Glucose-6-Phosphate Dehydrogenase Deficiency and COVID-19 Mortality, ICU Admission, and Length of Hospitalization.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has severe consequences in terms of mortality and morbidity. Knowledge of factors that impact COVID-19 may be useful in the search for treatments. OBJECTIVES: To determine the effect of glucose-6-phosphate dehydrogenase (G6PD) deficiency on morbidly and mortality associated with COVID-19. METHODS: All patients admitted to Hadassah Hebrew University Medical Center between 01 March 2020 and 03 May 2021 with a diagnosis of COVID-19 were included. We retrospectively retrieved demographic, clinical, and laboratory data from the hospital's electronic medical records. The main outcomes were mortality, intensive care unit (ICU) admission, and severity of COVID-19. RESULTS: The presence of G6PD deficiency emerged as an independent protective predictor for ICU admission (odds ratio [OR] 0.258, 95% confidence interval [95%CI] 0.077-0.619, P = 0.003) and the development of critical illness (OR 0.121, 95%CI 0.005-0.545, P = 0.006). Moreover, patients with G6PD deficiency had a trend toward lower mortality rates that did not reach statistical significance (OR 0.541, 95%CI 0.225-1.088, P = 0.10). CONCLUSIONS: Patients with G6PD deficiency were less likely to have a severe disease, had lower rates of ICU admission, and trended toward lower mortality rates.

Preventing all-cause hospitalizations in type 2 diabetes with sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists: A narrative review and proposed clinical approach.

Patients with type 2 diabetes (T2D) are at increased risk for hospital admissions, and acute hospitalizations are associated with a worse prognosis. However, outcomes related to all-cause hospital admissions (ACHAs) were often overlooked in trials that demonstrated the cardiovascular and kidney benefits of sodium-glucose cotransporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor agonists (GLP-1RAs). This review includes a contemporary literature summary of emerging data regarding the effects of SGLT2 inhibitors and GLP-1RAs on ACHAs. The role of SGLT2 inhibitors in preventing ACHAs was shown in exploratory investigations of several randomized controlled trials (RCTs) and was further supported by real-world evidence (RWE). However, the association between GLP-1RA use and lower ACHA risk was mainly shown through RWE, with minimal available RCT data. We also discuss the advantages and challenges of studying ACHAs. Finally, we propose an easily memorized ("ABCDE" acronym) clinical approach to evaluating T2D status and treatment in admitted patients, as they transition from hospital to community care. This systematic approach may assist clinicians in recognizing possible pitfalls in T2D management, thereby preventing subsequent hospitalizations and improving patient prognoses. While acute admission can sometimes be perceived as a management failure, it should also be viewed as an opportunity to take action to prevent the next hospitalization.

[IMMUNE CHECKPOINT INHIBITOR-INDUCED DIABETES MELLITUS].

INTRODUCTION: Immune checkpoint inhibitors (ICIs) have transformed the care of cancer patients, providing therapeutic options for advanced malignancies considered otherwise untreatable. However, these agents have been associated with immune-related adverse events (irAEs). ICI-induced diabetes (ICI-DM) is a rare complication of programmed death-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor therapy (~1%) and can be life-threatening, as patients often present with severe hyperglycemia and in diabetic ketoacidosis. We describe two patients with rapid-onset diabetes mellitus associated with anti PD-1 therapy followed by an in-depth review of the literature. We discuss the clinical presentation, potential mechanisms and optimal management of patients with ICI-DM. As ICI use continues to expand across a wide variety of malignancies, clinicians must be aware of this potentially life-threatening irAE to prevent significant morbidity and mortality.

[TO BE A RESIDENT IN THE DEPARTMENT OF MEDICINE].

INTRODUCTION: Sir William Osler is considered to be one of the fathers of modern medicine who pioneered the practice of bedside teaching of clinical medicine for medical students and residents. Osler was well known as a diagnostician and outstanding therapist with a humanized approach and rare didactic capabilities. Medical training at Hadassah is built on the central tenets of Osler's approach, incorporating the tremendous advances in science and medicine. Training for residents in Internal Medicine is designed to develop a broad base of medical and, if possible, scientific knowledge, as well as skills and competencies to deliver a high standard of patient care. In the past 7 years, 28 residents have undergone specialist training in Internal Medicine B. Among them, 71% were Israeli medical school graduates; 36% were women;18% were recent immigrants to Israel; 78% were Jewish. Among Jewish residents, 32% were religiously observant. Besides the usual assignments of the internal medicine ward, the medical staff of Internal Medicine B excelled in diagnosis of hard to diagnose diseases as described in eleven cases. The diagnosis in some of those cases was a result of listening to the patient, education on clinical reasoning and the use advanced diagnostic tools. The basic unit of the residency is the clinical mission with an emphasis on exposure to novel modalities such as the use of bedside ultra sound along with dealing with end-of-life dilemmas, the management of complex situations and development of communication and interpersonal skills needed to work with close relatives and families facing critical times. The medical training in the internal ward is not just the sum of arbitrary care of the hospitalized patients, but a well-structured plan with gradually increasing demands. Over the past 7 years, residents in Internal Medicine B have achieved successful passing grades of 38/38 on the first attempt oral and written board examinations, a record that attests to the quality of the trainees and the training process. Hadassah has a long history of providing state-of-the-art patient care, and training young physicians to maintain this high standard - but the education process necessitates longstanding efforts and continuous striving for excellence.

Adrenocorticotropic Hormone Secreting Pheochromocytoma Underlying Glucocorticoid Induced Pheochromocytoma Crisis.

CONTEXT: Pheochromocytomas are hormone secreting tumors of the medulla of the adrenal glands found in 0.1-0.5% of patients with hypertension. The vast majority of pheochromocytomas secrete catecholamines, but they have been occasionally shown to also secrete interleukins, calcitonin, testosterone, and in rare cases adrenocorticotropic hormone. Pheochromocytoma crisis is a life threatening event in which high levels of catecholamines cause a systemic reaction leading to organ failure. CASE DESCRIPTION: A 70-year-old man was admitted with acute myocardial ischemia following glucocorticoid administration as part of an endocrine workup for an adrenal mass. Cardiac catheterization disclosed patent coronary arteries and he was discharged. A year later he returned with similar angina-like chest pain. During hospitalization, he suffered additional events of chest pain, shortness of breath, and palpitations following administration of glucocorticoids as preparation for intravenous contrast administration. Throughout his admission, the patient demonstrated both signs of Cushing's syndrome and high catecholamine levels. Following stabilization of vital parameters and serum electrolytes, the adrenal mass was resected surgically and was found to harbor an adrenocorticotropic hormone secreting pheochromocytoma. This is the first documented case of adrenocorticotropic hormone secreting pheochromocytoma complicated by glucocorticoid induced pheochromocytoma crisis. CONCLUSION: Care should be taken when administering high doses of glucocorticoids to patients with suspected pheochromocytoma, even in a patient with concomitant Cushing's syndrome.

Handgrip Strength in Old and Very Old Adults: Mood, Cognition, Function, and Mortality.

OBJECTIVES: To determine the trajectory of handgrip strength (HGS) from age 70 to 90 and its association with mood, cognition, functional status, and mortality. DESIGN: Prospective follow-up of an age-homogenous representative community-dwelling cohort (born 1920-21) in the Jerusalem Longitudinal Cohort Study (1990-2015). SETTING: Home-based assessment. PARTICIPANTS: Subjects aged 70 (n = 327), 78 (n = 384), 85 (n = 1187), and 90 (n = 406), examined in 1990, 1998, 2005, and 2010, respectively. MEASUREMENTS: Handgrip strength (kg) (dynamometer), low HGS defined as sex-specific lowest quartile grip; geriatric assessment; all-cause mortality (1990-2015). RESULTS: Mean HGS declined between age 70 and 90 from 21.3 ± 7.2 to 11.5 ± 5.6 kg in women and from 35.3 ± 8.4 to 19.5 ± 8.2 kg in men. Cross-sectional associations were observed between low HGS and poor functional measures (age 70-90), lower educational and financial status, smoking, and diabetes mellitus (ages 78-90). After adjustment for baseline education, self-rated health, physical activity, diabetes mellitus, depression, and cognition, low HGS predicted subsequent activity of daily living dependence from age 78 to 85 (odds ratio (OR) = 2.68, 95% confidence interval (CI) = 1.04-6.89) and 85 to 90 (OR = 2.31, 95% CI = 1.01-5.30), whereas the adjusted ORs for activities of daily living difficulty and depression failed to achieve significance. HGS did not predict subsequent cognitive decline. Survival rates were significantly lower in participants with low HGS (Quartile 1) than in those with normal HGS (Quartiles 2, 3, 4) throughout follow-up from ages 78 to 85, 85 to 90, and 90 to 95. Similarly, after adjusting for sex, education, self-rated health, body mass index, hypertension, diabetes mellitus, ischemic heart disease, and smoking, a low HGS was associated with significantly higher mortality. CONCLUSIONS: Mean HGS declined progressively with age, and participants in the lowest age-specific quartile of HGS had a higher risk of subsequent functional decline and mortality.