Pancreatic cancer (PC) is often associated with a poor prognosis. Long-standing diabetes mellitus is considered as an important risk factor for its development. This risk can be modified by the use of certain antidiabetic medications. On the other hand, new-onset diabetes can signal towards an underlying PC in the elderly population. Recently, several attempts have been made to develop an effective clinical tool for PC screening using a combination of history of new-onset diabetes and several other clinical and biochemical markers. On the contrary, diabetes affects the survival after treatment for PC. We describe this intimate and complex two-way relationship of diabetes and PC in this review by exploring the underlying pathogenesis.

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SARS-CoV-2 pandemic has claimed millions of lives since its first identification in December 2019. Patients with diabetes are at a high risk of adverse outcomes after COVID-19 infection, whereas infection itself can be associated with severe hyperglycemia, including hyperglycemic emergencies. While the accelerated vaccine development and rollout have considerably decreased morbidity and mortality with reasonable safety, there are emerging reports of worsening of hyperglycemia in response to vaccination, with possible shared pathophysiology with COVID-19 infection-related hyperglycemia. We hereby report two young patients with type 1 diabetes (T1DM) who presented with severe diabetic ketoacidosis (DKA) after receiving second doses of COVISHIELD (ChAdOx1 nCoV-19) and COVAXIN (BBV152- inactivated whole virion) vaccines. Though a causal link cannot be established, post-vaccination immune response can potentially explain this transient worsening of hyperglycemia and hyperglycemic emergencies. We, hence report diabetic ketoacidosis (DKA) following COVID-19 vaccination in T1DM. We suggest that people with diabetes, particularly patients with T1DM with inadequate glycemic control should ideally be closely monitored for hyperglycemia and ketonemia for at least 2 weeks after receiving vaccination for COVID 19.

Dipeptidyl peptidase-4 inhibitors (DPP-4i) have an important place in the management of type 2 diabetes. The DPP-4 enzyme is ubiquitously distributed throughout the human body and has multiple substrates through which it regulates several important physiological functions. DPP-4 regulates several immune functions, including T-cell activation, macrophage function, and secretion of cytokines. Studies have reported an increase in autoimmune diseases like bullous pemphigoid, inflammatory bowel disease, and arthritis with DPP-4i use. The relationship of DPP-4i and autoimmune diseases is a complex one and warrants further research into the effect of DPP-4 inhibition on the immune system to understand the pathogenesis more clearly. Whether a particular cluster of autoimmune diseases is associated with DPP-4i use remains an important contentious issue. Nevertheless, a heightened awareness from the clinicians is required to identify and treat any such diseases. Through this review, we explore the clinical and pathophysiological characteristics of this association in light of recent evidence.

Chronic pancreatitis (CP) is characterized by progressive inflammation and fibrosis of the pancreas that eventually leads to pancreatic exocrine and endocrine insufficiency. Diabetes in the background of CP is very difficult to manage due to high glycemic variability and concomitant malabsorption. Progressive beta cell loss leading to insulin deficiency is the cardinal mechanism underlying diabetes development in CP. Alpha cell dysfunction leading to deranged glucagon secretion has been described in different studies using a variety of stimuli in CP. However, the emerging evidence is varied probably because of dependence on the study procedure, the study population as well as on the stage of the disease. The mechanism behind islet cell dysfunction in CP is multifactorial. The intra-islet alpha and beta cell regulation of each other is often lost. Moreover, secretion of the incretin hormones such as glucagon like peptide-1 and glucose-dependent insulinotropic polypeptide is dysregulated. This significantly contributes to islet cell disturbances. Persistent and progressive inflammation with changes in the function of other cells such as islet delta cells and pancreatic polypeptide cells are also implicated in CP. In addition, the different surgical procedures performed in patients with CP and antihyperglycemic drugs used to treat diabetes associated with CP also affect islet cell function. Hence, different factors such as chronic inflammation, dysregulated incretin axis, surgical interventions and anti-diabetic drugs all affect islet cell function in patients with CP. Newer therapies targeting alpha cell function and beta cell regeneration would be useful in the management of pancreatic diabetes in the near future.

Background: Coronary artery disease (CAD) takes the highest toll of lives across the world as well as India. Prompt diagnosis and effective treatment is lifesaving. Drug utilization studies scrutinize the appropriateness of treatment and provide favourable feedbacks to strengthen clinical practices. Several other studies have reported underuse of four evidence-based medicines namely aspirin, β-blockers, angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB), and statins in patients with CAD. Polypharmacy, injection overuse is some of the shortcomings. The objectives of this study was to describe treatment practices in terms of different disease spectrum and drug utilization (group-wise and individually) for inpatients with CAD using core prescription indicators by WHO.Methods: A cross-sectional study of 4-month duration was undertaken for patients with CAD admitted to cardiology indoor of a tertiary care hospital. A total no of 143 prescriptions was screened and analyzed.Results: Males (67.13%) were more in number than females (32.87%). Age group from (57-66) topped in frequency (61.05%) ahead of (67 to 76) group (38.46%). Average no of drugs per patient were 8.056±1.97 and 5.86±0.14 for cardiovascular drugs. Prescription in generics (45.49%), antibiotics (0.61%), fixed-dose combinations (FDCs) (0.52%) and injectables (28.47%) were noted. The most common categories of CAD were ST-segment elevated myocardial infarction (69.23%) followed by chronic stable angina (17.48%). Antiplatelets (100%), hypolipidemics (99.3%), antianginals (60.14%), β-blockers (37.06%) and ACE-I/ARBs (27.97%) were utilized. Drugs from the national list of essential medicines were 66.49%.Conclusions: Among four evidence-based drugs, use of β-blockers and ACE-I/ARBs were inappropriately low. Polypharmacy and overuse of Injectable drugs are noted.

Objectives: Chronic hypoparathyroidism is treated conventionally with active vitamin D and high doses of calcium. Recombinant human parathyroid hormone (PTH) replacement is an attractive option for treating patients with hypoparathyroidism since it can replace the physiological action of native PTH. The aim of our study was to perform a comprehensive evaluation of the effects of PTH replacement on calcium homeostasis, bone metabolism, and daily requirement of calcium and active vitamin D. Materials and Methods: Randomized controlled trials done in chronic hypoparathyroid patients were included in this meta-analysis. The PTH group included subjects receiving a subcutaneous injection of either PTH (1-84) or PTH (1-34) with oral calcium and/or active vitamin D. The control group included those receiving oral calcium and active vitamin D with/without subcutaneous placebo injection. The primary outcome of this meta-analysis was to compare serum calcium, 24-h urinary calcium, and severe adverse effects among PTH and control groups. Results: In this meta-analysis, we did not find any difference in serum calcium level between PTH and control groups [mean difference (MD) - 0.01; 95% confidence interval (CI) - 0.09, 0.06; P = 0.71]. Although there was a trend towards low 24-h urinary calcium in the PTH group, the difference was not statistically significant (MD - 1.43; 95% CI - 2.89, 0.03; P = 0.06). The incidence of serious adverse events was also similar in both groups (RR 1.35; 95% CI 0.58, 3.16; P = 0.49). Conclusion: Both PTH and active vitamin D therapies are associated with comparable serum and urine calcium levels with a similar incidence of serious adverse events in patients with chronic hypoparathyroidism.

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