VA Caribbean Healthcare System

It has become increasingly recognized that heart failure with a preserved ejection fraction (HFpEF) results from an inflammatory process, congestion, and metabolic dysbiosis rather than an intrinsic structural heart abnormality. Recent studies have highlighted the close link between the heart, the liver, and the pancreas, which are organically connected via the same inflammatory processes and pathways. Liver congestion and fibrosis are responsible for the inflammatory process and the lack of metabolic adaptation, whereas pancreatic ischaemia and insufficiency of the exocrine glands aggravate malnutrition and cachexia, worsening the heart condition. Acute pancreatitis may cause heart failure and arrhythmia through injury and systemic inflammatory response syndrome (SIRS), an inflammatory process mediated by the cytokines released during the injury process. Recognition of this hepato-pancreato-cardiac axis offers a paradigm shift towards integrated management of HFpEF, emphasizing anti-inflammatory, metabolic, and haemodynamic interventions. Future research integrating multi-organ imaging, inflammatory biomarkers, and therapeutic trials such as GLP-1 receptor agonists, SGLT2 inhibitors, and cytokine blockers will be critical to disrupt this tri-organ inflammatory circuit and improve outcomes in HFpEF.

Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer cases and is frequently diagnosed at advanced stages, leading to poor survival outcomes. Molecular analysis can identify actionable mutations, such as mesenchymal-epithelial transition (MET) exon 14 skipping mutations, which serve as therapeutic targets. Capmatinib, a selective MET tyrosine kinase inhibitor (TKI), has emerged as a promising targeted therapy for this molecular subtype. We present the case of an 83-year-old former smoker with a history of chronic obstructive pulmonary disease who was diagnosed with stage 4A metastatic lung adenocarcinoma. Molecular profiling revealed a MET exon 14 skipping mutation. The patient was initiated on capmatinib, resulting in sustained disease stability and a reduction in the lesion size over a three-year follow-up. This case highlights the clinical utility of molecular testing in NSCLC, particularly for identifying MET exon 14 alterations that guide targeted therapy. Capmatinib demonstrated durable disease control and was well tolerated, offering a viable alternative to conventional chemotherapy in an elderly patient with significant comorbidities. These findings support the integration of precision oncology into the management of advanced NSCLC and underscore the potential of MET TKIs to improve outcomes in this high-risk subgroup.

Abstract Introduction Obstructive sleep apnea (OSA) is prevalent among hospitalized patients and adversely impacts comorbidities and length of stay. In-hospital adherence may predict home PAP adherence. PAP therapy use during hospitalization has not been clearly established. We aim to assess inpatient PAP therapy prescription rates and use, and factors that influence them among hospitalized patients with OSA. Methods This retrospective study reviewed electronic records of all patients discharged from a Medicine ward during one month at the VA Caribbean Healthcare System. Records of patients with OSA were reviewed. Data collected included demographics, comorbidities, Epworth Sleepiness Scale (ESS), body mass index (BMI), home PAP adherence, PAP therapy prescriptions within 24 hours of admission and the proportion of patients prescribed PAP therapy that used it. Statistical analysis identified significant associations. Results Thirty five percent (n=120) of patients discharged (n=340) had a diagnosis of OSA. Of these 25.8% (n=31) were PAP-adherent at home. Of patients with OSA 44.2% (n=53) received PAP therapy within 24 hours of admission, 55.8% (n=67) did not. Factors associated with PAP prescriptions include home adherence (39.6% vs. 14.9%; p=0.002) and history of heart failure (50.9% vs. 20.9% p=0.001). Adherence among those prescribed PAP therapy was 73.6% (n=39). There was no significant difference in prescription rates or PAP use associated with AHI, obesity, insomnia, hypoventilation, BMI, ESS, hypertension, depression, anxiety, PTSD, substance use, cognitive disorders, chronic pain. Patients who did not use prescribed PAP therapy had a higher rate of home PAP compliance than in-hospital users (64.3% vs. 30.8%; p=0.028). Conclusion There was low timely PAP prescription rates among inpatients. Home PAP adherence predicted the in-hospital prescriptions. Non-adherent patients may be at greater risk of being untreated. A greater use of PAP during hospital admission might represent a window of opportunity to improve PAP treatment adherence. Factors associated with lower in-hospital adherence in home-adherent patients should be studied. Equipment issues (availability, differences between hospital and home devices and settings) may explain these differences. Education could enhance inpatient PAP use and increase awareness of the importance of treating OSA in patients with comorbidities besides CHF. Support (if any)

Abstract Chronic rhinosinusitis with nasal polyposis (CRSwNP) is a disease that can result in severe nasal congestion, hyposmia, facial pressure or pain. Disease recurrence is a known patient complication despite adequate medical and surgical management, but studies have observed it to occur many months after achieving after remission. Here we present a patient with an aggressive case of CRSwNP. This is a 39-year-old male with History of Aspirin-exacerbated respiratory disease (AERD), CRSwNP, and who has been followed by Allergy and ENT due to unrelenting sinusitis for the past ten years. Since 2014, he has been developing persistent nasal congestion with post-nasal drip, copious cough productive of yellow-green mucous phlegmons, facial pain, anosmia, dysgeusia, and multiple coughing episodes that also woke him at night. Physical examination of the nasal airways revealed multiple, bilateral polyps with mucosal edema, turbinate hypertrophy, and copious mucoid secretions. Bilateral endoscopic sinus surgery (FESS) and nasal septoplasty were then performed in 2015 after no relief with antihistamines and steroids. After 18 months, his symptoms recurred until 2019, when he was started on Omalizumab. He received Omalizumab and Dupilumab a year and a half each with no improvement seen. On April 2024 performed another FESS and provided temporary relief with elimination of the polyps, but the polyps and mucosal edema recurred in a three-week follow up. Polyp biopsy showed multiple neutrophils and low eosinophils. Nasal swab cultures taken on May were positive for P. aeruginosa MDS. Oral ciprofloxacin was provided, with no relief. New swab culture showed P. aeruginosa, now resistance to ciprofloxacin. ID was consulted and recommended 21 days of IV antibiotics, amikacin nasal rinses, and to start dupixumab. After finishing therapy, patient referred marked improvement for the first time ever in nasal congestion. Colonization of the upper respiratory tract by Pseudomonas species is that can contribute to local inflammation, mucosal barrier disruption, and mucociliary clearance dysfunction, leading to recurrence of disease even with optimal therapy. Symptom recurrence in less then a month after surgery suggests an active trigger in addition to his disease that is preventing healing of the mucosa. Highly-virulent organisms like Pseudomonas are known to infect CRS patients after surgeries, and require IV antibiotics to adequately treat, but are associated to immunocompromise states and Cystic fibrosis (CF). This case shows how Pseudomonas infection may also occur in an immunocompetent, non-CF patient, thus should remain in the differential in patient with recurrent disease.

Background: Ixekizumab is a monoclonal antibody that binds interleukin 17A (IL-17A) cytokine selectively and inhibits interaction with its receptor. This humanized monoclonal antibody is approved for the treatment of ankylosing spondylitis, non-radiographic axial spondyloarthritis, psoriatic arthritis and plaque psoriasis. Most common adverse reactions associated with this drug include injection site reactions, upper respiratory tract infections, nausea, and fungal infections. Development or exacerbations of inflammatory bowel diseases (IBD) is a rare adverse reaction of this medication. We report a case of new-onset ulcerative colitis in a 76-year-old man on ixekizumab for plaque psoriasis. Methods: This is the case of a 76-year-old man with past medical history of chronic plaque psoriasis of more than 20 years previously on methotrexate who initially presented with complaints of abdominal pain, anorexia, unintentional weight loss of 40 lbs. and watery diarrhea that later progressed to bloody. The patient denied having similar symptoms in the past. The patient had started ixekizumab 2 months prior to presentation, which was discontinued. Fecal calprotectin at the time was elevated >8000 mcg/g. Abdominal/pelvic CT with contrast was remarkable for concentric mural thickening of the distal transverse colon, descending colon, sigmoid colon, and proximal rectal region with surrounding fat stranding and associated mesenteric lymphadenopathy. Colonoscopy showed continuous marked erythema with associated ulcerations, exudates and loss of vascular pattern starting from distal descending (approx. 45 cm from anal verge) through sigmoid and rectum. The patient was admitted and started on steroids and initial dose of infliximab. The patient was discharged on steroid taper but had allergic reaction to the next infliximab dose. The patient was changed to upadacitinib and tapered off steroids with an adequate response. Results: In clinical trials, during the 12-week, placebo-controlled period, ulcerative colitis (0.2%) and Crohn’s disease (0.1%) occurred at a greater frequency in the ixekizumab 80 mg Q2W group than the placebo group (0%) in subjects with plaque psoriasis. A retrospective analysis demonstrated that IL-17 inhibitors are associated with new onset of IBD or exacerbations within 6 months of therapy. Conclusions: In this case, our patient did not have previous symptoms that suggested IBD, we hypothesize that he developed de novo ulcerative colitis associated with IL-17A inhibitor, ixekizumab. Although a rare adverse reaction, physicians should be aware of the potential association between exposure to anti-IL-17 and exacerbation or induction of IBD. All patients should be oriented about this adverse reaction and be counseled to monitor for new or worsening abdominal symptoms.

ASCVD is the principal cause of morbidity and mortality for Veterans in the VA Healthcare System. San Juan VA is one of 50 VA sites participating in a national quality improvement initiative called the VALOR QI: VA Lipid Optimization Reimagined Quality Improvement Project. Is a collaborative project between the U.S. Department of Veterans Affairs (VA) and the American Heart Association (AHA) with the goal of positively impacting Veterans’ cardiovascular (CV) health. VA sites work with an AHA QI consultant to develop and deploy a local quality improvement plan to help overcome site specific barriers preventing Veterans from achieving optimal cholesterol levels. The program’s objectives include improving clinical pathways and processes to impact ASCVD management through a Learning Healthcare System model of quality improvement designed to improve the management of dyslipidemia among those with high-risk ASCVD. The hypothesis is that patients who are part of the VALOR QI program will be more successful in reaching LDL-C target. This will help to reduce the risk of ASCVD and mortality for the patients, promoting better management of lipid levels through medications, diet and regular monitoring. As part of the methodology, the patients are enrolled to the program using the criteria of Veterans > 18 years of age with diagnosis of ASCVD and LDL-C > 70 mg/dl or non-HDL > 100 mg/dl. The Healthcare Coach has a full track of their lipid medications, assists the patients with refills, provides educational materials, follows up with their clinical appointments, and emphasizes the importance of having a good compliance with therapy, appointments and diets to maintain the target of LDL-C. Once the patient starts with a new lipid medication, they are followed in 3 months with labs. After reaching the target the patient is followed up closely in 6 months with labs to prevent relapse. The VALOR QI Program started at VA San Juan in June 2023 and, as of May 30, 2024, had directly engaged 282 Hispanic patients. 111 (39.4%) achieved target LDL-C; 268 (95%) have any statin use; 117 (41.5%) are on any non-statin lipid-lowering therapy (LLT); 116 (41%) are on statin plus LLT; 25 (8.9%) are on PCSK9, and 133 (47.2%) received educational materials. In conclusion, this initiative led to target LDL levels in 39% of patients which represents a significant population. As this program is further implemented in our institution, we expect improvement in patient outcomes and prognosis.

Introduction: Squamous cell carcinoma (SCC) of the rectum is an exceptionally rare variant, accounting for less than 2% of all rectal cancers. Due to its low prevalence and location lower in the rectum, SCC can be challenging to detect during colonoscopy, with estimates suggesting a detection rate of less than 2 per 1,000 individuals undergoing screening. Risk factors for SCC include chronic inflammation, Human papillomavirus (HPV) infection, and prior radiation therapy. This case highlights the importance of meticulous attention to detail during colonoscopy, particularly when performing retroflexion of the instrument to fully visualize the rectum. A thorough evaluation of the entire rectal surface is crucial to avoid missing a potential SCC. Case Description/Methods: A 61-year-old man with hypertension and a current smoker presented with 1-2 month history of changes in bowel habits. Stools were more frequent, non-bloody and pasty. Prior high-quality screening colonoscopy was unremarkable. Diagnostic colonoscopy revealed a large subepithelial mass in the upper rectum. Two additional smaller lesions were found throughout the rectum. Endoscopic ultrasound confirmed a 3 cm x 2.7 cm proximal rectal lesion with extension into perirectal tissues and suspicious lymph nodes. A distal rectal lesion (2.1 cm x 1.5 cm) was also identified within the rectal wall with surrounding inflammation. Biopsies from both lesions revealed poorly differentiated carcinoma with features most consistent with SCC. Discussion: This case emphasizes the importance of thorough colonoscopy with retroflexion in the rectum, especially when encountering atypical presentations of SCC. As seen here, SCC can arise in the upper rectum rather than the usual lower location. Additionally, the presence of multiple lesions and a negative prior colonoscopy highlight the potential for SCC to develop even with seemingly normal screening. Therefore, a high index of suspicion and meticulous examination during colonoscopy are crucial for diagnosing SCC, even in patients with atypical bowel habit changes like those presented here (more frequent, non-bloody, pasty stools). Early diagnosis and prompt treatment are crucial for optimal outcomes in these cases. This case also highlights the utility of endoscopic ultrasound in further characterizing suspicious lesions and guiding biopsies for further management (Figure 1).Figure 1.: Left: Endoscopic ultrasound of anorectal squamous carcinoma. Right: Subepithelial squamous cell carcinoma.

Introduction: Rapidly progressive glomerulonephritis is characterized by a rapid decline in renal function over days to weeks with U/A with proteinuria, hematuria, dysmorphic RBC's,and RBC casts. Incidence in the United States is 7 cases per 1 million persons,while in the United Kingdom it is 2 cases per 1 million. Common etiologies include immune complex-mediated RPGN, such as lupus, IgA vasculitis, or C3 glomerulonephritis. Here we present a difficult to treat case of a young woman with rapidly progressive glomerulonephritis. Case Description: This is a case of a 27-y/o female without medical history, who presented to the emergency room with nausea, vomiting, and diarrhea over two days. Vital signs revealed high blood pressure, tachycardia, hgb 6 g/dL. Labs revealed serum creatinine: 17, BUN: 116, Na:126, K: 5.5, CO2: 13. U/A with protein >500 mg/dL, large blood, microhematuria and urine protein/creatinine 6.6 g/day. After, patient developed pleuritic chest pain, with pericardial effusion and pericardial friction rub. Emergent hemodialysis was started with improvement after 4 days of HD and pulse steroids. Other labs revealed (+) Coombs test, high ferritin and LDH levels, (+) ANA/Ro pattern, low C3, (-) C4, (-) scleroderma AB, (-) anti-RNP AB, (-) anti-Sm AB, (+) anti-Ro AB, (-) anti-dsDNA AB, and (+) lupus anticoagulant. Kidney biopsy confirmed Diffuse Proliferative Lupus Nephritis Class IV. Treatment begun with Hydroxychloroquine, Mycophenolate and high dose steroids. After treatment patient remained dependent on HD. Discussion: Kidney biopsy is required for LN diagnosis, prognosis, and adequate management. Prognosis of disease worsens with advancing WHO histopathology classes, particularly in LN Class 4, where early initiation of therapy significantly improves disease outcomes. Treatment involves pulse steroids with methylprednisolone for 1-3 days followed by oral prednisone along with either cyclophosphamide (500 mg IV every two weeks for 3 months) or mycophenolate mofetil (2-3 g/day for 6 months). Monitoring disease includes assessments of blood pressure, renal function, proteinuria, urinary sediment, C3/C4 levels, and anti-dsDNA AB measured at least biannually. Earlier disease detection is vital as achieving complete kidney response during treatment provides a 5-year patient and kidney survival of more than 90% vs 69% (patient) and 45% (kidney) for those not achieving complete remission.

Introduction: Thrombus formation lies at the heart of Virchow’s triad. While portal vein thrombosis is common in cirrhotic patients, it can also occur without hepatocellular disease. Factors like Factor-V Leiden and prothrombin G20210A increase procoagulant activity, while deficiencies in antithrombin, protein C, or protein S reduce anticoagulant function. These factors can cause portal and mesenteric vein thrombosis in noncirrhotic patients. Rarely, blunt abdominal trauma can precipitate thrombosis, especially with undiagnosed thrombophilia. Clinical manifestations include upper abdominal pain, nausea, fever, anorexia, and jaundice. We present a rare case of multiple acute thromboses following blunt trauma in a patient without coagulability disorders. Case Description/Methods: A 56-year-old Hispanic man with no significant medical history presented with acute severe abdominal pain that began 4 days after a 2–3-meter fall while gardening. Initially diagnosed with acute gastritis and treated with PPIs, his pain progressed over 5 days. Physical exam showed epigastric and lower quadrant pain without hematoma or trauma signs. Labs revealed mild leukocytosis, stable hemoglobin and platelets, normal chemistry, elevated C-reactive protein (120.4 mg/L), and elevated fibrinogen degradation products (20 µg/mL). Coagulation studies were within normal limits. Abdominopelvic CT revealed thrombosis in the portal vein, portal splenic confluence, splenic vein, and superior mesenteric vein (Figure 1). The patient was started on subcutaneous enoxaparin and then transitioned to a direct oral anticoagulant. Hypercoagulability studies, including PNH and JAK-2 mutation, were unremarkable. Discussion: Virchow’s triad encompasses factors promoting thrombus formation. In this case, endothelial injury triggered thrombus formation. However, it's crucial to consider hypercoagulability disorders like Factor V Leiden, PNH, and JAK-2 mutation. Portal vein thrombosis typically presents with acute upper abdominal pain, vomiting, anorexia, fever, and abdominal distension. This rare clinical presentation has few reported cases. Symptoms could suggest other diagnoses like pancreatitis or gastritis, but thrombosis should be considered if there's blunt abdominal trauma. Adequate follow-up is critical to monitor for complications. Patients with PVT risk developing portal hypertension, potentially leading to cirrhosis. Compliance with anticoagulation and regular primary care follow-up is essential.Figure 1.: Abdomino-pelvic CT scan and doppler with evidence of occlusive thrombus.

Introduction: Acute-on-chronic liver failure (ACLF) is a process where an inflammatory event leads to decompensation of cirrhosis and extrahepatic organ failure. Approximately 60% of the events leading to ACLF are identified by physicians; alcoholic hepatitis and sepsis account for most of the cases. However, unusual events may lead to ACLF; spontaneous rupture of a pectoralis muscle was the culprit of the following case. Case Description/Methods: Case of a 61-year-old Hispanic man who presented to the ED due to a right-sided chest and arm pain that woke him up from sleep. Past medical history included cirrhosis secondary to cryptogenic steatotic liver disease and polym-year-oldsitis. Daily medications included azathioprine 50 mg, prednisone 5 mg, and vitamin E 1000 units. At the ED, the physical exam showed a right-sided hematoma involving the chest and entire upper extremity. Acknowledging that polym-year-oldsitis is an autoimmune condition against muscles, predisposing them to rupture and bleed, the emergency physician ordered bloodwork and imaging. Results included anemia (Hgb 7.1 g/dL.), right-sided pectoralis/subscapularis muscle rupture, and an 11 cm hematoma. The patient was admitted to the medical ward, where he developed acute moderate ascites and grade 1 encephalopathy. At the time, he had a Child-Pugh class C and MELD score of 23 due to hyperbilirubinemia (5.93 mg/dL), hypoalbuminemia (2 g/dL), a high INR (2.21), low creatinine levels (0.27 mg/dL), and normal sodium levels (136 mEq/L); also seen where mild elevations of AST and ALT (116 U/L and 60 U/L, respectively.) Despite aggressive management, the patient’s hematoma recurred, leading to the suspicion and eventual diagnosis of disseminated intravascular coagulation (DIC.) He decided to receive comfort care only; later, he was admitted to hospice. Discussion: In our patient, ACLF was evidenced by the sudden onset of ascites, encephalopathy, and DIC following the spontaneous rupture of his pectoralis muscle. Muscle rupture leads to ACLF via liver ischemia, hepatocyte necrosis, and an inflammatory process mediated by damage-associated molecular patterns. Consequently, the 28-day mortality rate of ACLF is 32.8%; thus, identifying unusual triggers is vital when facing the disease (see Figure 1).Figure 1.: On the left side of the image is our patient’s large hematoma. On the right side of the image, hematoma is seen on CT imaging.