United States

Background
Pembrolizumab is a humanized recombinant monoclonal antibody to the programmed cell death receptor-1 (PD-1) which has immunomodulatory activity and is approved for treatment of many cancers. Aside from side effects associated with infusion therapy patients can develop immune related adverse events (irAEs). IrAEs occur in approximately 15-25% of patients on pembrolizumab as a result of immune enhancement leading to inflammatory toxicity. In clinical trials of pembrolizumab, less than 1% of immune mediated hepatitis (IMH) was observed, making liver toxicity an extremely rare side effect of PD1 inhibition.


Case Presentation

An 68 year-old male with urothelial cell carcinoma (UCC) who underwent radical nephroureterectomy with negative margins was found to have a suspicious mass along the surgical bed during surveillance imaging. Follow-up PET/CT confirmed a 2.4 cm mass with subsequent biopsy confirming relapse. The patient was started on Enfortumab vedotin and Pembrolizumab. Two weeks after the first cycle of therapy the patient developed colitis, tumor lysis syndrome and Steven Johnson syndrome (SJS). His liver enzymes were also elevated. Liver ultrasound was obtained shortly after due to development of ascites which showed coarsened echotexture suggestive of diffuse hepatocellular process without focal hepatic lesions. Ascitic fluid studies were negative for malignancy. CT abdomen/pelvis revealed cirrhosis not seen on imaging two weeks prior.


Discussion and Conclusion

Pembrolizumab associated hepatic injury presents after 1-3 months after initiation of treatment. Studies have shown earlier onset of liver dysfunction resulted in shortened overall survival. The pattern of injury is usually hepatocellular however there have been cases of mixed or cholestatic. Even though histology usually reflects IMH with prominent lymphocytic infiltrates of activated T cells, immunoglobulin levels are usually normal and autoantibodies are not present. Historically, fatal cases associated with immune checkpoint inhibitors (ICI) have occurred in patients with cholestatic patterns of liver injury or severe irAEs such as SJS.

Due to potentially fatal outcomes associated with liver injury, monitoring with routine liver tests should be protocol for patients receiving ICI therapy. Rapid improvement of alkaline phosphatase and bilirubin has been seen with corticosteroid treatment. In instances of inadequate response to corticosteroids alone, addition of a second immunosuppressive agent may be beneficial. However, complete recovery is rare with long-term cholestasis or hepatic failure being the eventual outcome. As ICI use becomes more prevalent, prompt recognition and proper management of irAEs will aid clinical decision making and improve outcomes.


AMA Research Challenge 2024 

Single dose of pembrolizumab leading to rapid, irreversible hepatic injury

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Background
Rhabdomyosarcoma (RMS) is the most common soft-tissue tumor in children and adolescents but is rare in adults. RMS has three main subtypes: alveolar, embryonal, and pleomorphic. The embryonal subtype includes sarcoma botryoides, anaplastic type, and spindle cell type. Spindle cell rhabdomyosarcoma(SCR), comprising 5%-10% of RMS cases, is considered a distinct entity related to embryonal RMS. These tumors resemble leiomyomas histologically. With a 5-year survival rate of only 27% in adults, further research is needed. We report a case of a 21-year-old female with spindle cell rhabdomyosarcoma in the left frontal region.

Case Presentation
A 21-year-old female presented with a left frontal extracranial mass and intermittent headaches for the past year. Initial CT imaging revealed a 3.2 x 2.3 x 2.9 cm mass extending from the subcutaneous tissue through the bone intracranially. Initially suspected as a meningioma, MRI and angiogram later confirmed its growth and hypervascularity. Surgical resection was performed, and the pathology identified spindle cell rhabdomyosarcoma with FUS:TFCP2 fusion and positive IMHC markers (MYOD1, CKAE/AE, desmin, CD9, SSX-C, myogenin). Postoperatively, she developed a pulmonary embolism and was treated with apixaban. Subsequent visits for nausea, vomiting, and headaches led to observations of intracranial bleeding. Apixaban reversal was administered, and a six-week chemotherapy regimen (vincristine, adriamycin, cyclophosphamide) was initiated. A chest X-ray suggested possible pulmonary metastasis. Remaining treatment was continued at another facility.

Discussion
Sarcomas represent 1% of adult solid malignancies, with SCR being exceptionally rare (0.041 per 100,000). Predominantly found in the paratesticular region and head/neck of children, it is rarer in adults, especially in females. Diagnosis relies on histology, with MYOD1 as a primary marker, indicating poor prognosis when mutated. PIK3CA, involved in the mTOR pathway and also associated with SCR, was negative in this case. Spindle cell rhabdomyosarcoma in adults presents unpredictably, often forming in the lower extremities, abdomen, or inguinal region. Therefore, the frontal lobe tumor in this case demonstrates a distinct, uncommon location. Treatment follows general rhabdomyosarcoma guidelines, including cyclophosphamide and vincristine, with additional monitoring needed for metastasis and recurrence.

Spindle cell rhabdomyosarcoma in adults is a rare and complex malignancy. This case highlights the importance of recognizing its distinct pathological and immunohistochemical characteristics and demonstrates the effectiveness of surgical intervention followed by targeted chemotherapy. Understanding these nuances is crucial for enhancing diagnostic accuracy, optimizing treatment plans, and improving patient outcomes.


Spindle Cell Rhabdomyosarcoma in a Young Adult: A Rare Case with Unique Clinical Features

Objectives:
1. Outline the clinical background and pathophysiological mechanisms of spur cell hemolytic anemia
2. Discuss and highlight the presentation and interventions for a case of severe cirrhosis with associated end-stage hemolytic anemia
3. Evaluate and explore factors contributing to the unexpected clinical improvement of hemolytic anemia without liver transplantation

Background:
- Spur cell hemolytic anemia was first discussed in 1964 when a peripheral blood smear from a cirrhotic patient revealed erythrocytes with irregularly shaped projections
- Commonly associated with end-stage liver disease, this condition arises from disruptions in membrane lipid metabolism which leads to formation of acanthocytes— derived from the Greek word “acantho” meaning thorn
- Spur cell hemolytic anemia is a poor prognostic indicator, often requiring a liver transplant for clinical amelioration

Case Presentation: 
A 41-year-old female patient with decompensated cirrhosis secondary to chronic alcohol use (MELD 38) presented with jaundice and laboratory evidence of new onset acute anemia

Discussion:
- Cirrhosis disrupts lipid and cholesterol metabolism in the liver, leading to the accumulation of abnormal proteins, which alters the erythrocyte membrane and increases susceptibility to hemolysis
- The exact pathophysiology remains unclear, but it is believed that these membrane alterations result in the formation of abnormal red blood cells, such as target cells and acanthocytes, which are prone to hemolysis
- Liver transplantation is the only definitive treatment for spur cell hemolytic anemia, as it directly addresses the underlying cause of the condition
- The median survival for patients diagnosed with spur cell hemolytic anemia is approximately 1.9 years, with significantly higher mortality rates in those who are unable to undergo a liver transplant
- For patients ineligible for transplant, supportive care is the mainstay of management, aimed at minimizing symptoms and improving quality of life

Conclusion: 
- Spur cell hemolytic anemia, though associated with poor prognosis, can be managed with supportive care, including blood transfusions, liver disease management (albumin, diuretics), alcohol abstinence, and nutritional support
- The effectiveness of these treatments depends on the patient’s clinical status, MELD score, and the presence of comorbidities

Supportive Treatment of Spur Cell Hemolytic Anemia in the Setting of Decompensated Liver Failure

While Gastric cancer is the second leading cause of cancer-related mortality worldwide, its metastatic spread to the breast is extremely rare. This article illustrates a patient with primary diffuse-type gastric cancer which metastasized to the breast. 


A 52-year-old post-menopausal woman presented to the hospital with severe abdominal pain and constipation. Imaging showed lymphadenopathy gastric wall thickening, and a pulmonary nodule. Biopsy revealed diffuse type, poorly differentiated adenocarcinoma. A CT-PET showed hypermetabolic nodularity suspicious for primary breast malignancy versus metastatic disease. This was subsequently proven to be metastatic via immunochemistry staining. This case represents one of very few documented cases of gastric adenocarcinoma metastasizing to the breast and emphasizes the key role of immunohistochemistry in the diagnostic process.

Uncommon Pathways: A Rare Case of Breast Metastasis from Diffuse Gastric Cancer with Sporadic CDH1 Mutation


Abstract Title
A Cavernous Sinus Mass Resection Develops Into An Eye-Opening Complication

Background
Brain tumors are a rare disease in the general population, with a reported incidence of 5 – 13 out of 100,000. Cavernous sinus tumors are a subset of brain tumors and are also rare. Cavernous sinus tumors may impact internal carotid artery, cranial nerves 3 and 4, and the ophthalmic or maxillary branches of the trigeminal nerve. When tumors are located within this structure, ophthalmoplegia, proptosis, and paresthesias may develop. Management is affected by their involvement of surrounding structures and their mass effect which may cause significant pain.

Case Presentation
This is a case of a 35-year-old male with no past medical history but three months of constant headaches associated with left facial numbness and progressive diplopia. His diplopia progressed to persistent binocular diplopia in upgaze, right gaze, and down gaze. Physical exam was remarkable for left cranial nerve 3 palsy and decreased sensation to the left face. Labs were only remarkable for a cortisol of 0.5. During workup, magnetic resonance imaging of the brain demonstrated an extra-axial mass in the left Meckel’s cave, left cavernous sinus, and left middle cranial fossa. The differential diagnosis at that time included schwannoma, spindle cell tumor, lymphoma, meningioma, pituitary adenoma, and metastases. His biopsy was inconclusive. For his palsy, the patient was given a pirate patch. 
Upon progression of symptoms, he presented to the emergency department. He underwent transsphenoidal biopsy that demonstrated a spindle cell tumor. He was then discharged, and later saw neurosurgery in clinic, who scheduled him for an elective left craniotomy with mass resection. He underwent this procedure with a postoperative course complicated by a pseudomeningocele, complete ophthalmoplegia along with proptosis, inferior displacement and lagophthalmos, with severe exposure keratopathy. Ophthalmology recommended lubricant, steroid eye drops, moxifloxacin eye drops and completed a tarsorrhaphy. The patient lost vision in his left eye due to the significant exposure keratitis due to postoperative swelling of the cavernous sinus.

Discussion
Traditionally, management of ophthalmoplegia is achieved through use of lubricant eye drops and ointments. Surgical intervention can be considered depending on the severity and duration of lagophthalmos, in which a temporary vs permeant tarsorrhaphy is considered. Mild exposure keratopathy has a very good prognosis, while more severe disease can lead to permeant corneal scarring, perforation, and vision loss. Timely consultation and treatment for cavernous sinus masses are needed to prevent progression of these symptoms.


A Cavernous Sinus Mass Resection Develops Into An Eye-Opening Complication

Acquired methemoglobinemia is rare, however it could be fatal. Symptoms such as headache, fatigue, dyspnea, and syncope occur as methemoglobin levels rise, while levels above 50% can precipitate seizures, arrhythmias, coma, and even death. We are presenting a case where a middle-aged male ingested an energy drink named as “PWED super rush "for recreational purposes. Upon checking, it was noted that this drink contains isobutyl nitrite as the main ingredient that enhances sexual experience due to its vasodilatory properties.  
A 52-year-old male with past medical history of hypertension, hyperlipidemia, asthma, and alcohol use disorder presented via EMS with acute onset of lightheadedness, a near-syncopal episode shortly after drinking an energy drink followed by nausea and vomiting.  Vital signs in the ER showed significant hypoxia and otherwise unremarkable. CXR showed no findings concerning fluid overload or community acquired pneumonia. He tested negative for covid. The patient was started on nonrebreather, however, SpO2 remained in 84-88% with supplemental oxygen. To find out the cause of unexplained refractory hypoxia, blood gas analysis was obtained that showed pH of 7.357, pCO2 44, pO2 64, with methemoglobin 25.2%. Based on ABGs results and the initiation of sequence of events following ingestion of an energy drink, toxicology was consulted, and patient was started on methylene blue. He was admitted to ICU for close monitoring and after two doses of methylene blue 1mg/kg, his clinical symptoms significantly improved, successfully transitioned to nasal cannula. Repeat ABGs afterwards showed improvement in methemoglobin levels to 1.0%. His hospital course was uncomplicated, and he was discharged home in stable condition after counseling on substance use.  
Methemoglobinemia is treated with hyperbaric oxygen, methylene blue, ascorbic acid, riboflavin in high doses and exchange transfusion in refractory cases. The first line treatment-Methylene blue acts via the NADPH reductase pathway to regenerate ferrous heme and reduce further oxidation. This case emphasizes the need for a high index of suspicion for methemoglobinemia in cases of refractory hypoxia, especially in the setting of possible toxic ingestion. Point-of-care co-oximetry can quickly diagnose elevated methemoglobin levels when unavailable on ABG analysis.  Additionally, enhanced public awareness and restricting access to agents like isobutyl nitrite are needed to prevent further recreational cases that can overburden emergency departments, intensive care units, and hospitals.  


A Dangerous Rush: When Recreational Use Turns Life-Threatening​

Background: Amiodarone is a class III antiarrhythmic agent used for the management of certain cardiac arrhythmias. Although effective and relatively safe, amiodarone is associated with a spectrum of adverse effects including neurotoxicity. There have been sparse reports of drug-induced parkinsonism (DIP) as a consequence of amiodarone use; however, the mechanism and clinical implications remain an area of limited understanding and documentation. Parksinon’s disease (PD) is associated with degeneration of dopaminergic pathways in the basal ganglia, manifesting in the classic constellation of symptoms, including “pill-rolling” tremors. These dopaminergic pathways can also be disrupted by certain medications, notably antipsychotics, antiemetics, and antiepileptics, which may mimic the symptoms of PD.

Case Presentation: 92 year-old female with a past medical history of atrial fibrillation, hypothyroidism, heart failure, COPD, and dementia presented with resting tremors of the bilateral hands for 2 months. Pt endorsed no new bradykinesia, loss of balance, or muscle stiffness. Denied any fever, chills, myalgia, cough, dysuria, nausea, vomiting, diarrhea, or weight gain or loss. Physical exam demonstrated isolated bilateral resting tremors, with an otherwise unremarkable neurologic exam. There was no muscle rigidity, cerebellar dysfunction, motor/sensory deficits, or bradykinesia compared to baseline. Vital signs were normal and labwork including TSH, RPR, and vitamins B12 and B9 were unremarkable. Following review of the patient’s medication regimen, we reduced amiodarone dosing from 200mg to 100mg due to concern for neurotoxicity rather than late-onset PD. On follow up at 2 weeks and 1 month, resting tremors resolved completely and the patient had no further concerns.

Discussion: Despite the established neurotoxicity of amiodarone, reports of amiodarone-induced Parkinsonism remain sparse. Here, we present a case of Parkinsonism occurring in a patient receiving long-term amiodarone therapy. Through this case report, we aim to broaden understanding of potential neurotoxic effects of amiodarone and emphasize the importance of recognizing drug-induced parkinsonism (DIP). DIP is a reversible form of Parkinsonism caused by the blockade of dopamine receptors or interference with dopamine transmission in the basal ganglia, mimicking the dopaminergic deficiency seen in PD. Misdiagnosing DIP as Parkinson's disease could lead to inappropriate treatment, potentially causing harm. Hence, clinical vigilance is warranted in patients receiving long-term therapy with amiodarone. 


Amiodarone-Induced Parkinsonism: A Case Report Highlighting Neurotoxicity and Clinical Vigilance in Long-Term Therapy

Abstract Title
Atrial Fibrillation Presenting as Renal Infarction
Background
Renal infarction is caused by occlusion of renal artery or its branches, due to emboli from cardiac sources or in situ thrombosis. It presents as sudden flank or abdominal pain, with labs showing elevated LDH, hematuria, proteinuria. Prompt diagnosis is crucial to initiate timely revascularization therapies.

Case Presentation
A 78-year-old male with past medical history of hypertension, diabetes mellitus, hyperlipidemia, COPD, meningioma presented to the emergency department with complaints of pain in the left flank and umbilical region which started gradually over the past few days and was described as dull and non-radiating. Physical evaluation revealed stable vital signs with hypertension, chronic normocytic anemia, irregularly irregular pulse, Left costovertebral angle (CVA) tenderness, bilateral chronic hand tremors. No focal neurological deficits. Denies fever, nausea, vomiting, diarrhea, constipation, anorexia, alcohol use, changes with meal, similar pain, incontinence, dysuria, hematuria, changes with urine output, urinary frequency, chest pains, palpitations, syncope, orthopnea, PND, edema. Initial Diagnostic workup included negative troponin, COVID-19/flu/RSV tests, and a chest X-ray showing mediastinal widening. Further investigations with a CT angiography chest ruled out aortic aneurysm or dissection but noted a region of low density in the left kidney parenchyma suggestive of multiple cortical infarcts. Urinalysis was positive for microscopic blood and 1 RBC. An EKG demonstrated new-onset atrial fibrillation (Afib). Cardiology consulted recommended to start anticoagulation therapy for atrial fibrillation and electrophysiology with no immediate plan for cardioversion. Later, CTAP with and without contrast show findings consistent with multiple acute renal infarcts (ARI) in the left kidney. Urology was consulted and determined no surgical intervention was indicated, recommending anticoagulation to prevent further complications from kidney infarcts. The patient was educated about his condition and discharged with appropriate outpatient follow-up.

Discussion
ARI is potentially serious medical condition but its clinical presentation of is often
nonspecific, leading to delays in diagnosis and treatment. Autopsy studies suggest the incidence of renal infarction is 14 per 1000, or 1.4%. Other retrospective studies of ER admissions found an incidence of 0.004% to 0.007%. In our case, the patient's abdominal pain with no previous history of arrhythmias prompted further evaluation, revealing new-onset AFib on EKG and subsequent diagnosis of renal infarction on imaging. Afib can cause thrombotic complication to any body part, most commonly being ischemic stroke. Clinicians should suspect other systemic embolization phenomena in patients with Afib.


Atrial Fibrillation Presenting as Renal Infarction: A Case Report

Introduction. Variegate Porphyria (VP) is a rare autosomal dominant disorder characterized by mutations in the protoporphyrinogen oxidase (PPOX) gene, leading to diminished enzymatic activity, critical for heme biosynthesis. The clinical manifestations of VP are highly variable, with some patients exhibiting significant neurovisceral symptoms and others presenting with cutaneous photosensitivity, many with a combination of both. This variability reflects the disease's ability to often go undiagnosed, especially in pediatric populations, where the disease is not frequently seen in clinical practice.

Methods. This case study focuses on a 12-year-old male who presented with persistent photosensitivity, painful blistering, severe abdominal pain, and dark-colored urine. Despite normal renal and liver serology testing, elevated porphyrin levels in both urine and stool samples supported the presumptive diagnosis of VP, though the diagnosis was significantly delayed resulting in multiple unnecessary hospitalizations secondary to recurrent acute attacks.

Discussion. The complexity of VP, particularly in pediatric patients, often results in diagnostic delays due to the vague symptoms that oftentimes represent other medical conditions. Our case emphasizes the importance of a thorough clinical evaluation, family history, and awareness of this rare disorder. Management strategies, including sun protection and beta-carotene supplementation, were implemented to mitigate the risk of acute attacks.

Conclusion. This study emphasizes the need for increased awareness and understanding of VP, aiming to promote earlier diagnoses and improve patient outcomes through timely and appropriate interventions.

Case Study: Navigating the Complexities of Variegate Porphyria

Anti-TNF therapy has revolutionized the treatment of various autoimmune conditions. However, it has also been associated with an increased risk of bacterial infections. To our knowledge, no case of Acinetobacter baumannii bacteremia has been reported with adalimumab treatment.

A 63-year-old female with generalized pustular psoriasis (GPP) was referred to the ED by her dermatologist for worsening rash, severe weakness, and fatigue. Symptoms began a week prior and acutely worsened after adalimumab infusion a day before hospital presentation. This was her second infusion, the first had been two weeks earlier. In the ED, her vital signs and labs were unremarkable. However, she had chills, prompting the collection of two blood cultures at different sites, which were both positive for A. baumannii. She had no clear infection source. Infectious disease (ID) was consulted, and she was started on ampicillin-sulbactam. Her weakness and fatigue improved shortly after starting antibiotics. A transthoracic echocardiogram showed no vegetations, and repeat blood cultures were negative. Dermatology attributed her worsening rash to a GPP flare, and spesolimab was recommended. Her medical records showed a positive Quantiferon-TB Gold, with a low mitogen-nil value and a chest X-ray showing no evidence of past or current tuberculosis infection. ID suggested the result was a false positive, but a subsequent positive T-spot confirmed latent tuberculosis. Biologic treatment was suspended until completing one month of latent tuberculosis treatment. Outpatient ID planned to initiate once-weekly isoniazid plus rifapentine. Meanwhile, acitretin was started, with dermatology follow-up scheduled for one month later to begin spesolimab after latent tuberculosis treatment. She was discharged on ciprofloxacin to complete her antibiotic course.

Acinetobacter baumannii, part of the ESKAPE organisms, is predominantly associated with healthcare-related infections and known for developing antibiotic-resistant strains. In the US, community-acquired A. baumannii cases are rare, with most being hospital-acquired infections. Moreover, shaking chills is an independent predictor of bloodstream infection. Given that blood is generally sterile, there is a low likelihood it was a contaminant. This case highlights the importance of clinical exam findings to maintain a high index of suspicion for severe infections such as bacteremia in immunocompromised individuals, and the necessity for physicians to broaden differentials to include rare organisms even in the absence of recent clinical exposure. Fortunately, the isolate was pan-sensitive, as multidrug-resistant A. baumannii infections can be life-threatening. Additionally, we are not suggesting that the patient's symptoms were solely due to bacteremia; reactivation of latent tuberculosis may have contributed.



Community Acquired Acinetobacter baumannii Bacteremia After Receiving an Infusion of Adalimumab

Title: Delayed Diagnosis of Disseminated Coccidioidomycosis Due to Misdiagnosis
of Lymphoma: A Case Report.

Background:
Coccidioidomycosis, or valley fever, is a fungal infection caused by inhaling Coccidioides imitis/posadasii. These fungi are endemic to the southwestern USA, Mexico, and Central and South America. Incidence has been rising, likely due to population growth, climatechange, and increased awareness. The infection presents diversely, with most cases being asymptomatic. About one-third develop pulmonary illness, and a small percentage experience dissemination to other body areas, commonly to skin, bone, and CNS, particularly in immunocompromised individuals and certain ethnic groups.

Case presentation:
A 39-year-old Hispanic female with a history of non-Hodgkin's lymphoma and treated tuberculosis presented with painful ulcerative skin lesions. Initial labs showed mild leukocytosis, microcytic anemia, hypokalemia, and hypoalbuminemia. Imaging revealed bilateral pulmonary infiltrates, mediastinal adenopathy, and extensive lymphadenopathy. A skin biopsy report from Mexico indicated non-Hodgkin lymphoma, but no treatment was initiated at the time of diagnosis. A neck lymph node biopsy revealed fungal spherules and hyphae, consistent with coccidioidomycosis. Serology confirmed high titer IgG for Coccidioidomycosis. Further testing ruled out other conditions, including lymphoma. The patient started high-dose fluconazole. A lumbar puncture showed positive IgG for Coccidiomycosis in CSF, indicating CNS involvement. A repeated skin biopsy was negative for lymphoma, confirming disseminated coccidioidomycosis and ruling out
lymphoma diagnosis. The patient was discharged on oral fluconazole and prophylactic TMP-SMX. Two months later, she was readmitted with worsening weakness and altered mentation. Despite adequate treatment, the imaging showed new lytic lesions in the left scapula and T2 body. Repeated lumbar puncture confirmed CNS involvement. Her condition improved with continued antifungal. Not candidate for amphotericin B.

Discussion:
This case highlights the difficulty in diagnosing coccidioidomycosis, which is often
mistaken for other conditions. The patient's initial misdiagnosis of lymphoma while
undergoing care in Mexico led to a delay in appropriate treatment. Initially, treatment focused on a superimposed skin infection, assuming the underlying cause was NHL. However, even after diagnosing pulmonary coccidioidomycosis, the misdiagnosis of NHL persisted until a repeat skin biopsy ruled it out. This case highlights the challenge of differentiating reactive inflammatory changes from malignancy, which can delay a definitive diagnosis. The diagnosis was eventually confirmed through lymph node biopsy and subsequent serology testing, the most appropriate diagnostic methods. The initial treatment with fluconazole was appropriate as azoles remain the gold standard for therapy. The case underscores the need for timely and accurate diagnosis to initiate appropriate antifungal therapy and prevent complications.

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Spindle Cell Rhabdomyosarcoma in a Young Adult: A Rare Case with Unique Clinical Features

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