Being an outstanding physician and lifelong learner requires stoking the flames of clinical curiosity. In Chiefs’ Inquiry Corner (CIC) we attempt to succinctly answer actual clinical questions that have been raised on the wards and in the clinics of NYU’s teaching hospitals. Our answers are not meant to be all encompassing or practice changing but rather to serve as springboards for further exploration. For those of us with short attention spans, we hope CIC satisfies that craving for a morsel of knowledge in a digestible format.
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The Panton-Valentine Leukocidin (PVL) is a potent cytotoxin elaborated by some community acquired Staph
species, chief among them strains of Methicillin Resistant Staph Aureus
(MRSA). PVL is thought to contribute to MRSA virulence by forming pores in leukocyte membranes, promoting cell lysis and release of inflammatory factors. PVL-producing Staph
has been primarily implicated in skin and soft tissue infections, however also plays a role in especially aggressive forms of necrotizing pneumonia. Pulmonary infections caused by PVL-producing MRSA tend to be extremely severe and are characterized by extensive tissue necrosis and rapid progression, and are often preceded by influenza-like respiratory illnesses. While there is some clinical and in vitro evidence to suggest that addition of antibiotics with anti-toxin properties such as linezolid and clindamycin may be beneficial, the mechanism and magnitude of this benefit is poorly understood.
References: Lancet Staph PVL
Hypertrophic cardiomyopathy (HCM) is a genetic sarcomeric disorder with diverse phenotypic expression in which a subset of patients are at an increased risk of sudden cardiac death (SCD). Myocyte disarray, fibrosis and replacement scarring all serve as arrthythmogenic substrate that predispose to malignant ventricular arrhythmias. Several clinical markers have been organized into a risk stratification algorithm (ACCH/AHA) that is sensitive for identifying the majority of patients at increased risk for SCD. Major clinical risk factors
include: family history of HCM-related SCD, sustained VT causing syncope or hemodynamic compromise, unexplained syncope within the last six months, LV wall thickness > 30 mm, NSVT > 3 beats, and abnormal blood pressure response during exercise. Clinical risk modifiers
include: young age (<30 yrs), delayed hyperenchancement on cardiac MRI, LV outflow tract obstruction, LV aneurysm and LV ejection fraction <50%. Prophylactic defibrillator placement should be recommended for patients whose clinical profiles include family history of HCM-related SCD, increased wall thickness or recent syncope (IIa recommendation) and/or for patients who have NSVT or abnormal blood pressure response during exercise and one or more risk modifier
References: HCM and Sudden Cardiac Death
Zollinger-Ellison syndrome (ZES) is characterized by hypersecretion of gastrin by duodenal or pancreatic neuroendocrine gastrinomas causing severe acid-related peptic ulcer disease. It is a rare disease, with an incidence of about 0.5 to 2 per million annually, with about 80% occurring sporadically and another 20% in association with multiple endocrine neoplasia type I (MEN1). Almost all patients with ZES will present with abdominal pain; other common symptoms include diarrhea, heartburn, and peptic ulcers. Given these nonspecific symptoms, ZES is a difficult diagnosis to make, with an average time from onset of symptoms to diagnosis of more than 5 years. Diagnosis is made by confirming inappropriate hypergastrinemia. This can be done by concurrently measuring serum gastrin levels and gastric pH; if serum gastrin levels are high (10x the ULN) with low gastric pH (<2), the diagnosis is confirmed. If these tests are inconclusive, a secretin stimulation test can be performed. Secretin normally works by inhibiting gastric G cells from secreting gastrin; in contrast, secretin causes gastrinoma hypersecretion in cases of ZES, causing a large rise in serum gastrin levels.
References: Gastrointestinal neuroendocrine tumors: pancreatic endocrine tumors
Allergic rhinitis is a very common condition affecting approximately 20% of children and adults in the United States. It is characterized by nasal congestion, rhinorrhea, and sneezing as well as various other irritable symptoms. Allergic rhinitis contributes to a significant societal and economic burden as well given the cost of medical visits, pharmacotherapy, and sick days. Regarding treatment for allergic rhinitis, commonly used medications include antihistamine receptor antagonists as well as intranasal corticosteroids. A systematic review and meta-analysis from 2017 compared intranasal corticosteroids with oral antihistamines. Five randomized controlled trials were included in the meta-analysis with a total of 990 patients. The data were analyzed using standard mean differences (SMD) or mean difference for a single study or outcome. Intranasal corticosteroids were superior to oral antihistamines in regards to the following symptoms: total nasal symptoms score (SMD -0.70 [95% CI, -0.93 to -0.47]), nasal obstruction (SMD -0.56 [95% CI, -0.82 to -0.29]), rhinorrhea (SMD -0.47 [95% CI, -1.00 to 0.05]), nasal itching (SMD -0.42 [95% CI, -0.65 to -0.18]), sneezing (SMD -0.52 [95% CI, -0.73 to -0.32]), and quality of life (mean difference -0.90, 95% CI, -1.18 to -0.62). Thus, in the treatment of allergic rhinitis, intranasal corticosteroids should be first line pharmacologic therapy. Oral antihistamines may be used if the primary symptoms are itching, sneezing and rhinorrhea rather than nasal congestion or if intranasal corticosteroids alone are insufficient.
References: Allergic Rhinitis