Patient: Male, 68-year-old Final Diagnosis: 5-oxoproline toxicity • anion gap metabolic acidosis • starvation ketoacidosis Symptoms: Confusion • weakness Medication: — Clinical Procedure: — Specialty: General and Internal Medicine • Nephrology Objective: Rare coexistence of disease or pathology Background: Chronic acetaminophen toxicity has been known to cause anion gap metabolic acidosis (AGMA) due to accumulation of 5-oxoproline metabolites. This diagnosis requires a high index of suspicion because acetaminophen use is very common among patients, it is often difficult to gauge the extent of use, and patients often have multiple comorbid conditions complicating diagnoses. Case Report: A 68-year-old man with multiple medical comorbidities presented to the Emergency Department with recurrent generalized weakness. On all occasions, the patient denied focal weakness or infectious symptoms. He also denied ingestions other than prescribed medications, including acetaminophen 325 mg as needed, which he described taking “a couple times” a day. His vital signs were normal other than tachypnea to 28 breaths/min. The physical examination was notable for Kussmaul breathing pattern and slight confusion. The patient’s prior 3 presentations were notable for profound AGMA, hypernatremia, acute kidney injury, and ketosis. As the patient’s blood urea nitrogen, blood sugar, liver tests, lactic acid, and serum osmolality were normal, the patient was diagnosed with “starvation ketosis” and received supportive care each time with fluids and sodium bicarbonate. Further investigation at his final admission revealed an elevated 5-oxoproline level and a delayed diagnosis of chronic acetaminophen toxicity. Conclusions: This report emphasizes the need for a high index of suspicion related to chronic acetaminophen toxicity and other ingestions contributing to a metabolic acidosis in at-risk populations, even when routine history is unrevealing. Furthermore, severe acidosis should prompt more extensive investigation when out of proportion to obvious routine etiologies.
Clinical worsening or new manifestation of cryptococcal disease following initiation of anti-retroviral therapy (ART) in an HIV patient is a hallmark of cryptococcal immune reconstitution inflammatory syndrome (C-IRIS). However, it can be difficult to distinguish IRIS from worsening or new infection. Here, we present a case of severe C-IRIS involving multiple cerebellar, spinal, and intradural abscesses and spinal arachnoiditis 7 months after ART initiation in an AIDS patient with uncertain prior ART compliance. He had multiple prior episodes of cryptococcal meningitis with complications necessitating ventriculoperitoneal shunt placement and was on suppressive fluconazole when he developed worsening brain manifestations. He received empiric anti-cryptococcal re-induction without improvement. All cerebrospinal fluid cultures remained sterile, with negative Cryptococcus PCR testing, and his condition continued to worsen prior to corticosteroid initiation. Ultimately, C-IRIS was diagnosed by brain biopsy. This case demonstrates an extreme in severity of C-IRIS and in the timeline of presentation after ART initiation.
INTRODUCTION: Anal squamous cell carcinoma (SCC)typically presents as an anal mass. It rarely presentsin the rectumalone. Limited literature exists to discuss regarding optimal management for this unique presentation. We present a patient withanal SCC manifesting as a rectal mass and reviewher management. CASE DESCRIPTION/METHODS: A 73 year-old woman with esophageal reflux presented to our office with chronicrectal bleedingand constipation.She denied anal pain. Colonoscopy revealed a 1.2 cm massin the anterior rectum, 2 cm from the anal verge (Figure 1). Biopsies revealed focally invasive nonkeratinizing SCC (Figure 2). On rectal endoscopic ultrasound (EUS), the mass was confined to the anus andextended from the anorectal canal into the rectum (Figure 3). Submucosal invasion was noted, but not through the rectal muscularis propria. PET CT showed no perirectal invasion, lymphadenopathy, metastatic disease orother sources of primary SCC. Final staging was T2N0. She underwentchemoradiationwith5-fluorouricil and mitomycin. Surgery was deferred to preserve anal function.Her tumor showed a complete response after 6 weeks and she is currently being followed with routine surveillance. DISCUSSION: Anal SCC makes up2.6% of digestive system cancers in the United States, but its incidence is rising in men and women, possibly due to changes in sexual behavior and increasing rates of HPV exposure. Gastroenterologists should recognizeatypical presentations ofanal SCC, especially in high-risk populations: men who have sex with men, HIV positive patients, and women with high risk HPV. Rectal bleeding and altered bowel habits arethe most commonlyreported symptoms. Other symptoms include anal mass, pain, itching, and mucous discharge, but up to 20% of patients with anal cancer are asymptomatic. The absence of anal pain and external lesions as well as the rectal mass on in our patient suggested an alternative diagnosis. Given that management of rectal cancer has traditionally centered around resection, this emphasizes the utility of EUS to make the correct diagnosis and direct management. The management of this unique presentation of anal SCC has not been fully established, but our patient received standard chemoradiation with good results. Anal SCC has a range of presentations and can present as a rectal mass. Given that anal SCC rates are increasing, our case highlights the importance of disease screening, recognition, and prevention.
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