The rollout of the SARS-CoV-2 vaccine is underway, and millions have already been vaccinated. At least 25 reports of “immune thrombocytopenia” (ITP) or “thrombocytopenia” following the Moderna or Pfizer vaccine have been added to the Vaccine Adverse Event Reporting System (VAERS) in the US. ITP is a rare but known complication of several vaccinations. SARS-CoV-2 vaccine is new, with a novel mechanism of action, and understanding the epidemiology, clinical manifestations, treatment success and natural history of post-vaccination thrombocytopenia is evolving. We report a 74-year-old man who developed refractory thrombocytopenia within one day of receiving the Moderna SARS-CoV-2 vaccine. Several hours after vaccination, he developed significant epistaxis and cutaneous purpura. Severe thrombocytopenia was documented the following day, and he developed extremity weakness and encephalopathy with facial muscle weakness. Over a 14-day period, thrombocytopenia was treated first with high dose dexamethasone, intravenous immunoglobulin, platelet transfusions, rituximab, plasma exchange (for presumed acute inflammatory demyelinating polyneuropathy (AIDP)), and four daily doses of the thrombopoietin receptor agonist (TPO-RA) eltrombopag (Promacta™), without a platelet response. Three days later, he received the TPO-RA romiplostim (Nplate™). Five days later, his platelet count began to rise and by post-vaccination day 25, his platelet count was in the normal range. Thrombocytopenia was refractory to frontline and second-line treatment. The eventual rise in his platelet count suggests that one or both TPO-RAs may have impacted platelet recovery. Possibly, but less likely given the temporality, the drug-induced thrombocytopenia was subsiding. The aggressive use of immunosuppressive treatment may jeopardize the intended purpose of the SARS-CoV-2 vaccine, and earlier use of non-immunosuppressive second-line treatment for vaccine-related severe thrombocytopenia, such as with TPO-RAs, should be considered. While it is imperative to continue the global vaccination program, vigilance to the occurrence of post-vaccination severe thrombocytopenia is warranted.
Biliary angiodysplasia is extremely rare. Our background search revealed only a few case reports in the English literature. We present a case of angiodysplasia of the proximal common bile duct in a patient with subacute upper gastrointestinal bleeding and symptomatic anemia. A standard esophagogastroduodenoscopy with subsequent dedicated duodenoscopy revealed blood-stained bile draining from the major ampulla orifice. A contrast-enhanced magnetic resonance cholangiopancreatography was unrevealing for any pancreaticobiliary pathology. The patient subsequently underwent an endoscopic retrograde cholangiopancreatography and SpyGlass® cholangioscopy, which demonstrated intermittent bleeding from angiodysplasia in the proximal common bile duct.
A cluster of cefepime-induced neutropenia (CIN) was identified from June 2017 to May 2018 in a regional outpatient parenteral antimicrobial therapy population. Our data suggest prolonged courses of cefepime (≥2 weeks), administered by rapid intravenous push, were associated with a higher risk of CIN.
Patient: Male, 52Final Diagnosis: Cryptococcal ventriculoperitoneal shunt infectionSymptoms: Confusion • fever • LethargyMedication: Amphotericin B • FlucytosineClinical Procedure: Ventriculoperitoneal shunt removalSpecialty: Infectious diseaseObjective:Rare diseaseBackground:Ventriculoperitoneal shunting is an effective treatment for hydrocephalus. Ventriculoperitoneal shunt (VPS) infection is a common complication. Cryptococcus neoformans as an implicated organism is rare. In this report, we describe a patient with cryptococcal VPS infection.Case Report:A 52-year-old male with normal pressure hydrocephalus, status post implantation of VPS one year prior to the presentation; who was admitted with a fever, lethargy and confusion for three days. He was treated empirically with intravenous cefepime and vancomycin for VPS infection. The CSF analysis from both the lumbar puncture and the VPS was significant for a low white blood count, low glucose and high protein. Other work-up including India ink and cryptococcal antigen was unrevealing. He remained febrile despite antibiotic treatment for 5 days. The CSF from the shunt was sent for analysis again and it demonstrated similar results from the prior study, but the culture was now positive for Cryptococcus neoformans. The patient was started on oral flucytosine and intravenous liposomal amphotericin B. The VPS was removed and an externalized ventricular catheter was placed. The patient showed rapid resolution of the symptoms.Conclusions:To date, there was a total of nine reported cases of cryptococcal VPS infection upon review of the literature. Our presenting case and the literature review highlight the difficulties in making an accurate diagnosis of cryptococcal shunt infection. There were case reports of false negative cryptococcal antigen tests with culture proven cryptococcal meningitis. The CSF culture from the shunt remains a mainstay for identifying cryptococcal shunt infection. Cryptococcal shunt infections are rare and early diagnosis and treatment is essential for patient management which involves shunt replacement with concomitant administration of intravenous antifungal medication. High clinical suspicion is crucial and shunt culture preferably from the valve is recommended.
Drugs, toxins, and infections are known to cause acute eosinophilic pneumonia. Daptomycin and minocycline are the commonly reported antibiotics associated with acute eosinophilic pneumonia. In this study, we present a case of imipenem/cilastatin-induced acute eosinophilic pneumonia. The patient presented with fever, acute hypoxic respiratory distress, and diffuse ground-glass opacities on the chest CT a day after the initiation of imipenem/cilastatin. Patient also developed peripheral eosinophilia. A reinstitution of imipenem/cilastatin resulted in recurrence of the signs and symptoms. A bronchoscopy with bronchoalveolar lavage showed 780 nucleated cells/mm(3) with 15% eosinophil. The patient's clinical condition improved significantly after the discontinuation of imipenem/cilastatin therapy and the treatment with corticosteroid.
We present 23 cases of Pneumocystis jirovecii pneumonia (PCP) diagnosed with commercially available non-invasive plasma microbial cell-free deoxyribonucleic acid (mcfDNA) assay. Our findings suggest plasma mcfDNA testing resulted in positive clinical impact for the diagnosis and treatment for PCP and coinfections in 82.6% of the cases.
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