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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Patients with Hodgkin’s lymphoma and hypercalcemia are almost always found to have elevated levels of calcitriol (1,25-dihydroxyvitamin D). While dedicated studies in hematologic malignancies have not been performed, it is thought that the pathophysiology is similar to that of hypercalcemia of sarcoidosis. Malignant lymphocytes produce interferon-gamma, stimulating the 1-alpha-hydroxylase activity of monocytes and macrophages (one of the few cells outside of the kidney that have this enzyme), enhancing PTH-independent activation of vitamin D.
References: Calcitriol in Hodgkin’s Lymphoma
Standard pulse oximetry cannot distinguish between hemoglobin bound to oxygen and hemoglobin bound to carbon monoxide (HbCO), and therefore cannot be used to identify victims of carbon monoxide poisoning. Similarly, the partial pressure of O2 on an arterial blood gas reflects the level of dissolved oxygen, and therefore may be normal in patients with carbon monoxide poisoning. Instead, HbCO levels must be measured with specific spectrophotometric blood gas analysis, ordered as an “ABG with co-ox”. Greater than 3% HbCO is abnormal in non-smokers.
References: Carbon Monoxide
In healthy individuals, glucose is filtered by the glomerulus, and subsequently reabsorbed in the proximal tubule by sodium glucose cotransporters (SGLT) 1 and 2 in order to prevent loss of an energy substrate. SGLT2 represents the majority of filtered glucose reabsorption (80-90%), while SGLT1 represents a minority (10-20%). In humans/animals who have SGLT2 inhibited by either medications or via genetic mutation, SGLT1 reabsorption capacity increases and is capable of maintaining a minimum glucose absorption to maintain minimum serum glucose levels.
References: SGLT1 and SGLT2