Acute superior mesenteric vein thrombosis in the setting of cytomegalovirus mononucleosis: a case report and review of the literature.

Cytomegalovirus is a viral genus of the overarching family Herpesviridae, and is of particular importance because of its relevance to human disease. This association is predominantly due to human cytomegalovirus, a well-studied pathogen. In addition to the mononucleosis syndrome that can occur during acute cytomegalovirus viraemia, this virion has been recurrently implicated as a provoking factor for thromboembolic disease in the published scientific literature. As physicians increasingly forgo extensive laboratory investigation in the setting of clinical hypercoagulability, it has also become evident that in some circumstances whether or not a particular investigation alters clinical management is not necessarily the only important question. Viraemia as a provoking factor for thrombosis stands as such an example. The aim of this Grand Round is to further explore the role of cytomegalovirus as it pertains to thromboembolic disease, especially in the present era of viral-associated thromboembolism.

The concept of portal system obstruction in Avicenna's canon of medicine

Historical literature on portal hypertension is mainly focused on the contemporary advances in therapeutic methods, especially surgical ones. However, it seems that the origin of the human knowledge on the portal system, its association with the caval system, obstructive pathologies in this system and the gastrointestinal bleeding due to hepatic diseases might be much older than previously believed. Avicenna provided a detailed anatomy of the portal venous system and its feeding branches in the Canon of Medicine. Soddat al-Kabed va al-Masarigha (liver and mesenteric occlusion) is also a disease presented by Avicenna with clinical, etiological and therapeutic descriptions suggesting the fact that Soddat al-Kabed va al-Masarigha has multiple similarities with the currently identified concept of "portal hypertension". He presented sense of heaviness in the liver area with or without mild pain, anemia, pale and inappropriate body color, and loose stool which can be complicated with ascites, infection, fever and abdominal pain as clinical manifestations of this disease. He has also suggested therapeutic approaches including laxative and diuretic herbs to help excreting the obstructive material into stool or urine.

A Case of Idiopathic Mesenteric Phlebosclerosis with Progressive Intestinal Necrosis.

The patient was a 39-year-old woman who was referred to our department from her previous doctor with a 2-day history of right abdominal pain. Abdominal computed tomography showed wall thickening associated with calcification in the ascending colon. Contrast enhancement in the same portion of the intestinal wall was rather poor. Fluid accumulation was also seen around the intestine, so emergency surgery was performed under a provisional diagnosis of intestinal necrosis. Intestinal necrosis due to idiopathic mesenteric phlebosclerosis was diagnosed from postoperative histopathological tests. Idiopathic mesenteric phlebosclerosis displays a chronic course and in most cases conservative treatment is indicated. Bowel obstruction is common among patients who require surgical treatment, but rare cases such as the present one are also seen in which intestinal necrosis occurs. In recent years, an association with herbal medicine has been indicated as one potential cause of this disease, and this entity should be kept in mind when patients with acute abdomen and a history of taking herbal medicines are encountered.

Management of Acute Mesenteric Ischemia: A Critical Review and Treatment Algorithm.

BACKGROUND: Acute mesenteric ischemia (AMI) due to a sudden loss or decrease in blood perfusion to the mesentery represents a highly lethal condition. However, the optimal surgical management remains debatable and merits a more clear recommendation based on a higher level of evidence. METHODS: A systematic review of articles published between 2000 and 2013 was performed. Patients were divided into endovascular treatment (ET), open surgery (OS), and hybrid technique (HT) groups. Data of patients' demographics, procedural information, clinical outcomes including mortality, morbidity, primary patency rate, technique success, primary intestinal resection rate, and second-look laparotomy rate, and follow-up were all retrieved. Comparison between the ET and the OS groups was made using 2-sided Student t test and 2-sided χ(2) test or Fisher exact test where appropriate. RESULTS: Twenty-eight articles with a total of 1110 patients were included for the review. The ET group had lower in-hospital mortality and morbidity but similar survival rate during follow-up compared to the OS group. The primary patency rate was higher in the ET group. The overall bowel resection rate was lower in the ET group, and nearly every patient in the cohort who required second-look laparotomy required bowel resection. The HT group seemed to have the lowest mortality and acceptable second-look laparotomy rate and morbidity. Comparison between the HT group and other groups was not possible due to the limited number of cases available for review. CONCLUSION: Endovascular treatment may serve as a first-line therapy for select patients when there is a low suspicion for intestinal necrosis. Open surgery should be reserved for emergency conditions requiring exploratory laparotomy. Hybrid technique may be an especially effective approach for treating AMI, with low morbidity and mortality, although further studies are required comparing it to OS and ET.

Right-Side Colon Ischemia: Clinical Features, Large Visceral Artery Occlusion, and Long-Term Follow-Up.

CONTEXT: Large visceral artery occlusion (LVAO) could underlie right-side colon ischemia (RSCI) but is little known. OBJECTIVE: To assess patients with RSCI through long-term follow-up, including features and management of LVAO. MAIN OUTCOME MEASURES: Mesenteric ischemia and mortality. DESIGN: Retrospective observational study in an integrated health care system. RESULTS: Of 49 patients (30 women [61.2%]; mean [standard deviation] age, 69.4 [11.9] years), 19 (38.8%) underwent surgery­that is, 5 (83.3%) of 6 who developed RSCI in hospital following surgical procedures and 14 (32.6%) of 43 who had RSCI before hospitalization (p value = 0.03); overall, 5 (10.2%) died. Among 44 survivors with a median (range) follow-up of 5.19 (0.03-14.26) years, 5 (11.4%), including 3 (20.0%) of 15 operated cases, had symptomatic LVAO and underwent angioplasty and stent placement: 2 for abdominal angina that preceded RSCI, 1 for acute mesenteric ischemia 1 week after resection of RSCI, 1 for RSCI 6 weeks after resection of left-side ischemia, and 1 for abdominal angina that began 3 years after spontaneous recovery from RSCI. None had further mesenteric ischemia until death from nonintestinal disease or the end of follow-up (1.6 to 10.2 years later). Kaplan-Meier survival estimates for all 44 survivors at 1, 3, 5, and 10 years were 88.6%, 72.3%, 57.6%, and 25.9%, respectively. Thirty-one patients (70.4%) died during follow-up, 19 (61.3%) of a known cause; the 39 patients not treated for LVAO lacked mesenteric ischemia. CONCLUSION: Patients with RSCI may have symptomatic LVAO; therefore, we advise they undergo careful query for symptoms of abdominal angina and routine visceral artery imaging.

CT-guided injection of N-butyl cyanoacrylate glue for treatment of chylous leak after aorto-mesenteric bypass.

Lymphangiography and thoracic duct embolization are well-described techniques for the diagnosis and treatment of thoracic lymphatic leaks refractory to conservative treatment. However, thoracic duct embolization is not an option in patients with abdominal chylous leaks. The present report describes a 68-year-old man who underwent an aortomesenteric bypass complicated by a high-output postoperative chylothorax (>2,000 ml/day) and chylous ascites (>7,000 ml/paracentesis). Ultrasound-guided intranodal lymphangiography demonstrated a retroperitoneal lymphatic leak tracking along the vascular graft into the peritoneal cavity. Computed tomography-guided lymphatic duct occlusion with N-butyl cyanoacrylate glue was performed, resulting in successful treatment of both chylothorax and chylous ascites.

Intravenous administration of tetramethylpyrazine reduces intestinal ischemia-reperfusion injury in rats.

Intestinal ischemia-reperfusion injury (IIRI) is a life-threatening condition requiring prompt medical intervention. Tetramethylpyrazine (TMP) is a biologically active alkaloid isolated from Ligusticum wallichii. Previously, it was shown that TMP causes vasodilatation and inhibition of platelet aggregation as well as exhibits significant antioxidant effects. Therefore, the aim of the present study was to evaluate possible therapeutic effects of TMP in the prevention of IIRI. Wistar rats (n = 80) were randomly divided into eight experimental groups and subjected to a 1 h occlusion of cranial mesenteric artery followed by 0, 1, 12, and 24 h period of reperfusion. Thirty minutes before the IIRI animals received either TMP (30 mg/kg, i.v.) or identical volume of saline. In addition, a control group of 10 animals was not exposed to IIRI. Intestine morphology was evaluated by using histopathological injury index examination (HII), goblet and Paneth cells quantification as well as by applying immunofluorescent methods such as InSitu TUNEL and caspase-3 positivity assessment. Here we showed that preconditioning with TMP prior IIRI decreases the grade of injury. Significant reduction of HII was detected in TMP pretreated groups after 0, 1, and 12 h of reperfusion where injury reduction up to 75% was found. Lower histopathological damage in preconditioned groups was accompanied with increased number of secretory epithelial cells and decreased number of apoptotic cells. These results demonstrate the protective effect of TMP on the small intestine mucosa, suggesting administration of TMP as a molecule for pharmacological intervention against IIRI.

Effects of exogenous vasoactive intestinal peptide on mesenteric lymph pathway during early intestinal ischemia-reperfusion injury in rats.

Mesenteric lymph pathway serves as the primary route by which gut injury leads to systemic inflammation and distant organ injury. The inflammation of the intestinal tract is partially mediated by vasoactive intestinal peptide (VIP). Therefore, the aim of this study was to test whether exogenous VIP affects mesenteric lymph pathway during early intestinal ischemia-reperfusion (IIR) injury. Rats were randomized into control, control+VIP, IIR and IIR+VIP groups. The observation of mesenteric lymph flow was carried out by cannulation of mesenteric lymphatics. The distribution of in vivo lymphocyte trafficking was performed by (51)Cr labeled lymphocytes and was measured by γ-counter. Endotoxin concentration was assayed using the limulus test kit and TNF-α level was detected by ELISA. When IIR injury treated with VIP, the volumes of lymph flow increased by 80%, which caused the number of lymphocytes exiting in mesenteric lymphatic increased by 50% while the proportion of (51)Cr-lymphocytes in Peyer's patches, intestinal effector tissues, mesenteric nodes, large intestine, stomach decreased by 58%, 51%, 58%, 63%, 64% respectively at the 6th h after reperfusion following intestinal ischemia. Meanwhile, endotoxin and TNF-α levels in intestinal lymph decreased by 51% and 83%. These results suggest that exogenous VIP ameliorates IIR induced splanchnic organ damage via inhibition of toxic mediators reaching systemic circulation and reinforcement of the effective immune responses in gut-associated lymphoid tissues (GALT).

Mesenteric phlebosclerosis associated with long-term oral intake of geniposide, an ingredient of herbal medicine.

BACKGROUND: Idiopathic mesenteric phlebosclerosis (IMP) is a rare disease, characterised by thickening of the wall of the right hemicolon with calcification of mesenteric veins. However, the aetiology remains unknown. AIM: To investigate the possible association of herbal medicines with IMP. METHOD: The clinical data of four of our own patients were collected. Furthermore, we searched for previous reports about similar patients with detailed descriptions of herbal prescriptions that they had taken. We compared herbal ingredients to identify the toxic agent as a possible aetiological factor. RESULTS: Clinical data on a total of 25 patients were summarised. Mean age was 61.8 years and there was female predominance (6 men and 19 women). The used Kampo prescription, the number of cases, and the mean duration of use were as follows: kamisyoyosan in 12 cases for 12.8 years, inshin-iseihaito in 5 cases for 13.4 years, orengedokuto in 4 cases for 14.3 years, inchinkoto in 1 case for 20 years, kamikihitou in 1 case for 19 years, seijobofuto in 1 case for 10 years and gorinsan in 1 case for an unknown duration. Only one ingredient, sansisi, was common to the herbal medicines of all 25 patients. This crude drug called geniposide in English is a major constituent of the Gardenia fruits. CONCLUSION: The long-term use of geniposide in herbal medicines appears to be associated with mesenteric phlebosclerosis.

Effects of peripherally and centrally applied ghrelin in the pathogenesis of ischemia-reperfusion induced injury of the small intestine.

Ghrelin is an important hormone involved in the control of the human appetite center. Recently, protective properties of this hormone have been recognized in various models of impairment of the gastric mucosa, including stress, ischemia and reperfusion (I/R). Ghrelin is predominantly secreted by the gastric mucosa of stomach, but there are other sources of ghrelin, for example in the hypothalamus and various parts of the central nervous system (CNS) that should be taken into consideration. This hormone exerts biological effects via the activation of growth hormone secretagogue receptor (GHSR), the presence of which was confirmed in different parts of the gastrointestinal (GI) tract and midbrain structures. Although substantial evidence of the divergent biological effects of ghrelin and the mechanism of its action has been emphasized, the precise mechanisms of ghrelin which affords GI protection is still unclear. Particularly, there is a sparse amount of evidence concerning its action on the GI system. The major aim of the present study was to evaluate the importance of peripherally and centrally administered ghrelin at different times of the ischemia and reperfusion (I/R period in the modulation of resistance of the intestinal mucosa to the injury induced by ischemia and subsequent reperfusion. Secondly, we wanted to evaluate the possible mechanism of the action of ghrelin with a particular focus on its influence on the intestinal blood flow. Male Wistar rats were divided into 4 series (A-D) of the experimental groups (n=7). In series A the importance of peripherally administered ghrelin at different time of I/R period was studied. In series B the importance of centrally administered ghrelin at different time of I/R period was evaluated. In series C and D, the mechanisms of peripherally and centrally administered hormone were examined, respectively. Two models of the I/R period were selected: short lasting (30/60 min) and long lasting (60/120 min). The following drugs were used: ghrelin (50 µg/kg i.p. or 1 nmol in 10 µl i.c.v.), 6 hydroxy dopamine (50 mg/kg i.p.), nadolol (0.5 mg/kg i.p.), calcitonin gene related peptide fragment (CGRP(8-37), 100 µg /kg i.p.), capsaicin (5-10 mg/100 ml solution s.c.). The mesenteric blood flow (MBF-ml/min), the intestinal microcirculatory blood flow (LDBF-PU), the arterio-venous oxygen difference (AVO(2)-ml/O(2)/100 ml blood), and the intestinal oxygen uptake (VO(2)) in ml O(2)/min were measured. Mucosal impairment was assessed planimetrically with the use of a digital photo analyzer (LA) and histologically with the use of the six-point Park/Chiu scale. Peripheral administration of ghrelin evoked marked increase of MBF and LDBF by 42% and 48%, respectively, with significant reduction of LA by 38%. When ghrelin was administered at the beginning of the reperfusion period during the short I/R period or prior to the long lasting I/R period, the vascular reactions and protective effects were reduced, but not completely abolished. The central administration of ghrelin before the short I/R period significantly increased the MBF and LDBF by about 32% and 35%, respectively, as well as LA reduction by about 20% in comparison to the control group. However, when ghrelin was administered prior to the long I/R period or after the onset of completed ischemia, neither vascular nor protective effects were noticed. Sensory denervation and the blockade of the CGRP1 receptors totally blocked the protective and hyperemic effects of the peripherally administered ghrelin. Selective blockade of the adrenergic system or blunting of the vagal nerves (vagotomy) significantly but not totally eliminated the effects of centrally applied ghrelin, which were abolished when both adrenergic and parasympathetic pathways were ablated. These results indicate that ghrelin applied centrally or peripherally markedly increases resistance of the intestinal tissue during the I/R period induced mucosal and hyperemic impairment evoked by I/R. Ghrelin is an important mediator of the increase in the intestinal microcirculation and elevation of the intestinal metabolism, which seems to be, at least in part, responsible for the observed protection of the intestine subjected to I/R. Impairment of this microvasculature response due to I/R seems to be responsible for a markedly observed weaker effect of ghrelin when this hormone was administered after the ischemic period. The lack of a protective effect observed after central administration of this peptide against a long lasting I/R period is probably due to damage of neural pathways caused by I/R. Finally, the peripheral activity of ghrelin in the intestine is mediated by the sensory neurons with a prominent role of CGRP released from their endings. However, this peripheral action of ghrelin depends upon the proper functioning of both the sympathetic and parasympathetic system.

Diagnostic and prognostic value of procalcitonin and phosphorus in acute mesenteric ischemia.

BACKGROUND: In this study, using an animal model of acute mesenteric ischemia (AMI), we investigated the possible use of procalcitonin and phosphorus in the early diagnosis of AMI. METHODS: In this study, 21 New Zealand rabbits were used. Subjects were allocated into three groups as Control, Sham and Ischemia. No intervention was performed in the subjects in the Control group. In the subjects in the Sham and Ischemia groups, laparotomy was performed with midline incision. In the Ischemia group, the superior mesenteric artery was found and tied after laparotomy. Blood was drawn from the animals in all groups at 0, 1, 3 and 6 hours, and procalcitonin and phosphorus levels were studied in these samples. RESULTS: In the Ischemia group, the increase in the levels of serum phosphorus and procalcitonin was found to be statistically significant compared to the Control and Sham groups (p<0.05). The levels of phosphorus and procalcitonin were detected to increase from the 1st hour after ischemia onset, and the increase continued for the following 6 hours (p<0.05). CONCLUSION: Phosphorus and procalcitonin may be important parameters for use in the early diagnosis and prognosis of AMI.

A comparison of endovascular revascularization with traditional therapy for the treatment of acute mesenteric ischemia.

OBJECTIVES: Few centers have adopted endovascular therapy for the treatment of acute mesenteric ischemia (AMI). We sought to evaluate the effect of endovascular therapy on outcomes for the treatment of AMI. METHODS: A single-center, retrospective cohort review was performed on all consecutive patients with thrombotic or embolic AMI presenting between 1999 and 2008. Patients with mesenteric venous thrombosis, nonocclusive mesenteric ischemia, and ischemia associated with aortic dissection were excluded. Demographic factors, preoperative metabolic status, and etiology were compared. Primary clinical outcomes included endovascular technical success, operative complications, and in-hospital mortality. RESULTS: Seventy consecutive patients were identified with AMI (mean age, 64 ± 13 years). Etiology of mesenteric ischemia was 65% thrombotic and 35% embolic occlusions. Endovascular revascularization was the preferred treatment (81%) vs operative therapy (19%). Successful endovascular treatment was achieved in 87%. Endovascular therapy required laparotomy in 69% vs traditional therapy in 100% (P < .05), with a median 52-cm necrotic bowel resected (interquartile range [IQR], 11-140 cm) vs 160 cm (IQR, 90-250 cm; P < .05), respectively. Acute renal failure and pulmonary failure occurred less frequently with endovascular therapy (27% vs 50%; P < .05 and 27% vs 64%; P < .05). Successful endovascular treatment resulted in a mortality rate of 36% compared with 50% (P < .05) with traditional therapy, whereas the mortality rate for endovascular failures was 50%. Endovascular therapy was associated with improved mortality in thrombotic AMI (odds ratio, 0.10; 95% confidence interval, 0.10-0.76; P < .05). CONCLUSIONS: Endovascular therapy has altered the management of AMI, and there are measurable advantages to this approach. Using endovascular therapy as the primary modality for AMI reduces complications and improves outcomes.

Assessment of ischemic vascular damage.

This protocol describes a model convenient for acute experiments in anesthetized rats, performed by selective occlusion of the superior mesenteric artery. Such a model provides a means for assessing the role played by various pathophysiological mechanisms in the development of intestinal ischemic injury. It is especially suitable for studying different treatments, mainly pharmacological ones, to help cope with this problem in clinical practice. In the form of support protocols, this unit includes functional vascular and chemiluminescence studies, determination of vascular permeability and myeloperoxidase activity, transit time, and mortality.

The attenuation effect of 3,4-dihydroxy-phenyl lactic acid and salvianolic acid B on venular thrombosis induced in rat mesentery by photochemical reaction.

3,4-dihydroxy-phenyl lactic acid (DLA) and salvianolic acid B (SAB) are two major water-soluble components of Salvia miltiorrhiza (SM). Previous works have revealed the ability of DLA and SAB to scavenge oxygen free radicals, inhibiting the expression of adhesion molecules CD11b/CD18 in neutrophil. Cardiotonic pills (CP), which is a traditional Chinese medicine compound preparation containing DLA and SAB, was found to inhibit venular thrombosis induced by photochemical reaction (PR) in rat mesentery. The present study addressed the effect of DLA and SAB on PR-induced thrombosis in rat mesentery by utilizing a microcirculation dynamic viewing system. The result demonstrated that both DLA and SAB delayed thrombus-initiation time, while DLA also prolonged thrombus half-size time. The experiments explored the mechanism underlying that the dihydrorhodamine 123 (DHR) fluorescence in the mesenteric venular walls after PR challenge was diminished by pretreatment with either DLA or SAB, the expression of CD18 in neutrophils elicited by PR was depressed by administration of DLA, while mast cell degranulation in rat mesentery induced by PR was damped by SAB. The antioxidant potential of the two substances is likely to be responsible for their most beneficial effects on thrombosis, through either directly scavenging the peroxides produced and/or indirectly depressing the expression of adhesion molecules in neutrophil.

Mesenteric venous thrombosis with bowel infarction and hyperhomocysteinemia due to homozygous methylenetetrahydrofolate reductase C677T genotype.

The case of a 30-year-old man with bowel infarction due to mesenteric venous thrombosis and multiple risk factors, including mild hyperhomocysteinemia due to methylenetetrahydrofolate reductase C677T polymorphism and recent abdominal surgery, is reported. His clinical manifestation consisted of persistent abdominal pain; complementary examinations showed nonspecific findings such as leukocytosis and dilated loops of the bowel. The diagnosis of mesenteric venous thrombosis with bowel infarction was made during laparotomy and confirmed by anatomopathologic examination. He underwent segmental resection associated with lifelong anticoagulant therapy and vitamin B supplementation with a favorable course.

Time-dependent alterations in serum NO concentration after oral administration of L-arginine, L-NAME, and allopurinol in intestinal ischemia/reperfusion.

OBJECTIVE: To study the effect of oral administration of a nitric oxide (NO) donor L-arginine (L-Arg), a NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and an inhibitor of xanthine oxidase, allopurinol (Allo), on serum NO concentration and catalase activity after intestinal ischemia/reperfusion (I/R) in rats. METHODS: Male Wistar rats receivedper os L-Arg (800 mg/kg) or L-NAME (50 mg/kg) or Allo (100 mg/kg) 24 hrs, 12 hrs and 1 hr before underwent 1 hr occlusion of superior mesenteric artery followed by 1 hr of reperfusion (L-Arg(IR1), L-NAME(IR1) and Allo(IR1) respectively) or 1 hr occlusion followed by 8 hrs of reperfusion (L-Arg(IR8), L-NAME(IR8) and Allo(IR8) respectively). There was one group underwent 1 hr occlusion (I), a group underwent 1 hr occlusion followed by 1 hr reperfusion (IR1), a group subjected to 1 hr occlusion followed by 8 hrs of reperfusion (IR8) and a last group that served as control (C). Serum NO concentration and catalase activity were measured. RESULTS: After 1 hr of reperfusion serum NO concentration was elevated in IR1 and L-Arg(IR1) groups compared with group C but not in L-NAME(IR1) and Allo(IR1) group. Catalase activity was enhanced in L-NAME(IR1) group. Interestingly, serum NO concentration was increased after 8 hrs of reperfusion in all groups (IR8, L-Arg(IR8), L-NAME(IR8) and Allo(IR8)) compared with control while catalase activity did not show significant difference in any group. CONCLUSIONS: The results of the present study show that NO concentration is elevated in serum after intestinal I/R and the elevation sustained after administration of L-Arg but not after administration of L-NAME or Allo after 1 hr reperfusion. However, after 8 hrs of reperfusion NO concentration was increased in all groups studied, focusing attention on its possible important role in a complicated situation such as intestinal I/R that involves intestine and other organs. Serum catalase activity does not seem to be affected by per os supplementation of L-Arg or Allo in intestinal I/R.

Antioxidant activity of a novel extract from bamboo grass (AHSS) against ischemia-reperfusion injury in rat small intestine.

Production of free radical species in cells and body tissues is known to cause many pathological disorders. Therefore, free radical scavengers play an important role in the prevention of various human diseases. Bamboo grass, Sasa senanensis, is a native Japanese plant. Sasa has been used for medicine in Japan for many centuries. In this study, we investigated the antioxidative activity of Absolutely Hemicellulose Senanensis (AHSS), a novel extract from Sasa. In the first part of this study, we found that AHSS has antioxidant activities by the assay using superoxide anion-2-methyl-6-methoxyphenylethynylimidazopyrazynone (MPEC) reaction kit. We then confirmed its antioxidative activity using a rat ischemia and subsequent reperfusion (I/R) injury model. Breakdown of the intestinal wall caused by intestinal I/R was attenuated by pretreatment with AHSS. Moreover, AHSS inhibited the production of lipid peroxide by intestinal I/R. AHSS could be an important source of ingredients for use in functional foods and other applications.