Contrast-induced encephalopathy (CIE) is a rare but well-known complication of mostly intra-arterial contrast administration and presents with a variety of neurological deficits due to disruption of the bloodbrain barrier. We present a case of CIE after administration of intravenous contrast for computed tomography pulmonary angiogram (CTPE).A woman in her mid-70s with history of chronic obstructive pulmonary disease (COPD) presented with progressively worsening shortness of breath. She was diagnosed with multifocal pneumonia and started on IV antibiotics, IV steroids, and bilevel positive airway pressure (BiPAP) ventilation. A CTPE was done to rule out a pulmonary embolism during which she received 100 cc of Isovue 370 (iopamidol 76%), a low-osmolar, non-ionic, monomeric, iodine-based contrast agent. Within minutes of the contrast administration, the patient developed confusion and agitation with elevated blood pressure. Neurological evaluation revealed no gross focal motor or cranial nerve deficits and bilateral 2+ reflexes with mute plantar reflexes. Laboratory investigations were unchanged. She was shifted to the ICU but continued to remain drowsy and disoriented. CT brain done within two hours of onset revealed no intracranial abnormality. She was managed conservatively with IV fluids, neuro-checks, and blood pressure control. Her sensorium improved within 48 hours with supportive treatment. Repeat neuroimaging was not performed. She was discharged after four days with the resolution of her respiratory symptoms.CIE is a known but uncommon complication associated with the use of intraarterial contrast media but has been found to occur even after intravenous administration, which has been reported only once in literature. The presentation is highly variable, ranging from headache to coma, with transient cortical blindness being the most commonly identified. The diagnosis requires a high index of suspicion, and brain imaging is usually pathognomonic; however, cases in the absence of radiological signs have also been diagnosed. Typically, symptoms resolve within 48-72 hours and the disease runs a benign course, but cases of persistent neurological deficit and even cases of fatal cerebral edema have been reported. Treatment is usually supportive with intravenous hydration and anticonvulsants and the occasional use of IV steroids and mannitol with favorable outcomes.

Anthracosis is an environmental lung disease caused by carbon deposition and pigmentation in the airways. However, in rare instances, it can also have systemic involvement. We present a patient with B-symptoms and diffuse lymphadenopathy who was diagnosed with the infrequently described nodal anthracosis. A 64year-old Vietnamese gentleman with a 50-pack-year smoking history who was recently diagnosed with prostate cancer post-radical prostatectomy and awaiting radiation therapy presented with generalized weakness, low-grade fever, night sweats, and unquantifiable weight loss for a month. He was hemodynamically stable, and examination revealed bilateral inguinal and axillary lymphadenopathy. Computed tomography (CT) showed diffuse lymphadenopathy involving the mediastinum, hilar, axillary, mesenteric, retroperitoneal, and bilateral iliac chains with multiple diffuse pulmonary nodules. Laboratories disclosed anemia, thrombocytopenia, elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), albumin-globulin (A-G) reversal, and sterile blood cultures. The disseminated intravascular coagulation panel was negative with normal fibrinogen and mildly elevated D-dimer. Autoimmune workup, including antinuclear antibody (ANA), was negative. Infectious workup included Babesia, Ehrlichia, Anaplasma, Lyme serology, QuantiFERON-TB Gold, HIV, and hepatitis panel, and all were negative. He was managed with broad-spectrum antibiotics, which were discontinued after a negative infectious workup. He also complained of a new-onset holocranial headache with no features of meningitis; an MRI with contrast revealed focal occipital leptomeningeal involvement and cerebral edema with occipital lymphadenopathy. A lumbar puncture was planned but deferred at the patient's request. An excisional lymph node biopsy of the left axillary lymph node revealed reactive follicular hyperplasia with no evidence of malignancy, with flow cytometry negative for any evidence of B-or T-cell malignancies. He continued to have persistent low-grade fevers. A bone marrow biopsy showed 70% cellularity with paratrabecular interstitial lymphoid aggregates composed of both T and B cells, which was nonspecific, and flow cytometry could not be done due to dry tap. An F-18-fluorodeoxyglucose positron emission tomography (FDG PET) scan showed extensive hypermetabolic disease both above and below the diaphragm with bulky mediastinal adenopathy and splenomegaly. Subsequently, he underwent a mediastinoscopy and biopsy of the mediastinal lymph nodes, which demonstrated reactive hyperplasia and abundant anthracitic pigment on microscopic examination, consistent with the diagnosis of nodal anthracosis. He was managed conservatively, discharged, and found to have spontaneously resolved symptoms at a six-week follow-up. Nodal anthracosis with PET-positive mediastinal and hilar lymphadenopathy is a rare presentation of anthracosis that mimics infectious conditions, granulomatous diseases, and malignancies. The pigment deposition can cause persistent inflammatory...

INTRODUCTION Drug-induced immune thrombocytopenia (DITP) is a rare and often difficult-to-diagnose cause of thrombocytopenia, caused by drug-dependent platelet antibodies leading to increased platelet consumption and destruction. DITP evolves within 7 days of initiation of the offending drug and is characterized by thrombocytopenia, with or without bleeding manifestations. Immediate discontinuation of the inciting drug remains the cornerstone of management. Although the most commonly identified drugs are quinine, penicillamine, and valproic acid, isolated cases of ceftriaxone-induced immune thrombocytopenia have been reported. CASE REPORT A 60-year-old female presented with fever, dysuria, and fatigue for 3 days with associated proximal muscle weakness for a few weeks. She was diagnosed with right pyelonephritis with urine cultures growing non-ESBL (extended-spectrum beta-lactamase) Escherichia Coli for which she was started on Ceftriaxone 2g daily. She was also started on low-dose prednisone 20mg daily for fibromyalgia. Her platelet count continued to downtrend and on day 7 of treatment reached a nadir of 18K/μL. Heparin-induced thrombocytopenia (HIT) was excluded. She received one unit of platelets and ceftriaxone was switched to ceftazidime, with which her platelet counts improved. Owing to the temporal relationship between the development and resolution of thrombocytopenia with the commencement and withdrawal of ceftriaxone, drug-induced thrombocytopenia was diagnosed. Naranjo's algorithm revealed a probable adverse drug reaction but confirmatory tests for ceftriaxone-induced platelet antibodies could not be performed. DISCUSSION DITP remains a diagnosis of exclusion and poses a significant therapeutic challenge. Clinicians need to have a high index of suspicion to rule out common causes of unexplained thrombocytopenia before diagnosing DITP.

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Drug-induced pancreatitis is a rare and sometimes fatal cause of pancreatitis which is often difficult to diagnose. Acid suppressing medications include histamine-2 receptor antagonists and proton pump inhibitors have been linked to acute pancreatitis in several case-reports and recent systematic reviews. However, only one case of lansoprazole induced pancreatitis has been described in literature until date. A 67-year-old female presented with complaints of abdominal pain, nausea, vomiting and worsening generalized weakness for the past 1 week. She had recently been started on lansoprazole therapy for gastroesophageal reflux with no other change in medications. She denied any trauma, recent viral infection, alcohol intake, over-the-counter or herbal medication use. On presentation, she had abdominal distension with tenderness and epigastric guarding. Laboratory investigations were significant for leukocytosis and elevated amylase and lipase with normal triglyceride levels. Computed tomography of the abdomen and pelvis with contrast revealed features of acute interstitial pancreatitis with retroperitoneal lymphadenopathy and no other abnormality. She was diagnosed to have acute pancreatitis secondary to lansoprazole therapy and was managed conservatively. Her symptoms resolved after 3 days of discontinuation of the drug. There have been several cases reporting a potential link between acute pancreatitis and acid suppressing medications. However, drug-induced pancreatitis still remains a diagnosis of exclusion as it is difficult to establish causality. Almost all the acid suppressing medications have been linked to pancreatitis, but a case associated with lansoprazole has only been described once. Further studies are needed to establish causation.