Evaluating the effect of SARS-Cov-2 infection on prognosis and mortality in patients with acute pancreatitis.

INTRODUCTION: Acute pancreatitis (AP) is the leading cause of hospitalization among gastrointestinal disorders. The aim of our study is to compare the results between AP patients with and without COVID-19, and to reveal the effects of COVID-19 on the course, intensive care needs and mortality of AP patients. MATERIAL METHODS: This was a single-center, retrospective and observational study. Patients over 18 years of age, who were diagnosed with AP during the current pandemic. According to the RT-PCR test result, patients were divided into two groups: COVID-19 positive and COVID-19 negative. Gender, age, laboratory parameters, intensive care unit admission, length of hospital stay, severity and mortality of AP were compared between these two groups. RESULTS: We reviewed 562 patients presenting to the emergency department who were diagnosed with acute pancreatitis between 10.03.2020 and 31.12.2020 and included 189 patients in our study. Positive patients need for intensive care (7.23%) were higher compared to negative patients (0.94%). 32.53% of positive patients and 14.15% of negative patients had severe AP (p < 0.03). We established that being COVID-19 positive, CCI scores of ≥5, presence of COVID-19 compatible pneumonia on CT and BISAP scores had an effect on mortality (p < 0,05). CONCLUSION: The severity and mortality of AP increase in patients with both AP and COVID-19. This rate increases even more in the presence of COVID-19-associated pneumonia. We believe that new strategies should be developed for the follow-up and treatment of patients with both these conditions.

Effect of Changes in Intravascular Volume on Inferior Vena Cava and Aorta Diameters and the Caval/Aorta Index in Healthy Volunteers.

OBJECTIVES: Although inferior vena cava diameter (IVCD) measurement can be useful as a noninvasive method for monitoring the volume status, the benefit of abdominal aorta diameter (AAD) measurement is unclear. The purpose of this study was to determine the value of the combined use of the IVCD and AAD in blood loss monitoring. METHODS: This prospective observational study was conducted at the blood donor center of a training and research hospital. Standard blood donation criteria were followed during volunteer enrollment. Vital signs and ultrasound IVCD and AAD measurements were obtained before and after blood donation and after fluid resuscitation with 500 mL of 0.9% sodium chloride. Measurements before and after blood donation and after fluid resuscitation were compared by the paired t and Wilcoxon matched-pair tests. RESULTS: Thirty-nine volunteers were included in the study. With 500 mL of blood loss, percent changes in the shock index (SI; mean ± SD, 7% ± 6%), IVCD (6% ± 2%), and caval/aorta index (IVCD/AAD; 6.1% ± 3%) were similar and were higher (P < .001 for all parameters) than the changes in the pulse rate (3% ± 4%), AAD (0.5% ± 1.5%), systolic blood pressure (3% ± 4%), and diastolic blood pressure (2% ± 7%). Although IVCD and SI values changed significantly (P < .001 for both) after 500 mL of 0.9% sodium chloride resuscitation, no significant change was observed in the IVCD/AAD (P = .059). CONCLUSIONS: The IVCD/AAD, SI, and IVCD may have similar success rates in diagnosing early blood loss. Additionally, the SI and IVCD may be superior to the IVCD/AAD in bleeding patients requiring simultaneous fluid resuscitation.

Euglisemic diabetic ketoacidotic coma caused by dapagliflozin.

Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening acute complication of diabetes mellitus (DM). Sodium-glucose co-transporter-2(SGLT-2) inhibitors are new orally administered antihyperglycemic agents. These agents are related with rarely seen euglycemic diabetic ketoacidosis (eDKA) cases, which are difficult to diagnose in emergency department (ED) because of absence of an evident hyperglycemia and may result with potentially dangerous outcomes if missed. In this study, we present a clinical case of a patient, admitted to ED with altered mental status after SGLT2 inhibitor dapagliflozin administration.

The association of vitamin D deficiency with non-alcoholic fatty liver disease.

OBJECTIVE: Vitamin D deficiency has been related to diabetes, hypertension, hyperlipidemia and peripheral vascular disease. In this study, we aimed to investigate the role of vitamin D status in non-alcoholic fatty liver disease. METHODS: We included 211 consecutive subjects to examine the presence of non-alcoholic fatty liver disease. Of these subjects, 57 did not have non-alcoholic fatty liver disease and 154 had non-alcoholic fatty liver disease. RESULTS: The non-alcoholic fatty liver disease group had significantly higher fasting blood glucose (p = 0.005), uric acid (p = 0.001), aspartate aminotransferase (p<0.001), alanine aminotransferase (p<0.001), γ-glutamyltransferase (p<0.0001), alkaline phosphatase (p = 0.028), HbA1c (p<0.001), ferritin (p<0.001), insulin (p = 0.016), C-peptide (p = 0.001), HOMA-IR (p = 0.003), total cholesterol (p = 0.001), triglyceride (p = 0.001) and white blood cell (p = 0.04) levels. In contrast, the non-alcoholic fatty liver disease group had significantly lower 25(OH)D levels (12.3±8.9 ng/dl, p<0.001) compared with those of the control group (20±13.6 ng/dl). CONCLUSIONS: In this study, we found lower serum 25(OH)D levels in patients with non-alcoholic fatty liver disease than in subjects without non-alcoholic fatty liver disease. To establish causality between vitamin D and non-alcoholic fatty liver disease, further interventional studies with a long-term follow-up are needed.

The association of vitamin D deficiency with non-alcoholic fatty liver disease

OBJECTIVE: Vitamin D deficiency has been related to diabetes, hypertension, hyperlipidemia and peripheral vascular disease. In this study, we aimed to investigate the role of vitamin D status in non-alcoholic fatty liver disease. METHODS: We included 211 consecutive subjects to examine the presence of non-alcoholic fatty liver disease. Of these subjects, 57 did not have non-alcoholic fatty liver disease and 154 had non-alcoholic fatty liver disease. RESULTS: The non-alcoholic fatty liver disease group had significantly higher fasting blood glucose (p = 0.005), uric acid (p = 0.001), aspartate aminotransferase (p<0.001), alanine aminotransferase (p<0.001), γ-glutamyltransferase (p<0.0001), alkaline phosphatase (p = 0.028), HbA1c (p<0.001), ferritin (p<0.001), insulin (p = 0.016), C-peptide (p = 0.001), HOMA-IR (p = 0.003), total cholesterol (p = 0.001), triglyceride (p = 0.001) and white blood cell (p = 0.04) levels. In contrast, the non-alcoholic fatty liver disease group had significantly lower 25(OH)D levels (12.3±8.9 ng/dl, p<0.001) compared with those of the control group (20±13.6 ng/dl). CONCLUSIONS: In this study, we found lower serum 25(OH)D levels in patients with non-alcoholic fatty liver disease than in subjects without non-alcoholic fatty liver disease. To establish causality between vitamin D and non-alcoholic fatty liver disease, further interventional studies with a long-term follow-up are needed. .

Role of endogenous cortisol on Helicobacter pylori colonization.

BACKGROUND AND AIMS: Helicobacter pylori infects the gastric mucosa and can lead to chronic gastritis, gastric ulcer and gastric cancer. Colonization of H. pylori in the gastric mucosa is influenced by a variety of host, bacterial and environmental factors. Host defense mechanisms have been affected by endogenous glucocorticoids. We aimed to investigate the relationship between H. pylori and endogenous glucocorticoid. MATERIALS AND METHODS: Forty cases with endoscopically and histologically proven H. pylori and 26 patients who did not have H. pylori on gastric biopsy samples were enrolled in our study. Cortisol was tested from 24-h collected urine samples. RESULTS: H. pylori (+) and H. pylori (-) groups consisted of 40 (28 women, 12 men; aged 44.85+/-12.52 years) and 26 (22 women, 4 men; aged 52.27+/-15.15 years) patients, respectively. Age and gender were similar in both groups. Body mass index, C-reactive protein and erythrocyte sedimentation rate were not statistically different between the two groups (p>0.05). 24-h urine cortisol amount was lower in patients with H. pylori (+) than H. pylori (-) cases. CONCLUSIONS: Present study demonstrates that patients with gastric H. pylori colonization have significantly lower cortisol levels when compared with H. pylori negative cases. There is a negative correlation between H. pylori colonization and urine cortisol output.