Anomalies of the inferior vena cava (IVC) are an uncommon finding in the general population. A wide range of IVC anomalies has been described in the literature, the majority of which lack clinical significance.Agenesis of the IVC (AIVC) is a rare anomaly of the IVC in the general population. This anomaly may involve either complete agenesis of the IVC or agenesis of a segment of the IVC. Agenesis of the suprarenal segment is the most commonly occurring variant, while agenesis of the infrarenal and hepatic segments is less common. Here we report a case of agenesis of the intrahepatic segment of the IVC.

Gastrointestinal (GI) sarcoidosis is a rare manifestation of this multi-systemic granulomatous disorder. Esophageal involvement is extremely rare and there have been few case reports about this. Our article reports a case of esophageal sarcoidosis in which dysphagia was the main presenting symptom. The main initial treatment of symptomatic sarcoidosis in general and pulmonary sarcoidosis in specific usually involves corticosteroids, however, there are no specific guidelines for the management of GI sarcoidosis. Surprisingly, or maybe not, in our case, the dysphagia did not improve with steroid therapy which prompted further investigations as well as endoscopic intervention.

neurological deficits were noted. Liver enzymes were AST 9 U/L, ALT 3 U/L, total bilirubin 0.4 mg/ dL (direct 0.1), INR 1.2. Serum AFP one month prior to presentation was 24.5 ng/mL. CBC showed WBC of 3.7 K/UL, hemoglobin 8.2 g/dL and PLT 186 K/UL. Computed tomography showed a large expansile infiltration centered at the right ethmoid and upper nasal cavity extending to the superior medial aspect of the orbit, with associated mass effect upon the frontal lobes. Nasopharyngeal biopsies revealed poorly differentiated adenocarcinoma with immunostaining positive for heppar-1 compatible with metastatic HCC. The patient underwent bifrontal craniotomy for resection of the anterior skull base lesion, with a hospital course complicated by encephalopathy and sepsis necessitating ICU. The patient was discharged on comfort measures and hospice (Figure 1). Discussion: HCC metastasizing to the nasopharynx is exceedingly rare. The first case report documenting an isolated nasopharyngeal metastasis from a liver primary was described by Kattepur et al in 2014. In our case, the patient reported swelling behind the right eye as the initial presentation of a metastatic HCC after liver transplant. In patients with history of HCC, clinicians should maintain a broad differential with clinical suspicion for uncommon presentations of extra hepatic metastases, even after liver transplant.[3088] Figure 1. T1 weighted MRI orbit without contrast showing space occupying lesion extending through the right ethmoid sinuses with intracranial extension.

Boerhaave’s syndrome is a rare yet serious condition associated with high mortality and morbidity. Diagnosis of this syndrome is usually done with the aid of imaging and prompt management should be initiated to improve the outcomes. Treatment for this syndrome has been mainly surgical since its discovery by Herman Boerhaave; however, multiple endoscopic approaches have been successfully used recently with the advancement of this field. Here, we describe two cases of Boerhaave’s syndrome that were endoscopically managed along with a brief literature review of the different endoscopic methods used to manage this syndrome.

Metformin is considered an initial oral pharmacotherapy of choice for treating hyperglycemia in type 2 diabetes mellitus (T2DM). Although safe in the vast majority of the population, rare side effects will come to light as the prevalence of T2DM continues to rise. We present a rare case of metformin-induced hepatotoxicity and possibly the first reported case of dose-dependent metformin-induced hepatotoxicity. This case report aims to make clinicians aware of this infrequent yet significant adverse reaction that can arise with metformin therapy.

No abstract

Sweet syndrome (SS) is also known as acute febrile neutrophilic dermatoses. Clinically, SS features fever, arthralgias, and the sudden onset of an erythematous rash. The morphologies of skin lesions in SS are heterogenous, varying from papules, plaques, and nodules to hemorrhagic bullae, which sometimes makes the diagnosis of SS more challenging. We report a 62-year-old obese male with a history of chronic myeloid leukemia in remission for 10 years who presented with a rash for five days. The patient reported prodromal flu-like symptoms with subjective fever, malaise, cough, and nasal congestion followed by a sudden onset, painful, non-pruritic rash. The rash was associated with bilateral hip arthralgias and abdominal pain. The patient denied any recent travel, exposure to sick contacts, or the use of any new medications. Physical examination showed a well-demarcated, non-blanching, confluent, erythematous plaque involving the bilateral buttocks and extending to the lower back and flanks with coalescent "juicy"-appearing plaques and flaccid bullae. No oral or mucosal involvement was noted. Laboratory investigations revealed mild leukocytosis, elevated inflammatory markers, and acute kidney injury. The patient was started on antibiotics given the cellulitis-like skin lesions, leukocytosis with neutrophilia, and elevated inflammatory markers. Dermatology was consulted, who attributed the patient's rash to shingles and recommended initiating acyclovir and obtaining a skin biopsy. However, the patient's rash and arthralgias worsened with anti-viral treatment while awaiting pathology results. Antinuclear antibodies, complement, human immunodeficiency virus, hepatitis panel, blood cultures, and tumor markers were all negative. Flow cytometry showed no evidence of hematopoietic neoplasms. The skin punch biopsy revealed dense neutrophilic infiltration in the dermis with no evidence of leukocytoclastic vasculitis, consistent with acute neutrophilic dermatoses.The diagnosis of giant cellulitis-like Sweet syndrome was established, and the patient was started on prednisone 60 milligrams daily. His symptoms improved promptly with steroid treatment. Our case suggests that SS can camouflage a wide spectrum of diseases, including cellulitis, shingles, vasculitis, drug eruptions, leukemia cutis, and sarcoidosis, which emphasizes the importance of keeping a high index of suspicion for SS when assessing the clinical constellations of fever, neutrophilia, and erythematous plaques suggesting atypical cellulitis. Approximately 21% of Sweet syndrome is associated with malignancy. Sweet syndrome can precede, concur with, or follow the onset of malignancy. Due to the lack of a systematic approach to patients with SS, under-investigation and diagnostic delays are common. Therefore, further screening and continuous monitoring in patients with SS becomes especially important in facilitating the early detection of a potential underlying malignancy and assists in initiating adequate therapy.

Introduction: Colorectal cancer (CRC) ranks second as a cause of cancer mortality and is the third most prevalent cancer in both men and women in the US. CRC screening efforts are directed towards the detection and removal of adenomas and sessile serrated lesions (SSLs), which reduces CRC incidence and CRC mortality significantly. In our Internal Medicine clinic at a tertiary care hospital, a deficient colorectal cancer screening compliance rate was identified in 2019. We performed individual patient calls to increase the screening rates and evaluated the efficacy of these interventions. Methods: We screened patients aged 50-75 in our clinic. Patient due for CRC screening was defined as having had their screening colonoscopy more than 10 years ago or stool-DNA test more than 3 years ago with normal results. Patients with a history of colon cancer or familial cancer syndromes were excluded. For the next year, patients due for screening were called by resident physicians to provide counseling regarding different screening options and the risks and benefits of each test. If the patient agreed, a stool test or a referral to a gastroenterologist was ordered. We hypothesized that if patients underwent a screening test within 1 year after the phone calls, it was because of the interventions. Results: A total of 572 patients were eligible for the study. 418 patients were satisfied with screening at the start. 154 patients due for CRC screening were called, 18 patients responded to have received screening on time from other facilities; hence satisfied and 2 patients were deceased at the time of intervention. Out of 134 patients eligible for screening, 96 agreed to undergo a screening colonoscopy after the discussion, 22 patients refused screening and 16 patients were unable to be contacted via phone. Among 96 patients who agreed to screen, 54 received screening for CRC within a year of the intervention. Phone call intervention revealed a 45.7% (54/134-16) response rate. The baseline CRC screening compliance before interventions was 76.2% (418118/572), and post-intervention compliance rate was 85.6% (418118154/ 572). (Figure ) Conclusion: A phone call intervention increased colorectal cancer screening compliance by 9.4% in our cohort. We concluded that internal medicine clinics can play an active part in CRC prevention by counseling patients during regular wellness visits, sending reminder letters and/or phone calls to eligible patients.