Severe and fatal COVID-19 is characterised by increased circulating glucagon like peptide 1 and procalcitonin modulated by type 2 diabetes.

AIMS: Endotoxemia commonly occurs in severe and fatal COVID-19, suggesting that concomitant bacterial stimuli may amplify the innate immune response induced by SARS-CoV-2. We previously demonstrated that the endogenous glucagon like peptide 1 (GLP-1) system in conjunction with increased procalcitonin (PCT) is hyperactivated in patients with severe Gram-negative sepsis and modulated by type 2 diabetes (T2D). We aimed to determine the association of COVID-19 severity with endogenous GLP-1 activation upregulated by increased specific pro-inflammatory innate immune response in patients with and without T2D. MATERIALS AND METHODS: Plasma levels of total GLP-1, IL-6, and PCT were estimated on admission and during hospitalisation in 61 patients (17 with T2D) with non-severe and severe COVID-19. RESULTS: COVID-19 patients demonstrated ten-fold increase of IL-6 levels regardless of disease severity. Increased admission GLP-1 levels (p = 0.03) accompanied by two-fold increased PCT were found in severe as compared with non-severe patients. Moreover, GLP-1 and PCT levels were significantly increased in non-survived as compared with survived patients at admission (p = 0.01 and p = 0.001, respectively) and at 5 to 6 days of hospitalisation (p = 0.05). Both non-diabetic and T2D patients demonstrated a positive correlation between GLP-1 and PCT response (r = 0.33, p = 0.03, and r = 0.54, p = 0.03, respectively), but the intensity of this joint pro-inflammatory/GLP-1 response was modulated by T2D. In addition, hypoxaemia down-regulated GLP-1 response only in T2D patients with bilateral lung damage. CONCLUSIONS: The persistent joint increase of endogenous GLP-1 and PCT in severe and fatal COVID-19 suggests a role of concomitant bacterial infection in disease exacerbation. Early elevation of endogenous GLP-1 may serve as a new biomarker of COVID-19 severity and fatal outcome.

[A RARE CASE OF RELAPSING GUILLAIN-BARRE SYNDROME PRESENTING AS BRAIN DEATH].

INTRODUCTION: Acute immune-mediated polyneuropathies classified as Guillain-Barre Syndrome (GBS) constitute a wide range of clinical manifestations characterized by ascending symmetrical limbs paralysis along with possible involvement of the respiratory muscles. Paralysis of facial and eye muscles including unresponsive pupils, which may mimic a brain death is rare, though previously described. This presentation is challenging because it masks the correct diagnosis and delays or prevents appropriate treatment. A 69-year-old female patient was hospitalized with progressive bilateral limb paralysis with involvement of the respiratory and facial muscles necessitating intubation. Plasmapheresis resulted in significant motor and respiratory improvement and the patient was sent for further rehabilitation. Six weeks later she was hospitalized again with complete muscle paralysis including involvement of the eye muscles and pupils. In the absence of ocular, corneal, and swallowing reflexes, a working diagnosis of brain death was initially made. However, a repeated and meticulous physical examination revealed that her consciousness was preserved. An EEG test showing brain activity ruled out brain death. EMG showed extensive axonal damage supporting the diagnosis of GBS. Repeated plasmapheresis failed to improve her condition but she had partially responded to treatment with immunoglobulins. Clinicians should be aware of those patients diagnosed as brain dead but who in fact suffer from another treatable disease that needs to be diagnosed.

Increased Incidence of Symptomatic Cholelithiasis After Bariatric Roux-En-Y Gastric Bypass and Previous Bariatric Surgery: a Single Center Experience.

BACKGROUND: Bariatric surgery predisposes patients to cholelithiasis and therefore the need of a subsequent cholecystectomy; however, the incidence of cholecystectomy after bariatric surgery is debated. AIM AND METHODS: Medical records of 601patients hospitalized for bariatric surgery between January 2010 and July 2018 were reviewed. Our aim was to evaluate the incidence of cholecystectomy following different types of common bariatric procedures. All patients who developed cholelithiasis and a subsequent cholecystectomy were included. Cholelithiasis was diagnosed by clinical criteria and characteristic ultrasound findings. RESULTS: We retrospectively evaluated 580 patients with an average follow-up of 12 months (range 6-24 months). Twenty-one patients were excluded because of missing data. Mean age was 48 ± 19 years (78% females). Twenty-nine patients (5%) underwent laparoscopic cholecystectomy (LC) before the bariatric surgery, and 58 patients (10%) performed concomitant LC with the bariatric procedure due to symptomatic gallstone disease (including stones, sludge, and polyps). There were 203 laparoscopic sleeve gastrectomy (SG) (35%), 175 laparoscopic gastric band (LAGB) (30%), 55 Roux-en-Y gastric bypass (RYGB) (9.5%), and 147 (25%) mini gastric bypass (MGB) procedures during the study period. At the follow-up period, 36 patients (6.2%) developed symptomatic cholelithiasis, while the most common clinical presentation was biliary colic. There was a significant difference between the type of the bariatric procedure and the incidence of symptomatic cholelithiasis after the operation. The incidence of symptomatic gallstone formation in patients who underwent RYGB was 14.5%. This was significantly higher comparing to 4.4% following SG, 4.1% following LAGB, and 7.5% following MGB (p = 0.04). We did not find any predictive risk factors including smoking; BMI at surgery; change in BMI; comorbidities such as diabetes, hyperlipidemia, hypertension, and COPD for gallstone formation; or a subsequent cholecystectomy. Interestingly we found that previous bariatric surgery was a risk factor for gallstone formation and cholecystectomy, 13/82 patients (15.8%) compared to 23/492 patients (4.6%) among those without previous bariatric operation (p < 0.001)]. CONCLUSION: Our data demonstrate that patients with previous bariatric surgery or patients planned for RYGB are at high risk to develop postoperative symptomatic gallbladder disease. Concomitant cholecystectomy during the bariatric procedure or alternatively UDCA treatment for at least for 6 months to avoid the high incidence of postoperative symptomatic gallstones should be considered in those asymptomatic patients.