Coronary artery ectasia (CAE) is a rare form of aneurysmal coronary heart disease. It is defined as a dilatation of the coronary artery by more than one-third of its length and with a diameter 1.5 times of a normal coronary artery adjacent to it. This condition increases the risk of angina pectoris and acute coronary syndrome. Hence, we discuss the pharmacologic options for primary and secondary prevention of CAE complications. Antiplatelets such as aspirin are considered the mainstay of treatment in patients with CAE. Anticoagulants such as warfarin are warranted on a case-by-case basis to prevent thrombus formation depending on the presence of concomitant obstructive coronary artery disease and the patient's risk of bleeding. Since atherosclerosis is the most common cause of CAE, statins are indicated in all patients for primary prevention. Angiotensin-converting enzyme (ACE) inhibitors may be indicated, especially in hypertensive patients, due to their anti-inflammatory properties. Beta-blockers may be indicated due to their antihypertensive and anti-ischemic effects. Calcium (Ca) channel blockers may be needed to prevent coronary vasospasm. Nitrates are generally contraindicated as they may lead to worsening of symptoms.Other antianginal medications such as trimetazidine can improve exercise tolerance with no reported adverse events in these patients.

The emergence of food allergies in children is crucial for various medical fields seeking a viable strategy for allergy prevention. The most well-recognized approach adopted by numerous health care and government institutions hinges on the delay in the introduction of food allergens, which supposedly protects infants from sensitization and decreases the possibility of allergy development. However, recent experimental findings indicate that the benefits of this approach might be overestimated, as early exposure to allergenic foods has been shown to yield more advantageous outcomes. Multiple investigations on the causes of allergic diseases report that avoiding food allergies might be related to early consumption of these allergens. Alternatively, delaying the contact with allergenic nourishments, explored in contemporary research, has been proven to result in a higher prevalence of allergies among children, originating such conditions as atopic diseases and extreme sensitization to foods. The current paper compares the two prominent strategies of allergenic food introduction, gathering the most pertinent modern evidence to distinguish whether exposure to food allergens should be delayed or advanced.

Anorexia nervosa (AN) is a persistent psychiatric disorder that is marked by abnormal reduced weight and amenorrhea, which may be primary or secondary. AN affects multiple endocrine axes such as gonadal, thyroid, and adrenal axis, growth hormone, and insulin-like growth factor-1, adipokines such as leptin, gut peptides like ghrelin, peptide YY, and amylin. As a result of these changes bone mineral density is reduced, which increases the risk of bone fracture in patients. In this review, we focus on substantial endocrine alterations in AN with a particular emphasis on the severe bone loss associated with this condition and current bone therapies. The disorder primarily affects girls and women, who are the focus of this review. Although the majority of AN-related endocrinopathies improve over time, long-term consequences such as short stature, osteoporosis, and infertility may occur. To avoid serious consequences, nutrition therapy in these patients requires a full understanding of bone complications, and new therapeutic options for treatment should be researched.

Multiple myeloma is a pathology of plasma cells, with one of the most common side effects of its treatment is heart failure. In addition, cardiac amyloidosis could cause heart failure by itself. Even though mechanisms of cardiac amyloidosis are known, and they involve lysosomal dysfunction, reactive oxygen species (ROS) accumulation, and infiltrative effect by fibrils, there is no specific agent that could protect from these effects. While the molecular mechanism of doxorubicin cardiotoxicity via topoisomerase II β is established, the only FDA-approved agent for treatment is dexrazoxane. Liposomal doxorubicin can potentially improve response and decrease the development of heart failure due to microscopic liposomes that can accumulate and penetrate only tumor vasculature. Supplements that enhance mitochondrial biogenesis are also shown to improve doxorubicin-induced cardiotoxicity. Other agents, such as JR-311, ICRF-193, and ursolic acid, could potentially become new treatment options. Proteasome inhibitors, novel agents, have significantly improved survival rates among multiple myeloma patients. They act on a proteasome system that is highly active in cardiomyocytes and activates various molecular cascades in malignant cells, as well as in the heart, through nuclear factor kappa B (NF-kB), endoplasmic reticulum (ER), calcineurin-nuclear factor of activated T-cells (NFAT), and adenosine monophosphate-activated protein kinase (AMPKa)/autophagy pathways. Metformin, apremilast, and rutin have shown positive results in animal studies and may become a promising therapy as cardioprotective agents. This article aims to highlight the main molecular mechanisms of heart failure among patients with multiple myeloma and potential treatment options to facilitate the development and research of new preventive strategies. Hence, this will have a positive impact on life expectancy in patients with multiple myeloma.

Biliary cancer (BC) is a rare disease. It is formed from the biliary epithelium of the small ducts in the liver periphery (intrahepatic) and the main ducts of the hilum (extrahepatic). The incidence of intrahepatic carcinoma is rising in the western world, and the incidence of gallbladder cancer is declining. Surgical treatment is the primary treatment option for localized forms of these tumors, but only a small group of patients is eligible for it. Palliative therapy is the standard treatment option for those with advanced cases, and it mainly relies on chemotherapy. The advanced form's five-year survival of BC does not exceed 5%. However, targeted therapy aimed at tumors with fusion mutations of the fibroblast growth factor receptor (FGFR), isocitrate dehydrogenase (IDH) 1 and 2, the genes encoding the B-Raf protein (BRAF), breast cancer (BRCA1/2), epidermal growth factor receptor 2 (HER2), and the neurotrophic receptor tyrosine kinase gene (NTRK), is gradually changing the paradigm in the treatment of this disease. This can be seen especially in approaches to treating intrahepatic cholangiocarcinoma, which is associated with a high incidence of mutations. This literature review aims to provide the latest scientific evidence regarding targeted therapy in treating cholangiocarcinoma.