Amantadine, which is known for its antiviral activity, is presently used as therapy for Parkinson's disease. Adverse effects, such as cardiac arrhythmias, have been described in patients after ingestion of amantadine. Here, we present a patient who suffered a cardiac arrest following ingestion of a low dose of amantadine. A 71-year-old man was admitted to the emergency department for a witnessed cardiac arrest. He had developed an upper respiratory tract infection the preceding week and was prescribed 100 mg of amantadine. Within half an hour of taking the first dose, the patient collapsed. He was found to be in asystole by emergency medical services, and advanced cardiac life support protocols were initiated, including cardiopulmonary resuscitation and intubation for airway protection. However, he sustained multiple recurrences of cardiac arrest, and despite all resuscitation efforts, the patient expired.

Enteritis associated with systemic lupus erythematosus (SLE) is a rare and unusual manifestation of the gastrointestinal (GI) consequences of SLE itself. Complications of the enteritis component include mesenteric vasculitis, intestinal pseudo-obstruction, and protein-losing enteropathy. Lupus enteritis is very responsive to treatment with pulse steroids in almost 70% of the patients, but it is critical to diagnose it early to prevent devastating organ damage. The case describes a 21-year-old Caucasian female with a past medical history of uncomplicated laparoscopic appendectomy (one month prior to the time of presentation), major depressive disorder, asthma, iron deficiency anemia, pelvic inflammatory disease secondary to sexually transmitted Chlamydia trachomatis infection, and SLE (diagnosed two weeks prior to presentation). She had been transferred from an outside facility with complaints of severe right upper quadrant (RUQ) abdominal pain for one day. The patient had run out of her prescription for steroids and hydroxychloroquine two days prior to the presentation. Her abdominal pain was accompanied by nausea, bilious vomiting, non-bloody diarrhea, a photosensitive facial rash, left-sided pressure-type periorbital headache, diplopia, oral ulcers, inappetence, joint stiffness, and muscle weakness. A CT of the abdomen and pelvis from an outside facility showed enteritis involving the proximal jejunum with associated mesenteric edema and ascites, suggesting infectious versus inflammatory or autoimmune etiology. A repeat CT scan a few days later confirmed these findings along with adjacent mesenteric fat stranding. Her autoimmune workup confirmed the serological diagnosis of SLE, and assessment of the SLE Disease Activity Index (SLEDAI) confirmed the diagnosis of a severe SLE flare. Upper endoscopy detected edematous mucosa in the duodenum and jejunum without active bleeding, gastropathy, or ulceration. No surgical intervention was required. Her symptoms resolved with supportive care, pulse steroids, and hydroxychloroquine. She was discharged with instructions for outpatient follow-up with gastroenterology and rheumatology.

Opioid addiction is a major public health problem. Through a commitment to individualized treatment plans meant to help patients meet personal goals, behavioral therapy can encourage abstinence and help prevent relapses that can have debilitating consequences. This case describes a 31-year-old male with heroin relapse who presented with flaccid quadriparesis as well as loss of sensation below the T2-3 spinal level, loss of rectal tone, and urinary retention. A urine drug screen (UDS) was positive for opiates and amphetamines. Autoimmune serologies were negative. Cerebrospinal fluid (CSF) analysis was negative for any acute ongoing infectious process. Magnetic resonance imaging (MRIs) of the cervical and thoracic spine showed increased intramedullary signals with spinal cord expansion from C2-T2, indicating acute transverse myelitis. Upon completion of the aforementioned work-up, idiopathic transverse myelopathy (TM) was diagnosed, and the patient was started on intravenous (IV) methylprednisolone; he also received five sessions of plasmapheresis. By process of elimination, suspicion remained of a diagnosis of opioid-induced myelopathy. The patient showed mild improvement in his original sensory deficits and flaccid quadriplegia.

Many drugs are known to potentially cause liver injury; however, only a few reports investigate the association between levofloxacin and acute liver failure (ALF).  The case describes a 65-year-old man who was admitted with primary diagnoses of cerebrovascular accident (CVA) and acute coronary syndrome (ACS) who developed an upper respiratory tract infection for which he was started on levofloxacin. Following its administration, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) increased more than 100-fold above the upper limit of normal. Over the next 24 hours, AST peaked at 9334 U/L, ALT at 4525 U/L, prothrombin time to 24.6 seconds, international normalized ratio (INR) to 2.22, and serum ammonia to 157 µmol/L. The patient developed signs and symptoms of decompensated liver disease, namely hepatic encephalopathy (HE). Levofloxacin was discontinued immediately, and evidence-based treatment per society guidelines from The American Association for the Study of Liver Diseases consisting of IV n-acetylcysteine as well as lactulose and rifaximin was initiated. Such medical management resulted in clinical resolution of his ALF, but he had a poor overall prognosis and eventually succumbed to critical illness.