The objective of this report is to discuss a case of drug-induced acute pancreatitis in a patient on a combination of dulaglutide and glipizide. The patient was a 61-year-old African American male with a past medical history of diabetes mellitus type 2 and essential hypertension, who was admitted for acute pancreatitis after presenting with upper abdominal pain. He was initially on glipizide but dulaglutide was added to improve control. The patient was a social drinker and an ex-cigarette smoker. He had serum lipase greater than 900 U/L, serum alcohol was negative, and abdominal computed tomography reported significant pancreatic edema consistent with acute pancreatitis but without features of necrotizing pancreatitis and no evidence of cholelithiasis or choledocholithiasis. His clinical state deteriorated after being complicated by paralytic ileus. He was managed conservatively, improved clinically, and was discharged home.Seeing that the incidence of pancreatitis is higher in patients with diabetes when compared to non-diabetics, it is important to counsel and monitor patients for risk factors of pancreatitis including medications. In the absence of other common causes in this case and considering the temporal relationship between presentation and the addition of dulaglutide to ongoing glipizide regimen, the combination of both drugs may have induced acute pancreatitis.
The ubiquitously present gram-negative bacteria Pantoea agglomerans is not a commonly known human pathogen. Recently, increasing recognition of the species as a human pathogen has led to controversy as limited documented cases of P. agglomerans bacteremia and infections have been reported in the literature, with most cases reported among immunocompromised patients or the pediatric population. Here, we present the case of a 54-year-old female with P. agglomerans and Enterococcus faecium bacteremia along with chronic obstructive pulmonary disease.
Septic arthritis leads to significant hospital burden in the United States adult patient population. Bacteria are the leading cause of septic arthritis with Staphylococcus aureus being the most common. Of the staphylococcal species, Staphylococcus schleiferi, primarily found in carnivores, rarely causes septic arthritis. We here report the presentation, diagnosis, treatment, and discharge of a 39-year-old male with S. schleiferi septic arthritis. Due to biochemical similarities, S. schleiferi are commonly misidentified as S. aureus, and correct identification is increasingly relevant for the selection of appropriate therapy due to the rise in cases of multidrug-resistant microorganisms.
Hyperammonemic encephalopathy (HE) can be broadly defined as an alteration in the level of consciousness due to elevated blood ammonia level. While hepatic cirrhosis is the most common cause of HE, non-hepatic causes like drugs, infections, and porto-systemic shunts can also lead to the presentation. In this case, we highlight an unusual occurrence of recurrent non-cirrhotic HE from obstructive urinary tract infection (UTI) with urea-splitting micro-organisms in an elderly male patient. The patient exhibited altered mentation, and elevated ammonia levels with normal hepatic function at presentation. Urine culture revealed Proteus mirabilis resistant to extended spectrum beta-lactamases (ESBL). Successful management of obstructive UTI was achieved through Foley’s catheterization and intravenous (IV) antibiotics, resulting in the resolution of HE. This outcome further supports the significance of UTI as a potential cause of hyperammonemia. Thus, UTI as one of the non-hepatic causes of hyperammonemia should always be explored among elderly patients presenting with altered mentation.
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