PDMS) SPME fiber and determined by GC-NPD. Salt addition, extraction temperature, preheating and extraction time were optimized to enhance the recovery of the extraction from aqueous solution spiked with venlafaxine. Finally the developed procedure was applied to post-mortem biological samples of a fatally poisoned woman by venlafaxine. The drug was quantified in post-mortem blood gastric and oesophagus contents of the deceased woman. A simple and rapid procedure using HS-SPME was developed for sample preparation of venlafaxine in post-mortem biological samples prior to GC-NPD determination. Validation data was satisfactory, thus enabling application in the toxicological analysis of forensic samples.

Acute paraplegia in painless aortic dissection. Rich imaging with poor outcome.

STUDY DESIGN: Case report. OBJECTIVE: To describe the clinical and imaging findings of a patient with painless aortic dissection. SETTING: University Neurology Department, Thessaloniki, Greece. PATIENT, METHODS, RESULTS: A 46-year-old man was transferred to our Department for emergent evaluation of paraplegia, from the local hospital of the nearby town, where he was admitted complaining from sudden, painless, bilateral leg weakness, 24 h earlier. He presented complete flaccid paraplegia with urinary retention, loss of pain and temperature sensation below the TH7 level and well-preserved vibration and position sense bilaterally. He had no pain and general physical examination was unremarkable. Chest X-rays first raised the suspicion of an aortic lesion. Thoracic MRI revealed cord dilation, with no enhancement on T1-weighted images (wi) and increased signal on T2-wi at the TH9-TH12 levels, suggesting cord ischemia. At the same MR sequences, the double lumen of the descending aorta indicated dissection in both sagittal and axial images. Later the same day, the patient died, and autopsy verified dissection of the descending aorta up to the aortic valve. CONCLUSION: The rapid evolution of our case further points out that radiologists, neurologists, as well as internal specialists should be vigilant for this emergency, which despite rich imaging could have a fatal outcome.

[Gingival hyperplasia induced by nifedipine. Report of two cases]. / Yperplasia oulon apo niphedipine (Parousiase dyo periptoseon).

Two cases of gingival hyperplasia associated with the administration of nifedipine are presented in this paper. Case 1, a 66 years old woman appeared with severe gingival enlargement, which was located at the right anterior and premolar region. Both attached gingivae and interdental papillae were hyperplastic, and the enlargement was more pronounced at the labial surfaces. The patient discontinued nifedipine, and after scaling and root planning, gingivectomy was performed. One month postoperatively the gingivae were in perfect health. Case 2, a 68 years old man presented with gingival enlargement mainly of the interdental papillae of the anterior and posterior region, which was more pronounced at the labial surfaces. Gingivectomy was performed at the upper anterior region after deep scaling, but the patient did not discontinue nifedipine. Three weeks postoperatively, recurrence of hyperplasia was noticed. In both cases histologically the gingival epithelium was parakeratininized and exhibited elongated rete pegs. The underlying connective tissue comprised of dense collagen fibres and the inflammatory cells which were present in the connective tissue, were mainly plasma cells and lymphocytes.