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Introduction The most typical presentation of COVID-19 is an acute respiratory syndrome whose most common symptoms include fever, cough, and dyspnea. However, gastrointestinal symptoms, such as diarrhea and nausea/vomiting, are increasingly reported in patients affected by COVID-19. This study aimed to describe the prevalence and time of onset of gastrointestinal symptoms in patients affected by COVID-19 and to find potential associations between gastrointestinal symptoms and clinical outcomes. Methods We performed a prospective single-center cohort study, enrolling patients who received diagnosis of COVID-19 at our institution between March 23, 2020, and April 5, 2020. We collected patient demographics and medical history, laboratory data, and clinical outcomes. Furthermore, we used a specifically designed questionnaire, administered to patients at time of diagnosis, to obtain data on the presence and time of onset of fever, typical respiratory symptoms, gastrointestinal symptoms, and other symptoms (fatigue, headache, myalgia/arthralgia, anosmia, ageusia/dysgeusia, sore throat, and ocular symptoms). Results In our cohort, 138 (69%) of 190 patients showed at least 1 gastrointestinal symptom at diagnosis; if excluding hyporexia/anorexia, 93 patients (48.9%) showed at least 1 gastrointestinal symptom. Gastrointestinal symptoms, in particular diarrhea, were associated with a lower mortality. At multivariate analysis, diarrhea was confirmed as independent predictive factor of lower mortality. Discussion Gastrointestinal symptoms are very frequent in patients with COVID-19 and may be associated with a better prognosis. These data suggest that, in some patients, the gastrointestinal tract may be more involved than the respiratory system in severe acute respiratory syndrome coronavirus 2 infection, and this could account for the less severe course of disease.

Pancreatic polypeptide (PP) islet cell tumors are usually not associated with a distinct clinical syndrome, although some reports suggest that they can cause a watery diarrhea syndrome similar to vasoactive intestinal polypeptide (VIP) cell tumors. We report the case of a young woman with an unusual presentation of a pancreatic neuroendocrine tumor mainly secreting PP. The patient developed a reversible hypokalemic rhabdomyolysis very likely secondary to the presence of the tumor. The myopathy resolved following the restoration of normokaliemia using potassium supplementation and a partial laparoscopic pancreasectomy. Isolated cases of hypokalemic rhabdomyolysis induced by intestinal diseases have been described in literature but these did not include gastroenteropancreatic neoplasms. We suggest that pancreatic neuroendocrine tumors should be added to the list of intestinal diseases capable of producing hypokalemic myopathy.

OBJECTIVES: Hypofibrinolysis has been proposed as a possible mechanism underlying the known risk of thrombosis observed in patients with inflammatory bowel diseases (IBD). Thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently described inhibitor of fibrinolysis. Increased TAR plasma levels are associated with a risk for venous thrombosis. The objective was to evaluate TAR plasma levels and their possible correlations with clinical features and acute-phase reactants in IBD patients. METHODS: Eighty-one IBD patients (47 Crohn's disease and 34 ulcerative colitis) and 81 sex- and age-matched healthy controls were enrolled in the study; moreover, we studied 30 inflammatory controls (13 Reiter's syndrome, 4 Behget's syndrome, and 13 patients with newly diagnosed celiac disease). TAR plasma levels were assessed by means of a commercially available ELISA kit. Erythrocytes sedimentation rate, C-reactive protein, and alpha1-acid glycoprotein were measured as acute-phase reactants. Statistical analysis was performed by means of nonparametric tests and Fisher's exact test and chi(2) test for independence. RESULTS: Median TAR plasma levels were significantly higher in IBD patients (116.0%, range: 39.0-232.0%) and in inflammatory controls (176.0%, 50.0-435.0%) than in healthy controls (99.0%, 40.0-170.0%) (p < 0.05 and p < 0.001, respectively). TAR plasma levels higher than the 95th percentile of control values were significantly more frequent in IBD patients (19.7%) and in inflammatory controls (53.3%) than in healthy controls (4.9%) (p < 0.008 and p < 0.0001, respectively) and more frequent in clinically active IBD than in clinically quiescent IBD (31.4% vs 10.9%, p < 0.03). Finally, in IBD, significant correlations were observed between TAR plasma levels and erythrocytes sedimentation rate (p < 0.02), C-reactive protein (p < 0.001), and a1-acid glycoprotein (p < 0.05). CONCLUSIONS: TAR plasma levels are increased in IBD patients and correlate with acute-phase reactants. Increased TAR plasma levels might contribute to the prothrombotic state observed in IBD through the induction of hypofibrinolysis.

OBJECTIVE: Little is known about the clinical features and natural history of segmental colitis associated with diverticula. Our aim was to evaluate the incidence of segmental colitis associated with diverticula in patients undergoing colonoscopy, its clinical picture, and its outcome. METHODS: This was a multicenter, prospective study. Patients with inflammatory bowel disease (IBD)-like lesions limited to colonic segments with diverticula were enrolled. Patients were treated with oral and topical 5-aminosalicylic (5-ASA) until remission was achieved; clinical and endoscopic follow-up was planned at 6 wk and 12 months. RESULTS: A total of 5457 consecutive colonoscopies were recorded at five participating institutions; 20 patients (0.36%) met the endoscopic criteria for segmental colitis associated with diverticula. All had lesions in the left colon, and one also had lesions in the right colon. In six cases, a specific diagnosis was made thereafter. The remaining 14 patients (0.25% of colonoscopies; eight men; age range, 49-80 yr) were in clinical and endoscopic remission at the first follow-up visit. At onset, 13/14 had hematochezia, seven had diarrhea, and five had abdominal pain; only one had weight loss. No subject had fever. In all but one case, blood chemistries were normal. Five patients had had similar symptoms previously. Thirteen of 14 patients were in clinical and endoscopic remission at 12 months. CONCLUSIONS: This endoscopic picture is not an exceptional finding. Hematochezia was the main clinical feature, and no relation with gender, age, or smoking habit was found. Blood chemistries were generally normal and the rectum was spared. The histological features were not diagnostic and most patients did not complain of any abdominal symptoms 12 months after enrollment.

Inflammation and coagulation play crucial roles in the pathogenesis of multiple chronic inflammatory disorders. Growing evidence highlights a tight mutual network in which inflammation, coagulation, and fibrinolysis play closely related roles. Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel disease (IBD), are chronic inflammatory conditions, characterized by a hypercoagulable state and prothrombotic conditions, and accompanied by abnormalities in coagulation. From a pathophysiological point of view, cells and molecules classically implicated in the physiological process of coagulation have now been shown to behave abnormally in IBD and possibly to also play an active role in disease pathogenesis and/or disease progression. This paper reviews studies performed on the coagulation profile and risk factors for thrombosis in IBD. In particular, an overview is provided of the epidemiology, clinical features, and etiology of thromboembolic complications in IBD. Furthermore, we review hemostatic abnormalities in IBD, as well as the cell types involved in such processes. Finally, we highlight the coagulation system as a dynamic participant in the multifaceted process of chronic intestinal inflammation. Overall, an overview is provided that the coagulation system represents an important, though previously underestimated, component of IBD pathogenesis, and may be a possible target for therapeutic intervention. Inflammation and coagulation play crucial roles in the pathogenesis of multiple chronic inflammatory disorders. Growing evidence highlights a tight mutual network in which inflammation, coagulation, and fibrinolysis play closely related roles. Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel disease (IBD), are chronic inflammatory conditions, characterized by a hypercoagulable state and prothrombotic conditions, and accompanied by abnormalities in coagulation. From a pathophysiological point of view, cells and molecules classically implicated in the physiological process of coagulation have now been shown to behave abnormally in IBD and possibly to also play an active role in disease pathogenesis and/or disease progression. This paper reviews studies performed on the coagulation profile and risk factors for thrombosis in IBD. In particular, an overview is provided of the epidemiology, clinical features, and etiology of thromboembolic complications in IBD. Furthermore, we review hemostatic abnormalities in IBD, as well as the cell types involved in such processes. Finally, we highlight the coagulation system as a dynamic participant in the multifaceted process of chronic intestinal inflammation. Overall, an overview is provided that the coagulation system represents an important, though previously underestimated, component of IBD pathogenesis, and may be a possible target for therapeutic intervention.

BACKGROUND: Inflammatory bowel diseases (IBD) are characterized by an increased risk for venous and arterial thrombosis. Although the pathogenetic mechanisms of this predisposition are unclear, a possible role of inherited risk factors for thrombosis in determining this predisposition has been suggested. AIM: To evaluate the role of factor V Leiden (G1691A) and G20210A prothrombin gene mutations in determining the occurrence of thrombosis in IBD patients. PATIENTS AND Forty-seven IBD patients (30 ulcerative colitis and 17 Crohn's disease) with a positive history for METHODS: thrombosis (9 at arterial sites and 38 at venous sites) were enrolled in the study. For each patient, two non-IBD subjects matched for sex and age, type, and site of thrombosis were used as controls. Peripheral blood DNA specimens were amplified by PCR using appropriate primers and analyzed by restriction analysis on agarose gel electrophoresis. Statistical analysis was performed by means of Fisher's exact test. RESULTS: The total number of subjects with one or both mutations was significantly lower in IBD patients with thrombosis than in control subjects (12.8% vs 29.8%, respectively; p = 0.035, OR = 0.34, 95% Cl 0.13-0.90). The total frequency of the mutated alleles was also significantly lower in IBD than in controls (7.4% vs 16.5%, respectively; p = 0.041, OR = 0.40, 95% Cl 0.17-0.96). Prothrombotic mutations were particularly unfrequent in IBD patients with active disease at the time of thrombosis compared with patients with quiescent disease (8.0% vs 36.4%, respectively; p = 0.057, OR = 0.15, 95% Cl 0.02-1.01). CONCLUSIONS: The major inherited risk factors for thrombosis are significantly less frequent in thrombotic IBD patients than in thrombotic non-IBD subjects, suggesting that acquired risk factors play the most relevant role in determining thromboembollc events observed in IBD patients, particularly during active phases of the disease.

Individuals with inflammatory bowel disease (IBD) are at increased risk for thrombosis and vitamin deficiencies. Low plasma levels of vitamin B(6) are an independent risk factor for thrombosis and may cause hyperhomocysteinemia, another recognized risk factor for thrombosis. The aim of this study was to evaluate vitamin B(6) plasma levels in IBD patients.We studied 61 IBD patients: 32 with Crohn's disease and 29 with ulcerative colitis. For each patient, three sex- and age-matched healthy control subjects were studied.Median vitamin B(6) levels were significantly lower in IBD patients (22.0 pmol/L, range 3.6-231.0) than in controls (31.1 pmol/L, 3.7-363.4; p0.01). In all, 13.1% IBD patients and 5.5% controls had plasma vitamin B(6) levels lower than the 5th percentile of distribution in normal controls (p0.05). Low vitamin B(6) levels were significantly more frequent in patients with active disease than in patients with quiescent disease (seven of 26, 26.9%, vs one of 35, 2.9%; p0.001). Moreover, patients with active disease had significantly lower median vitamin B(6) levels (13.4 pmol/L, range 3.6-124.0) than patients in a quiescent phase (27.0 pmol/L, 7.8-231.0; p0.001). Low vitamin B(6) levels were significantly correlated with serum concentrations of C-reactive protein (r = -0.36, 95% CI = -0.59 to -0.09, p0.01) and alpha(1)-acid-glycoprotein (r = -0.37, 95% CI = -0.59 to -0.10, p0.01). Hyperhomocysteinemia was more frequent in patients with low vitamin B(6) levels (three of eight, 37.5%) than in patients with normal levels (nine of 53, 17.0%; p = 0.18). There was no statistically significant correlation between vitamin B(6) and homocysteine plasma levels (r = -0.13, 95% CI = -0.37 to +0.14, p = 0.33).Low vitamin B(6) plasma levels, an independent risk factor for thrombosis, are frequent in patients with IBD, especially those with active disease.

TO THE EDITOR: We are glad of the interest to our article (1) expressed in the letter by Koutroubakis and colleagues and we appreciate their comments. However, we do not agree with many of their considerations, which may result from a misunderstanding of our article. It is true that in our study we have shown that the prothrombotic factors are significantly less frequent in IBD than in controls when considered together. Indeed, when the number of patients who are carriers of one and/or the other factor was evaluated, a significantly lower prevalence of this condition was observed in IBD; we also feel that this finding is not due to the mixed types of thrombotic events enrolled in our study, as suggested by Koutroubakis, since this difference is even more significant when only patients with venous thrombosis are considered. We agree that the prevalence of factor V Leiden in our thrombotic IBD population is rather low, but we also know that the prevalence rate of this mutation is very variable in the previous papers on IBD and thrombosis, and that this variability is probably largely due to the small size of most reported series (2): in this direction, our study reports one of the largest thrombotic IBD groups in the literature. As far as the composition of the control population is concerned, our control group is the first to be carefully selected, being matched (in a proportion of 2:1) for sex, age, type, and site of thrombosis with the cases. We feel, indeed, that this is a relevant point of our study, since our findings may have resulted from the comparison of thrombotic IBD patients with equally young thrombotic subjects without IBD.