Identifying Clinical Characteristics of Hypoparathyroidism in Turkey: HIPOPARATURK-NET Study.

Hypoparathyroidism is an orphan disease with ill-defined epidemiology that is subject to geographic variability. We conducted this study to assess the demographics, etiologic distribution, treatment patterns and complication frequency of patients with chronic hypoparathyroidism in Turkey. This is a retrospective, cross-sectional database study, with collaboration of 30 endocrinology centers located in 20 cities across seven geographical regions of Turkey. A total of 830 adults (mean age 49.6 ± 13.5 years; female 81.2%) with hypoparathyroidism (mean duration 9.7 ± 9.0 years) were included in the final analysis. Hypoparathyroidism was predominantly surgery-induced (n = 686, 82.6%). The insulting surgeries was carried out mostly due to benign causes in postsurgical group (SG) (n = 504, 73.5%) while patients in nonsurgical group (NSG) was most frequently classified as idiopathic (n = 103, 71.5%). The treatment was highly dependent on calcium salts (n = 771, 92.9%), calcitriol (n = 786, 94.7%) and to a lower extent cholecalciferol use (n = 635, 76.5%) while the rate of parathyroid hormone (n = 2, 0.2%) use was low. Serum calcium levels were most frequently kept in the normal range (sCa 8.5-10.5 mg/dL, n = 383, 46.1%) which might be higher than desired for this patient group. NSG had a lower mean plasma PTH concentration (6.42 ± 5.53 vs. 9.09 ± 7.08 ng/l, p < 0.0001), higher daily intake of elementary calcium (2038 ± 1214 vs. 1846 ± 1355 mg/day, p = 0.0193) and calcitriol (0.78 ± 0.39 vs. 0.69 ± 0.38 mcg/day, p = 0.0057), a higher rate of chronic renal disease (9.7% vs. 3.6%, p = 0.0017), epilepsy (6.3% vs. 1.6%, p = 0.0009), intracranial calcifications (11.8% vs. 7.3%, p < 0.0001) and cataracts (22.2% vs. 13.7%, p = 0.0096) compared to SG. In conclusion, postsurgical hypoparathyroidism is the dominant etiology of hypoparathyroidism in Turkey while the nonsurgical patients have a higher disease burden with greater need for medications and increased risk of complications than the postsurgical patients.

Interleukin 18, soluble cluster of differentiation 40, platelet factor 4 variant 1, and neutrophil gelatinase-associated lipocalin can be used as biomarkers to aid activity and diagnosis in ocular Behçet's disease.

PURPOSE: The molecules human interleukin (IL-18), the soluble cluster of differentiation (sCD40), platelet factor 4 variant 1 (PF4V1), and neutrophil gelatinase-associated lipocalin (NGAL) are all markers of inflammation in biological systems and are linked to prognosis in several inflammatory diseases as well. Since there is no study in which the above-mentioned molecules are studied together in ocular Behçet's disease (OBD), the aim of this study is to reveal whether these molecules are activity markers in active (OABD) and inactive (OIBD) disease. METHODS: 30 OABD and 30 OIBD and 30 healthy individuals were included in the study. IL-18, sCD40, PF4V1, and NGAL molecules were studied in blood samples by the ELISA method. RESULTS: When OABD and OIBD were compared to healthy individuals, the levels of IL-18, sCD40, PF4V1, and NGAL molecules were found to be statistically significant. These values were even more significantly higher in patients with OABD. CONCLUSION: When ROC values of IL-18, sCD40, PF4V1, and NGAL are evaluated, it is clear that these four molecules can be used as biomarkers to aid activity and diagnosis in OBD.

Subfatin and asprosin, two new metabolic players of polycystic ovary syndrome.

Asprosin and subfatin are recently discovered two new hormones of adipocyte origin that play a role in the regulation of glucose metabolism. Polycystic ovary syndrome (PCOS) is a gynaecological syndrome presenting with energy turbulence. The aim of this study was to investigate whether asprosin and subfatin play a role in PCOS disease. Thirty participants with a diagnosis of PCOS and thirty control group participants were included in this case-control study. Hormone profiles of the participants (subfatin, asprosin, insulin, prolactin, thyroid-stimulating hormone (TSH), oestradiol (E2), follicle-stimulating hormone (FSH), luteinising hormone (LH), dehydroepiandrosterone sulphate (DHEA-SO4), lipid profiles [(total testosterone, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride, cholesterol)], fasting blood sugar (FBS) and high-sensitivity C-reactive protein (hs-CRP) values were measured. While the levels of asprosin, LDL and triglyceride, TSH, E2, FSH, LH, DHEA-SO4 were found to be significantly higher in patients with PCOS compared to controls (p = .005; p = .01), subfatin and HDL levels were found to be low. Significantly decreasing subfatin and increasing asprosin levels in circulation in PCOS may play a role in the etiopathology of this disease and that they may also be new candidate molecules in addition to classical laboratory parameters in the diagnosis and follow-up of PCOS in the future.Impact statementWhat is already known on this subject? The studies investigating the relationship between PCOS and asprosin are contradictory. Although subfatin has been studied in many metabolic diseases, it has not been studied yet whether it is associated with PCOS. Furthermore, whether there is a mutual relationship between subfatin and asprosin in patients with PCOS has not been studied yet.What do the results of this study add? This available data indicates that significantly decreasing subfatin and increasing asprosin levels in the circulation in PCOS may play a role in the etiopathology of this disease.What are the implications of these findings for clinical practice and/or further research? The findings are promising in that decreasing subfatin and increasing asprosin levels will shed new light on reproductive endocrinology changes caused by PCOS and may help to clarify the pathophysiology of PCOS. Furthermore, in our study, the asprosin/subfatin ratio was above three in PCOS disease. This ratio reported here is anticipated to contribute to the course or follow-up of the disease in the future. Also, subfatin has been investigated here for the first time, may also be a new candidate molecule in addition to classical laboratory parameters in the diagnosis and follow-up of PCOS.

Intra-ovarian stem cell transplantation in management of premature ovarian insufficiency: towards the induced Oogonial Stem Cell (iOSC).

The specialized resident-stem cells in gonads are tasked with restorating damaged ovarian cells following injury to maintain sequential reproductive events. When we talk about premature ovarian insufficiency (POI) we accept the existence of decreased stem cell and their regenerative abilities. The present study was to explain how restorating damaged ovarian cells following injury to maintain sequential reproductive events in evidence-based medicine indexed in PubMed and Web of Science. The exact mechanism is unclear stem cells transfer may improve compromised ovarian function and fertility outcome in women with POI. Soluble factors secreted by stem cell may rescue impaired mitochondrial function in oogonial stem cells, enhance metabolic capacity of resident stem cells, induce local neovascularization in the ovary, and activate gene shifting between transferred stem cells and germ cell precursors. This review may provide insight into how stem cells show some of their beneficial effects on compromised ovarian microenvironment and germ cell niche and paves the way for clinical trials for improving ovarian function of women with POI. We also had the opportunity to share our hypothesis about the design and development of induced oogonial stem cell (iOSC) and its use in POI.

Combating sars-cov-2 through lipoxins, proteasome, caveolin and nuclear factor-κb pathways in non-pregnant and pregnant populations.

It can be misleading to think that the new severe acute respiratory syndrome coronavirus (SARS-CoV2) which has a very strong mutation and adaptation capabilities, uses only the angiotensin-converting enzyme II (ACE2) pathway to reach target cells. Despite all the precautions taken, the pandemic attack continues and the rapid increase in the number of deaths suggest that this virus has entered the cell through different pathways and caused damage through different mechanisms. The main reason why the ACE2 pathway comes to the fore in all scientific studies is that this receptor is located at the entry point of basic mechanisms that provide alveolo-capillary homeostasis. SARS-CoV-2 has to use nuclear factor-κB (NF-kB), caveloae, clathrin, lipoxin, serine protease and proteasome pathways in addition to ACE2 to enter the target cell and initiate damage. For this reason, while new drug development studies are continuing, in order to be beneficial to patients in their acute period, it is imperative that we are able to come up with drugs that activate or inhibit these pathways and are currently in clinical use. It is also critical that we adopt these new pathways to the treatment of pregnant women affected by SARS-CoV-2, based on the scientific data we use to treat the general population.

ALTERED BLOOD AND AQUEOUS HUMOR LEVELS OF ASPROSIN, 4-HYDROXYNONENAL, AND 8-HYDROXY-DEOXYGUANOSINE IN PATIENTS WITH DIABETES MELLITUS AND CATARACT WITH AND WITHOUT DIABETIC RETINOPATHY.

PURPOSE: Diabetic retinopathy (DRP) is the formation of edema and small vessels in the retina due to high blood glucose levels. Asprosin is a hormone that stimulates the release of glucose from the liver into the circulation. Considering the relationship between oxidative stress and DRP, our study aimed to determine the levels of the oxidative stress markers 4-hydroxynonenal (4-HNE) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as asprosin, in the blood and aqueous humor (Aq) of patients with and without DRP. METHODS: Thirty patients with single-eye DRP and cataract (DRP + C), 30 patients with diabetes mellitus and cataract without DRP (DM + C), and 30 healthy control (CON) participants were enrolled into this retrospective study. Except for healthy controls, Aq and blood samples were taken from these patients during their cataract operation. Asprosin, 4-HNE, and 8-OHdG concentrations were analyzed using enzyme-linked immunosorbent assays. RESULTS: In patients with DRP, the levels of asprosin, 4-HNE, and 8-OHdG were significantly higher in both Aq and blood samples compared with the group of patients without DRP. CONCLUSION: These findings suggest that the measurement of asprosin, 4-HNE, and 8-OHdG levels may support clinicians in determining the risk of DRP development.

Nppc/Npr2/cGMP signaling cascade maintains oocyte developmental capacity.

The follicle must fulfill the following criteria if it is to survive the period between early embryonic life and the luteinizing hormone (LH) peak. It should (i) be surrounded by pregranulosa cells; (ii) complete the first meiotic division and become dormant; and (iii) continue metabolism during the dormant stage. Interaction between the natriuretic peptide precursor type C (Nppc) and its receptor, natriuretic peptide receptor 2 (Npr2), affects female fertility through the production of oocytes with developmental capacity and maintain oocyte meiotic arrest. While Nppc is expressed in mural cells, cumulus cells express Npr2. Nppc/Npr2 system exerts its biological function on developing follicles by increasing the production of intracellular cyclic guanosine monophosphate (cGMP). This pathway not only contributes to the development of ovary and the uterus, but aids the formation of healthy eggs in terms of their morphological and genetic aspects. A defect in this pathway leads to asmall ovarian size, string-like uterine horns, and thin endometrium and myometrium. Disorganized chromosomes, abnormal cumulus expansion and early meiotic resumption occur in animals with defective Nppc/Npr2 signaling. The types and number of oocytes also decrease when there is incompetent Nppc/Npr2 signaling. This paper extends on most recent and relevant experimental evidence regarding Nppc/Npr2/cGMP signaling with regard to its crucial role in maintaining oocyte meiotic arrest and the production of oocytes with developmental capacity. We further discuss whether the agonist or antagonist forms of the members of this exciting pathway can be usedfor triggering final oocyte maturation.

Molecular role of peptides/proteins in subfertility of polycystic ovarian syndrome.

Obesity and hyperandrogenemia are known to have adverse effects on both developing follicle and endometrium receptivity in polycystic ovarian syndrome (PCOS). Insulin resistance also contributes to this dilemma as a cause or a consequence and leads to worsening of the clinical picture. The difficulty in obtaining pregnancy despite the presence of a large number of oocyte has concentrated our attention on oocyte quality and development. However, the occurence of subfertility has also caused us to investigate the presence of different etiologic agents in non-obese PCOS women with normal androgen and insulin levels. In this context peptides have become the most accused and investigated molecules in cases of impaired fertility due to PCOS. Most of the studies investigating the relationship between PCOS and peptide did not support each other. The difficulties in measuring peptide levels as well as the individual variations in peptide synthesis and release are possible causes of this incongruity. For all these reasons, the incorporation of studies investigating the relationship between PCOS, peptide and subfertility in an article has become critical to pioneering future work. Understanding the association between peptides and subfertility will help us to understand the effects of peptides on failed fertility in PCOS. Moreover, updating our knowledge about peptides may allow us designing new drugs to to treat subfertility in PCOS. This review provides a general summary of the mechanisms of action of neuroendocrine peptides in regulating reproductive events. Since it is not usual to discuss all peptides in this context, only the effects of key central and peripheral peptides on fertility in PCOS have been extensively addressed.

Evaluation of elabela, apelin and nitric oxide findings in maternal blood of normal pregnant women, pregnant women with pre-eclampsia, severe pre-eclampsia and umbilical arteries and venules of newborns.

Pre-eclampsia is multisystem metabolic diseases, commonly accompanied by hypertension and proteinuria, which are among the important causes of maternal and perinatal mortality and morbidity worldwide. In a pre-eclampsia animal model study in the last year, Elabela (ELA) infusion was reported to correct hypertension and proteinuria and to normalise the birth weights of the offspring. Therefore, our main goal in this human study is to compare ELA, apelin (APLN) and nitric oxide (NO) levels in the maternal blood of pregnant women with pre-eclampsia and severe pre-eclampsia and in their newborns' venous-arterial cord blood with maternal blood of healthy pregnant women and their newborns' venous-arterial cord blood. Thirty controls, 28 pre-eclampsia and 24 severe pre-eclampsia cases and their newborns participated in this study. Maternal blood and newborn venous-arterial cord blood samples were collected from these patients. ELA, APLN and NO levels in these samples were measured by ELISA method. When the maternal blood ELA, APLN and NO amounts were compared with control groups, there was a significant decrease in both pre-eclamptic and severe pre-eclamptic women and this was more prominent in the women with severe pre-eclampsia. When ELA, APLN and NO levels in the newborn venous-arterial cord blood of control group was compared with that of severe pre-eclamptic and pre-eclamptic women; it was parallel with maternal findings. ELA, APLN and NO levels appear to play a role in the pathophysiology of pre-eclampsia. It is predicted that if these molecules, which are reduced due to pre-eclampsia and severe pre-eclampsia, are brought to physiological limits in the future; pre-eclampsia related maternal and perinatal mortality and morbidity can be reduced. Impact Statement What is already known on this subject? There are two studies (one human and one animal) in the literature evaluating only maternal elabela (ELA) levels in pre-eclamptic pregnancies. The animal study demonstrated decreased blood ELA levels in pre-eclamptic animals and the human study found increased blood ELA levels in pre-eclamptic patients. There are no studies evaluating maternal ELA levels in severe pre-eclampsia patients and also there are no studies evaluating maternal ELA levels in pre-eclampsia and severe pre-eclampsia patients. There are no studies evaluating newborns' venous-arterial blood APLN and NO levels. Apelin (APLN) and nitric oxide (NO) results were controversial in pre-eclampsia and severe pre-eclampsia patients. What the results of this study add? The present study, for the first time, demonstrates that decreased blood ELA, APLN and NO levels in maternal blood of pregnant women with pre-eclampsia and severe pre-eclampsia and in their newborns' venous-arterial blood. Furthermore, we have also demonstrated for the first time that decreased ELA, APLN and NO are also related with low birth weights. What the implications are of these findings for clinical practice and/or further research? The low levels of ELA, APLN and NO in maternal blood and newborns' venous-arterial blood may be the result or the cause of pathologic changes in pre-eclampsia and severe pre-eclampsia. Also, ELA, APLN and NO may be new indicator parameters of systemic endothelial dysfunction together. More studies are needed to evaluate the relationship between of ELA, APLN and NO and pre-eclampsia and severe pre-eclampsia and in newborns' venous-arterial blood.

Pentraxin-3: A new parameter in predicting the severity of diabetic foot infection?

This study was undertaken to evaluate the diagnostic and prognostic values of pentraxin-3 (PTX-3) in patients with infected diabetic foot ulcers (IDFU) as well as to assess the association between PTX-3 levels and IDFU severity. This study included 60 IDFU patients (Group 1), 45 diabetic patients without DFU (Group 2), and 45 healthy controls. Patients with IDFU were divided into mild, moderate, and severe subgroups based on classification of clinical severity. Patients who underwent amputation were also documented. Blood samples were collected to determine PTX-3 levels. PTX-3 levels in healthy controls, Group 1, and Group 2 were 5.83 (3.41-20) ng/mL, 1.47 (0.61-15.13) ng/mL, and 3.26 (0.67-20) ng/mL, respectively. A negative correlation between plasma PTX-3 and glucose levels was found. There were significant differences in terms of procalcitonin (PCT) and PTX-3 levels in the subgroup analysis of Group 1. The PTX-3 level in patients who did or did not undergo amputation was 4.1 (0.8-13.7) and 1 (0.6-15.1) ng/mL, respectively. Results suggest that PTX-3 is a particularly effective marker in patients with IDFU, both in terms of predicting disease severity and assisting in the decision to perform amputation.

Patatin-like phospholipase domain containing 3-gene (adiponutrin), preptin, kisspeptin and amylin regulates oocyte developmental capacity in PCOS.

This study was planned to test whether follicular fluid (FF) levels of patatin-like phospholipase domain containing 3-gene (PNPLA3:adiponutrin), preptin, kisspeptin, and amylin change in polycystic ovarian syndrome (PCOS). A total of 40 infertile volunteers undergoing IVF/ICSI were included in the study. They were divided into two groups as PCOS (n=20) and control group without PCOS (n=20). The controls were recruited from subjects with a poor ovarian response. The PCOS and control participants were matched according to their body mass index (BMI). Each group of participants underwent ovarian stimulation with GnRH antagonist protocol. Blood and FF samples of one dominant follicle were obtained from each subject during the oocyte pick-up. FF and serum levels of PNPLA3, preptin, kisspeptin and amylin were measured through ELISA. Amylin and adiponutrin median values were not different according to study groups (p>0.05). FF-preptin median values in the control group were similar to the serum preptin values of control and PCOS groups (Z=0.970, p=1.000 and Z=2.631, p=0.051, respectively). Medians of the serum preptin in control and PCOS groups were the same (Z=1.649; p=0.595). FF-preptin median values of PCOS group were significantly lower than the preptin median values of the control group. Serum preptin levels were positively correlated with HOMA-IR, but not with pregnancy rates and the number of retrieved oocytes. Serum kisspeptin levels were negatively correlated with the number of retrieved oocytes and pregnancy rates. While amylin and adiponutrin have no role in the folliculogenesis, kisspeptin and preptin work together for regulating follicle developmental capacity in PCOS.

Hepatoprotective properties for Salvia cryptantha extract on carbon tetrachloride-induced liver injury.

The present study was designed to determine the possible hepatoprotective effects of Salvia cryptantha (black weed) plant extract against carbon tetrachloride (CCl4)-induced hepatic injury in rats. Animals were grouped as follows: control group (Group I), CCl4 group (Group II), olive oil group (Group III), CCl4 + S. cryphantha 200 mg/kg group (Group IV), and CCl4 + S. cryptantha 400mg/kg group (Group V). Rats were injected intraperitoneally with CCl4 diluted in olive oil (50% v/v) at a dose of 1ml/kg body weight.  Bax and Caspase3 were determined by immunohistochemical staining, while apoptotic index was evaluated using TUNEL assay. Total mRNA was isolated from liver tissues, and the levels of BCL2, Caspase3, SOD, CAT, and glutathione peroxidase (GPx) were determined by using PCR, while MDA level were determined using a colorimetric assay. The antioxidant and anti-apoptotic gene transcripts were decreased in all of the control and treatment groups, while Caspase3 levels were not statistically different. The S. cryptantha plant extract treatment was also found to improve SOD, GPx, and catalase levels, while reducing the serum levels of MDA. The extract of S. cryptantha supplementation had a protective effect against CCl4-induced liver damage. S. cryptantha extract as a supplement may be useful as a hepato-protective agent to combat the toxic effects caused by CCl4 and other chemicals.

Effects of irisin and exercise on adropin and betatrophin in a new metabolic syndrome model.

Metabolic syndrome (MetS) is a prevalent public health problem. Uric acid (UA) is increased by MetS. We investigated whether administration of UA and 10% fructose (F) would accelerate MetS formation and we also determined the effects of irisin and exercise. We used seven groups of rats. Group 1 (control); group 2 (sham); group 3 (10% F); group 4 (1% UA); group 5 (2% UA); group 6 (10% F + 1% UA); and Group 7, (10% F + 2% UA). After induction of MetS (groups 3 -7), Group 3 was divided into three subgroups: 3A, no further treatment; 3B, irisin treatment; 3C, irisin treatment + exercise. Group 4, 1% UA, which was divided into three subgroups: 4A, no further treatment; 4B, irisin treatment; 4C, Irisin treatment + exercise. Group 5, 2% UA, which was divided into three subgroups: 5A, no further treatment; 5B, irisin treatment; 5C, irisin treatment + exercise. Group 6, 10% F + 1% UA, which was divided into three subgroups: 6A, no further treatment; 6B, irisin treatment; 6C, irisin treatment + exercise. Group 7, 10% F + 2% UA, which was divided into three subgroups: 7A, no further treatment; 7B, irisin treatment; 7C, irisin treatment + exercise., Irisin was administered 10 ng/kg irisin intraperitoneally on Monday, Wednesday, Friday, Sunday each week for 1 month. The exercise animals (in addition to irisin treatment) also were run on a treadmill for 45 min on Monday, Wednesday, Friday, Sunday each week for 1 month. The rats were sacrificed and samples of liver, heart, kidney, pancreas, skeletal muscles and blood were obtained. The amounts of adropin (ADR) and betatrophin in the tissue supernatant and blood were measured using an ELISA method. Immunohistochemistry was used to detect ADR and betatrophin expression in situ in tissue samples. The duration of these experiments varied from 3 and 10 weeks. The order of development of MetS was: group 7, 3 weeks; group 6, 4 weeks; group 5, 6 weeks; group 4, 7 weeks; group 3, 10 weeks. Kidney, liver, heart, pancreas and skeletal muscle tissues are sources of adropin and betatrophin. In these tissues and in the circulation, adropin was decreased significantly, while betatrophin was increased significantly due to MetS; irisin + exercise reversed this situation. We found that the best method for creating a MetS model was F + UA2 supplementation. Our method is rapid and simple. Irisin + exercise was best for preventing MetS.

The Course of Diabetic Foot Infection in Elderly Patients: Data of Patients From Turkey.

With the aging population, it is expected that diabetes and related complications will increase rapidly. The aim of this study was to examine the signs and symptoms of diabetic foot infection in elderly individuals. Patients with diabetic foot infection were grouped as mild, moderate, and severe. Patients aged <65 years and those who did not meet the diagnosis of diabetic foot infection were excluded from the study. Only the first applications of patients who applied to the hospital multiple times with diabetic foot infection diagnosis were evaluated. 314 patients were included in the study. The mean age of the patients was 71.5 (±12). The number of patients aged 75 and over was 125 (39.8%). Of the patients, 25.7% had mild, 61.7% moderate, and 12.4% severe clinical forms. 131 (41.7%) of the patients had osteomyelitis. Amputation was performed in 112 of the patients. Antibiotic treatment was given to 102 patients only. While 89 patients died, a significant correlation was found between all groups between amputation rate and mortality frequency and clinical severity of diabetic foot infection (P < .001). In our study, it was observed that the clinical severity of diabetic foot infection was more severe and the overall mortality rate was higher in geriatric patients. In light of all these data, it can be concluded that an early and comprehensive roadmap should be followed in geriatric patients with diabetic foot infection who have an increased risk of morbidity and mortality.

Betatrophin, elabela, asprosin, glucagon and subfatin peptides in breast tissue, blood and milk in gestational diabetes.

We investigated the presence of asprosin (ASP), betatrophin, elabela (ELA), glucagon and subfatin (SUB) in the milk of mothers with gestational diabetes mellitus (GDM) and compared their levels with blood levels. We also investigated whether these peptides are synthesized by the breast. We investigated 12 volunteer mothers with GDM and 14 pregnant non-GDM control mothers. The peptides were measured using ELISA and their tissue localization was determined using immunohistochemistry. Breast milk contains ASP, betatrophin, ELA, glucagon and SUB. The amount of the peptides ranged from highest to the lowest in colostrum, transitional milk and mature milk. The amount of peptides in the milk was greater than for blood. The peptides, except for ELA, were increased in milk and blood by GDM. Betatrophin and ELA are synthesized in the connective tissue of the breast. ASP, glucagon and SUB are synthesized in the alveolar tissue of the breast. These peptides in breast milk may contribute to the development of the gastrointestinal tract of newborns and infants.

A New Inflammatory Marker of Clinical and Diagnostic Importance in Diabetic Foot Infection: Systemic Immune-Inflammation Index.

Diabetes and associated complications still pose an important public health problem. Osteomyelitis as especially seen in patients with diabetes is associated with increased rates of morbidity and mortality. The present study aimed to investigate the clinical and diagnostic significance of inflammatory markers, including the systemic immune-inflammation index (SII) and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin (PCT) to differentiate osteomyelitis and cellulitis. The present study included 96 patients with osteomyelitis (Group 1) and 151 patients with cellulitis (Group 2). Inflammatory markers were significantly elevated in Group 1 compared to Group 2 patients (p < 0.05). Furthermore, the correlation coefficients (rho) between SII and ESR, CRP, and PCT were 0.466 (p < 0.001), 0.627 (p < 0.001), and 0.501 (p < 0.001), respectively, as a result of Spearman's Rho analysis. Accordingly, a moderately positive relationship was found between the variables. The area under the curve (AUC) values for SII, ESR, CRP, and PCT in diabetic foot infection patients with osteomyelitis were 0.687, 0.722, 0.692, and 0.641, respectively. As a result of the Likelhood Ratio (LR) test, the cut-off values were 2.182 for SII (sensitivity: 39.8% and specificity: 79.8%), 76.5 mm/h for ESR (sensitivity: 59.1% and specificity: 73.1%), 109.5 mg/mL for CRP (sensitivity: 40.9% and specificity: 79.8%), and 0.44 ng/mL for PCT (sensitivity: 26.1% and specificity: 88.2%). In conclusion, given that the patients with osteomyelitis had much higher ESR, CRP, PCT, and SII levels combined with the fact that SII is a low-cost and easy-to-measure index, suggests that the same may serve as an effective and novel marker alternative to other inflammatory markers for predicting diabetic foot osteomyelitis.

Sonoelastrographic finding of Achilles tendon in patients with ankylosing spondylitis and acromegaly.

OBJECTIVES: Achilles tendinopathy can be noticed in both acromegaly and ankylosing spondylitis (AS). Acromegaly patients presenting with tendinopathy findings may be confused with AS findings. In this study, sonoelastrographic findings of Achilles tendon are explored in patients with AS and acromegaly. METHODS: 25 patients with AS, 30 patients with acromegaly, and 18 healthy controls were enrolled in the study. Achilles tendon was evaluated by sonoelastography in all the study participants. RESULTS: The thickness of Achilles tendon in neutral positions was higher in acromegaly patients than those in AS patients. The sonoelastography measurement of Achilles tendon was increased in acromegaly patients when compared to the control group and AS patients. CONCLUSION: The thickness of Achilles tendon can increase in patients with acromegaly and AS. However, the sonoelastographic features of Achilles tendon can be similar in patients with AS and acromegaly.

Association Between Dermcidin, Salusin-α, Salusin-ß Molecules and Diabetic Foot Infections.

Dermcidin, salusin-α, and salusin-ß are three recently discovered molecules that confer antimicrobial properties. The present study aims to investigate the association between dermcidin, salusin-α, and salusin-ß in the etiopathology of patients with diabetic foot infection. The study included three groups: Group 1 - diabetic foot infection; Group 2 - diabetes without history of diabetic foot; and Group 3 - the control group. Plasma dermcidin, salusin-α, and salusin-ß levels were compared across the groups. Median (Q1-Q3) values of plasma dermcidin levels in Groups 1, 2, and 3 were 3.45 (0.8-4.4), 5.2 (3.7-6.4), and 5.8 (3.1-10) ng/mL, respectively. Diabetic foot infection group had significantly lower plasma dermcidin levels compared to diabetes only group and control group (P = .000, ANOVA), whereas there was no statistically significant difference between the Group 2 and Group 3 (P = .163, ANOVA). Salusin-α and salusin-ß levels were significantly higher in the Group 3 compared to the other groups. Based on our findings, diabetic foot infection group had significantly lower plasma dermcidin levels and salusin-α and salusin-ß levels were significantly higher in the control group. These molecules (dermcidin specifically) can be researched as an adjuvant therapeutic agent in addition to conventional treatments in diabetic foot diabetic foot infections. Also, it can be searched this may prevent many complications including amputation.

Biochemical characteristics and calcium and PTH levels of patients with high normal and elevated serum 25(OH)D levels in Turkey: DeVIT-TOX survey.

Vitamin D intake over the recommended dose is usually associated with high serum 25(OH)D levels and generally not associated with symptoms of hypercalcemia. High doses of cholecalciferol need to be avoided to protect against vitamin D toxicity and related complications. Strict adherence to the clinical guidelines for treating vitamin D deficiency can ensure safe and effective treatment. PURPOSE: We observed a tendency to use high doses of cholecalciferol for vitamin D deficiency treatment or vitamin D supplementation. We aimed to determine the biochemical characteristics of patients with high normal and elevated serum 25(OH)D levels. METHODS: An online invitation was sent to all tertiary endocrinology clinics in Turkey to complete an online retrospective survey (DeVIT-TOX Survey) for patients diagnosed with high serum 25(OH)D levels (> 88 ng/mL) between January 2019 and December 2019. The patients were evaluated according to the presence of signs and symptoms of hypercalcemia and doses of vitamin D intake, evaluated into the following three groups according to their 25(OH)D levels: group 1, > 150 ng/mL; group 2, 149-100 ng/mL; and group 3, 99-88 ng/mL. RESULTS: A total of 253 patients were included in the final analysis (female/male: 215/38; mean age, 51.5 ± 15.6 years). The average serum 25(OH)D level was 119.9 ± 33 (range, 88-455) ng/mL, and the average serum calcium level was 9.8 ± 0.7 (range, 8.1-13.1) mg/dL. Most (n = 201; 75.4%) patients were asymptomatic despite having high serum 25(OH)D and calcium levels. The serum 25(OH)D level was significantly higher in the symptomatic groups than in the asymptomatic groups (138.6 ± 64 ng/mL vs. 117.7 ± 31 ng/mL, p < 0.05). The most common cause (73.5%) associated with high serum 25(OH)D levels was the inappropriate prescription of a high dose of oral vitamin D (600.000-1.500.000 IU) for treating vitamin D deficiency/insufficiency in a short time (1-3 months). The cut-off value of 25 (OH) D level in patients with hypercalcemia was found to be 89 ng/mL [median 116.5 (89-216)]. CONCLUSIONS: High dose of vitamin D intake is associated with a high serum 25 OH D level, without symptoms of hypercalcemia. Inappropriate prescription of vitamin D is the primary cause for elevated 25(OH) D levels and related hypercalcemia. Hypercalcemia may not be observed in every patient at very high 25(OH) D levels. Adherence to the recommendation of guidelines is essential to ensure safe and effective treatment of vitamin D deficiency.