Presence of retained calcified fibrin sheath after central venous catheter removal: A systematic literature review.

Central venous catheters (CVC) are used in many clinical settings for a variety of indications. We performed a systematic literature review concerning case reports of retained calcified fibrin sheaths after dialysis CVC removal. The aim of our study was to systematize the knowledge regarding clinical management of this phenomenon, placing special emphasis on diagnostic radiological features in different imaging modalities, including chest radiography, echocardiography, computed tomography, and magnetic resonance imaging. We discuss the most common risk factors associated with this CVC complication. In our review, we found eight cases of hemodialysis patients. The most common risk factors associated with calcified fibrin sheath formation in the analyzed cases were pro-thrombotic and pro-calcification factors related to patient comorbidities, and prolonged catheter dwell time. Differentiating between a calcified fibrin sheath (present in about 6% of patients with long-term indwelling CVC as diagnosed by computed tomography) and a retained catheter tip can be challenging. The initial diagnosis based on imaging methods was incorrect in most of the analyzed cases. This suggests that some cases of retained fibrin sheaths may remain undetected or misinterpreted. This is important in patients with known pro-thrombotic and pro-calcification risk factors and prolonged catheter dwell time. Therefore, implementation of preventive strategies, familiarity with radiological findings of this phenomenon, comparison with previous imaging studies, and an overall comprehensive assessment with clinical data is imperative.

Influence of omalizumab therapy on airway remodeling assessed with high-resolution computed tomography (HRCT) in severe allergic asthma patients.

INTRODUCTION: Airway remodeling is an important factor in persistent obstruction in severe asthma. High resolution computed tomography (HRCT) is an effective method of detecting changes in airway structure. Our aim was to use HRCT to assess changes in airway remodeling in patients with severe allergic asthma who are treated with omalizumab. MATERIAL AND METHODS: In 12 patients with severe allergic asthma, HRCT was performed before and after treatment with omalizumab. In selected bronchi airways, parameters were calculated: bronchial wall area (BA), also corrected for body surface area (BSA); percentage of wall area (WA%); and the ratio of luminal area to total bronchial area (Ai/Ao). Clinical response to treatment was assessed using an asthma control questionnaire (ACQ), asthma quality of life questionnaire (AQLQ), and number of exacerbations per year. Assessment included spirometry and blood eosinophilia. RESULTS: Treatment resulted in significant improvement in ACQ (p = 0.035) and AQLQ (p = 0.001). We observed significant reduction in exacerbations per year (p = 0.002) and reduction of daily systemic steroid dose (p = 0.032). FEV1 and peripheral blood eospinophilia did not change (p = 0.846 and p = 0.221). Airway dimensions (Ai/Ao) of particular bronchi were consistent with the mean of the parameters calculated for all bronchi measured. Although we observed a significant decrease in WA (p = 0.002) and WA/BSA (p = 0.002), WA% and Ai/Ao did not improve (p = 0.39 and p = 0.49). We found no correlations between changes in airways and changes in spirometry or clinical parameters. CONCLUSION: Despite clinical effectiveness of omalizumab, its effect on airway remodeling may be limited.

Cardiac computed tomography compared with two-dimensional transesophageal echocardiography for the detection and assessment of atrial septal pouches.

The aim of this study is to compare the two-dimensional transesophageal echocardiography (2D-TEE) with multi-slice computed tomography (MSCT) and with autopsied material to evaluate the ability and precision of the imaging methods for the detection and assessment of septal pouch (SP). One hundred and fifty patients that underwent both 2D-TEE and MSCT and 50 autopsied human hearts were investigated. In MSCT, the interatrial septum was classified as a left SP in 37.3%, right SP in 3.3%, and patent foramen ovale (PFO) channel in 3.3%. In 2D-TEE, the interatrial septum was classified as a left SP in 39.3%, right SP in 11.3%, double SP in 4.7%, and PFO channel in 2.0%. The weighted kappa coefficient between MSCT and 2D-TEE in assessing the septum morphology was 0.59. The prevalence of the left SP is lower when it is evaluated by MSCT or 2D-TEE than by anatomical study, but this difference is insignificant (37.3% vs. 44.0%, p = 0.40, and 39.3% vs. 44.0%, p = 0.56, respectively). The prevalence of left SPs is lower when detected by MSCT or 2D-TEE than during autopsy, but the difference is statistically insignificant (37.3% vs. 44.0%, p = 0.40, and 39.3% vs. 44.0%, p = 0.56, respectively). Both 2D-TEE and MSCT are comparable techniques for detecting left-sided SPs with the insignificant lower prevalence of detecting left-sided SPs compared to autopsied material. However, TEE with the contrast seems to be superior over MSCT due to the possibility of unambiguous PFO channel detection. Therefore, TEE with contrast should be preferred over MSCT in the identification of left-sided SPs.

Left atrial accessory appendages, diverticula, and left-sided septal pouch in multi-slice computed tomography. Association with atrial fibrillation and cerebrovascular accidents.

BACKGROUND: The aim of this study is to provide a morphometric description of the left-sided septal pouch (LSSP), left atrial accessory appendages, and diverticula using cardiac multi-slice computed tomography (MSCT) and to compare results between patient subgroups. METHODS: Two hundred and ninety four patients (42.9% females) with a mean of 69.4±13.1years of age were investigated using MSCT. The presence of the LSSP, left atrial accessory appendages, and diverticula was evaluated. Multiple logistic regression analysis was performed to check whether the presence of additional left atrial structures is associated with increased risk of atrial fibrillation and cerebrovascular accidents. RESULTS: At least one additional left atrial structure was present in 51.7% of patients. A single LSSP, left atrial diverticulum, and accessory appendage were present in 35.7%, 16.0%, and 4.1% of patients, respectively. After adjusting for other risk factors via multiple logistic regression, patients with LSSP are more likely to have atrial fibrillation (OR=2.00, 95% CI=1.14-3.48, p=0.01). The presence of a LSSP was found to be associated with an increased risk of transient ischemic attack using multiple logistic regression analysis after adjustment for other risk factors (OR=3.88, 95% CI=1.10-13.69, p=0.03). CONCLUSIONS: In conclusion LSSPs, accessory appendages, and diverticula are highly prevalent anatomic structures within the left atrium, which could be easily identified by MSCT. The presence of LSSP is associated with increased risk for atrial fibrillation and transient ischemic attack.

Cough-induced lung intercostal hernia.

A 73-year-old male with marked emphysema was admitted to the 2nd Department of Internal Medicine, University Hospital in Krakow because of chronic obstructive pulmonary disease (COPD) exacerbation. His medical history was significant for total laryngectomy due to laryngeal cancer in 2010.

Bradycardia as a rare symptom of cisplatin cardiotoxicity: A case report.

Cisplatin (DDP) is one of the most frequently used chemotherapeutic agents, and has a characteristic toxicity profile. For DDP, complications affecting the cardiovascular system, which are typical for certain other agents, are rare; however, their occurrence may lead to life-threatening conditions. To the best of our knowledge, there are few reported cases of DDP-induced bradycardia in the relevant medical literature. The current report presents the case of a 58-year-old patient diagnosed with metastatic neuroendocrine carcinoma with a primary lesion in the posterior mediastinum, who was treated with DDP and etoposide chemotherapy. Following the initial chemotherapy cycle, the patient experienced severe symptomatic bradycardia (a drop in heart rate to 40 bpm), with the corrected QT interval prolonged to 424 msec. The patient's condition required close monitoring and treatment. Similar symptoms occurred following each of the three cycles of chemotherapy. Imaging studies performed following the third treatment cycle revealed disease progression, and the patient was referred for palliative care. Reports have indicated that damage to the cardiovascular system, including cardiac ischemia, diastolic disturbances, hypertension and microalbuminuria, may be associated with DDP-based therapy. However, the mechanism of DDP-associated cardiac toxicity remains to be elucidated. It may be induced by factors including direct toxicity, ion imbalance, heart infiltration and, in the case of neuroendocrine tumors, the influence of tumor excretions.

Effects of exercise of different intensity on gut peptides, energy intake and appetite in young males.

UNLABELLED: INTRODUCTION AND RESEARCH AIMS: The aim of the work was an evaluation of the impact of physical exertion on the regulating of food intake and digestive system hormone release as well as the partly connected phenomenon of evaluating the subjective sensation of hunger and the amount of food consumed at various time following physical exercise. MATERIALS AND METHODS: The tests covered 12 young, healthy men, for whom the effects of physical exertion of a moderate and high intensity on the subjective sensation of hunger/satiety, evaluated by means of visual analogue scales, on food intake as well as on the metabolic and hormonal parameters were tested. RESULTS: Physical exertion resulted in a fall in the subjective sensation of hunger, but only following intensive exertion was this statistically significant. The intake of food was greater after exertion when compared to the control group. Moderate exertion resulted in a statistically significant but short-lived increase in the ghrelin level. This effect was not observed after intensive exertion, while in those tests during the post-meal period there occurred a fall in the concentration of ghrelin in the plasma. After exertion a physical fall was observed in the concentration of insulin in the plasma, for the intake of food resulted in a notable increase in its level. CONCLUSIONS: Physical highly intensive exertion, results in a temporary reduction in the subjective sensation of hunger but leads to an increased food intake. The current research suggests that moderate but not intensive physical exertion stimulates the secretion of ghrelin.

Helicobacter pylori promotes apoptosis, activates cyclooxygenase (COX)-2 and inhibits heat shock protein HSP70 in gastric cancer epithelial cells.

OBJECTIVE: Apoptosis plays an important role in the regulation of gastric epithelial cell number and gastrointestinal disorders induced by Helicobacter pylori (Hp). Heat shock proteins (HSPs) are involved in cell integrity, cell growth and in gastric mucosa colonized by Hp. COX-2 was implicated in Hp-induced carcinogenesis but the effects of this germ and CagA cytotoxin on HSP70, COX-2, Bax and Bcl-2 in gastric cancer epithelial cells have been little studied. MATERIAL AND METHODS: We determined the expression for HSP70, Bax and Bcl-2 in human gastric epithelial MKN7 cells incubated with live strain Hp (cagA + vacA+) with or without co-incubation with exogenous CagA and NS-398, the selective COX-2 inhibitor. After 3-48 h of incubation, the expression of HSP70, COX-2, Bax and Bcl-2 mRNA and proteins were determined by RT-PCR and immunoprecipitation. RESULTS: Hp inhibited expression for HSP70 and this was significantly potentiated by exogenous CagA. Co-incubation of epithelial cells with Hp, without or with CagA increased Bax expression and simultaneously decreased expression for Bcl-2. The increase in COX-2 mRNA and Bax expression were significantly inhibited by NS-398. We conclude that Hp promotes apoptosis in adenocarcinoma gastric epithelial cells in vitro and this is associated with activation of COX-2 and inhibition of HSP70.

Lipoxins, the novel mediators of gastroprotection and gastric adaptation to ulcerogenic action of aspirin.

Previous studies revealed that prostaglandins contribute to the mechanism of maintenance of gastrointestinal integrity and mediate various physiological aspects of mucosal defense. The suppression of prostaglandin synthesis in the stomach is a critical event in terms of the development of mucosal injury after administration of various NSAID including aspirin (ASA). A worldwide use of ASA is now accepted due to its remarkable analgesic, antipyretic and anti-thrombotic prophylactics against myocardial infarct and coronary disorders despite the fact that the use of NSAIDs is associated with the risk of gastrointestinal bleedings, haemorrhagic lesions and ulcerations. It has become clear that other mediators besides prostaglandins can similarly act to protect the gastrointestinal mucosa of experimental animals and humans from injury induced by ASA. For instance, nitric oxide (NO) released from vascular epithelium, epithelial cells of gastrointestinal tract and sensory nerves can influence many of the same components of mucosal defense as do prostaglandins. This review was designed to provide an updated overview based on the experimental and clinical evidence on the involvement COX-2 derived products, lipoxins in the mechanism of gastric defense, gastroprotection and gastric adaptation to ASA. Lipoxins were recently considered as another group of lipid mediators that can protect the stomach similarly as NO-donors known to exert protective influence on the stomach from the injury under condition where the mucosal prostaglandin levels are suppressed. The new class of NO-releasing NSAIDs, including NO-aspirin or NO-naproxen, represent a very promising approach to reducing the toxicity of their parent NSAIDs. Aspirin-triggered lipoxin (ATL) synthesis, via COX-2, acts to reduce the severity of damage induced by this NSAID. Lipoxin analogues may prove to be useful for preventing mucosal injury and for modulating mucosal inflammation. Evidence presented in this review documents that ATL also play in important role in gastric adaptation during chronic ASA administration. Suppression of COX-2 activity by selective COX-2 inhibitors such as rofecoxib or celecoxib was shown to abolish the production of ATL and to diminish the gastric tolerability of ASA and gastric adaptation developed in response to repetitive administration of this NSAID. Synthetic analogues of lipoxins as well as newer class of NSAIDs releasing NO may be used in the future as the therapeutic approach to counteract adverse effects in the stomach associated with NSAIDs ingestion.

Involvement of orexigenic peptides in the mechanism of gastric mucosal integrity and healing of chronic gastric ulcers.

Orexigenic peptides are group of endocrine hormones exerting a pleiotropic influence on many physiological functions including regulation of the feeding behaviour and energy expenditure, release of growth hormone (GH) and inotropic effects on the heart. Some of these peptides such as ghrelin, originally identified in the gastric mucosa, has been involved not only in control of food intake and growth hormone release but also exerts the immunomodulatory and anti-inflammatory properties. This review summarizes the recent attempts to prove the concept that orexigenic peptides such as ghrelin, orexin-A and obestatin besides playing an important role in the mechanism of food intake, exhibit a potent gastroprotective action against the formation of acute gastric mucosal injury induced by various ulcerogens. This protective effect depends upon vagal activity and hyperemia mediated by NOS/NO and COX/PG systems and CGRP released from sensory afferent nerves. In addition, the appetite peptides such as ghrelin and orexin-A are implicated in the mechanism of the healing of preexisting gastric ulcers due to an activation of specific GHS-R1a and OX-R1 receptors and PG/COX system.

[A case of sepsis in ILBW infant caused by Bacillus cereus]. / Zakazenie bacillus cereus u noworodka z niewiarygodnie mala urodzeniowa masa ciala.

Bacillus cereus is an aerobic or facultative anaerobic Gram-positive rod which is ubiquitous in the environment. The incidence of neonatal infections is very low. The clinical course is serious, usually life- threatening or permanently damaging the central nervous system. The immature immune system, subjected to invasive procedures, increases the morbidity risk in this age group, especially in extremely low birth weight infants. Diagnostic difficulties and insusceptibility to ''first- line'' antibiotics can delay effective therapy and increase the risk of its failure. We report a 730 g preterm neonate, delivered at 27 weeks gestation with late- onset sepsis due to Bacillus cereus. The disease course was complicated by development of brain abscesses. We describe the clinical course of infection, diagnostic difficulties and the treatment. After the 140 days of hospitalization and relatively long period of therapy with different antibiotics, the patient was discharged from hospital in good condition. Despite of transmission of infection to the central nervous system, the introduced therapy prevented severe neurological disabilities as confirmed during the evaluation according to the Bayley Scale of Infant Development, performed at 29 months of life.

Involvement of sensory nerves in the protective effect of growth hormone on acute pancreatitis.

UNLABELLED: Growth hormone (GH) has been shown to protect the intestinal barrier integrity and to stimulate the production of insulin-like growth factor 1 (IGF-1), which inhibits the development of acute pancreatitis. Sensory nerves are implicated in the protection of pancreatic tissue against acute inflammation. The aim of this study was to investigate the influence of exogenous GH on acute pancreatitis (AP) and to assess the involvement of sensory nerves and IGF-1 in above effect. Studies were performed on Wistar rats. AP was induced by subcutaneous administration of caerulein (25mug/kg) to the conscious animals. GH (1 or 2mg/kg) was administered to the rats as an intraperitoneal injection 30min prior to the start of AP. To deactivate sensory nerves capsaicin was given at total dose of 100mg/kg 10days before the experiments. AP was confirmed by histological examination and manifested by the significant rises of pancreatic weight, and serum activities of lipase, TNFalpha and IL-10 (by 550%, 300% and 50%, respectively), whereas IGF-1 blood concentration was markedly reduced. Administration of GH prior to the caerulein infusion significantly increased GH, IGF-1 and IL-10 blood levels, attenuated harmful effects of AP and reduced histological manifestations of pancreatitis in the rats with intact sensory nerves. This was accompanied by the reduction of serum lipase, and TNFalpha activities. In the AP rats with capsaicin-deactivated sensory nerves GH failed to protect the pancreas against acute damage and, as a consequence of above deactivation, IGF-1 was low. CONCLUSION: GH modulates the development of acute pancreatitis in the presence of active sensory nerves probably via stimulation of IGF-1 release.

Dual, time-dependent deleterious and protective effect of anandamide on the course of cerulein-induced acute pancreatitis. Role of sensory nerves.

Some recent studies indicate that cannabis may induce acute pancreatitis in humans and administration of anandamide increases the severity of acute pancreatitis; whereas another study exhibits some therapeutic effects in acute pancreatitis. Aim of the present study was to discover what is the reason for these opposite confusing results and to determine the role of sensory nerves in this effect. Acute pancreatitis was induced in rats by cerulein. Anandamide, an endogenous cannabinoid, was administered i.p. (1.5 micromol/kg) before or 2 h after cerulein administration. Stimulation of sensory nerves was performed by capsaicin (0.5 mg/kg s.c.). In rats treated with combination of anandamide plus capsaicin, capsaicin was given 10 min after each dose of anandamide. After the last injection of cerulein or 4 h later, the study was terminated. In our study we observed that stimulation of sensory nerves by capsaicin, before administration of cerulein, reduced the severity of acute pancreatitis. Anandamide, administered alone before cerulein, increased pancreatic damage in acute pancreatitis. Anandamide administered in combination with capsaicin, before cerulein, abolished the capsaicin-induced protective effect on the pancreas. Opposite effects were observed when capsaicin and anandamide were administered after injection of cerulein. Capsaicin increased the severity of acute pancreatitis, whereas anandamide reduced pancreatic damage and reversed the deleterious effect of capsaicin. We conclude that the effect of anandamide on the severity of acute pancreatitis depends on the phase of this disease. Administration of anandamide, before induction of pancreatitis, aggravates pancreatic damage; whereas anandamide administered after induction of pancreatitis, reduces the severity of acute pancreatitis. Sensory nerves are involved in the mechanism of this biphasic effect of anandamide.

Gastroprotective action of orexin-A against stress-induced gastric damage is mediated by endogenous prostaglandins, sensory afferent neuropeptides and nitric oxide.

Orexin-A, identified in the neurons and endocrine cells in the gut, has been implicated in control of food intake and sleep behavior but little is known about its influence on gastric secretion and mucosal integrity. The effects of orexin-A on gastric secretion and gastric lesions induced in rats by 3.5 h of water immersion and restraint stress (WRS) or 75% ethanol were determined. Orexin-A (5-80 microg/kg i.p.) increased gastric acid secretion and attenuated gastric lesions induced by WRS and this was accompanied by the significant rise in plasma orexin-A, CGRP and gastrin levels, the gastric mucosal blood flow (GBF), luminal NO concentration and an increase in mRNA for CGRP and overexpression of COX-2 protein and the generation of PGE(2) in the gastric mucosa. Orexin-A-induced protection was abolished by selective OX-1 receptor antagonist, vagotomy and attenuated by suppression of COX-1 and COX-2, deactivation of afferent nerves with neurotoxic dose of capsaicin, pretreatment with CCK(2)/gastrin antagonist, CGRP(8-37) or capsazepine and by inhibition of NOS with L-NNA. This study shows for the first time that orexin-A exerts a potent protective action on the stomach of rats exposed to non-topical ulcerogens such as WRS or topical noxious agents such as ethanol and these effects depend upon hyperemia mediated by COX-PG and NOS-NO systems, activation of vagal nerves and sensory neuropeptides such as CGRP released from sensory nerves probably triggered by an increase in gastric acid secretion induced by this peptide.

Therapeutic potential of 1-methylnicotinamide against acute gastric lesions induced by stress: role of endogenous prostacyclin and sensory nerves.

1-Methylnicotinamide (MNA) is one of the major derivatives of nicotinamide, which was recently shown to exhibit antithrombotic and antiinflammatory actions. However, it is not yet known whether MNA affects gastric mucosal defense. The effects of exogenous MNA were studied on gastric secretion and gastric lesions induced in rats by 3.5 h of water immersion and water restraint stress (WRS) or in rats administered 75% ethanol. MNA [6.25-100 mg/kg intragastrically (i.g.)] led to a dose-dependent rise in the plasma MNA level, inhibited gastric acid secretion, and attenuated these gastric lesions induced by WRS or ethanol. The gastroprotective effect of MNA was accompanied by an increase in the gastric mucosal blood flow and plasma calcitonin gene-related peptide (CGRP) levels, the preservation of prostacyclin (PGI(2)) generation (measured as 6-keto-PGF1alpha), and an overexpression of mRNAs for cyclooxygenase (COX)-2 and CGRP in the gastric mucosa. R-3-(4-Fluoro-phenyl)-2-[5-(4-fluoro-phenyl)-benzofuran-2-ylmethoxycarbonylamino]-propionic acid (RO 324479), which is the selective antagonist of IP/PGI(2) receptors, reversed the effects of MNA on gastric lesions and GBF. MNA-induced gastroprotection was attenuated by suppression of COX-1 [5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole; SC-560] and COX-2 [4-(4-methylsulfonylphenyl)-3-phenyl-5H-furan-2-one; rofecoxib] activity, capsaicin denervation, and by the pretreatment with CGRP(8-37) or capsazepine. Addition of exogenous PGI(2) or CGRP restored the MNA-induced gastroprotection in rats treated with COX-1 and COX-2 inhibitors or in those with capsaicin denervation. WRS enhanced MDA content while decreasing superoxide dismutase (SOD) activity in the gastric mucosa, but pretreatment with MNA reversed these changes. MNA exerts potent gastroprotection against WRS damage via mechanisms involving cooperative action of PGI(2) and CGRP in preservation of microvascular flow, antioxidizing enzyme SOD activity, and reduction in lipid peroxidation.

[Protective role of leptin in acute gastric ulcers]. / Ochronna rola leptyny w ostrych wrzodach zoladka.

There are few data concerning protective effects of leptin on gastric epithelium treated with necrotic factors: ethanol, bile salts and hiperosmotic solutions. Further investigations are needed to establish the role of hormone leptin in gastroprotection and in the process of chronic gastric ulcers healing in animals. Exogenous leptin administration plays protective effects against 75% ethanol damage in gastric epithelium. Nitric oxide is involved in gastroprotective effects of leptin and CCK.