Anal skin tags: removal made simple.

AIM: Anal skin tags are a common finding. They are found in one-third of patients with bening anal disorders. We describe a simple method of anal skin tag removal during stapled anopexy. This involves utilizing the circular anal dilator provided with the stapling kit. METHOD: Skin tags are brought through the perforations of the circular anal dilator of the stapling kit. The skin tags are removed by cautery. RESULTS: Minimal pain has been noticed in patients under going this procedure. CONCLUSION: Anal skin tags can be removed in a simple manner using components provided with the stapling kit. We decribe a simple method of anal skin tag removal during stapled anopexy. This involves utilizing the circular anal dilator provided with the stapling kit.

Management of concurrent colorectal cancer and vascular disease in the endovascular era.

UNLABELLED: Concurrent colorectal cancer (CRC) and vascular disease, such as abdominal aortic aneurysm, represents a challenging clinical situation. Both lesions may lead to the demise of the patient and therefore should be treated. Endovascular techniques may enhance decision-making and even permit single-stage treatment. PATIENTS AND METHODS: Retrospective review of patients in a university department with extensive endovascular experience. Between 2004 and 2010, seven patients with synchronous vascular disease and colorectal cancer were identified. RESULTS: The mean age was 73 years, and all patients were men. Five patients had concurrent CRC and aneurysmal disease. Two had synchronous critical carotid artery stenosis and CRC. All vascular lesions were treated with endovascular techniques. All CRC were resected with open techniques. In four patients, endovascular repair followed by staged CRC resection was performed. In three patients, single-stage procedures were performed. There was one perioperative death, for a mortality of 14.3% in our series. There were no graft infections. CONCLUSIONS: Priority of treating concurrent vascular disease and CRC remains a dilemma. Combined treatment with a single-stage procedure is feasible. Risk of graft infection may be lower than expected.

Sacral nerve stimulation for fecal incontinence. First successful case in Greece.

INTRODUCTION: Sacral nerve modulation (SNM) is an established and successful treatment for fecal incontinence. We present the first successful case in Greece, performed in our department. PATIENTS AND METHODS: A 60-year-old female patient presented with a 5-year-old history of fecal incontinence. The Cleveland Clinic Florida (CCF) Incontinence Score was 15. Endoanal ultrasound did not show defects of the internal or external anal sphincter. Conservative and pharmacological therapy was unsuccessful. The patient subsequently underwent a total pelvic floor repair, which was also unsuccessful. After discussing further options, the patient gave consent for percutaneous nerve evaluation (PNE), for possible permanent stimulator implantation. RESULTS: A quadripolar lead was placed percutaneously through the dorsal S3 foramen under local anesthesia. This was connected to a test stimulator (Medtronic Interstim Model 3625, Minneapolis, MN). The stimulator was activated for a period of 4 weeks. At the end of the test period, the CCF Incontinence score was 5. This was considered successful. A permanent stimulator (Medtronic Interstim Implantable Pulse Generator Model 3058, Minneapolis, MN) was then implanted under local anesthesia. Two months after permanent implantation, the Wexner Score has not increased. CONCLUSION: SNM is a relatively simple, safe and minimally invasive technique for the treatment of fecal incontinence.

Priority of resection in concomitant abdominal aortic aneurysm (AAA) and colorectal cancer (CRC): review of the literature and experience of our clinic.

The concomitant occurrence of abdominal aortic aneurysm (AAA) and colorectal cancer (CRC), although rare, always represents a therapeutic dilemma. The incidence of coexistence ranges between 0.49 and 2.1%. Both lesions should be treated to achieve best life expectancy. But the main controversy revolves around whether to treat them simultaneously or as staged procedures. In our institution, we treated seven cases of concomitant AAA and CRC. In five of them, synchronous conventional resection was preferred. In the latest two, which we present, endovascular aortic repair was chosen. No graft infection was documented.

Dynamics of neutrophil aggregation in couette flow revealed by videomicroscopy: effect of shear rate on two-body collision efficiency and doublet lifetime.

During inflammation, neutrophil capture by vascular endothelial cells is dependent on L-selectin and beta(2)-integrin adhesion receptors. One of us (S.I.S.) previously demonstrated that homotypic neutrophil aggregation is analogous to this process in that it is also mediated by these receptors, thus providing a model for studying the dynamics of neutrophil adhesion. In the present work, we set out to confirm the hypothesis that cell-cell adhesion via selectins serves to increase the lifetimes of neutrophil doublets formed through shear-induced two-body collisions. In turn, this would facilitate the engagement of more stable beta(2)-integrin bonds and thus increase the two-body collision efficiency (fraction of collisions resulting in the formation of nonseparating doublets). To this end, suspensions of unstimulated neutrophils were subjected to a uniform shear field in a transparent counter-rotating cone and plate rheoscope, and the formation of doublets and growth of aggregates recorded using high-speed videomicroscopy. The dependence of neutrophil doublet lifetime and two-body collision-capture efficiency on shear rate, G, from 14 to 220 s(-1) was investigated. Bond formation during a two-body collision was indicated by doublets rotating well past the orientation predicted for break-up of doublets of inert spheres. A striking dependence of doublet lifetime on shear rate was observed. At low shear (G = 14 s(-1)), no collision capture occurred, and doublet lifetimes were no different from those of neutrophils pretreated with a blocking antibody to L-selectin, or in Ca(++)-depleted EDTA buffers. At G > or = 66 s(-1), doublet lifetimes increased, with increasing G reaching values twice those for the L-selectin-blocked controls. This correlated with capture efficiencies in excess of 20%, and, at G > or = 110 s(-1), led to the rapid formation of large aggregates, and this in the absence of exogenous chemotactic stimuli. Moreover, the aggregates almost completely broke up when the shear rate was reduced below 66 s(-1). Partial inhibition of aggregate formation was achieved by blocking beta(2)-integrin receptors with antibody. By direct observation of the shear-induced interactions between neutrophils, these data reveal that steady application of a threshold level of shear rate is sufficient to support homotypic neutrophil aggregation.

Differential effect of histamine 3 receptor-active agents on brain, but not peritoneal, mast cell activation.

The activation of presynaptic histamine 3 (H(3)) receptors inhibits the release of histamine and other neurotransmitters from central nervous system neurons. Rat brain mast cells (MCs) release histamine and 5-hydroxytryptamine (5-HT) in response to neuropeptides and neurotransmitters secreted from adjacent neurons. Dura MCs also degranulate in response to antidromic trigeminal nerve stimulation and with acute psychological stress. Such findings have implicated brain MCs in certain neuroinflammatory disorders, such as migraines. We investigated the ultrastructural appearance of control and stimulated thalamic/hypothalamic (brain) MCs before and after treatment with the H(3) receptor agonist N(alpha)-methylhistamine (N(alpha)-mH) and the H(3) receptor antagonist thioperamide (Th). Ultrastructural investigation of brain MCs stimulated with compound 48/80 revealed extensive intragranular changes that paralleled 5-HT secretion but without degranulation by exocytosis typical of connective tissue MCs. N(alpha)-mH significantly reduced these morphological changes, as well as 5-HT release from brain MCs and neurons stimulated with KCl; conversely, Th augmented both histamine and 5-HT release from brain neurons and MCs. Neither N(alpha)-mH nor Th had any effect on peritoneal MCs. Simultaneous addition of both drugs largely antagonized each other's effects on brain MC activation and 5-HT secretion. Ultrastructural observations and lack of lactic dehydrogenase release in the perfusate excluded any cytotoxic effect. The ability of H(3) agonists to inhibit brain MC activation, as well as secretion of 5-HT from both brain MCs and neurons, may be useful in the management of migraines.

Stress-induced bladder mast cell activation: implications for interstitial cystitis.

PURPOSE: To investigate whether acute psychological stress may activate bladder mast cells which appear to play a significant role in the pathophysiology of interstitial cystitis, a syndrome that occurs primarily in females and is characterized by urinary urgency, frequency and suprapubic pain, all of which often worsen with stress. MATERIALS AND METHODS: Non-traumatic immobilization stress was used as a model of acute emotional stress by placing a rat in a plexiglass immobilizer, after first bringing each rat in the laboratory daily for 4 days to reduce the stress of handling. The rat was then anesthetized, decapitated and the bladder removed and fixed for light and electron microscopy. RESULTS: This type of stress resulted in activation of over 70% of bladder mast cells within 30 minutes, as evidenced by light and electron microscopy. Pretreatment of the animals with intraperitoneal administration of polyclonal antiserum to corticotropin releasing hormone had no effect on bladder mast cell activation and no nerve fibers positive for this hormone were identified in the bladder. Stress-induced bladder mast cell activation was, however, substantially reduced in animals treated neonatally with capsaicin suggesting that sensory neuropeptides, such as substance P, of which increased positive nerve fibers have been localized close to bladder mast cells, are involved in this response. CONCLUSIONS: This is the first time that psychological stress is shown to activate bladder mast cells, apparently via the action of at least some sensory neuropeptides. These findings have implications for the pathophysiology and possible therapy of interstitial cystitis.

Carbachol-induced bladder mast cell activation: augmentation by estradiol and implications for interstitial cystitis.

OBJECTIVES: Interstitial cystitis (IC) is a painful, sterile bladder disorder that occurs primarily in women, many of whom also experience allergies with symptoms that worsen perimenstrually. Increased numbers of activated bladder mast cells have recently been implicated in the pathophysiology of IC. These mast cells express high-affinity estrogen receptors and are located close to increased bladder nerves, many of which contain the neuropeptide substance P (SP). We therefore investigated whether the neurotransmitter acetylcholine (ACh) and SP could activate bladder mast cells and whether estradiol could influence this effect. METHODS: Bladder pieces from male Sprague-Dawley rats were perfused with carbachol (the stable analogue of ACh), SP, or the mast cell secretagogue compound 48/80 (C48/80) with or without preincubation with beta-estradiol. The effect of carbachol was also investigated after pretreatment with the muscarinic antagonist atropine. Mast cell activation was assessed by release of 3H-serotonin and morphologic evidence of secretion by light and electron microscopy. RESULTS: Carbachol triggered rat bladder mast cell serotonin release in a dose-dependent manner, an effect increased by tissue pretreatment with estradiol and blocked by atropine. The effect of carbachol was accompanied by ultrastructural evidence of mast cell activation and was stronger than that obtained by either C48/ 80 or SP. CONCLUSIONS: Bladder mast cell activation is neurogenically mediated and augmented by estradiol, findings that could possibly explain the painful symptoms of IC and its prevalence in women, as well as the worsening of symptoms perimenstrually.

Stress-induced intracranial mast cell degranulation: a corticotropin-releasing hormone-mediated effect.

Stress is known to precipitate or worsen a number of disorders, such as migraines, in which mast cells are suspected of being involved by releasing vasoactive, nociceptive, and proinflammatory mediators. However, no functional association has been demonstrated yet between a migraine trigger and brain mast cell activation. Nontraumatic immobilization (restrain) stress has been shown to stimulate the hypothalamic-pituitary-adrenal axis and to cause redistribution of immune cells. Here, restrain stress caused degranulation in 70% of rat dura mast cells within 30 min, as shown both by light and electron microscopy. These morphologic findings were accompanied by cerebrospinal fluid elevation of rat mast cell protease I, but not II, indicating secretion from connective tissue type mast cells. Mast cell activation due to stress was abolished in animals that had been treated neonatally with capsaicin, indicating that neuropeptides in sensory nerve endings are involved in this response. Complete inhibition was also achieved by pretreating the animals ip with polyclonal antiserum to CRH. Mast cells in the dura were localized close to nerve processes containing substance P, but no CRH-positive fibers were identified even though these were found close to mast cells in the median eminence. This is the first time that stress is shown to activate intracranial mast cells; apparently through the sequential action of CRH and sensory neuropeptides. These findings may have implications for the pathophysiology and possible therapy of neuroinflammatory disorders such as migraines, which are induced or exacerbated by stress.