United States

Introduction:
Essential thrombocythemia (ET) is a BCR-ABL1 negative myeloproliferative neoplasm with an incidence of 1-2.5/100,000 population per year. It is caused by mutations in the JAK2, CALR, or MPL genes. ET is considered benign, with a low risk of leukemic transformation, a good prognosis, and long-term survival. However, severe complications such as myelofibrosis (MF) and acute myeloid leukemia (AML) can occur. Recent studies indicate ET progresses to MF in 4.8% of cases and to AML in 3.3% of cases. Additionally, leukemia cutis occurs in 3% of AML patients. Here, we report an extremely rare case of ET that progressed to MF and subsequently transformed into leukemia cutis.

Case presentation:
We present a unique case report highlighting the clinical progression of a 75-year-old female diagnosed with JAK2-positive Essential Thrombocythemia (ET) in 1990. Initially, she presented in 2014 for thrombocytosis evaluation, and a bone marrow biopsy revealed a hypercellular marrow with megakaryocytic hyperplasia, confirming ET. Treatment with hydroxyurea yielded variable responses. In 2021, abnormal WBC results prompted further investigation. Flow cytometry revealed myeloid left shift, increased myeloblasts, and teardrop-shaped red blood cells, confirming Post-ET myelofibrosis. Trisomy 8 and a 1:21 translocation were detected with FISH. Her condition was stabilized with Ruxolitinib (Jakafi) therapy. In July 2023, she presented with hepatosplenomegaly and multiple skin nodules on her upper abdomen, back, and face. A bone marrow biopsy in January 2024 revealed a hypocellular marrow, severe reticulin fibrosis (MF-3), and &gt;20% blasts, indicating progression to acute myeloid leukemia. Flow cytometry revealed an aberrant CD34-positive blast population expressing several monocytic markers. Subsequent histopathological examination of the nodules demonstrated perivascular infiltration of immature mononuclear cells resembling blasts immunoreactive to MPO, CD117, CD163, and C68 surface markers, confirming leukemia cutis. In February 2024, the patient began treatment with venetoclax and completed one cycle of Azacitidine. Due to an inadequate response, Azacitidine was switched to Decitabine combined with Cedazuridine (Inqovi) and low-dose Jakafi. Despite undergoing six cycles of Inqovi, the patient remains unresponsive to treatment.

Conclusion:
This case report illustrates the rare clinical progression of essential thrombocythemia (ET) into acute myeloid leukemia (AML), manifesting as leukemia cutis. The transition from ET to AML, while uncommon, is frequently associated with unfavorable cytogenetics and a poor prognosis. This emphasizes that close monitoring, early identification, and appropriate intervention are critical in the management of leukemic transformation.

AMA Research Challenge 2024 

Essential Thrombocythemia to Leukemia Cutis: A Blood-to-Skin Transformation

The 27th International Conference on Systems, Signals and Image Processing.

IWSSIP 2020

Introduction:
Essential thrombocythemia (ET) is a BCR-ABL1 negative myeloproliferative neoplasm with an incidence of 1-2.5/100,000 population per year. It is caused by mutations in the JAK2, CALR, or MPL genes. ET is considered benign, with a low risk of leukemic transformation, a good prognosis, and long-term survival. However, severe complications such as myelofibrosis (MF) and acute myeloid leukemia (AML) can occur. Recent studies indicate ET progresses to MF in 4.8% of cases and to AML in 3.3% of cases. Additionally, leukemia cutis occurs in 3% of AML patients. Here, we report an extremely rare case of ET that progressed to MF and subsequently transformed into leukemia cutis.

Case presentation:
We present a unique case report highlighting the clinical progression of a 75-year-old female diagnosed with JAK2-positive Essential Thrombocythemia (ET) in 1990. Initially, she presented in 2014 for thrombocytosis evaluation, and a bone marrow biopsy revealed a hypercellular marrow with megakaryocytic hyperplasia, confirming ET. Treatment with hydroxyurea yielded variable responses. In 2021, abnormal WBC results prompted further investigation. Flow cytometry revealed myeloid left shift, increased myeloblasts, and teardrop-shaped red blood cells, confirming Post-ET myelofibrosis. Trisomy 8 and a 1:21 translocation were detected with FISH. Her condition was stabilized with Ruxolitinib (Jakafi) therapy. In July 2023, she presented with hepatosplenomegaly and multiple skin nodules on her upper abdomen, back, and face. A bone marrow biopsy in January 2024 revealed a hypocellular marrow, severe reticulin fibrosis (MF-3), and >20% blasts, indicating progression to acute myeloid leukemia. Flow cytometry revealed an aberrant CD34-positive blast population expressing several monocytic markers. Subsequent histopathological examination of the nodules demonstrated perivascular infiltration of immature mononuclear cells resembling blasts immunoreactive to MPO, CD117, CD163, and C68 surface markers, confirming leukemia cutis. In February 2024, the patient began treatment with venetoclax and completed one cycle of Azacitidine. Due to an inadequate response, Azacitidine was switched to Decitabine combined with Cedazuridine (Inqovi) and low-dose Jakafi. Despite undergoing six cycles of Inqovi, the patient remains unresponsive to treatment.

Conclusion:
This case report illustrates the rare clinical progression of essential thrombocythemia (ET) into acute myeloid leukemia (AML), manifesting as leukemia cutis. The transition from ET to AML, while uncommon, is frequently associated with unfavorable cytogenetics and a poor prognosis. This emphasizes that close monitoring, early identification, and appropriate intervention are critical in the management of leukemic transformation.

poster

Welcome to the **largest national, multi-specialty research** event featuring research from more than 750 medical students, residents, fellows, and international medical graduates.

Use the buttons below or navigation menu to access the event.
 

[![](https://assets.underline.io/markdown_image/1/image/20e1e77aa954efeac7a15d84c85eb383.jpg)](https://underline.io/events/468/sessions?searchGroup=all)
 
[![](https://assets.underline.io/markdown_image/1/image/068522d81aca0b68a369787c7dfccd1b.jpg)](https://underline.io/events/468/posters?searchGroup=all)
 
[![](https://assets.underline.io/markdown_image/1/image/d3971ece79d5e5575b178bdc2c8bbfae.jpg)](https://underline.io/events/468/help-desk)
 

#### Event Details

The 2024 American Medical Association Research Challenge includes a poster symposium hall and a semifinals hall with the top scored research. **Log in at any time throughout the event to:**

* **View posters and presentations** on a variety of topics and specialties
* **Score posters in the semifinals** to help decide the top five finalists (AMA member exclusive opportunity)
* **Connect with participants** and provide feedback to help advance their research

At the conclusion of this event, the AMA will announce the top five finalists who will advance to the AMA Research Challenge finals, present their research to an elite panel of judges, and compete to win a $10,000 grand prize presented by Laurel Road. 

### Grand Prize Sponsor

AMA would like to thank Laurel Road for sponsoring a $10,000 grand prize for the winner of the AMA Research Challenge. Laurel Road is not involved in winner selection process. The winner will be announced on February 20, 2025 during the AMA Research Challenge finals. Payment of the grand prize will be directly from Laurel Road. See the AMA Research Challenge Official Rules for terms and conditions.

[![](https://assets.underline.io/uploads/markdown_image/1/image/611e331d4a0eba0920f240cfc04b4d77.png)](https://www.laurelroad.com/)

You need to log in with the email address you registered with. Access credentials have been sent to your email. 

Please be sure to check your spam and other email folders if you do not see an email confirmation right away.

Please log in to explore this event.

**There is no registration fee for this event! **

If you have used the AMA Research Challenge platform previously, please click the ‘Log-in’ button below. If you do not remember your password, please click “forgot password” and follow prompts to reset your password. After resetting your password, please refresh your webpage to access the platform.

Register to explore research in a variety of topics. AMA members get exclusive access to score posters in the semifinals. 

**Please use this link [here](https://www.ama-assn.org/member-benefits/events/ama-research-challenge) to register for free.**

Registration Is Required

Join the AMA Research Challenge poster symposium and semifinals to explore top research posters and score posters in the semifinals (an AMA member exclusive opportunity).

Background
Malaria is a parasitic infection transmitted by the Anopheles mosquito, with Plasmodium falciparum being the most severe species. Initial symptoms include fever, headaches, and nausea, often leading to a robust immune response. Diagnostic challenges arise in non-endemic regions, and cross-reactivity with other tests may occur.
Case Presentation
A 49-year-old woman traveling from Yemen via Djibouti presented in the Midwest with irregular fluctuating fevers, cough, headache with behavioral changes, and abdominal pain with emesis. Initial workup showed pancytopenia, hemolysis, and significant splenomegaly on CT scan. Blood smear confirmed Plasmodium falciparum malaria, classified as severe due to cerebral involvement and hyperparasitemia. Despite a positive fourth-generation HIV test, confirmatory HIV differentiation test and HIV nucleic acid amplification were negative, indicating a false positive likely due to severe malaria. The patient was successfully treated with three days of artemether-lumefantrine, and symptoms subsided.

Discussion
This case highlights the potential for false positive fourth-generation HIV tests in the context of severe malaria. The high sensitivity (99.8%) and specificity (99.5%) of these tests are generally reliable, but cross-reactivity can occur, necessitating confirmatory testing to avoid misdiagnosis. Previous cases have reported similar findings. For instance, a 2019 case report described a tourist returning from West Africa with severe P. falciparum malaria who tested false positive on the fourth-generation HIV test, but confirmatory testing was negative. Another case in 2023 documented a woman with P. malariae presenting a false positive HIV test, which was subsequently negated by differentiation testing. These false positives are thought to occur due to the immune system's response to malaria, which can produce antibodies or immune complexes that cross-react with HIV test antigens. Studies have shown that younger patients with malaria might produce more nonspecific antibodies, leading to higher rates of false positives. Historical enzyme immunoassay tests also reported similar issues, with significant rates of false positives in malaria patients. The unique presentation of our patient shows the necessity of considering false positives in regions where malaria is rare but HIV testing is common. This case reinforces the need for thorough diagnostic evaluations and the importance of reflexive confirmatory testing to prevent misdiagnosis and unnecessary treatment.


False Positive Fourth Generation HIV Test in a Woman with Severe Malaria

Abstract

Background: Actinomyces neuii is a gram-positive, non-branching rod-shaped bacteria, It rarely causes infection in humans. We report potentially the first case of primary actinomycosis of both breasts with Actinomyces neuii in an immunocompetent male.
Case description: A 40-year-old man reported chronic green bilateral nipple discharge. The patient underwent incision and drainage of the left breast abscess in the outpatient setting as well as a course of Clindamycin, Trimethoprim / Sulfamethoxazole (TMP-SMX), and short-term Penicillin. The patient continued to have drainage while on antibiotics. A culture of exudate in blood agar media was positive for Actinomyces neuii. A thorough history revealed nipples were pierced years earlier. A breast mammogram confirmed an abscess. Then the patient received an extended course of penicillin. When the prolonged course of penicillin was administered without improvement, the patient was put on oral linezolid; the induration continued even after the bilateral breast drainage stopped.
Conclusion: Actinomycosis is an invasive, progressive, and occasionally recurrent granulomatous infection caused by this genus. Actinomyces (A.) israelii is the common cause of actinomycosis whereas A. neuii relatively rarely causes it. This case of primary actinomycosis involving both breasts with Actinomyces neuii in a healthy male patient highlights the potential for this organism to cause significant pathology, particularly in the context of compromised barriers such as previous nipple piercings. This unusual presentation prompts considerations regarding the etiology, diagnosis, and management of A. neuii infections, which typically require prolonged antibiotic therapy and may necessitate surgical intervention in refractory cases. 



First Case Of Bilateral Breast Abscess By Actinomyces neuii In An Immunocompetent Male

Background
Ovarian cancer is the fifth-leading cause of cancer related deaths for women worldwide, and women have a lifetime risk of 1.3%. Factors known to increase your risk are familial genetic syndromes such as BRCA1/BRCA 2 tumor suppressor gene mutations, increasing age, obesity, and post-menopausal hormone therapy. Women present with abdominal pain/pressure, fatigue, and early satiety (1). Ovarian cysts have an unknown prevalence since most women are asymptomatic and they tend to be found incidentally while performing imaging for another cause. However, if causing symptoms, the patient may complain of pelvic pain/pressure, vaginal bleeding, and early satiety with or without nausea. Cancer antigen 125 (CA125) is a glycoprotein antigen present on various tissues including those lining the ovaries, fallopian tubes, and non-gynecological organs such as stomach and colon. It can be present in healthy tissue and malignant tissue. The normal range is between 5–35 IU/mL and values > 35 IU/mL are present in 6% of ovarian cysts (3). 

Case Presentation
Our patient was a 43-year-old female who presented with a chief complaint of abdominal fullness and dyspnea. She had been having ongoing increasing abdominal girth and pressure for the past nine months with new onset dyspnea at rest. On physical exam she was cachectic, abdomen was firm/distended, and she had 3+ bilateral lower extremity edema up to the knees bilaterally. The CT abdomen was significant for a left sided adnexal mass 20x20x30cm with severe abdominal distention and ascites. She underwent paracentesis on three consecutive days (day 1: 2.3L, day 2: 15L, and day 3: 2L) for a total removal of 19.3L. The ascitic fluid studies showed bloody fluid with >400,000 red blood cells without malignant cells present. Blood tests were unremarkable and subsequent cancer antigens were obtained. The results were: cancer antigen 125 (CA125) 114, carcinoembryonic antigen (CEA) 4.2, and cancer antigen 19-9 (CA19-9) 93. Patient underwent total abdominal hysterectomy (TAH) and bilateral salpingo-oophorectomy (BSO). After excision of the mass, the final histopathology showed a benign epithelial cyst measuring 27cm.

Discussion
Rapid onset worsening abdominal pressure accompanied with diffuse ascites and elevated CA125 leads one to the differential diagnosis of gynecological malignancy, mainly ovarian in origin. However, giant ovarian cysts defined as >10cm have a similar presentation. CA125 is associated with malignant ovarian cancer, but the specificity of this marker is low and can be falsely elevated in benign conditions and premenopausal women (4).

From Fear to Relief: A Case of Ovarian Cyst Masquerading as Malignancy

Abstract Title
How Did It Get There? A Case of Thoracic discitis and paraspinal abscesses caused by a vaginal flora in a 73-year-old man.

Background
Gardnerella vaginalis (G. vaginalis) is a small, gram-variable rod typically part of the vaginal flora. The overgrowth of G. vaginalis is a well-known cause of bacterial vaginosis. Only a few cases document infection with G. vaginalis in men, the most common source being genitourinary. We present a case of a 73-year-old man with altered mental status and sepsis who was found to have multilevel thoracic discitis/osteomyelitis with paraspinal and mediastinal abscesses secondary to G. vaginalis.

Case Presentation
A 73-year-old man presented to Loyola University Medical Center (LUMC) as a transfer for escalated care for septic shock. He initially presented to an outside hospital after being found down for two days. He had altered mental status, chest discomfort, shortness of breath, and an inability to move his bilateral lower extremities (LE). He was afebrile, hypotensive, tachycardic, and tachypneic with cold LE bilaterally. Computed tomography of chest, abdomen and pelvis revealed T7-T10 discitis/osteomyelitis, a complex fluid collection along the left posterior mediastinum, and emphysematous cystitis. Magnetic resonance imaging of the thoracic spine confirmed the presence of discitis/osteomyelitis, mediastinal and paraspinal abscesses and revealed an epidural abscess (T1-T7-8) and canal stenosis (T9-10). He was empirically treated with vancomycin and piperacillin-tazobactam. He rapidly decompensated requiring intubation and was therefore transferred to LUMC.

At LUMC, neurosurgery was consulted for concerns of acute cord compression. He underwent T7-T10 laminectomy, T8-9 transpedicular decompression and T5-11 fusion for spinal infection with unstable T8 spine fracture. Frank purulence was noted upon fascial opening. Intraoperative cultures of thoracic epidural fluid, epidural swab and deep fascia wound cultures grew few colonies of G. vaginalis. Blood cultures were negative. After treatment of emphysematous cystitis, he was transitioned to ampicillin-sulbactam for 6 weeks. He remained afebrile with improved leukocytosis and negative blood cultures but was still unable to move his bilateral LE upon discharge (hospital day 27). Later, he was unfortunately readmitted to an outside hospital for unknown reasons and was lost to follow up. 

Discussion
This case demonstrates the pathogenic ability of G. vaginalis to cause extensive spinal abscesses and osteomyelitis. Although G. vaginalis can cause bacterial vaginosis and treatment for this is well-established, the management of this case is much more complex. This patient’s diagnosis is uncommon, so being aware of the pathogenicity of G. vaginalis to cause substantial infection and analyzing treatment outcomes for these cases is important for management of future cases. 


How Did It Get There? A Case of Thoracic Discitis and Paraspinal Abscesses Caused by a Vaginal Flora in a 73-year-old Man

Hydralazine-Associated Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Lupus with Crescentic Pauci-Immune Rapidly Progressive Glomerulonephritis - A Case Report
Cynthia Andrade, Adam Ostrovsky, Nairuti Sanghavi, Eunae Ko, Vandana Bandari, Sangeetha Satyan

Introduction
Hydralazine, a commonly prescribed medication for hypertension and heart failure, has been linked with anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis and lupus. We present a unique case of hydralazine associated ANCA vasculitis and lupus with crescentic pauci-immune type rapidly progressive glomerulonephritis (RPGN) requiring renal replacement therapy treated with immunosuppression and Avacopan.

Case Presentation
A 58-year-old male with hypertension treated with hydralazine 100 mg three times a day for about three years presented to the hospital with fatigue, poor appetite, twenty-pound weight loss, exertional dyspnea, intermittent fevers, and erythematous rash for about three months.
Serum creatinine was elevated at 2.4 mg/dL on admission with a previous baseline of 1.0 mg/dL four months prior to hospitalization. Urinalysis showed proteinuria and microscopic hematuria. Hemoglobin was 11.8 g/dL. Urine protein/creatinine ratio was 0.6 g/g. Renal ultrasound revealed normal sized echogenic kidneys. Further evaluation revealed elevated inflammatory markers, high anti-nuclear antibody (ANA) in a homogeneous pattern (titer of 1:1280), normal anti-ds DNA, hypocomplementemia with low C3 and lower limits of normal C4, positive anti-histone antibody at 3.1 U, and anti-cardiolipin IgM antibodies at 30.8 MPL-U/mL. Kidney biopsy revealed focal segmental necrotizing and crescentic pauci-immune type glomerulonephritis (GN) with mild tubular atrophy and interstitial fibrosis and severe acute tubular injury. Immunofluorescence revealed low level immune complex deposition; electron microscopy revealed global small electron dense deposits in mesangial areas and rare endothelial tubulo-reticular inclusions. ANCA screen was positive for p-ANCA (titer of > 1: 640) with high anti-MPO and anti-PR3 antibodies at 652.7 and 5.5 AI, respectively.
Hydralazine was discontinued. He was treated with high dose methylprednisolone along with rituximab for induction therapy followed by prednisone taper. Renal function progressively worsened requiring initiation of renal replacement therapy. He was also treated with Avacopan. Hemodialysis was discontinued after about four months due to renal recovery but with residual stage four chronic kidney disease. ANA and ANCA titers decreased with treatment and anti-MPO and anti-PR3 antibodies were 3.5 and 0.3 Units respectively at four months. 

Discussion 
Hydralazine induced Lupus and ANCA vasculitis with pauci-immune type RPGN is rare. Certain serologic markers and pathologic features are suggestive of drug associated ANCA-GN rather than primary ANCA-GN as demonstrated in our case. ANCA-GN including that complicated by hydralazine has high morbidity and mortality. Vigilance, prompt diagnosis, discontinuation of the offending medication, and immunosuppressive treatment for severe disease are necessary. Clinicians must be cognizant of this potentially life-threatening condition associated with hydralazine and consider alternative available treatments for hypertension and heart failure when feasible.


Hydralazine-Associated Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Lupus with Crescentic Pauci-Immune Rapidly Progressive Glomerulonephritis - A Case Report

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.


Internal Medicine Resident PGY-3

We report a case of Lemierre Syndrome caused by Arcanobacterium haemolyticum bacteremia in a previously healthy immunocompetent 29-year-old male. Two blood cultures revealed the exclusive presence of A. haemolyticum. 

A 29-year-old male with no past medical history presented with a 5-day history of fever, chills, and severe odynophagia. Physical exam revealed asymmetrical tonsillar swelling and a CT Neck with contrast showed an infectious process surrounding the left palatine tonsil and inflammatory phlegmonous changes and gas abutting the left carotid sheath. Given this, patient was to be transferred to a tertiary care center for further evaluation by ENT. 
His symptoms continued to worsen, and he presented to the tertiary care center the following day. Initially, the patient was afebrile with a leukocytosis 13.5. A CT neck showed an infectious abscess around the left parapharyngeal and left carotid spaces with thrombophlebitis of the left internal jugular vein with complete thrombosis suggestive of Lemierre’s syndrome. Septic emboli were also noted in the upper lungs. Antibiotics were broadened to linezolid and piperacillin-tazobactam. The patient was taken to the OR for left neck exploration, left peritonsillar abscess drainage, and excision of the left jugular vein. During the procedure, it was noted that the thrombosed internal jugular vein had purulent material expressed. 
Two blood cultures were positive exclusively for Arcanobacterium haemolyticum at 3.6 days and the BCID panel was negative for all targets including Streptococcus. Intra-operative cultures had no growth. His leukocytosis gradually returned to normal range, and he remained afebrile. Patient was discharged with plan for 2 weeks of IV ampicillin-sulbactam and 4 additional weeks of PO amoxicillin/clavulanate. 

In 1936, Andre Lemierre described a series of cases of septicemia caused by Fusobacterium necrophorum and complicated with internal jugular vein thrombophlebitis and septic emboli to distant organs. F. necrophorum is the most common causative agent of Lemierre’s syndrome, followed by Fusobacterium nucleatum. Lemierre's syndrome is a rare condition, estimated to affect approximately one in a million individuals annually. Typically, affected individuals are young, previously healthy adults, with a male-to-female ratio of 2:1. 
To date, only 6 cases of Lemierre’s syndrome caused exclusively by A. haemolyticum have been reported in the medical literature and no cases have been reported from the United States. We present the first case of Lemierre's disease stemming from infection solely involving A. haemolyticum.

Lemierre Syndrome caused by Arcanobacterium haemolyticum: First reported case in the United States

Abstract Title
Losing Fat or Muscle? A Case of Rhabdomyolysis Following Initiation of Semaglutide (Wegovy)
Background
GLP-1 receptor agonist semaglutide has gained popularity due to its glycemic control, positive cardiovascular effects, and role in weight management. Common side effects include fatigue, headache, injection site reactions, and gastrointestinal symptoms, like abdominal pain, nausea, and gastroparesis.
Case Presentation
A 56-year-old female with past medical history of systemic lupus erythematosus (SLE) on hydroxychloroquine (HCQ) for 30 years, gastroesophageal reflux disease, autoimmune hepatitis on budesonide, asthma, and fibromyalgia presented to the emergency department (ED) with five days of worsening fatigue, bilateral lower extremity weakness, and pain. One week prior, she experienced nausea, heartburn, and pruritus of the breast, back, and buttocks. Primary care visit labs revealed a creatine kinase (CK) above 27,000 u/L (n=30-184 u/L) prompting ED evaluation. On admission, she endorsed worsening pain, weakness, and decreased appetite. She denied new excessive exertion, foods or supplements, trauma, or statin use but did disclose starting semaglutide (Wegovy) 0.25 mg injections two weeks prior for weight loss. Family history includes polymyositis in her father. Admission vital signs were notable for pulse 113 beats per minute, blood pressure 137/99 mmHg, and BMI 36.85 kg/m2. Physical exam demonstrated bilateral calf tenderness, positive Homan’s sign, hip flexor weakness, normal range of motion, and no joint tenderness. Serum studies demonstrated CK above 34,000 u/L, aspartate aminotransferase (AST) 1018 u/L, alanine aminotransferase (ALT) 297 u/L, creatinine 0.60 mg/dL, estimated glomerular filtration rate (eGFR) >90 mL/min/1.73m2, and no leukocytosis. Rheumatological studies including C3/C4, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), urine protein-creatinine ratio, and double-stranded DNA (dsDNA) were within normal limits. Aldolase was elevated to 176.5 u/L (normal <7.7 u/L). Duplex doppler ultrasonography showed no venous thromboembolism bilaterally. She was diagnosed with rhabdomyolysis and admitted for three days during which her HCQ was held, and she received aggressive IV fluids. CK levels dropped nearly 10,000 u/L daily. At discharge, CK was below 6,000 u/L with no renal injury and improved liver enzymes; she reported near resolution of symptoms. Repeat CK four days post-discharge was 192 u/L.
Discussion
Limited information exists on the association between semaglutide and rhabdomyolysis; one case report details a similar presentation, both in timing and symptomology. This patient had significantly elevated CK levels and liver enzymes. Despite stable autoimmune conditions on long-term treatment, laboratory results suggest her rhabdomyolysis is attributable to recent semaglutide initiation instead of another etiology.

Losing Fat or Muscle? A Case of Rhabdomyolysis Following Initiation of Semaglutide (Wegovy)

Title: Lurasidone (LATUDA)-Induced Pancreatitis: A Case Report

Background: Lurasidone (LATUDA) is a second-generation antipsychotic used in the management of schizophrenia and bipolar disorder. There have been reports of drug-induced pancreatitis (DIP) associated with antipsychotics such as haloperidol, olanzapine and clozapine. However, there is limited documented literature on the association between Lurasidone and pancreatitis. Although rare, DIP is a severe adverse effect of various medications. Here, we present a compelling case of
Lurasidone-induced pancreatitis that sets itself apart from other cases of DIP.

Methods: A 60-year-old African-American woman with a past medical history of Type-1 bipolar disorder presented to the ER with complaints of nausea, multiple episodes of vomiting, and constant, sharp abdominal pain that radiates to her back. These symptoms began approximately a month after she started taking Lurasidone. A thorough examination revealed tenderness to palpation in the umbilical and lower abdominal area without rebound tenderness or guarding. Laboratory tests
showed significantly elevated serum Lipase (997 U/L) and serum Amylase (533 U/L), consistent with the diagnosis of acute pancreatitis. We considered a diagnosis of Lurasidone-induced pancreatitis due to the correlation between the initiation of Lurasidone therapy and the manifestation of her symptoms. Subsequently, we discontinued the patient's Lurasidone therapy and initiated supportive management, including bowel rest, intravenous fluids, and pain control. Her symptoms improved progressively and successive laboratory assessments revealed downward
trending pancreatic enzyme concentrations (serum Lipase of 25 U/L after a week).

Results: Despite the absence of documented literature linking Lurasidone specifically to pancreatitis, patient presentation and laboratory findings confirmed drug-induced pancreatitis. Much like the other antipsychotics implicated in drug-induced pancreatitis (DIP), the mechanism of this reaction, although unclear, is believed to stem from either direct toxicity on pancreatic cells, immune-mediated mechanisms, or hypertriglyceridemia.

Conclusion: Since there are no documented cases of Lurasidone-induced pancreatitis, this case report necessitates healthcare providers to maintain a high index of suspicion for DIP in patients presenting with acute abdominal pain when they are on Lurasidone therapy. The patient's clinical presentation, laboratory findings, and the temporal relationship between the start of Lurasidone
treatment and the onset of symptoms, combined with the lack of any other identifiable causes for pancreatitis, established the diagnosis of Lurasidone-induced pancreatitis. Further studies are warranted to elucidate the underlying pathophysiological mechanisms and guide appropriate clinical practice for prompt patient management.

Lurasidone (LATUDA)- Induced Pancreatitis: A case Report

In-stent thrombosis (ISR) is one of the dreaded complications of percutaneous coronary angioplasty. Despite marked reductions in ISR since the transition from bare metal stents to drug-eluting stents, ISR still occurs at a rate of 1%-2% per year. 

We present the case of a 64-year-old Caucasian male who was admitted for staged angioplasty after a left heart catheterization had shown significant stenosis to the LAD and mid ramus intermedius. He had DES placed to the mid-LAD and mid-ramus intermedius. Despite being placed on dual antiplatelet therapy after the stent placement, six hours later, he complained of chest pain and EKG showed new ST elevations in leads I, aVL, and V2-V6. Repeat LHC showed thrombosis to recently placed LAD and mid ramus-intermedius stents, so a new set of stents was placed, and the patient was loaded with eptifibatide and then restarted on dual antiplatelet therapy after the procedure.

However, only 48 hours later, the patient started complaining of chest pain again. EKG showed new ischemic changes and a high sensitivity troponin of 5000. He was taken to the catheterization lab, and LHC once again revealed late stenosis of the previously stented LAD and mid-ramus intermedius. He underwent percutaneous coronary angioplasty to these stents. Post-LHC, he was started on prasugrel and aspirin instead of the 2 other times when he was on clopidogrel and aspirin, then ticagrelor and aspirin.

In addition to the dual antiplatelet therapy, he was also started on a Factor X inhibitor, rivaroxaban. Our hypercoagulability investigations did not yield any positive results; however, we found out the patient was on testosterone replacement.

This case is very unique in that we had early re-stenosis of a drug-eluting stent, and it did not only occur once, it occurred twice. One of the questions raised in this unique case is: when you have patients who have early restenosis of their stents, what is the preferred antiplatelet agent, and is a Factor Xa inhibitor indicated in this scenario? In the case of our patient, we went for prasugrel + aspirin + rivaroxaban, and we did not have any re-stenosis.


Premium content

Next from AMA Research Challenge 2024

False Positive Fourth Generation HIV Test in a Woman with Severe Malaria

Similar lecture

Convolution Neural Network Models for Acute Leukemia Diagnosis