Chronic pain is ongoing pain that has persisted beyond standard tissue healing time along with comorbidities such as depression. This article discusses studies that have shown the prevalence of chronic pain and chronic pain-induced depression and explained methods of prevention for these conditions. The molecular mechanisms such as monoamine neurotransmitters, brain-derived neurotrophic factor, inflammatory factors, and glutamate that are similar in chronic pain and depression have also been discussed. This article reviews the methods of management that utilize the identification of these molecular mechanisms to treat this condition further. It also emphasizes the importance of the awareness of chronic pain-induced depression for the upcoming advances in the subject of mental health.

There has been an established relationship between hypothyroidism and depression. Studies have demonstrated that somatostatin and serotonin influence the hypothalamus-pituitary-thyroid axis, which links hypothyroidism to depression. Multiple studies concluded that undiagnosed, untreated, undertreated patients with hypothyroidism are at increased risk of developing depression. Autoimmune thyroiditis is also associated with an increased risk of depression. Elevated thyroid-stimulating hormone (TSH), antithyroglobulin (TgAb), and thyroid peroxidase antibodies (TPOAb) levels have all been linked to depression and an increased risk of suicide. Moreover, hypothyroidism is known to be one of the leading causes of treatment-resistant depression. Treating underlying hypothyroidism with thyroid replacement therapy could significantly improve mood disorders such as depression. Levothyroxine therapy is also used as adjunctive therapy to antidepressants in the management of depression, and it is known to improve the symptoms of depression rapidly when compared to antidepressants alone. This review strengthens the link between hypothyroidism and depression, and it also demonstrates how treating the underlying hypothyroidism in people who have been diagnosed with depression will be very beneficial.

Anastomotic leakage is a common yet one of the most feared complications following colorectal surgery. Dehiscence of the anastomosis can result in fatal complications such as peritonitis, abscess formation, and sepsis, thereby increasing morbidity and mortality, cost and length of hospital stay. Multiple factors contribute to the development of anastomotic dehiscence. Several studies have been published identifying various risk factors that may play a role in causing AL. Our study reviewed prospective and retrospective studies and summarized the risk factors into three categories: preoperative, intraoperative, and postoperative. Among these are various risk factors such as age, gender, comorbidities, American Society of Anesthesiologists (ASA) scores, operative time, smoking, alcohol use, obesity, nutritional status, mechanical bowel preparation, and steroid use. It is crucial for surgeons to have a thorough understanding of the risk factors associated with anastomotic leakage to identify patients at high risk preoperatively. It may also be relevant to intraoperative decision-making when establishing an anastomosis, such as considering proximal diversion or placing a drain if such high-risk features are present. Knowing high-risk features also helps to detect leaks as early as possible postoperatively.

The combination of stereotactic body radiation therapy (SBRT) plus immune checkpoint inhibitors (ICI) must be explored to treat advanced primary liver tumors such as hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA). Limited retrospective reviews and case reports/series suggest this combination can be effective and safe in both cancer types. With ICIs moving into the first line (IMbrave 150, HIMALAYA, and TOPAZ-1) to manage these cancers, identifying a suitable population for this approach is challenging. Patients with macrovascular invasion (MVI)-positive HCC (especially if larger veins are involved) or recurrent HCCs post-locoregional therapies (such as transarterial radioembolization (TARE), transarterial chemoembolization (TACE), or ablation), as well as those ineligible for bevacizumab or tyrosine kinase inhibitors (TKIs), should be the focus of exploring this combination in HCC. Unresectable or oligometastatic CCA patients who cannot tolerate gemcitabine/cisplatin (GC) or those who progressed on GC without durvalumab and do not have targetable mutations could also be considered for this approach. In both HCC and CCA disease groups, SBRT plus ICI can be examined post-ICI as these two modalities act synergistically to enhance anti-tumor activity (based on pre-clinical studies). Large-scale randomized trials are needed to identify the subsets of primary liver cancers suitable for this approach and to clearly define its clinical benefit.

Cell-free DNA (cfDNA) testing currently does not have a significant role in PDA management: it is insufficient to diagnose PDA, and its use is primarily restricted to identifying targetable mutations (if tissue is insufficient or unavailable). cfDNA testing has the potential to address critical needs in PDA management, such as pre-operative risk stratification (POR), prognostication, and predicting (and monitoring) treatment response. Prior studies have focused primarily on somatic mutations, specifically KRAS variants, and have shown limited success in addressing prognosis and POR. Recent studies have demonstrated the importance of other less prevalent mutations (ERBB2 and TP53), but no studies have provided reliable mutation panels for clinical use. Methylation aberrations in cfDNA (epigenetic markers) in PDA have been relatively less explored. However, early evidence has suggested they offer diagnostic and, to some extent, prognostic value. The inclusion of epigenetic markers of cfDNA adds another dimension to genomic testing and may open new therapeutic avenues beyond addressing critical areas of need in PDA treatment. For cfDNA to substantially influence PDA management, concerted efforts are required to include less frequent mutations and epigenetic markers. Furthermore, relying on KRAS mutations for PDA management will always be inadequate.

Sickle cell disease (SCD) is a hematological disorder that is inherited in an autosomal recessive (AR) fashion. It is caused by mutations in the genes encoding for the globin apoprotein of hemoglobin (Hb), leading to diminished oxygen-carrying ability. Its pathophysiologic mechanism affects multiple organ systems, making it crucial to understand the complications of SCD and find the best ways to prevent and treat them. Some important ways that SCD manifests in the respiratory system are acute chest syndrome (ACS), pulmonary hypertension (PH), asthma, and venous thromboembolism (VTE). This article summarizes their salient features, including pathogenesis related to the adverse outcomes, screening practices, and management guidelines, with the intent to provide greater insight into forming better practices that increase the quality of life in SCD patients.