This Week in The New England Journal of Medicine

January 25, 2001

"Intracoronary beta-
radiation therapy
produces a significant
dose-dependent decrease
in the rate of restenosis
after angioplasty."

Endoluminal Beta Irradiation for the Prevention of Coronary Restenosis after Balloon Angioplasty

Restenosis is the principal problem limiting the long-term clinical benefit of balloon angioplasty. Beta radiation reduces vascular neointimal proliferation, which is a pivotal cellular event in coronary restenosis. In this study, coronary endoluminal irradiation was performed after completion of angioplasty by positioning a catheter equipped with a yttrium-90 source at the site dilated by the balloon. Irradiation was effective in reducing the incidence of restenosis at six months.

This interesting new approach to the problem of coronary restenosis warrants further investigation in larger randomized trials. The follow-up in the current study was short, and long-term observations will be needed to document the durability of the beneficial effect on restenosis and to assess possible long-term complications.

Related Editorials, pages 295 and 297

Localized Intracoronary Gamma Radiation to Inhibit Restenosis after Stenting

Although the incidence of restenosis after coronary angioplasty has been reduced by stenting, restenosis -- even when a stent has been placed -- is still a troublesome problem. In this study, localized intracoronary radiation therapy was used in an attempt to prevent a second episode of restenosis. Over nine months of follow-up, irradiation was effective in reducing the need for repeated revascularization but resulted in an increased risk of late coronary thrombosis and myocardial infarction.

Localized intracoronary irradiation is an interesting new approach to the prevention of coronary restenosis after angioplasty and other revascularization procedures. However, the risk of late coronary thrombosis must be overcome before the procedure can be recommended for routine use.

Related Editorials, pages 295 and 297

A Molecular Marker for Chloroquine-Resistant Falciparum Malaria

In the malaria parasite, point mutations that are correlated with chloroquine resistance have been described in transmembrane proteins of the digestive vacuole. This clinical study of falciparum malaria in Mali found that the mutant pfcrt T76 allele had a base-line prevalence of 41 percent in samples obtained from patients before treatment with chloroquine but was present in all 60 samples from patients who had persistent or recurrent infection after treatment (odds ratio for resistant infection, 18.8).

These findings indicate that this mutation is a marker with a high sensitivity but a low specificity for chloroquine-resistant malaria due to Plasmodium falciparum. It may be most useful in helping to survey for chloroquine-resistant malaria in sub-Saharan Africa.

Related Editorial

"Children with
diabetic ketoacidosis
who had higher serum
urea nitrogen
concentrations and
more severe hypocapnia
. . . were at increased
risk for cerebral edema."

Risk Factors for Cerebral Edema in Children with Diabetic Ketoacidosis

Cerebral edema occurs in 1 to 5 percent of children with diabetic ketoacidosis. In this casecontrol study of children with diabetic ketoacidosis, the risk factors for cerebral edema were a higher initial serum urea nitrogen concentration, a lower initial partial pressure of arterial carbon dioxide, a smaller increase in the serum sodium concentration during treatment, and treatment with sodium bicarbonate. Cerebral edema was not associated with the initial serum glucose concentration, the change in the serum glucose concentration during therapy, or the rate of infusion of insulin or sodium.

This is a comprehensive analysis of a large number of children with diabetic ketoacidosis who had cerebral edema. Overall, the differences between these children and the control groups indicate that brain ischemia caused by marked dehydration and hypocapnia has an important role in the pathogenesis of cerebral edema in such children. In terms of therapy, the findings translate into the need for vigorous fluid replacement with isotonic saline and avoidance of sodium bicarbonate.

Related Editorial

Duodenal-biopsy specimen

Characterization of Malabsorption in Autoimmune Polyglandular Syndrome Type I

Autoimmune polyglandular syndrome type I is a rare inherited disease characterized by a variety of endocrine disorders and candidiasis. Fat malabsorption develops in about one fifth of patients. This case report describes a patient with the syndrome in whom severe malabsorption was caused by a deficiency of cholecystokinin-producing enteroendocrine cells in the mucosa of his proximal small intestine.

Although fat malabsorption associated with autoimmune polyglandular syndrome type I is uncommon, this report suggests that a deficiency of cholecystokinin-producing enteroendocrine cells in the proximal small bowel can cause severe malabsorption. Bile acid secretion, which is stimulated by cholecystokinin, was low in the patient when malabsorption was severe.

Mechanisms of Disease: Estrogen and the Risk of Breast Cancer

Estrogen has an important role in the pathogenesis of breast cancer, and treatment is often directed at altering estrogen production or action. This review summarizes what is known about the role of variations in the production, metabolism, and action of estrogen and the sensitivity of breast tissue to estrogen as determinants of the risk of breast cancer in women.

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