Internal Pancreatic Stent Causing Irreversible Dilatation of Pancreatic Duct

A 28-year-old woman underwent a pylorus preserving Whipple procedure for pancreatic serous cystadenoma located on the head of the pancreas. During the operation, an internal stent (7F silastic catheter, 9 cm in length) was placed within the pancreatic duct in the area of pancreaticojejunal end-to-end Dunking type anastomosis to prevent development of fistula. The stent was positioned so that one third of its length would lie into the pancreatic duct, and it was anchored to the periductal pancreatic tissue with only one rapidly absorbable chromic suture. Leakage from the anastomosis was not observed, and she was discharged without any complaint. Early postoperative abdominal CT examination revealed that the stent was retained within the normal caliber pancreatic duct (Fig. 1a). Six months after the operation, she began to complain to epigastric pain triggered by the meals. The laboratory analysis was normal, particularly liver biochemical tests and serum amylase. The internal pancreatic stent within the dilated pancreatic duct was detected by an additional CT examination (Fig. 1b). The stent was removed endoscopically at the third attempt. The pain was resolved after its removal. Control CT examination which was taken at the 18th month after removal of the stent showed dilatation of the pancreatic duct (Fig. 2a). The patient remained free of any complaint, although regressed pancreatic duct dilatation has persisted over 4 years of follow-up (Fig. 2b).     

Investigation of inflammation related gene polymorphism of the mannose-binding lectin 2 in schizophrenia and bipolar disorder

Objectives:To investigate the association between mannose-binding lectin 2 (MBL2) codon 54 polymorphism and clinical features of patients diagnosed with schizophrenia (SCZ) or bipolar disorder (BD).Methods:One hundred and eighteen patients with SCZ, 100 patients with BD, and 100 healthy volunteers were included in the case-control study. The patients consecutively admitted to the outpatient clinic in December 2017-May 2018 and were evaluated with some scales for clinical parameters. Polymerase chain reaction and RFLP were used to determine MBL2 polymorphism in DNA material.Results:The MBL2 gene polymorphism distributions in SCZ or BD patients were significantly different from the control group. The heterozygous genotype percentages were significantly higher in the control group than in the SCZ or BD patients (OR: 0.450; 95% Cl: 0.243-0.830; p=0.010; OR: 0.532; 95%Cl: 0.284-0.995; p=0.047, respectively), and there were statistically significant differences in the MBL2 polymorphism distributions between treatment-responsive SCZ or BD patients and treatment-resistant patients diagnosed with SCZ or BD. The heterozygous genotype percentages were also significantly higher in the treatment-responsive group than in the treatment-resistant group in SCZ or BD patients (OR: 7.857; 95% Cl: 1.006-61.363; p=0.023; OR: 8.782; 95% Cl: 1.114-69.197; p=0.016, respectively).Conclusion:The presence of a heterozygous MBL2 genotype seems to be favorable both in terms of the absence of SCZ and BD in the healthy population and treatment response for Turkish patients.

Schizophrenia (SCZ) and bipolar disorder (BD) are chronic psychiatric disorders that cause substantial disruptions in psychosocial capacity and occur in approximately 1% of the world population.¹ Genome-wide association studies (GWAS) of Psychiatric Genomics Consortium for SCZ recognized more than a hundred common single nucleotide polymorphisms (SNPs) with minor individual effects presenting susceptibility to the SCZ.² A similar mega-analysis for BD, although including a more moderate sample, identified common risk variants specific to BD.³ The long-lasting alterations in gene expression patterns after environmental exposures imply that epigenetic mechanisms might also play a critical role in chronic psychiatric disorders.⁴ Again, previous researches have constantly reported shared genetic etiology between SCZ and BD. Researches showing the genetic overlap between SCZ and BD have improved from studying family and twin inheritance to determine genetic correlation and performing polygenic risk score analysis from GWAS data in large case-control samples.⁵ Despite these researches with large sample size, the cause of both disorders is still relatively unknown; recent studies have shown that uncontrolled activity of microglia and excessive inflammatory responses caused by pro-inflammatory cytokines are among the factors that play a role in the development of SCZ and BD based on genetic susceptibility.^1,6 A relationship between SCZ and many autoimmune diseases and an increase in the prevalence of an autoimmune disease occurrence by about 45% have been found. Moreover, infections of embryonic and early childhood periods lead to delays in fetal brain development and excessive synaptic pruning during adolescence, are among the possible risk factors of psychosis.^7,8 Systemic inflammation and central inflammation are thought to be associated with episodes, remission, and prognosis of BD. Neuroendocrine irregularities, neurotransmitter abnormalities, and glial cell dysfunctions cause plastic alterations in the mood-regulating brain areas. The high rate of comorbid autoimmune diseases also supports this claim.⁹Mannose-binding lectin (MBL) has a vital function in the innate immune system by stimulating the complement system’s lectin pathway. Therefore, it is the only collectin that binds to microorganisms, serves as an opsonin, promotes phagocytosis, and stimulates macrophages. MBL2 gene, which consists of 4 exons in the q11.2-q21 region of the long arm of chromosome 10, encoded MBL. Mutation at codon 54 follows in a replacement of glycine to aspartic acid (allele B), and the normal MBL2 allele is defined by allele A.^10-12 In heterozygous mutants, serum MBL decreases almost 10-fold, whereas, in homozygous mutants, the level decreases to an undetectable level. MBL deficiency is the most common immune defect in humans, affecting approximately 5-7% of individuals.¹³ A decrease in serum MBL level can cause recurrent spontaneous miscarriage,¹⁴ premature birth,¹⁵ and exacerbation of chronic diseases such as ischemic heart disease,¹⁶ and severe infections such as sepsis and systemic inflammatory response syndrome (SIRS).¹⁷ Besides, previous studies suggested that MBL plays an essential role in the pathogenesis of autoimmune diseases.^12,18 We believe that this is the first case-control study comparing MBL2 genotype distributions in patients with SCZ or BD according to treatment resistance, clinical characteristics, and scale scores in detail.Aims of the studyWe aimed to examine whether MBL2 codon 54 polymorphism was involved in the etiopathogenesis and treatment response of SCZ and BD compared with healthy controls.     

Management of orthopedic oncology patients during coronavirus pandemic

The new measures implemented in hospitals also altered the operation of orthopedics and traumatology departments. The main purpose of this article is to discuss how orthopedic oncology clinics should be organized during the pandemic and to present the process management scheme for patients requiring orthopedic surgery, including trauma surgery, from diagnosis to treatment, together with our experiences. Instead of thinking about the global emergence of the epidemic, it is time to act decisively. At first glance, the coronavirus disease 2019 (COVID-19) pandemic and orthopedics may seem to be unrelated disciplines, but the provision of healthcare services to patients who require them proves that these two fields are parts of the same whole. Our experiences in treating neutropenic, lymphocytopenic, and chemotherapy patients seem to have proven beneficial during this process. We operated on 10 biopsy patients, 15 primary bone sarcomas, 9 soft tissue sarcomas, and 82 trauma patients within this time frame. Only three patients were suspected to have COVID-19 before admission. The early identification, strict isolation, and effective treatment of these patients prevented any nosocomial infections and disease-related comorbidities. This success is the result of the multidisciplinary cooperation of the Ministry of Health, our hospital, and our clinic.     

Laparoscopic versus open resection of colorectal liver metastasis

Background

Findings have shown laparoscopic liver resection (LLR) to be feasible and safe, but the data in the literature regarding oncologic outcomes are scant. This study aimed to compare the perioperative and short-term oncologic outcomes between LLR and open resection of colorectal liver metastasis (CLM).

Methods

Between January 2006 and April 2012, 40 patients underwent LLR of CLM. These patients were compared with a consecutive matched group of 40 patients who underwent open resection within the same period. Data were obtained from a prospective institutional review board (IRB)-approved database. Statistical analysis was performed using t test, Chi-square, and Kaplan–Meier survival.

Results

The groups were similar in terms of age, gender, tumor size, number of tumors, and type of resections performed. The operative time was similar in the two groups, but the estimated blood loss was less in the LLR group than in the open resection group. The length of stay was shorter in the LLR group (3.7 vs 6.5 days; p < 0.001). The 2-year overall survival rate was 89 % for LLR and 81 % for open resection. The median disease-free survival time was 23 months in each group.

Conclusions

The findings suggest that LLR is associated with less blood loss and a shorter hospital stay than open resection for CLM. According to our short-term results, LLR is equivalent to open resection in terms of oncologic outcomes.     

Insulin counteracts glucotoxic effects by suppressing thioredoxin-interacting protein production in INS-1E beta cells and in Psammomys obesus pancreatic islets

Aims/hypothesis  In type 2 diabetes, glucose toxicity leads to beta cell apoptosis with decreased beta cell mass as a consequence. Thioredoxin-interacting protein (TXNIP) is a critical mediator of glucose-induced beta cell apoptosis. Since hyperglycaemia leads to elevated serum insulin, we hypothesised that insulin is involved in the regulation of TXNIP protein levels in beta cells. Methods  We studied the production of TXNIP in INS-1E beta cells and in islets of Psammomys obesus, an animal model of type 2 diabetes, in response to glucose and different modulators of insulin secretion. Results  TXNIP production was markedly augmented in islets from diabetic P. obesus and in beta cells exposed to high glucose concentration. In contrast, adding insulin to the culture medium or stimulating insulin secretion with different secretagogues suppressed TXNIP. Inhibition of glucose and fatty acid-stimulated insulin secretion with diazoxide increased TXNIP production in beta cells. Nitric oxide (NO), a repressor of TXNIP, enhanced insulin signal transduction, whereas inhibition of NO synthase abolished its activation, suggesting that TXNIP inhibition by NO is mediated by stimulation of insulin signalling. Treatment of beta cells chronically exposed to high glucose with insulin reduced beta cell apoptosis. Txnip knockdown mimicking the effect of insulin prevented glucose-induced beta cell apoptosis. Conclusions/interpretation  Insulin is a potent repressor of TXNIP, operating a negative feedback loop that restrains the stimulation of TXNIP by chronic hyperglycaemia. Repression of TXNIP by insulin is probably an important compensatory mechanism protecting beta cells from oxidative damage and apoptosis in type 2 diabetes. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorised users.     

Role of cyclic AMP in glucagon-induced stimulation of hepatic glucose output in man

The interrelationship between glucagon action on splanchnic glucose output and cyclic AMP production was studied in healthy volunteers after hepatic venous catheterization. Glucagon was infused according to four different protocols to achieve arterial levels ranging from 300 to 9000 ng/I. Infusion of glucagon which resulted in arterial levels of the hormone of 4000-9000 ng/1 was associated with a marked increase in net splanchnic cyclic AMP production and in the arterial levels of the cyclic nucleotide. The rise in cyclic AMP efflux from the splanchnic area was transient but an augmented splanchnic production was still evident after 30 min of glucagon infusion. Splanchnic glucose output rose 3-5 fold. Infusion of glucagon at lower rates, resulting in arterial levels of 300-900 ng/I, did not measureably stimulate the efflux of cyclic AMP from the splanchnic area. In spite of this, splanchnic glucose output rose 2-3 fold and the blood glucose level increased 20-50% during glucagon infusion at these lower rates.

It is concluded that (1) factors other than cyclic AMP are rate limiting in the stimulation of hepatic glucose production, and (2) although cyclic AMP is an established 'second messenger' of glucagon action, other factors may also be of importance in mediating the physiological response of this hormone.