Is SARS-CoV-2 infection an emerging risk factor for splanchnic venous thrombosis?

OBJECTIVE: Thrombosis represents one of the most feared complications of the COronaVIrus Disease-2019 (COVID-19). Although pulmonary embolism and deep venous thrombosis are the most described complications, some investigations reported thrombotic localization also in the splanchnic venous district. METHODS: We describe the case of a patient with SARS-CoV-2 infection presenting with abdominal pain and diagnosed with portal vein thrombosis. In addition, we shortly review available literature supporting the possible role of COVID-19 as leading cause of splanchnic venous thrombosis. RESULTS: After in-depth diagnostic workup, we excluded the commonest causes of portal thrombosis and concluded that SARS-CoV-2 infection represented the main explanation of this finding. CONCLUSIONS: Our study warns the clinicians to maintain a high index of suspicion for thrombosis in patients diagnosed with SARS-CoV-2 infection manifesting gastrointestinal symptoms. An appropriate diagnostic work-up could allow to obtain an early diagnosis and consequently improve the clinical outcome of patients.

Serum C3 is a stronger inflammatory marker of insulin resistance than C-reactive protein, leukocyte count, and erythrocyte sedimentation rate: comparison study in an elderly population.

OBJECTIVE: This study was performed to ascertain the relative relevance of some inflammatory markers in insulin resistance. RESEARCH DESIGN AND METHODS: Four inflammatory markers (leukocyte count, erythrocyte sedimentation rate [ESR], high-sensitivity C-reactive protein [CRP], and C3 complement) were assessed as possible determinants of the homeostasis model assessment (HOMA) index, together with the five elements of the metabolic syndrome (National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults [Adult Treatment Panel III] definition), total cholesterol, physical activity, and four indicators of adiposity (BMI, waist circumference, percent body fat, and hepatic steatosis) in an unselected population of 990 subjects aged 65-91 years (the Pianoro Study). RESULTS: In univariable analysis, C3, CRP, and leukocyte count, but not ESR, were significantly correlated with HOMA index. In multivariable analysis, C3 remained associated with insulin resistance with the highest partial R(2) value (0.049), independently of all other covariates. The other most significant (P < 0.0001) determinants of HOMA index were total cholesterol (inverse association, R(2) = 0.026), waist circumference (R(2) = 0.023), triglycerides (R(2) = 0.022), and hepatic steatosis (R(2) = 0.021) (R(2) = 0.450 for the whole model). The adjusted relative risks of having the metabolic syndrome for the subjects with inflammatory markers in the high tertile, with respect to those with lower values, were (prevalence ratio [95% CI]): 1.77 (1.41-2.22) for C3, 1.38 (1.12-1.70) for leukocyte count, 1.17 (0.94-1.46) for CRP, and 1.13 (0.91-1.40) for ESR. CONCLUSIONS: Of the four inflammatory markers simultaneously assessed in our elderly population, only C3 was strongly associated with insulin resistance, independently of the components of the metabolic syndrome and the main indexes of abdominal and general obesity.

Postprandial splanchnic haemodynamic changes in patients with liver cirrhosis and patent paraumbilical vein.

OBJECTIVE: The haemodynamic changes induced by a meal on collateral vessels in portal hypertensive cirrhotic patients are not well characterized. We aimed to study the postprandial modifications of splanchnic circulation in patients with a patent paraumbilical vein (PUV). METHODS: We studied 10 cirrhotic patients with patent PUV and 10 matched cirrhotic patients without PUV, by using echo colour Doppler at baseline and 15, 30 and 45 min after a standard mixed liquid meal (400 ml; 600 kcal). Calibre and blood flow velocities of the superior mesenteric artery, portal vein and PUV were obtained; congestion index of portal vein, portal blood flow, paraumbilical blood flow and effective portal liver perfusion were calculated; intrahepatic and intrasplenic arterial resistance and pulsatility indexes were recorded. RESULTS: We observed a postprandial splanchnic hyperaemia (superior mesenteric artery and portal vein blood flow increased after the meal in both groups; ANOVA P < 0.05), with no changes of hepatic impedance. In PUV patients, PUV constricted significantly postprandially, maximally at 30 min (calibre -17.5 +/- 7.0%; P = 0.003). Intrasplenic impedance, which may reflect portal pressure, increased, maximally at 30 min (pulsatility index +22.6 +/- 27.0%; P = 0.01), and inversely correlated with PUV vasoconstriction (R = 0.75, P = 0.01). In non-PUV patients intrasplenic impedance did not change. Portal liver perfusion increased similarly in both groups. CONCLUSIONS: PUV constricts after the meal, and this vasoconstriction is associated with an increase of splenic impedance which may indicate the postprandial increase of portal pressure observed in cirrhosis. The increase in postprandial portal liver perfusion in the PUV group is allowed by a paradox constriction of the collateral vessel.