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INTRODUCTION: Hereditary hemochromatosis is commonly caused by mutation of the HFE protein (C282Y/H63D), leading to iron overload and deposition in the liver, heart, pancreas, and pituitary. Manifestations of Hereditary hemochromatosis differ based on the primary site of iron deposition, ranging from cirrhosis, cardiomyopathy, to diabetes and immunosuppression. which increases susceptibility to opportunistic infections including disseminated mycoplasma. Even with its estimated prevalence of 15% of all community acquired pneumonias, mycoplasma pneumonia is not well recognized for its multitude of rare extrapulmonary manifestations (Figure 1). CASE DESCRIPTION/METHODS: 43 year old male was found unresponsive at home. On admission, diffuse mucosal sloughing and bleeding with numerous small, flat, erythematous lesions on the trunk and extremities. Throat swab Polymerase Chain Reaction: positive for mycoplasma pneumonia, with IgM serum confirmatory test. These skin lesions would blister and ulcerate on following days. Skin biopsy revealed Steven Johnson Syndrome. On hospital day 6 patient was noted to have left hemiplegia, Head imaging, Right Middle Cerebral Artery ischemic stroke and hemorrhagic conversion. Cardiac Imaging showed No patent Foramen Ovale, no atrial thrombi or valvular pathology, leading to a diagnosis of cryptogenic stroke. In the presence of elevated liver function testing and diffuse hyperattenuation of the liver on non-contrast CT, Iron studies were obtained. Ferritin of 10,086 ng/ml, % Iron saturation of 78.7. Genetic testing returned homozygous for C282Y gene. Liver biopsy confirmed hemochromatosis. Appropriate antibiotics and serial phlebotomies started, after which he clinically improved. DISCUSSION: The liver plays a central role in the clearance of bacteria from the bloodstream as hepatic phagocytosis accounts for more than 80% of all reticuloendothelial system function. In hemochromatosis, patients have increased portocaval shunting from liver injury. Therefore, bypassing the liver, and reducing clearance of mycoplasma, predisposing patients to a more virulent clinical course. Mycoplasma's activity in an Iron rich environment is poorly understood. It is known that mycoplasma binds to lactoferrin, a protein largely responsible for iron sequestration in the body for bacteriostasis. This leaves room for further research regarding its evolutionary pathogenicity. Therefore, patients with unexplained opportunistic infections and elevated transaminases should be investigated for hemochromatosis.

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Cefepime is a 4th generation cephalosporin often used for its ability to cover gram-positives, gram negatives, anaerobic bacteria, and, most importantly, pseudomonas. Prior to initiation of cefepime, the medication is dosed based on the renal function to avoid a multitude of its toxicity profiles, including encephalopathy, aphasia, myoclonus, seizures, and nonconvulsive status epilepticus. These risks are increased in the presence of renal impairment. We present a case of a 65-year-old woman who had presented to the emergency department (ED) two weeks after initiation of outpatient IV cefepime therapy with concerns of altered mentation and decreased oral intake. In the ED, the patient was noted to have a creatinine: 5.77 (baseline of 0.76) and urea: 94. During evaluation by the ED provider, the patient was noted to have transient slurring of speech, speech arrest, and tonic-clonic movements on the right. CT of the head, followed by CT angiography of the head and neck, demonstrated no acute intracranial pathology. Spot EEG revealed generalized slowing with unclear left-sided epileptiform discharges. There was a concern for complex partial seizures. Neurology and nephrology were consulted. The patient was given 1 g of levetiracetam, and emergent dialysis was performed. After dialysis, no other epileptiform activity was noted with the improvement of her encephalopathy. The patient returned to her baseline mentation. Here we emphasize the importance of recognizing cefepime's toxicity profile while triaging patients. In the rare event of toxicity, immediate treatment is discontinuing the offending agent and initiation of emergent hemodialysis.

Mitral valve prolapse (MVP) affects approximately 170 million people worldwide; however, phenotypically, there is a wide variety of heterogeneity. In particular subsets, the incidence of sudden cardiac death is calculated to be 998 per 100,000 person-years, which is significantly increased when compared with the general population of MVP patients. Individuals with high-risk features have been identified as young females with bileaflet MVP and electrocardiogram findings of frequent complex ectopy, ST-T wave changes, and inferior T wave inversions. Supplemental imaging modalities in this subgroup demonstrate redundant leaflets and chordae on 2-dimensional transthoracic echocardiography along with varying severity of mitral annular disjunction. Detailed morphologic assessment by 3-dimensional echocardiography provides a quantitative assessment of annular disjunction along with left ventricular longitudinal and basal circumferential strain patterns. Late gadolinium enhancement on cardiac magnetic resonance imaging identifies diffuse and isolated left ventricle fibrosis involving the fascicles and papillary muscles, which has been visualized in isolation during autopsy. Findings of this review propose that sudden cardiac death as a result of malignant arrhythmias arises from automaticity, complex ectopy, and reentry at the level of the fascicles and papillary muscles. The repetitive mechanical stress provides a nidus for the development of both micro- and macrofibrosis easily identified by late gadolinium enhancement on cardiac magnetic resonance imaging. Escalation to electrophysiology studies and early intervention could provide new targeted lifesaving therapies.

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