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Advances in the field of oncology have led to the advent of doxorubicin (DOX), an anthracycline chemotherapeutic agent, through which cancer survival rates have remarkably improved. There has, however, been a rise in adverse effects from the use of DOX, most notably cardiotoxicity. DOX-induced cardiotoxicity is thought to arise through the generation of reactive oxygen species (ROS), causing mitochondrial dysfunction in the cardiomyocytes. This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards and focused on cancer patients undergoing DOX therapy. The research question addressed interventions aimed at preventing DOX-induced cardiotoxicity. Google Scholar, PubMed, and ScienceDirect databases were used to conduct a systematic search. Next, screening was carried out by reviewing the title and abstract of various articles to exclude irrelevant studies, followed by the retrieval of full-text articles. Scale for the assessment of narrative review articles 2 (SANRA 2) for narrative reviews, a measurement tool to assess systematic reviews (AMSTAR) checklist for systematic reviews, and the Cochrane risk of bias tool for randomized controlled trials (RCTs) were the tools employed for quality assessment. This systematic review provides convincing evidence about preventive interventions to counteract DOX-induced cardiotoxicity. Primary prevention strategies against DOX-induced cardiotoxicity include pharmacological and non-pharmacological measures. Dexrazoxane reduces cardiotoxicity without therapeutic compromise. Beta-blockers showed mixed results in preserving cardiac function. The research on renin-angiotensin-aldosterone system (RAAS) inhibitors suggests that most of these agents can reduce the risk of DOX-induced cardiotoxicity. The liposomal formulation of DOX decreases cardiotoxicity without sacrificing effectiveness. Chemotherapy regimens should be supplemented with cardioprotective medications to increase therapeutic efficacy and lower cardiac risks. Exercise is an essential non-pharmacological strategy for decreasing DOX-induced cardiotoxicity. It acts by lowering oxidative stress, maintaining mitochondrial function, and averting apoptosis. Other non-pharmacological interventions through antioxidative, anti-apoptotic, and mitochondrial protective mechanisms, such as resveratrol, vitamin E, curcumin, and visnagin, show promise in lowering DOX-induced cardiotoxicity and may be useful as supplementary therapy during cancer treatment. In conclusion, this review highlights the need for a multimodal strategy that incorporates different tactics, as well as the need for additional research and strong clinical trials, with the ultimate goal of protecting cardiac health in patients receiving chemotherapy with DOX.
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Castleman disease (CD) comprises a rare spectrum of disorders characterized by benign lymphoepithelial proliferation, classified into unicentric and multicentric forms. The idiopathic multicentric Castleman disease (iMCD) subtype, specifically, is challenging to diagnose and treat due to its variable manifestations and unpredictable disease course. We report a case of a 23-year-old female with a history of iron deficiency anemia presenting with concurrent antiphospholipid syndrome (APS) and human herpesvirus-6 (HHV-6) positivity. Investigations revealed a gastric mass, with a biopsy suggestive of the plasma cell variant of CD. This case report aims to understand the possible association of HHV-6 positivity with CD and the significance of diagnosing APS early in patients with the disease. Treatment with siltuximab and tocilizumab proved effective, highlighting the role of interleukin 6 (IL-6) in the elusive etiology of this condition.
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Evans syndrome (ES) is characterized by a combination of autoimmune hemolytic anemia (AIHA) and immune thrombocytopenia (ITP). Immune dysregulation, which results in the development of antibodies against blood cells, is its defining feature. ES being a diagnosis of exclusion requires a thorough workup to rule out other probable illnesses like lymphoproliferative diseases and systemic lupus erythematosus (SLE). We present the case of a 38-year-old male who experienced shortness of breath, chest discomfort, and generalized weakness. His medical history included recurrent anemia, thrombocytopenia, and pulmonary tuberculosis in remission. Hemolysis, thrombocytopenia, and a large pericardial effusion were discovered during the physical examination and investigations. An initial treatment strategy that included pericardiocentesis was performed. In combination with AIHA and ITP, the clinical and laboratory findings strongly suggested ES, which improved with prednisolone therapy. First-line treatments consist of corticosteroids and intravenous immunoglobulin; refractory cases may also require rituximab, thrombopoietin receptor antagonists, and sirolimus. Achieving remission and lowering relapse rates need careful patient monitoring and customized treatment programs.
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Key Clinical Message: Identifying pulmonary pathology while evaluating electrolyte disorders is crucial for optimal patient management. Physicians working in endemic regions of tuberculosis should consider this pathology as a differential for electrolyte imbalances. Abstract: Hyponatremia, a common electrolyte imbalance, can arise from various underlying etiologies such as diuretics, diarrhea, vomiting, congestive heart failure, and liver and renal disease. We present a case report of a 74-year-old man highlighting the association between pulmonary tuberculosis (TB) and the development of hyponatremia. GeneXpert assay of the patient's sputum sample led to the identification of underlying active pulmonary TB as the cause of hyponatremia. The patient was started on anti-TB therapy, and concurrent fluid restriction and sodium supplementation were initiated to correct the electrolyte imbalance. Over the next 3 days, the patient demonstrated clinical improvement with the resolution of hyponatremia. This case also highlights the importance of considering TB as a potential etiology in patients presenting with hyponatremia, especially in endemic areas. Further research is warranted to explore the mechanistic pathways linking pulmonary TB and hyponatremia, aiding in the development of targeted therapeutic interventions.
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[This corrects the article DOI: 10.7759/cureus.50541.].
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Key Clinical Message: Peripheral eosinophilia is a rare but potential sign of TB infection. Physicians should assess patients for TB, especially if they display related symptoms or risk factors, and consider TB as a differential diagnosis, especially in idiopathic cases. Abstract: Millions of new tuberculosis (TB) cases are reported annually. Peripheral eosinophilia is rare in tuberculosis. We describe a rare case of tuberculosis with a high peripheral eosinophil count. A 9-year-old male presented with fever, cough, and respiratory discomfort for a month. The patient's cough did not respond to treatment, along with weight loss and a loss of appetite. A physical examination revealed cervical lymphadenopathy and bilateral lung crepitations. A hematological investigation showed a high eosinophil count of 25,920 cells per cubic millimeter and medical imaging abnormalities consistent with TB. Some malignancies, allergies, and parasitic infections produce peripheral eosinophilia. However, medical literature rarely discusses TB-induced eosinophilia. Several studies attribute it to mycobacterium antigen hyperreactivity. Eosinophilic release of cytotoxic chemicals may cause tissue damage, and TB patients' eosinophil levels may fluctuate. This case report emphasizes the need to investigate TB in peripheral eosinophilia patients after ruling out other explanations. Our patient benefited from early detection and anti-TB medication. More studies are required to investigate the causes of TB eosinophilia and its consequences. A detailed medical history and physical examination are essential to diagnose and treat atypical presentations of TB.
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Helicobacter pylori has been reported as a health problem worldwide, affecting a sizable portion of people. Peptic ulcers, gastric cancer, and various extra gastric conditions are associated with this bacterium. The rampant overprescribing of antibiotics has led to the emergence of H. pylori strains resistant to multiple antibiotics, causing a decline in the effectiveness of current treatments. Recently, there has been growing interest in researching alternative treatment options for H. pylori infections that do not respond to initial therapy. Rifabutin, a rifamycin derivative initially designed for tuberculosis treatment and preventing Mycobacterium avium complex infection, has gained attention as a potential rescue medication. It has shown efficacy against H. pylori and the potential to eradicate the bacterium when combined with other antibiotics. This systematic review article focuses on using rifabutin-based regimens as a treatment option after initial treatments have failed. The authors screened literature published in the last five years, between 2017 and 2022, across various search engines and closely examined relevant studies following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. The search covered a variety of electronic databases and focused on H. pylori gastritis, rifabutin-based treatment plans, and in vivo investigations in healthy individuals. The comprehensive review provides convincing evidence that rifabutin-based regimens are effective rescue treatments for H. pylori infections. Multiple studies in various areas consistently demonstrated high eradication rates, ranging from 70% to 90%, when rifabutin-containing regimens were used. The analysis found that only a tiny percentage of H. pylori strains (1%) were resistant to rifabutin therapy, further supporting the viability of Rifabutin as an alternative when other antibiotics failed to eradicate H. pylori. The cost of Rifabutin is a significant factor that may limit its accessibility, particularly in resource-constrained settings where H. pylori infection is common. Moreover, the potential side effects of Rifabutin, such as hematological problems, rashes, and digestive issues, need to be considered. However, these side effects are typically manageable and can be reduced by combining Rifabutin with other antibiotics. In conclusion, this systematic review provides evidence supporting the effectiveness of regimens derived from Rifabutin in eliminating H. pylori infections after initial therapy failure. Due to the observation that Rifabutin effectively eradicates resistant H. pylori infections, it can be considered a suitable choice for rescue therapy. Rifabutin-containing regimens should be reserved as fourth- or later-line therapy options, considering economic factors, the risk of microbial resistance, potential side effects, and the availability of alternative medications. Future research should focus on optimizing rifabutin-based regimens and investigating combination therapies that have better H. pylori eradication rates while also addressing the problem of resistant strains.