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Introduction:Myocardial infarction with nonobstructive coronary artery disease (MINOCA) is a group of conditions that share common characteristics and is characterized by the absence of ≥50% stenosis of coronary arteries and without any evidence of atherosclerotic plaque rupture [1]. A study conducted by Waller et al. reported that 4% to 7% of all patients diagnosed with AMI, do not have underlying atherosclerotic coronary disease on autopsy or angiography [2].Coronary artery embolism is a rare and important non-atherosclerotic cause of acute myocardial infarction (AMI), and the first case of AMI secondary to coronary embolism was reported in 1856 by Rudolf Virchow and was classified initially as a precipitating factor for type-II MI, now recognized as one of the cause of MINOCA [3]. Coronary embolism (CE) is more frequently reported in infective endocarditis patients and it mainly involves the left main coronary artery system due to flow characteristics and aortic morphology [4, 5]. CE may also originate from mural thrombus within the left-sided cardiac chambers, but it has rarely been reported in the literature [6]. Most cases of coronary embolism in the literature have been reported secondary to infective endocarditis, valvular heart diseases, and atrial fibrillation [7-9]. Here, we are reporting a case of a 74-year-old female, who had a chronic history of atrial fibrillation on anticoagulation with questionable compliance and was admitted with sepsis and takotasubo cardiomyopathy and later developed AMI secondary to coronary embolism to the left anterior descending artery.

Introduction: Spontaneous coronary artery dissection (SCAD) is a tear or separation within the coronary artery wall forming an intraluminal hematoma reducing downstream blood flow leading to myocardial ischemia (MI)(Figure 1A-C)1 . Intraluminal hematomas may develop from ”inside-out” due to endothelial-intimal injury or ”outside-in” due to injury within the vasa vasorum leading to bleeding in the wall. The subsequent false lumen from either mechanism can extend and compress the true lumen to cause MI [2]. Unlike other luminal etiologies of MI, SCAD is not caused by atherosclerotic plaque rupture, coronary intervention, or trauma [3]. With significant MI from intraluminal hematoma, patients can present with signs and symptoms that mimic MI including chest pain with and without radiation, dyspnea, nausea and vomiting. It can also include elevated troponin with electrocardiogram (ECG) changes consistent with ST segment elevation or non-ST segment elevation MI. The diagnosis is made when other etiologies of acute coronary syndrome (ACS) are ruled out and there is an angiographic evidence of non-iatrogenic or non-atherosclerotic radiolucent intimal flap and contrast staining [1]. Left anterior descending (LAD) artery is the most commonly affected branch of the left main coronary [4]. Severe stenosis can lead to heart failure as well as cardiogenic shock amongst other post-MI complications including ventricular arrhythmias, ventricular free wall or septal wall rupture. If angiography is inconclusive, then intracoronary imaging with optical coherence tomography or intravascular ultrasound may be considered before repeat angiography [5].The etiology of SCAD is thought to be multifactorial without a clear underlying cause. Risk factors associated include fibromuscular dysplasia (FMD), peri and postpartum period, hormonal fluctuations, and arteriopathies. SCAD is a rare cause of ACS, although when present, there is a higher prevalence in young females without cardiac risk factors [6]. Stable patients are treated conservatively with medication while percutaneous coronary intervention (PCI) and coronary artery bypass graft are reserved for severe stenosis and acute change in hemodynamics. Use of antiplatelet therapy remains controversial as medications such as acetylsalicylic acid (i.e. aspirin) and P2Y12 receptor blockers can worsen intraluminal hematoma. Dual antiplatelet therapy is recommended for those who undergo stent placement [5]. Similarly, guideline directed medical therapy is initiated for new onset of heart failure. Review of literature reveals 90% recovery within one month with coronary computed tomography angiography [5]. Many cases of SCAD have been reported in young females with ischemic symptoms and angiographic findings in the distal LAD but only few cases highlight proximal coronary involvement. We present a case of a young woman with extensive left main and proximal LAD SCAD requiring intervention.

Varicella Zoster is a neurotropic virus which leads to acute varicella or it may lay dormant in the spinal root ganglion. Reactivation of varicella zoster causes Herpes Zoster (HZ) and occurs commonly in immunosuppressed conditions like COPD. Severity of Herpes Zoster is also higher among those with comorbidities like COPD. Even among COPD patients, the severity of HZ is said to be higher among those using oral corticosteroids than those using inhaled steroids due to greater immunosuppressive effect. It has also been found that incidence rate of COPD exacerbations, transient ischemic attack and stroke are higher among COPD patients with HZ compared to those without HZ. Herpes zoster vaccinations prevent reactivation of latent HZ and reduce the associated complications. Live attenuated and recombinant vaccines are available for vaccination among which recombinant vaccine is found to be more effective. The cost burden due to HZ among COPD patients was also higher compared to those without HZ. Childhood varicella vaccination is cost effective, however cost effectiveness of adolescent vaccination is unclear.

Introduction:Sebaceous cysts, often known as epidermoid cysts, are keratin-containing unilocular retention cysts. It frequently appears on the head, neck, scalp, scrotum, earlobe, and breast, and can range in size from a few millimetres to less than a few centimetres. When an epidermal cyst exceeds more than 5 cm in diameter, it is considered a giant cyst. The development of cancer is more likely in giant epidermal cysts, which are uncommon.1Conventional sebaceous cysts are typically small, slowly expanding, non-sensitive lesions with a dome shape. Unless it becomes infected or enlarges to the point where it damages nearby anatomical structures, an epidermal cyst is typically asymptomatic. Authors have previously described enormous epidermal cysts with diameters greater than 5 cm.2,3A well-developed granular cell layer lines epidermoid cysts, which are also lined by stratified squamous epithelium. On rare occasions, the cyst wall may also contain pseudostratified ciliated columnar epithelium. The cyst wall may have calcification of a dystrophic type. The preferred course of action is excision. Studying the occurrence of enormous sebaceous cysts was the goal.4Epidermal inclusion cysts, ganglion cysts, neurogenic tumors, myxoid tumors, nodular fasciitis, and dermatofibrosarcoma protuberans are among the possible diagnoses. The reported incidence of malignant degeneration to squamous-cell carcinoma is 2.2%. 5The present study reported a case of a giant sebaceous cyst over the posterior upper back in a 75-year-old male.

Introduction:Varicella-zoster virus (VZV) is the causative agent of chickenpox, a viral rash that is generally benign and self-limiting, requiring minimal treatment. However, in rare cases, complications can arise. Although chickenpox is commonly associated with mild thrombocytopenia in children, severe thrombocytopenia resulting in bleeding is uncommon [1]. Immune Thrombocytopenia (ITP) is a blood disorder characterized by the destruction of platelets through immune-mediated mechanisms, leading to a decrease in platelet count below 100×10^9/L. Viral infections and live virus vaccinations are frequent triggers of ITP. It presents as acute, self-limiting episodes of bleeding, usually minor, but with the potential for intracranial hemorrhage (ICH). Compared to other causes of thrombocytopenia, ITP typically results in less severe bleeding. Diagnosis is based on clinical presentation and laboratory findings, and it is a diagnosis of exclusion [2]. The primary goal of treating a patient with ITP is to raise their platelet count to a safer level, reducing the risk of severe bleeding, particularly intracranial hemorrhage (ICH). Corticosteroids have been effectively used since the 1950s, reducing the production of anti-platelet antibodies and enhancing the clearance of opsonized platelets. Intravenous immunoglobulin (IVIG), introduced by Imbach et al., has also shown high efficacy in increasing platelet counts in over 80% of patients, with a faster onset of action compared to steroids [3].The coexistence of chickenpox and ITP presents a clinical conundrum, as the underlying mechanisms linking these conditions remain elusive. Although there are sporadic reports in the medical literature of patients developing ITP following chickenpox, the incidence of this simultaneous presentation is exceedingly rare. Furthermore, the majority of these reported cases lack comprehensive hematologic data, hindering a thorough understanding of the clinical course and management strategies.We thus present one such intriguing and rare case of chickenpox with simultaneous ITP purpura.

IntroductionIBD is a chronic systemic inflammatory disease that predominantly involves the gastrointestinal tract. At the same time, it exerts numerous cardiovascular manifestations, like atherosclerotic cardiovascular disease and thromboembolic events, due to a hypercoagulable state. Although the disease mechanism is unclear, factors responsible, like the disruption of the normal coagulation cascade, hyperhomocysteinemia, abnormalities in platelet-endothelial cell interactions, and increased fibrinolysis, are implicated.

Silicosis unveiled: Improving diagnostic accuracy and distinguishing it from tuberculosis: A case report from a low and middle-income countryChapagain, Sanskriti1 , Shrestha,Abhigan Babu2 ,Shrestha ,shumneva 3,Shrestha, sajina4,jaiswal ,vikash5,yadav,Hritik Raj 2, Shrestha ,Nilasma61. Devdaha Medical College and Research Institute, Bhaluhi, Rupandehi, Nepal2.M Abdur Rahim Medical Medical College Hospital, Department Of Internal MedicineDinajpur, Bangladesh3. Tribhuvan University Institute of Medicine Maharajgunj Medical Campus ,Nepal4. KIST Medical College, Department Of Internal Medicine, patan Imadol, Lalitpur,Nepal5. Medical AMA School of Medicine, Medicine Bangkal makati, Philippines Makati City, Luzon6.Kathmandu Medical College,Kathmandu,NepalCorresponding author :Chapagain,SanskritiDevdaha Medical College and Research Institute, Bhaluhi, Rupandehi, Nepalsanskritichapagain527@gmail.com

Japanese Encephalitis (JE) is a viral disease caused by the Japanese Encephalitis Virus (JEV) which is a mosquito-borne, single-stranded, RNA flavivirus belonging to the Flaviviridae family. It is imperative to note that JE can cause severe inflammation of the brain, leading to long-term neurological complications or even death in some cases. JE vaccine provides a crucial defense against this potentially fatal disease. Given the high prevalence of JE in Bangladesh, widespread vaccination campaigns and public health initiatives are necessary to promote awareness and ensure that individuals at risk receive the vaccine. The commentary emphasizes on how crucial it is that individuals who are at risk of JE infection receive the vaccine through nation wide immunization campaign in Bangladesh.

Aspirin induced urticaria in a recently diagnosed ischemic stroke patient: A case report and literature review. Abhinav Dahal : Sukraraj Tropical and Infectious Disease Hospital, Teku, Kathmandu, Nepal Email: abhinav.dahal333@gmail.comSushant gautam: Nepalgunj medical college, banke,Nepalemail: gautamsushant1941@outlook.comAliza Shakya : Manipal college of medical sciences, Pokhara, Nepalemail: shakyaaliza@gmail.comAshmita pant: Manipal college of medical sciences, Pokhara, Nepalemail: ashmita.pant@gmail.comKriti Bhandari , Nepal Medical College, Jorpati, Kathmandu, Nepal itirkbhandari977@gmail.comAbhigan Babu Shrestha, M Abdur Rahim Medical College, Dinajpur, Bangladesh. Abigan17@gmail.comCorresponding author:ABS; M Abdur Rahim Medical College, Dinajpur, Bangladesh. Abigan17@gmail.comAbstract: Aspirin and urticaria correlation has not been fully understood. The pharmacological inference is suspected to be the diversion of arachidonic acid metabolism. Aspirin sensitivity can aggravate pre-existing chronic urticaria and in some instances causes acute urticaria. We report a case of a 53-year old male, recently diagnosed with stroke, who presented with complaints of multiple rash over trunk and upper extremity with aspirin. NSAIDs induced urticarial are usually neglected by physicians during diagnosis. Keywords: Aspirin, urticarial, stroke, hemiplegiaIntroduction: Aspirin is a drug which is widely used to reduce the risk of stroke, transient ischemic attack, and cardiovascular events. This is due to its antithrombotic properties by irreversibly inhibiting the cyclooxygenase enzyme, reducing the synthesis of Thromboxane A2 and thus subsequently reducing platelet aggregation [1– 3]. Aspirin and NSAIDs’ pharmacological properties also result in adverse reactions like GI upset, renal toxicity, and hemorrhagic complications, as well as potentiate hypersensitivity reactions [4]. Aspirin Hypersensitivity is reported by 0.9 to 1.5% of the general population [5]. Hypersensitivity reactions to NSAIDs are classified on the basis of their involvement of the skin, like urticaria or angioedema, the airways or other organs, their acute or delayed onset, the presence of underlying diseases, and their cross reactivity[6]. In this report, we document a case of aspirin induced urticaria in a patient with a recent history of Ischaemic stroke and Hypertension.Case Description: A 53 years old male presented to the emergency department with a chief complaint of multiple rashes with burning and itching sensation over trunk and extremities. Figure 1 and 2. The patient was a known case of hypertension with recent diagnosis of left sided ischemic stroke with right sided hemiparesis 7 days back for which he was admitted for 3 days. There were no significant reactions to the treatment noticed during the hospital stay. He was discharged with a daily dose of aspirin 75 mg o.d., enalapril 10 mg o.d., atorvastatin 20 mg o.d., omeprazole 20 mg b.d. He was advised for proper bed rest with two hourly posture changes & physiotherapy. He was solely on prescribed medications for the past 4 days. On the next day, he was admitted following the appearance of cutaneous manifestations with no other associated symptoms such as angioedema or shortness of breath. He had no prior history of allergic reactions. On further enquiry, he denied any changes to diet or environmental stimuli including no exposure to any pets or animals. He also gave a negative history of family members having such allergic manifestations. On examination, multiple, pruritic, erythematous, blanching macules were present on bilateral upper extremities and trunk(Figure 1). His vital signs were within normal limits. Leukocytosis (wbc:12,000 cells/mm3) with higher eosinophil count ( 550 per ml of blood) was noted while other complete blood count and comprehensive metabolic panels were unremarkable. Medical history revealed he was taking enalapril 10 mg o.d. for the past 3 years for hypertension. As ACE inhibitors are commonly responsible for causing the side effects such as allergies, drug rash & even angioedema, it was replaced with amlodipine 5 mg o.d. He was started on histacin 4 mg b.d for symptomatic management. However, there was no significant improvement in his condition. Therefore, we decided to stop the current medication one at a time to identify the culprit drug. Aspirin was replaced with clopidogrel 75 mg o.d. & given daily. He was kept under observation & followed up the next day with improvement. Patient told that his itching and the degree of rash spread throught his body were diminished. Three days later, the rashes almost fully subsided & he was advised to continue histacin for 1 more week without stopping clopidogrel intake. Aspirin was identified as the sole cause for the rashes. He was discharged following complete recovery of cutaneous symptoms after 3 days with proper counselling regarding his condition and precaution to be taken for future aspirin use.Discussion: Aspirin and other NSAID are known to cause hypersensitivity reactions. One of the manifestation of such reactions is urticaria. The prevalence of aspirin induced urticaria is estimated to be around 0.3% excluding individuals with recurrent urticaria, hay fever and chronic chest disease [7]. Aspirin induced Urticaria(AIU) can be classified into two types as aspirin intolerant acute urticaria(AIAU) and aspirin intolerant chronic urticaria(AICU). The symptoms develop within minutes to 24 hour in AIAU and lasts for less than 6 weeks whereas, in AICU symptoms typically last for more than 6 weeks.[8] Elevated IgE levels and atopy are suggested as a common predisposingfactors for AIU according to a genetic study done in Korean population[8]. In addition, HLA-DRB1 * 1302 - DQB1*0609 also has been identified as a genetic marker[9]. Besides this, various genetic studies have reported that high affinity IgE receptor[10] , histamine N‐methyltransferase[11] and adenosine A3 receptor[12] are other genetic determinants for AIU. These findings allude that, causes leading to the release of inflammatory mediators either by increased histamine release, faulty histamine degradation or augmented mast cell signalling, contributes to the manifestation of AIU. NSAIDs and Aspirin are known to be one of the common drugs causing hypersensitivity drug reactions.(13) Drug Hypersensitivity Reactions constitute about one third of all adverse drug reactions and affects 10-20% of hospitalized patients and 7% of outpatients.[14] Depending on the type of hypersensitivity reaction, patient can develop an array of cutaneous manifestations ranging from urticaria/ angioedema, fixed drug eruption, maculopapular exanthem to more severe manifestations such as DRESS or SJS/TEN.[15] We have previously encountered a case of Stevens Johnson Syndrome, Type III Hypersensitivity Reaction due to an antibiotic namely Cefixime.[16] In this case, we have encountered a case of Single NSAID Induced Urticaria/ Angioedema or Anaphylaxis, a Type I Hypersensitivity Reaction. Figure 3.To date, there are only few case reports published in pubmed highlighting the association of aspirin with urticaria. This may be due to the fact that aspirin sensitivity is often neglected because of the cross reaction with NSAIDs. One case report has documented urticaria in three patients caused by aspirin where pharmaceutical excipients present in the formulation of drug was found to be the sole cause for the hypersensitivity reaction in two of those patients.[17]However, acute urticaria is not uncommon and when patients present with an urticarial reaction clinicians do not consider NSAIDs as the cause, as the reaction occurs in context of different triggers and is thus difficult to establish.Beyond drug induced urticaria, differential diagnosis of acute urticaria includes urticaria attributed to infections, foodstuffs, contact dermatitis, solar urticaria, cholinergic urticaria, arthropod bite reactions, autoimmune disorders, small vessel vasculitis. Diagnostic workup for many of these etiologies rely on laboratory parameters and histological evidence in addition to history. Initial laboratory investigations revealed lekocytosis with a predominance of eosinophils. However, access to further testing was limited due to patient’s refusal and unfortunately no blood investigations or skin biopsy was taken at presentation. Management of NSAID induced urticaria includes strict culprit NSAID avoidance along with symptomatic management of acute urticaria.[18] Antihistamines are the first line treatment for management of acute urticaria. In severe cases, corticosteroids can be added to control symptoms.[19,20] Some types of NSAID hypersensitivity are known to exhibit cross reactivity thus strict NSAID avoidance should be done until potential of cross-intolerance is ruled out. If patient has history suggesting selective NSAID induced urticaria, challenge to chemically unrelated strong COX-1 inhibitor may be done to rule out crossreactivity type hypersensitivity.[21] Once diagnosis of SNIUAA is established, use of drug allergy passport and patient education help both the medical provider and the patient know about the NSAID hypersensitivity status, avoidance of the culprit NSAID as well as use of chemically unrelated NSAIDs as safe alternatives. In this entity, alternative drug to aspirin must be sought.[18,21] Therefore our clinical reasoning is composed from detailed patient’s history, physical examination and clinical course. Our patient did not have any history of multisystem involvement, recent infection, past medical history of atopy, inducible urticaria due to heat, cold or stress, recent contact with common irritants or insect bite. The patient had been taking Aspirin, Enalapril and Atorvastatin following the diagnosis of Ischemic Stroke with Right Sided Hemiparesis. The urticaria and pruritus should not be caused by Enalapril, since the patient was tolerating the medication well for the past 3 years and the patient’s symptoms worsened even after withdrawing of the drug. The temporal correlation between the appearance of urticarial rash and aspirin intake, and the resolution of urticarial rash and pruritus following aspirin discontinuation suggests the possibility of Aspirin Induced Urticaria. The causality assessment of the adverse drug reaction (ADR) was carried out using the Naranjo Scale, a method for estimating the probability of adverse drug reactions. The assessment revealed the ADR to be ‘Probable’(+6) to be associated with Aspirin.[22]The patient’s history notably lacked presence of chronic urticaria. While the drug provocation test for cross intolerance was not done, the patient’s history reveals previous tolerance to other NSAIDs like ibuprofen and paracetamol.

Heterotaxy pattern associated with Sinus Node Dysfunction in an adult: A case report.Authors : Naman Shah MBBS1, Sankalp Acharya2, Apoorva Tripathi MBBS2, Himanshi Bisht MBBS2,Maitri Shah MBBS1, Aayushi Pareek MBBS3, Asmit Gera MBBS4, Abhigan Babu Shrestha, MBBS5, Vikash Jaiswal MD61. GMERS Medical college Sola, Ahmedabad, India2. B. J. Medical College, Ahmedabad, India3. RHUS College of Medical Science, Jaipur, Rajasthan4. JCCR Cardiology Research, Varanasi, India5. M Abdur Rahim Medical College, Dinajpur, Bangladesh6. AMA School of Medicine, Makati, Philippines

Harlequin Ichthyosis is a rare autosomal recessive disorder occurring in 1: 3,000,000 birth characterized by thick keratin skin with scaly appearance. Preterm deliveries, early marriage and consanguinity of marriage are some risk factors. Antenatal checkup of DNA for ABCA12 mutation helps in diagnosis but USG in places where not available.