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Item A Case of Refractory Hypoglycemia with DPP-IV Inhibitors in a Patient with CKD and Paraproteinemia(Society of Hospital Medicine, 2020-11-05) Lugo, Adrian; Cho, Elizabeth; MacKay, Keir; Thothala, NiranjanItem Combined Hormonal Contraceptives: The Culprit of Acute Portal Vein Thrombosis(2021-06-10) Ayala Castillo, Crystal; Lugo, Adrian; Lingamurthy, Manjesh; Rascon-Aguilar, IvanOral contraceptive medications are known to increase the risk of developing blood clots. Most commonly, these thrombi are found as deep vein thrombi (DVTs) or pulmonary emboli (PEs). The incidence of portal vein thrombosis is much rarer in patients without comorbidities like liver cirrhosis, malignancies, and hematologic disorders. In this case report, we present the cause of a female's epigastric abdominal pain to stem from portal vein thrombosis while on combination oral contraceptive pills (OCPs). A 34-year-old Caucasian female with a history of hypothyroidism, obesity, and oral contraceptive use presented to the emergency room complaining of epigastric abdominal pain for two days. The pain radiated to her back, and she described it as pressure-like in nature with intermittent episodes of nausea. She reported taking norethindrone-ethinyl estradiol for contraception for several years prior. No history of blood clots in the past. Physical examination was pertinent for tenderness in the epigastric area. Vital signs were stable. A blood pregnancy test was negative. Liver enzymes were within normal limits. A complete abdominal ultrasound was unremarkable. Computerized tomography of the abdomen without contrast revealed left portal vein hyperattenuation which was suggestive for acute portal vein thrombosis (Figure 1). Serological testing performed to rule out inherited thrombophilia were negative (Table 1). The patient was subsequently started on anticoagulation and was discharged hemodynamically stable with close outpatient follow up. Portal vein thrombosis can present acutely or exist in chronic states in a broad array of underlying causes. Risk factors include: liver cirrhosis, malignancy, hematologic disorders, thrombophilia, inflammatory disease, and while on hormonal therapies. In the current literature, the most typical sites to find venous thromboembolisms while on OCPs are in the deep veins of the legs and the pulmonary vasculature. Finding a thrombus in the portal vasculature is rare when there is no associated liver disease. Other contributing factors in our patient were obesity and the presence of hypothyroidism. We believe this case report is noteworthy as it helps clinicians suspect portal vein thrombi in patients that are chronically on OCPs. This will help decrease morbidity and mortality and will help guide future management of birth control, possibly by helping form a guideline for contraceptive use in the setting of unusual thrombus locations.Item Cyclical Hematochezia in a 30-Year-Old Female Linked to Endometriosis(2021-06-10) Lugo, Adrian; Martyn, Colin; Cho, Isaac S.; Fraser, Scott; Gislason, GardarClinical manifestations of gastrointestinal (GI) dysfunction are diverse. However, many of these symptoms such as abdominal pain and hematochezia are nonspecific and can be caused by a variety of ailments. As such, it is imperative to develop a broad differential diagnosis including conditions outside of the GI system. In this case report, we demonstrate how endometriosis was inadvertently discovered as the culprit in a patient with abdominal pain and hematochezia. A 30-year-old female with a history of endometriosis, total laparoscopic hysterectomy with left salpingo-oophorectomy, and right salpingectomy presented to the clinic with abdominal pain. It was gradual in onset, occurred 3 to 4 days monthly, and was associated with diarrhea, tenesmus, and mild hematochezia with clots. Alleviating factors included defecation and warmth. No weight loss was noted. Physical exam was significant for right lower quardrant and subprapubic tenderness. A colonoscopy was performed which demonstrated an infiltrative, submucosal, non-bleeding 3 cm mass in the proximal rectum. The terminal ileum and colon were unremarkable. An endoscopic ultrasound with biopsy via fine need aspiration of the mass was then performed. The biopsy demonstrated glands within smooth muscle bundles positive for cytokeratin 7, Ber-EP4, weak to moderate staining of the estrogen receptor, and very weak focal positivity for PAX-8, all of which was most consistent with endometriosis. The patient was subsequently referred to a surgeon for removal of the affected rectum, but she ultimately declined surgery. Her symptoms were mildly controlled with oral contraceptives, but the hematochezia persisted during her menstrual cycles. Patients often present with vague GI symptoms that are manifestations of non-GI processes. This case report demonstrates how an extra-intestinal condition was able to infiltrate through the intestinal wall to cause abdominal pain and hematochezia. We believe the patient’s symptoms stemmed from her endometriosis as she has an intact right ovary and the hematochezia was cyclical in nature. Other investigations have reported multiple segments of the bowel being affected by endometriosis, but the literature is scarce in the standardization of treatment for these cases. This report highlights the importance of potentially resecting bowel segments that are affected by endometriosis as these lesions may cause significant morbidity if the underlying condition is not treated accordingly.Item Extensive Intestinal Lymphangiectasia Results in Hemorrhagic Duodeno-Jejunitis(2021-06-20) Lugo, Adrian; Alomari, Mohammad; Tandon, Kanwarpreet; Ruiz, Claudia; Schneider, Alison; Asad Ur Rahman, FnuIntestinal lymphangiectasia is a rare disorder in which the lymph vessels that supply the lining of the small intestine are occluded. When this occurs, malabsorption ensues from a protein-losing enteropathy. To date, only a few cases of small bowel bleeding have been linked to intestinal lymphangiectasia. We highlight a case of intestinal lymphangiectasia causing both hemorrhagic duodeno-jejunitis and refractory blood loss anemia. A 68-year-old male with a history of hypothyroidism and dyslipidemia was referred to our institution for melena. Previous upper endoscopy (EGD) revealed hemorrhagic duodenitis, and a colonoscopy was unremarkable. Patient was requiring blood transfusions every 3 days for a total of 36 units of blood. His serum albumin was 1.5 g/dL. On computed tomography angiography of the abdomen/pelvis, the celiac trunk was severely stenosed with a hook-like appearance, suggestive of median arcuate ligament syndrome (MALS). Exploratory laparotomy was done to evaluate for MALS, but there were findings of extensive lymphatic vessels. An abdominal angiogram showed good perfusion to the stomach, celiac trunk, and duodenum, and a lymphangiogram of the abdomen/pelvis ruled out lymphatic blockage. A follow-up EGD with push enteroscopy revealed congestive duodenojejunopathy with numerous lymphangiectasia which appeared to be the source of bleeding. As the patient remained transfusion-dependent, he was scheduled for small bowel resection of the involved segment assisted by intraoperative enteroscopy. Intestinal lymphangiectasia is a rare disease characterized by focal or diffuse dilated enteric lymphatics. This case portrays a potential pathologic link between protein-losing enteropathy and refractory gastrointestinal bleeding. Although there is paucity in literature discussing this entity, it is hypothesized that increased pressure within the lymphatic system can cause venous congestion, and therefore gastrointestinal bleeding. In our case, we attempted to hold enteral nutrition and added octreotide to decrease lymphatic pressure and subsequently control his bleeding. Unfortunately, although his bleeding frequency decreased, it did not stop completely. Our case is unique as it highlights a rare entity that can result in a disabling, life-incompatible outcome. It also emphasized the need to better understand the underlying pathophysiology to effectively treat this condition. Regardless, a multidisciplinary approach proved to be beneficial in management.Item Histoplasmosis: Fever of Unknown Origin Disseminated to Bone Marrow(2021-06-09) Lugo, Adrian; Adjapong, Andrews; Ahmad, WaseemHistoplasmosis capsulatum is a dimorphic fungus highly endemic to the Mississippi and Ohio River valleys of North America. Infection develops when Histoplasma microconidia are inhaled and transform into their yeast form inside the lungs. In this report, we highlight the importance of including histoplasmosis as a differential diagnosis for a fever of unknown origin. A 42-year-old female with a PMH of HIV presented to the ED in Southwest Indiana for a fever. Her last known CD4 count was 4 and viral load was 601,000. She was found to have pancytopenia. Her platelets were refractory to platelet transfusion and she had several episodes of epistaxis requiring packing. She failed IV antibiotics as her fever persisted. Blood cultures were initially negative, chest x-ray was insignificant, urinalysis was unremarkable, and a respiratory panel was negative, but a urine blastomyces antigen test came back positive and a month later the blood culture subsequently grew presumptive histoplasma capsulatum. She subsequently underwent a bone marrow biopsy as part of her pancytopenia workup which demonstrated histiocytes containing fungal organisms. Her pancytopenia was therefore declared to be secondary to disseminated mycosis. She was treated with IV amphotericin B per infectious disease with improvement. Extrapulmonary disease has been well reported in patients with blastomycosis and histoplasmosis, but bone marrow infiltration is rare. In fact, according to one epidemiological study, only 4% of cases have bone involvement. Our case report is unique as the patient had evidence of fungus in the bone, and it was only through inadvertently obtaining a bone marrow sample for hematologic testing that we were able to find the source for her fever. Although CT of the chest would later demonstrate lung involvement, the case of disseminated mycosis was made by both blood cultures and bone marrow aspirate, indicating osteomyelitis and, hence, disseminated disease that would have otherwise gone unnoticed. This case report highlights the importance of keeping histoplasmosis and other fungal infections on the list of differential diagnoses given the demographic and geographical region as it can potentially be the source for acute illness.Item Hunter Accidentally Stumbles Upon Leprosy in West Florida(American College of Physicians: 2021 National Conference, 2021-05-14) Lugo, Adrian; Studsrud, Taylor; Lugo, Yulie; Beliveau-Ficalora, Margaret; DeMaio, JamesLeprosy is caused by acid-fast bacilli of the M. leprae complex, which includes M. leprae and M. lepromatosis. Transmission in the U.S. is rare, but has been documented in hunters who handle wild nine-banded armadillo. The origins of M. leprae infection among armadillos, the geographic range of the infected animals, and the potential risks infected armadillos present to people have been topics of concern. The infection originated amongst armadillos decades before they were ever used in leprosy research, and numerous surveys have confirmed that armadillos in the southern United States are a large natural reservoir for M. leprae; its prevalence exceeds 20% in some locales. In this case report, we highlight a rare case of leprosy and the importance of keeping leprosy in the differential diagnosis of a pruritic, urticarial rash. A 54-year-old male with no significant past medical history or foreign travel history presented to the clinic with a diffuse, pruritic rash. Patient is a wild boar hunter who handled fresh armadillo carcasses without the use of gloves. Patient was born in Pennsylvania and moved to Florida at 6 months of age, no history of overseas travel or recent travel outside of Florida. PCR was positive for M. leprae and negative for M. lepromatosis. A skin biopsy was positive for borderline lepromatous leprosy with an early type 2 erythema nodosum leprosum reaction. This case report demonstrates how a rare zoonotic infection was inadvertently acquired by a human host in West Florida by handling nine-banded armadillos without proper equipment. Most of the leprosy cases reported in the U.S. came primarily from Southern states, but 93% of the cases reported in the Americas came from Brazil. In the U.S., approximately 200 cases of leprosy are reported each year, and about 175 of those cases are diagnosed for the first time. Florida contributes a small number of these, but recent data is showing an increasing incidence. Studies from other southern U.S. states demonstrate infection with the same strain of Mycobacterium leprae, thus confirming the nine-banded armadillo as the main risk factor. Because of this bacteria’s rarity in the region and the nonspecific symptoms that manifest in a new host, this case report highlights the importance of including leprosy in the differential diagnosis in patients with a high exposure to wildlife in Florida.Item A Near-Fatal Case of Ruptured Pulmonary Artery After an Elective Diagnostic Right and Left Heart Catheterization(CHEST Journal, 2020-10) Alzaiem, Firas; Al-Obaydi, Sarah; Lugo, Adrian; DiGregorio, Joshua; Asi, Zyad; Dabage-Forzoli, Nemer; Restrepo, RicardoItem The Repercussions of Hereditary Pancreatitis in a 29-Year-Old Male and His Family(2020-10-01) Lugo, Adrian; Martyn, Colin; Fraser, Scott; Ahmed, KhanThe etiology of chronic pancreatitis is multifactorial, but it can frequently be attributed to an inciting factor such as alcohol use, biliary cholelithiasis, or hypertriglyceridemia. In rare cases, inherited mutations in cationic trypsinogen (PRSS1) can lead to hereditary pancreatitis (HP) and increase the risk of pancreatic cancer. In this report, we demonstrate the case of a 29-year-old male with hereditary pancreatitis who inherited a PRSS1 mutation from his mother. A 29-year-old male with a past medical history of hypertriglyceridemia, tobacco use, hypothyroidism, and hereditary pancreatitis presented with epigastric pain and nausea. Liver function tests were unremarkable. Lipase was 760 U/L (range 8-78 U/L). Triglyceride level was 163 (15-150 mg/dL). Computerized tomography imaging of the patient’s abdomen and pelvis from a year prior demonstrated parenchymal calcifications within the pancreas. The patient's symptoms abated within 4 days of aggressive IV fluid resuscitation and supportive care. Regarding his history, at the age of 8, the patient was found to possess a mutated R117H allele in the PRSS1 gene upon PCR analysis of exon 3 from chromosome 7. His mother carried this gene and underwent pancreatectomy for recurrent pancreatitis and numerous pancreatic parenchymal calcifications. In adulthood, the patient has averaged 4 to 5 episodes of pancreatitis annually and has used pancrelipase, indomethacin suppositories and injectable octreotide for symptom control. Of note, the patient’s son did not possess the PRSS1 gene mutation. Mutations in the PRSS1 gene are associated with hereditary pancreatitis due to unrestricted action of trypsin which leads to pancreatic autodigestion. Our patient inherited a mutated PRSS1 allele from his symptomatic mother, but his male offspring did not manifest such symptoms. The literature shows that penetrance of the PRSS1 gene ranges between 40-90%, which implies a high probability of passing these alleles to offspring. More importantly, patients with HP tend to also be carriers of the SPINK1 and CFTR mutations, which are linked to pancreatic cancer and cystic fibrosis, respectively. This case report highlights the importance of genetic testing as mutations can lead to both a perpetual cycle of pancreatitis and increase the risk of developing pancreatic cancer. Proper anticipation can prompt the use of pancreatic enzyme supplementation, octreotide, and indomethacin to help control symptoms and reduce chronicity.Item Systemic Sclerosis Sine Scleroderma(American College of Physicians: Florida Chapter, 2020-03) Lugo, Adrian; Cappiello, Andrew; Ramamurthy, GuruswamyScleroderma and systemic sclerosis are autoimmune phenomena that can cause progressive and permanent damage to the organs of the human body. Rarely, the only manifestation of systemic sclerosis is severe hypertension with renal failure, a subset known as systemic sclerosis sine scleroderma. In this case report, a 39-year-old Hispanic female with a past medical history of GERD and gestational hypertension had presented for nausea and vomiting. She was a Jehovah's witness. Upon review of admission labs and studies from years prior, her chemistries had shown signs of progressive renal failure and proteinuria, but the cause of such abnormalities was never pursued. On admission, she was immediately transferred to the intensive care unit for severe metabolic acidosis requiring emergent hemodialysis, treatment for hypertensive emergency, severe anemia, and electrolyte derangements. Moreover, due to her religion, she declined blood products, so she required erythropoietin and iron products instead. She remained in the intensive care unit for three days for severe metabolic acidosis with a chronic, non-oliguric nephrotic syndrome pattern. An extensive immune panel was positive for the antinuclear antibody, the Scl-70 antibody, and low C3. A renal biopsy was not attempted because the patient's hemoglobin was too unstable at the time. She was briefly placed on captopril, but due to an ongoing dry cough the patient declined to remain on it. The patient has since been receiving tri-weekly hemodialysis treatments, but her progressive renal failure over the years sequentially led to irreversible, chronic kidney disease. This case report demonstrates a rare incidence of systemic sclerosis sine scleroderma in a patient who was positive for the Scl-70 antibody and had multiple contraindications to appropriate treatments. It also highlights the importance of pursuing abnormalities on routine blood studies because it can ultimately prevent irreversible kidney damage and can aid in anticipating further internal organ involvement.Item A Truth Unraveled: Unpredictable Collagenous Gastritis Explains Vague Upper Abdominal Symptoms(2021-06-11) Lugo, Adrian; Cho, Isaac S.; Martyn, Colin; Fraser, Scott; Lynch, Lori; Gislason, GardarCollagenous gastritis (CG) is a rare disease characterized by subepithelial deposition of collagen bands and inflammatory cell infiltrates in the lamina propria. Owing to the rare occurrence, little is known about its clinical manifestations which are both diverse and nonspecific. Furthermore, the pathogenesis of CG remains unclear although there are reported associations with autoimmune conditions including celiac disease and type I diabetes. Currently, there is no effective treatment for this disease. A 64-year-old female with a history of gastroesophageal reflux disease and hypothyroidism presented to the clinic for evaluation of nausea, bilious emesis, early satiety, and an unintentional weight loss of 10 pounds within the past few months. There were no alleviating or aggravating factors and she denied any changes in her bowel function or a familial history of colon cancer. Physical exam demonstrated left lower quadrant fullness. A stool-DNA screening test was negative. Esophagogastroduodenoscopy (EGD) demonstrated a diffusely nodular and congested appearance mainly in the antrum without bleeding, consistent with gastritis. Biopsies were obtained which revealed collagenous gastritis but negative immunoperoxidase staining for lymphoma, Congo red stain for amyloid, and immunohistochemical staining for Helicobacter pylori. A repeat EGD with biopsy demonstrated patchy, mild villous blunting with very few intraepithelial lymphocytes. Antibodies could not be obtained as the patient was lost to follow-up. Patients often present to the clinic with vague gastrointestinal symptoms that warrant endoscopic evaluation. In this case report, we were able to demonstrate the findings of collagenous gastritis, a rare condition that has been reported less than 300 times at the time of this report. This particular case highlights the importance of obtaining the histopathology as it may allow clinicians to rule out reversible causes that may be amenable to treatment prior to making a diagnosis of an untreatable condition such as CG. Furthermore, the second biopsy of our patient suggests that this disease may be linked to celiac disease which is consistent with other reports that suggest CG being related to other autoimmune conditions. Thus, it is of vital importance to create a wider recognition of this condition’s histopathologic features and to examine its clinical associations in order to standardize a more effective therapy for this untreatable disease.