Tumor-associated macrophages derived exosomes; from pathogenesis to therapeutic opportunities.

Tumor-associated macrophages (TAMs) exert profound influences on cancer progression, orchestrating a dynamic interplay within the tumor microenvironment. Recent attention has focused on the role of TAM-derived exosomes, small extracellular vesicles containing bioactive molecules, in mediating this intricate communication. This review comprehensively synthesizes current knowledge, emphasizing the diverse functions of TAM-derived exosomes across various cancer types. The review delves into the impact of TAM-derived exosomes on fundamental cancer hallmarks, elucidating their involvement in promoting cancer cell proliferation, migration, invasion, and apoptosis evasion. By dissecting the molecular cargo encapsulated within these exosomes, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and proteins, the review uncovers key regulatory mechanisms governing these effects. Noteworthy miRNAs, such as miR-155, miR-196a-5p, and miR-221-3p, are highlighted for their pivotal roles in mediating TAM-derived exosomal communication and influencing downstream targets. Moreover, the review explores the impact of TAM-derived exosomes on the immune microenvironment, particularly their ability to modulate immune cell function and foster immune evasion. The discussion encompasses the regulation of programmed cell death ligand 1 (PD-L1) expression and subsequent impairment of CD8 + T cell activity, unraveling the immunosuppressive effects of TAM-derived exosomes. With an eye toward clinical implications, the review underscores the potential of TAM-derived exosomes as diagnostic markers and therapeutic targets. Their involvement in cancer progression, metastasis, and therapy resistance positions TAM-derived exosomes as key players in reshaping treatment strategies. Finally, the review outlines future directions, proposing avenues for targeted therapies aimed at disrupting TAM-derived exosomal functions and redefining the tumor microenvironment.

Performance of existing diagnostic criteria for palindromic rheumatism.

BACKGROUND: Four criteria have been proposed for the diagnosis of palindromic rheumatism (PR), including those of Hannonen et al., Passero and Barbieri, Guerne and Weisman, and Gonzalez-López. But none of these criteria has been validated. In this research, we investigated the performance of these diagnostic criteria for diagnosing PR. METHODS: In this study, PR and control groups were consecutively recruited from a prospective cohort of intermittent arthritis. Inclusion criteria for PR group were diagnosing PR by an expert rheumatologist, age ≥ 18, having at least 6 months follow-up, and ruling out of other causes of intermittent arthritis. These criteria were applied to both groups. Sensitivity, specificity, positive predictive value, negative predictive value, diagnostic odds ratio (DOR), and Youden's index were calculated for each criteria. RESULTS: This study included 197 consecutive subjects diagnosed with PR and 208 subjects with a diagnosis other than PR. The sensitivity of Hannonen et al. criteria was higher than the Gonzalez-Lopez, Guerne and Weisman, and Pasero and Barbieri criteria (96.4% versus 95.4%, 79.2%, and 35.5%, respectively). The specificity of the Pasero and Barbieri criteria was higher than the other criteria. Hannonen al. criteria with a DOR of 325.7, had the highest DOR. In descending order, the best accuracy belonged to Hannonen et al., Gonzalez-Lopez, Guerne and Weisman, and Pasero and Barbieri criteria (94.3%, 94.1%, 86.4%, and 66.9% respectively). CONCLUSION: This study showed that the Hannonen et al. and Gonzalez-Lopez criteria have a better performance in diagnosing PR. Key Points • The sensitivity of Hannonen et al. criteria and the specifity of Passero and Barbieri criteria are higher than other proposed criteria for diagnosis of palindromic rheumatism. • Hannonen et al. criteria with a sensitivity of 96.4%, specifity of 92.3% and accuracy of 94.3% has the best performance in diagnosis of palindromic rheumatism between existing diagnostic criteria for palindromic rheumatism.

Inhibitory effect of microRNA-21 on pathways and mechanisms involved in cardiac fibrosis development.

Cardiac fibrosis is a pivotal cardiovascular disease (CVD) process and represents a notable health concern worldwide. While the complex mechanisms underlying CVD have been widely investigated, recent research has highlighted microRNA-21's (miR-21) role in cardiac fibrosis pathogenesis. In this narrative review, we explore the molecular interactions, focusing on the role of miR-21 in contributing to cardiac fibrosis. Various signaling pathways, such as the RAAS, TGF-ß, IL-6, IL-1, ERK, PI3K-Akt, and PTEN pathways, besides dysregulation in fibroblast activity, matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs cause cardiac fibrosis. Besides, miR-21 in growth factor secretion, apoptosis, and endothelial-to-mesenchymal transition play crucial roles. miR-21 capacity regulatory function presents promising insights for cardiac fibrosis. Moreover, this review discusses numerous approaches to control miR-21 expression, including antisense oligonucleotides, anti-miR-21 compounds, and Notch signaling modulation, all novel methods of cardiac fibrosis inhibition. In summary, this narrative review aims to assess the molecular mechanisms of cardiac fibrosis and its essential miR-21 function.

Unraveling cardiac fibrosis: insights into microRNA-21's key role and promising approaches for controlCardiac fibrosis poses a significant global health threat and plays a central role in cardiovascular diseases. This examination delves into recent research revealing the participation of microRNA-21 (MiR-21) in the progression of cardiac fibrosis, providing insight into its critical function in this process. The investigation explores diverse molecular interactions, underscoring MiR-21's contribution to the development of cardiac fibrosis. Various signaling pathways, including the Renin-Angiotensin-Aldosterone System, TGF-ß, IL-6, IL-1, ERK, PI3K-Akt, and PTEN pathways, coupled with disturbances in fibroblast activity, matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs (TIMPs), contribute to cardiac fibrosis. MiR-21's influence on growth factor secretion, apoptosis, and endothelial-to-mesenchymal transition further emphasizes its crucial role. What adds promise to MiR-21 is its capacity for regulation, providing potential insights into controlling cardiac fibrosis. The review also investigates various methods to modulate MiR-21 expression, such as antisense oligonucleotides, anti-miR-21 compounds, and Notch signaling modulation ­ innovative approaches showing potential in inhibiting cardiac fibrosis. In summary, this narrative review aims to dissect the complex molecular mechanisms behind cardiac fibrosis, explicitly emphasizing the indispensable role of MiR-21. By comprehending these mechanisms, researchers can lay the groundwork for inventive interventions and therapeutic strategies to hinder cardiac fibrosis, ultimately contributing to advancing cardiovascular health.

Sudden onset of symptoms in concurrent Takayasu arteritis and Ulcerative colitis: A case report with neurological complications.

Key Clinical Message: The rare co-occurrence of takayasu arteritis (TAK) and ulcerative colitis (UC), presenting with asymptomatic onset and neurological complications, highlights the importance of an integrated diagnostic approach for overlapping autoimmune conditions. Abstract: We present a rare case of a 44-year-old female diagnosed with both UC and TAK, characterized by an unusual acute asymptomatic onset accompanied by neurological manifestations. The patient exhibited symptoms of acute ischemic stroke along with vascular abnormalities, as well as colon inflammation associated with UC. The patient's asymptomatic presentation at the onset differs from previously reported cases. The presence of additional complications, such as hepatocellular adenoma and primary sclerosing cholangitis, further complicated the diagnostic challenges. The patient's treatment involved a combination of methylprednisolone, azathioprine, and prednisolone leading to improved clinical outcomes. This case emphasizes the complexity involved in diagnosing overlapping conditions and highlights the significance of TAK in presenting atypical manifestations in relation to UC. Furthermore, this case contributes to the limited literature, underscoring the need for early detection and comprehensive treatment approaches.

Challenging in leprosy relapse with antiphospholipid syndrome diagnosis: A case report.

Key Clinical Message: Infectious diseases like leprosy can cause antiphospholipid antibodies, leading to blood clots. Clinicians should consider this for patients with unusual thrombotic events and prior infectious disease history. Abstract: This case report details the diagnostic challenge of a 42-year-old man with a history of treated leprosy who presented with clinical features suggestive of antiphospholipid syndrome (APS). Vascular angiography revealed thrombosis, and serological tests were positive for APS antibodies. However, the patient subsequently developed symptoms, including thenar atrophy, paresthesia, and hypopigmented skin patches, which prompted further investigation. Electromyography detected sensorimotor polyneuropathy, while a nerve biopsy indicated a resurgence or chronic presence of leprosy. Despite initial APS management, the case evolved into a leprosy relapse confirmation after 20 years of remission, underscoring the diagnostic intricacies when concurrent autoimmune antibodies and infectious disease manifestations are present. This report emphasizes the importance of considering a broad differential diagnosis, including the potential for infectious disease relapse, in the presence of antiphospholipid antibodies. It illustrates the necessity of an interdisciplinary treatment approach in complex clinical scenarios.

Acute myeloid leukemia with unreported translocation (x; 3) (q24; p13): A case report.

Key Clinical Message: Novel and rare chromosomal aberrations in AML are important to understand, particularly if associated with tumorigenesis and how they contribute to prognostic risk. It is important that acute leukemia be treated right away. Herein, novel (x; 3) (q24; p13) is described. Abstract: Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow. It is the most common type of acute leukemia in adults. This type of cancer usually gets worse quickly if it is not treated. Here, we report an unusual case of AML with an unreported translocation associated with AML.

The Hepatoprotective Effects of Ginsenoside from Ginseng: A Review of Molecular Mechanisms and Therapeutic Potentials.

Treatment of hepatic diseases presents a significant challenge due to their diverse nature. Ginsenosides, bioactive compounds derived from the root of Panax ginseng and widely used in traditional Chinese medicine, offer multifaceted protection to various organs in the body. Their versatile effects, including antioxidant, anti-inflammatory, anti-apoptotic and more, make them a promising approach for addressing hepatic disorders. This review explores the intricate molecular mechanisms and properties of ginsenosides in the prevention and treatment of liver ailments, from mild conditions to severe damage and liver fibrosis. Given the increasing prevalence of hepatic disorders, this article sheds light on the significant pharmaceutical potential of ginsenosides in the realm of hepatic disease management.

Advances in Monoclonal Antibody Therapies for Triple-Negative Breast Cancer: Immunotherapeutic and Targeted Strategies.

Triple-negative breast cancer (TNBC) presents considerable obstacles because of its highly aggressive characteristics and limited availability of specific therapeutic interventions. The utilization of monoclonal antibody (mAb)-based immunotherapy is a viable approach to tackle these difficulties. This review aims to examine the present state of mAb-based immunotherapy in TNBC, focusing on the underlying mechanisms of action, clinical applications, and existing challenges. The effectiveness of mAbs in reducing tumor development, regulating immune responses, and changing the tumor microenvironment has been demonstrated in many clinical investigations. The challenges encompass several aspects such as the discovery of biomarkers, understanding resistance mechanisms, managing toxicity, considering costs, and ensuring accessibility. The future is poised to bring forth significant advancements in the field of biomedicine, particularly in the areas of new mAbs, personalized medicine, and precision immunotherapy. In conclusion, mAb-based immunotherapy has promise in revolutionizing the treatment of TNBC, hence providing a possible avenue for enhanced patient outcomes and quality of life.

A case of familial Mediterranean fever presenting with ankylosing spondylitis: A rare case-report.

Key Clinical Message: The association of familial Mediterranean fever and ankylosing spondylitis is rare, but it is essential to consider this diagnosis in patients with a history of FMF who develop symptoms of back pain or other rheumatologic conditions. Abstract: Familial Mediterranean fever (FMF) is an inherited inflammatory disorder characterized by recurrent fever episodes, abdominal pain, and arthralgia. Ankylosing spondylitis (AS) is a chronic inflammatory disease that affects the spine's joints. The association of FMF and AS is rare. We report the case of a 22-year-old male patient with a history of FMF and a positive family history of FMF in his father, who presented with inflammatory back pain. The patient was found to have sacroiliitis on MRI, which is a characteristic feature of AS. The patient was negative for HLA-B27, a genetic marker often associated with AS. This case report highlights the importance of considering AS in patients with a history of FMF who develop back pain symptoms or other rheumatologic conditions.

Axonal sensory-motor polyneuropathy in ankylosing spondylitis: A case report.

Key Clinical Message: In ankylosing spondylitis cases, axonal-type sensory-motor polyneuropathy is a rare manifestation and should be considered an underlying etiology in patients with unexplained neuropathy. Abstract: This case report discusses a 45-year-old male diagnosed with ankylosing spondylitis (AS), a chronic inflammatory disorder affecting the axial skeleton and peripheral joints. The patient presented with polyneuropathy, characterized by tingling and numbness in the upper and lower limbs, which is an uncommon manifestation of AS. After undergoing various tests, including CT scans and EMG-NCV, no secondary cause for the neuropathy was identified; AS was considered the etiology of the patient's axonal-type sensory-motor polyneuropathy.

Don't eat me/eat me signals as a novel strategy in cancer immunotherapy.

Cancer stands as one of the prominent global causes of death, with its incidence burden continuously increasing, leading to a substantial rise in mortality rates. Cancer treatment has seen the development of various strategies, each carrying its drawbacks that can negatively impact the quality of life for cancer patients. The challenge remains significant within the medical field to establish a definitive cancer treatment that minimizes complications and limitations. In the forthcoming years, exploring new strategies to surmount the failures in cancer treatment appears to be an unavoidable pursuit. Among these strategies, immunology-based ones hold substantial promise in combatting cancer and immune-related disorders. A particular subset of this approach identifies "eat me" and "Don't eat me" signals in cancer cells, contrasting them with their counterparts in non-cancerous cells. This distinction could potentially mark a significant breakthrough in treating diverse cancers. By delving into signal transduction and engineering novel technologies that utilize distinct "eat me" and "Don't eat me" signals, a valuable avenue may emerge for advancing cancer treatment methodologies. Macrophages, functioning as vital components of the immune system, regulate metabolic equilibrium, manage inflammatory disorders, oversee fibrosis, and aid in the repair of injuries. However, in the context of tumor cells, the overexpression of "Don't eat me" signals like CD47, PD-L1, and beta-2 microglobulin (B2M), an anti-phagocytic subunit of the primary histocompatibility complex class I, enables these cells to evade macrophages and proliferate uncontrollably. Conversely, the presentation of an "eat me" signal, such as Phosphatidylserine (PS), along with alterations in charge and glycosylation patterns on the cellular surface, modifications in intercellular adhesion molecule-1 (ICAM-1) epitopes, and the exposure of Calreticulin and PS on the outer layer of the plasma membrane represent universally observed changes on the surface of apoptotic cells, preventing phagocytosis from causing harm to adjacent non-tumoral cells. The current review provides insight into how signaling pathways and immune cells either stimulate or obstruct these signals, aiming to address challenges that may arise in future immunotherapy research. A potential solution lies in combination therapies targeting the "eat me" and "Don't eat me" signals in conjunction with other targeted therapeutic approaches. This innovative strategy holds promise as a novel avenue for the future treatment of cancer.

Castleman disease presenting as lymphadenopathy in a female with systemic lupus erythematosus: A rare case report.

Castleman disease is an infrequent disease that affects the lymph nodes and related tissues. The condition may manifest with lymphadenopathy, characterized by the enlargement of the lymph nodes, alongside additional symptoms such as high fever, nocturnal sweating, exhaustion, and loss of body mass. The diagnosis of Castleman disease typically entails a multifaceted approach that includes a physical examination, imaging modalities, and a biopsy of the lymph nodes that are affected. The selection of treatment modalities is contingent upon the classification and extent of the disease. Systemic lupus erythematosus (SLE) has been identified as a potential risk factor for the development of lymphoma, a condition that may manifest with lymphadenopathy resembling Castleman disease. Hence, it is crucial for individuals diagnosed with SLE and exhibiting lymphadenopathy to undergo a comprehensive assessment to exclude the possibility of any other associated disease. Although lymphadenopathy is a common symptom shared by both Castleman illness and SLE, these diseases have distinct etiologies and are treated in different ways. Seeking advice from a healthcare practitioner is crucial in order to obtain an accurate diagnosis and effective treatment. A 39-year-old female patient with a history of SLE since 18 years ago and lupus nephritis since 6 years ago which treated with Mycophenolic Acid 2 g daily, Hydroxychloroquine 400 mg daily, and low doses of Prednisolone. Also, Mycophenolic Acid has discontinued for her 5 months ago due to the reduction of proteinuria and the control of the disease. Although the association of Castleman Disease with SLE is infrequent, establishing a connection between them could prove advantageous in the treatment and etiology of diseases.

Outcomes of undifferentiated peripheral inflammatory arthritis in real-world practice. A longitudinal cohort study.

OBJECTIVES: Undifferentiated peripheral inflammatory arthritis (UPIA) may have 3 different courses, including evolution to differentiated arthritis, remaining undifferentiated, and self-limited course. The purpose of this study was to provide a real-world evidence for predictors of outcomes in UPIA in a longitudinal cohort of patients. METHODS: Patients enrolled in the CTDRC-UA cohort were screened for eligibility. Inclusion criteria were: (i) having synovitis in ≥ 1 joint, (ii) not meeting the criteria of any other rheumatic disease, (iii) having at least 2 visits per year, iv) included in the cohort during the period of 2004 to 2021, and (v) having active disease at cohort entry. Two hundred and three patients who met the inclusion criteria were followed up until January 2023. RESULTS: Medication-free remissions occurred in 42 (20.7%) cases. In 24 (11.8%) cases, the disease met the criteria of other rheumatic diseases, of which rheumatoid arthritis (RA) was the most common. In addition, joint damage occurred in 33 (16.3%) cases. Predictors of medication-free remissions were absence of comorbidity, starting a sustained remission at ≤ 6 months, and having no flare. Factors associated with disease evolution to RA were anti-citrullinated peptide antibody (ACPA) positivity, non-adherence to therapy, not going into sustained remission and having flare. Delay in treatment for > 3 months and being ACPA positive were the predictors of joint damage. CONCLUSION: Although the majority of UIPA cases treated with step-up combination therapy with DMARDs do not progress to RA, most require continued treatment and a few achieve medication-free remissions. Key Points • Undifferentiated peripheral inflammatory arthritis (UPIA) can progress to rheumatoid arthritis in 11% of cases; and lack of sustained remission, being anti-citrullinated peptide antibody positive, non-adherence to therapy, and having flare are its predictors. • Medication-free remissions occur in 21% of patients with UPIA; and absence of comorbidity, starting a sustained remission at ≤ 6 months, and having no flare are its predictors. • Initiating treatment in the window of opportunity may lead to a better joint outcome.

TTP-like syndrome and its relationship with complement activation in critically ill patients with COVID-19: A cross-sectional study.

Background: The covid-19 disease has caused many deaths worldwide since December 2019. Many thromboembolic events, such as VTE and TTP, have been reported since the beginning of this pandemic. Considering the prominent role of complement in developing TTP and TTP-like syndrome in recent studies, this study aimed to assess the prevalence of TTP-like syndrome and its relationship with complement activity in critically ill patients with COVID-19. Method: This study was conducted on 77 COVID-19 patients admitted to the ICU wards of Tabriz Imam Reza hospital from March to June 2021. TTP-like syndrome was diagnosed using a blood specimen for evidence of thrombocytopenia, microangiopathic hemolysis (low hemoglobin, increased LDH level, schistocytes in a peripheral blood smear, and negative direct agglutination test), and end-organ injury, including acute kidney injury or neurological deficit. ADAMTS 13 activity levels could not be achieved owing to logistic issues; therefore, we could not accurately diagnose TTP and TTP-like syndrome based on ADAMTS 13 levels, so to increase the accuracy of diagnosis, we have included people with classical pentad evidence in the TTP-like syndrome group. Complement parameters, including C3, C4, and CH50, were measured. Result: Seven cases of TTP-like syndrome were diagnosed using the previously mentioned criteria, which stands for 9.1% of the study population. Compared with patients without TTP-like syndrome, C3 was significantly lower in patients with TTP-like syndrome (p-value = 0.014), and C4 and CH50 demonstrated insignificant differences between the two groups (p-value = 0.46, p-value = 0.75). Conclusion: Our study showed that the TTP-like syndrome was present in a significant percentage of critically ill patients with COVID-19. Lower C3 levels in TTP-like syndrome-diagnosed patients can indicate complement activation as one of the influential factors in initiating TTP-like syndrome in COVID-19 patients. More studies are recommended to clarify the exact mechanism to achieve adequate therapeutic methods and better manage the disease and its complications.

Prevalence and predictors of long-term remission in rheumatoid arthritis in real-world practice: a longitudinal study.

OBJECTIVES: The aim of the present study was to provide real-world evidence for factors predicting long-term remission in a longitudinal study of rheumatoid arthritis (RA) patients. METHODS: Long-term remission was defined by meeting American Rheumatism Association (ARA) criteria for remission and prednisolone dose ≤ 5 mg/d for at least 5 years. Patients in this cohort were treated by tight control strategy using step-up combination therapy with conventional synthetic DMARDs (csDMARDs), biologic DMARDs. The parameters associated with long-term remission were subjected to univariate analysis, and parameters with P-values of < 0.1 in univariate analysis were included in a multivariate regression analysis. RESULTS: One thousand two hundred and eighty-six RA subjects were considered for eligibility, and finally, 499 patients were included in the study. Median duration of follow-up was 108 months. Long-term remission occurred in 157 (31.5%) patients. Median time to long-term remission was 8 (5, 41) months. Predictors of long-term remission were absence of flare during the course of disease, occurrence of sustained remission during 6 months after starting therapy, age at the disease onset > 60, being anti-citrullinated protein antibodies (ACPA) negative, and Disease Activity Score-28 (DAS28) at cohort entry ≤ 5.1. CONCLUSION: In real-world practice, long-term remission occurs in 31.5% of patients treated with a tight control strategy. Absence of flare during the course of disease, occurrence of sustained remission during 6 months after starting therapy, age at the disease onset > 60, being ACPA negative, and DAS28 at baseline ≤ 5.1 are independent predictors of long-term remission. Key Points • In real-world practice, long-term remission occurs in 31.5% of patients treated with a tight control strategy. • Median time to long-term remission was 8 months. • Absence of flare during the course of disease, occurrence of sustained remission during 6 months after starting therapy, age at the disease onset >60, being ACPA negative, and DAS28 at baseline ≤ 5.1 are independent predictors of long-term remission.

Circulating glucagon-like peptide-1 level in patients with liver cirrhosis.

BACKGROUND: Glucagon-like peptide-1 (GLP-1), a gut-derived incretin hormone, plays a pivotal role in glucose-induced insulin secretion. Currently, the role of incretin hormones in the pathogenesis of cirrhosis is not clearly defined. This study aimed to investigate circulating levels of GLP-1 in liver cirrhosis and its association with the severity of liver disease. METHODS: A total of 80 participants including 39 patients with a definite diagnosis of liver cirrhosis and 41 healthy controls recruited in this cross-sectional study. Circulating levels of GLP-1 were determined using the ELISA method. The severity of liver cirrhosis was assessed according to the Child-Pugh, MELD (i), MELD-Na, MELD New, and UK end-stage liver disease score (UKELD) criteria. RESULTS: The mean age of patients and healthy subjects was 42.51 ± 12.80 and 42.07 ± 10.92 years, respectively (p value = .869). The mean MELD (i), MELD-Na, MELD New, UKELD, and Child-Pugh scores were 14.36 ± 4.26, 15.26 ± 4.81, 14.74 ± 4.66, 52.33 ± 3.82, and 7.28 ± 1.50, respectively. In this study, circulating levels of GLP-1 were statistically lower in cirrhotic patients compared with healthy controls (95.26 ± 17.15 vs 111.84 ± 38.14 pg/mL; p value = .017). CONCLUSION: Larger prospective studies are needed to explore the incretin effect in cirrhosis patients compared with healthy individuals.

Immune checkpoints and their promising prospect in cholangiocarcinoma treatment in combination with other therapeutic approaches.

Cholangiocarcinoma (CCA) is one of the malignant tumors that has shown rapid development in incidence and mortality in recent years. Like other types of cancer, patients with CCA experience alterations in the expression of immune checkpoints, indicating the importance of immune checkpoint inhibitors in treating CCA. The results of TCGA analysis in this study revealed a marginal difference in the expression of important immune checkpoints, Programmed cell death 1 (PD-1) and Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and their ligands in CCA samples compared to normal ones. This issue showed the importance of combination therapy in this cancer. This review considers CCA treatment and covers several therapeutic modalities or combined treatment strategies. We also cover the most recent developments in the field and outline the important areas of immune checkpoint molecules as prognostic variables and therapeutic targets in CCA.

Pulse pressure and inferior wall ST-segment elevation myocardial infarction: investigating mortality, hospital major cardiovascular events, and long-term prognosis.

Inferior Wall ST-Segment Elevation Myocardial Infarction (INF STEMI) is a severe condition with high mortality. Rapid treatment with Primary Percutaneous Coronary Intervention (PPCI) is preferred. Pulse Pressure (PP) is a known risk factor for both cardiovascular disease and may be a valuable predictor of outcomes in these patients. The study aims to evaluate the relationship between PP and long-term prognosis, mortality, and major cardiovascular events after inferior STEMI in cases who underwent PPCI. This cross-sectional study included subjects with a confirmed diagnosis of inferior STEMI who underwent PPCI. Patient data were gathered from hospital records and analyzed for the relationship between PP and MACE during hospitalization and one-year follow-up. Statistical analysis was performed using SPSS. This cross-sectional study of 320 cases found that DM, DBP, and Cr patients had a higher incidence of MACEs (P-value #x003C;0.05). Subjects with higher LVEF and SBP had fewer MACEs (P-value #x003C;0.05). Cases with a PP of ≤50 had a higher mortality and heart failure incidence during hospitalization than those with a PP >50 (P-value #x003C;0.05). However, the two groups had no significant difference in one-year MACE rates. The study found that increasing DBP, Cr, and DM and decreasing LVEF and SBP impacted MACE incidence. PP ≤50 had more heart failure incidence and mortality during hospitalization in patients with inferior STEMI.

SLE-associated myelitis successfully treated by rituximab.

Systemic lupus erythematosus (SLE) is an autoimmune disease. Transverse myelitis (TM) is one of the rare neurological manifestations of SLE. Here, we present a case of SLE in which TM precede other symptoms and successfully treated by Rituximab.

Diagnostic Performance of Magnetic Resonance Imaging for Detection of Acute Appendicitis in Pregnant Women; a Systematic Review and Meta-Analysis.

Introduction: The diagnosis of acute appendicitis (AA) in pregnant women is commonly challenging owing to the normal results of laboratory tests, organ displacement, and normal physiological inflammatory alterations. This meta-analysis aimed to investigate the accuracy of magnetic resonance imaging (MRI) in diagnosis of AA in pregnant women. Methods: Two investigators independently performed a comprehensive systematic literature search of electronic databases including MEDLINE, Cochrane Central, EMBASE, Web of Science, Scopus, and Google Scholar to identify studies that reported accuracy of MRI for diagnosis of AA in pregnant women from inception to April 1, 2022. Results: Our systematic search identified a total of 525 published papers. Finally, a total of 26 papers were included in the meta-analysis. The pooled sensitivity and specificity of MRI in diagnosis of AA in pregnant women were 0.92 (95% CI: 0.88-0.95) and 0.98 (95% CI 0.97-0.98), respectively. The pooled positive likelihood ratio and negative likelihood ratio were 29.52 (95% CI: 21.90-39.81) and 0.10 (95% CI: 0.04-0.25), respectively. The area under hierarchical summary receiver operating characteristic (HSROC) curve indicated that the accuracy of MRI for diagnosis of AA in pregnant women is 99%. Conclusion: This meta-analysis showed that MRI has high sensitivity, specificity, and accuracy for diagnosis of AA in pregnant women and can be used as a first-line imaging modality for suspected cases of AA during pregnancy. Furthermore, it should be noted that when the result of ultrasonography is inconclusive, the use of MRI can reduce unnecessary appendectomy in pregnant patients.