The New England Journal of Medicine

Journal Information
ISSN / EISSN: 00284793 / 15334406
Total articles ≅ 198,982

Latest articles in this journal

The New England Journal of Medicine; https://doi.org/10.1056/nejmicm2205584

Abstract:
A 77-year-old man had a 2-day history of a diffuse rash that spared an area of his right torso. Two weeks earlier, herpes zoster infection had developed on his right chest; he subsequently began taking celecoxib for back pain.
Richard L. Schilsky, Dan L. Longo
The New England Journal of Medicine; https://doi.org/10.1056/nejmp2210638

Abstract:
Genomic analysis of tumor tissue and circulating tumor DNA is an increasingly important component of cancer care. But evidence indicates underutilization of tumor genomic testing.
Robert Shireman
The New England Journal of Medicine; https://doi.org/10.1056/nejmp2117605

Abstract:
The nonprofit-governance requirement for medical schools was a core component of U.S. medical care’s transformation. But recently, several for-profit schools have been provisionally or fully accredited.
The New England Journal of Medicine; https://doi.org/10.1056/nejmp2210418

Abstract:
During an awake craniotomy for resecting part of her astrocytoma, a patient-investigator faces a high-stakes decision that she will make in collaboration with her neurosurgeon.
The New England Journal of Medicine, Volume 387, pp 2074-2074; https://doi.org/10.1056/nejmicm2027922

Abstract:
A 70-year-old woman with long-term bismuth subsalicylate use presented with altered mental status, shortness of breath, nausea, and vomiting. An abdominal radiograph showed intraluminal radiopaque material.
The New England Journal of Medicine, Volume 387, pp 2101-2103; https://doi.org/10.1056/nejmc2212742

Abstract:
To the Editor: With respect to the review article on chronic urticaria by Lang (Sept. 1 issue),1 angioedema may be of special interest. Bradykinin-mediated angioedema was not addressed in the review. This rare chronic hereditary urticaria mediated by bradykinin may be life-threatening, and treatments for this condition have been developed.2 Clinicians may also see angiotensin-converting–enzyme (ACE) inhibitor–induced angioedema that does not respond to treatment with antihistamines and glucocorticoids. To the Editor: In the review article on chronic urticaria, Figure 3 describes stepped care. The author states that the information in this figure was synthesized from recommendations based on clinical guidelines. . . .
Julie R. Ingelfinger
The New England Journal of Medicine, Volume 387, pp 2083-2084; https://doi.org/10.1056/nejme2214315

Abstract:
Blockade of the renin–angiotensin system (RAS) is renoprotective beyond the effect of lowering blood pressure, especially in patients with mild-to-moderate chronic kidney disease (CKD).1,2 However, such renoprotection is far more effective when patients with CKD have proteinuria.1,2 As nephrologists, we struggle about whether to continue prescribing RAS inhibitors to patients with advanced (stage 4 or 5) CKD, given the perceived risks. We hope that stopping such treatment may lead to an increase (however modest) in the estimated glomerular filtration rate (eGFR), and we worry about possible drug-related hyperkalemia and other adverse events if RAS inhibition is continued. Although recent retrospective . . .
Douglas Galasko, Tanya Simuni
The New England Journal of Medicine, Volume 387, pp 2087-2088; https://doi.org/10.1056/nejme2213120

Abstract:
There are no treatments that convincingly slow the progression of Parkinson’s disease. One avenue of investigation is based on iron deposition in the brain, which occurs with aging but is also implicated in neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis.1 Iron levels are regulated by binding to transferrin and ferritin, and intracellular iron is partitioned in neurons to prevent toxic effects. Ferroptosis refers to iron-dependent toxicity that triggers lipid peroxidation and other oxidative stresses that lead to cell death.2 Furthermore, cellular iron may exacerbate aggregation of α-synuclein, the neuronal protein that forms Lewy body inclusions . . .
William E. Whitehead, Howard L. Weiner
The New England Journal of Medicine, Volume 387, pp 2067-2073; https://doi.org/10.1056/nejmra2116504

Abstract:
Enlarged ventricles early in life cause developmental delay and acute neurologic signs. Shunting of the ventricles is the definitive treatment but has many problems, and there are temporizing approaches.
David Devos, Julien Labreuche, Olivier Rascol, Jean-Christophe Corvol, Alain Duhamel, Pauline Guyon Delannoy, Werner Poewe, Yaroslau Compta, Nicola Pavese, Evžen Růžička, et al.
The New England Journal of Medicine, Volume 387, pp 2045-2055; https://doi.org/10.1056/nejmoa2209254

Abstract:
Iron content is increased in the substantia nigra of persons with Parkinson’s disease and may contribute to the pathophysiology of the disorder. Early research suggests that the iron chelator deferiprone can reduce nigrostriatal iron content in persons with Parkinson’s disease, but its effects on disease progression are unclear.
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