Objective: The aim of this study was to determine the associations of the neutrophil–lymphocyte ratio (NLR) and C-reactive protein (CRP)–albumin ratio (CAR) with the duration of hospital stay and fatality rate in geriatric patients with coronavirus disease 2019 (COVID-19). Methods: Patients older than 65 years with polymerase chain reaction-positive COVID-19 were included. Neutrophil, lymphocyte, CRP, albumin, and demographic data and the duration of hospitalization were recorded. Results: The mean length of stay was 15 days. NLR and CAR were significantly higher in patients who died than in those who survived. The cutoffs predictive of mortality were 4.02 (area under the curve [AUC] = 0.717) for NLR and 23 for CAR (AUC = 0.781). The fatality rate among patients who required inpatient treatment was 33%. Conclusion: NLR and CAR, which can be calculated inexpensively and quickly at the first admission to the hospital, are extremely useful for estimating the duration of hospitalization and risk of mortality in geriatric patients with COVID-19. Using these data, treatment can quickly be intensified when needed.

Chanarin Dorfman syndrome is a multisystem, very rare, autosomal recessive lipid storage disorder, characterized by the accumulation of lipid vacuoles in neutrophils, and was first described by Dorfman in 1974. Due to a mutation in the ABHD5 gene of the short arm of chromosome 3, lipid is stored in the granulocytes at various sites in the human body, such as the muscle, liver, eye, ear, central nervous system, and bone marrow. Clinically, the disease is presented with ichthyosis, hearing loss, hepatomegaly, splenomegaly, cirrhosis, cataract, keratopathy, myopathy, and mental retardation. A 38-year-old male patient was referred to our Internal Medicine Clinic for consultation with laboratory findings as follows: high aspartate aminotransferase (AST; 203 U/L), alanine aminotransferase (ALT; 151 U/L), gamma-glutamyl transferase (GGT; 167 U/L), creatine kinase (CK; 1127 U/L) levels and low platelet levels (108000). After ultrasonography and gastroscopy, the patient was diagnosed with liver cirrhosis. Bilateral mixed-type hearing loss on audial tests and bilateral punctuate keratopathy, ectropion, and cataract in the left eye on ophthalmological tests were found. For the definitive diagnosis of Chanarin Dorfman syndrome, peripheral blood was examined, which revealed lipid accumulation in the neutrophils (Jordan’s anomaly). We emphasize that if a patient has unusual findings, such as ichthyosis, hearing loss, hepatomegaly, splenomegaly, cirrhosis, cataract, keratopathy, myopathy, and mental retardation, the possibility of Chanarin Dorfman syndrome should be considered. Cite this article as: Kalyon S, Gökden Y, Demirel N, Erden B, Türkyılmaz A. Chanarin-Dorfman syndrome. Turk J Gastroenterol 2019; 30: 105-8.

Background: Much research has demonstrated that there is a relation between depression and chronic diseases. Type 2 diabetes mellitus (T2DM) is one of the most common chronic diseases, and it is an expanding global health problem. This study aims to explore the relationship between glycemic control (GC), antidiabetic agents, and depression in T2DM, focusing on how depression affects treatment adherence and GC. Methods: This prospective study included 250 patients with T2DM. Demographic information and laboratory results were obtained from the patients as well as from the hospital’s laboratory system. Beck’s Depression Inventory (BDI) scores, GC indicator HbA1c levels, and antidiabetic agents used by the patients were compared. Results: Upon analyzing the findings, we found a statistically significant positive correlation between the severity of depression and HbA1c levels (p < 0.001). Additionally, no significant relationship was observed between depression and the use of oral antidiabetic medications, except for metformin. However, a significant association between depression and insulin use was found even in patients with good GC (p < 0.001), regardless of whether HbA1c was high. Conclusions: Regardless of the type of antidiabetic treatment, diabetic patients receiving intensive insulin therapy, whether they have good or poor GC, should be carefully evaluated for depressive symptoms. Appropriate psychiatric support should be provided to help achieve GC and enhance their quality of life. Our study is the first to emphasize the importance of close monitoring for diabetic patients using insulin, even those with good GC. Understanding these interactions may improve disease management, patient outcomes, and quality of life.

Apelin is a peptide known for its insulin-sensitizing effect. This study aimed to examine the relationship between apelin and fatty liver disease. Non-diabetic patients were evaluated by ultrasound in this prospective, single-center, case-control study between 1 April 2020 and 1 April 2021. Serum apelin levels were measured, and the relationship with ultrasonography results and degree of hepatosteatosis was examined. Statistical analysis was carried out using NCSS 2007. This study was conducted with 80 non-diabetic participants, 53 females and 27 males. The mean age of the cases was 40.55 ± 13.82 (interquartile range = 27–51) years, and their mean body mass index (BMI) was 29.34 ± 7.44 (interquartile range = 23.4–35.2) kg/m². There was no hepatosteatosis according to ultrasound in 42% (n = 34) of the cases. When patients with or without hepatosteatosis were compared, there was no difference in terms of gender, alanine aminotransferase (ALT), and hemoglobin levels, whereas fasting blood glucose (FBG), HOMA-IR, triglycerides, LDL-cholesterol, BMI, creatinine, and age were higher in the group with hepatosteatosis. Apelin was found to be lower in patients with non-diabetic hepatosteatosis than in those without hepatosteatosis ( p = .001). As the degree of fatty liver increased, the apelin level decreased further. There was also a negative correlation between apelin and age. However, the relationship between apelin and hepatosteatosis was independent of age. In non-diabetic patients with fatty liver disease, compared to those without fatty liver disease, serum apelin level was lower and was negatively correlated with the degree of steatosis, independent of age.

Aim: Pentraxin 3 is a molecule that is known to show inflammation, however few studies with contradictory results have been conducted in current literature in Inflammatory Bowel Disease patients regarding PTX3. We aimed to investigate whether PTX3 can be used in the discrimination of Crohn’s disese and Ulcerative colitis patients and whether there is a correlation of PTX3 with disease activity, involved intestinal segments and their length. Method: Ethical committee approval was obtained for this a prospective, single-centered, single-blind study. IBD patients who were older than 18 years old, without pregnancy, malignancy, acute/chronic infections or inflammatory diseases were included. Healthy volunteers were included in study as a control group. PTX3 levels were measured in the blood. Shapiro-Wilk, Mann-Whitney U, Kruskal Wallis, Bonferroni-Dunn, Spearman tests were used with NCSS 2007 program. Results: The median age of the 56 male and 42 female participants was 37 years (25 CD, 43 UK and 30 controls). In the UK group, PTX3, which did not have relationship with the Trulove Witts score or the Mayo score; was a statistically significant higher in patients with pancolitis. There was no relationship between PTX3 levels and involvement, behavior pattern, CDAI scores and activity of the disease in CD group. Conclusion:PTX3 is not an appropriate biomarker for monitoring the activation of İBD and it can’t distinguish two subtypes from eachother. PTX3 is insufficient to indicate both the behavior pattern and the location of involvement in CD patients. Only, until the control endoscopy times of the patients with UK, it can be monitored whether the disease affects the entire colon by following the PTX3 levels in the interim period. '+st+' Chen J, Xu X, Xia L, Xi X, Liu B, Yang M. Serum pentraxin 3 is a novel marker in Crohn’s disease. Mol Med Rep. 2015 Jul;12(1):543-6. doi:10.3892/mmr.2015.3451. Epub 2015 Mar 6. Muthas D, Reznichenko A, Balendran CA, Böttcher G, Clausen IG, Kärrman Mårdh C, et al. Neutrophils in ulcerative colitis: a review of selected biomarkers and their potential therapeutic implications. Scand J Gastroenterol. 2017 Feb;52(2):125-135. doi: 10.1080/00365521.2016.1235224. Epub 2016 Sep 27. Leitner GC, Vogelsang H. Pharmacological- and non-pharmacological therapeutic approaches in inflammatory bowel disease in adults. World J Gastrointest Pharmacol Ther. 2016;7(1):5-20. Burisch J, Munkholm P. The epidemiology of inflammatory bowel disease. Scand J Gastroenterol. 2015;50(8):942-51. Klouche M, Peri G, Knabbe C, Eckstein HH, Schmid FX, Schmitz G, at al. Modified atherogenic lipoproteins induce expression of pentraxin 3 by human vascular smooth muscle cells. Atherosclerosis 175: 221 228, 2004. Fazzini F, Peri G, Doni A, Dell'Antonio G, Cin ED, Bozzolo E, et al. PTX3 in small vessel vascu¬litides: an independent indicator of disease activity produced at sites of inflammation. Arthritis Rheum 44: 2841 2850, 2001. Baldini M, Maugeri N, Ramirez GA, Giacomassi C, Castiglioni A, Gonzalez SP, et al. Selective up regu¬lation of the soluble pattern recognition receptor pentraxin 3 and of vascular endothelial growth factor in giant cell arteritis: relevance for recent optic nerve ischemia. Arthritis Rheum 64: 854 865, 2012. Kato S, Ochiai M, Sakurada T, Ohno S, Miyamoto K, Sagara M, et al. Increased expression of long pentraxin PTX3 in inflammatory bowel diseases. Dig Dis Sci. 2008;53(7):1910-6. Savchenko AS, Inoue A, Ohashi R, Jiang S, Hasegawa G, Tanaka T, et al. Long pentraxin 3 (PTX3) expression and release by neutrophils in vitro and in ulcerative colitis. Pathol Int. 2011 May;61(5):290-7. doi: 10.1111/j.1440-1827.2011.02651.x. Epub 2011 Mar 17. Kato S, Ochiai M, Sakurada T, Ohno S, Miyamoto K, Sagara M, et al. Increased Expression of Long Pentraxin PTX3 in Inflammatory Bowel Diseases. Dig Dis Sci. 2008 Jul;53(7):1910-6. Epub 2007 Nov 8. Copyright (c) 2020 Semih Kalyon, Yasemin Gökden, Fırat Oyman This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.