Hydrochlorothiazide-induced acute pulmonary edema.

OBJECTIVE: To describe a patient with noncardiogenic acute pulmonary edema induced by hydrochlorothiazide. CASE SUMMARY: A 70-year-old woman in generally good health, except for mild pedal edema, developed acute pulmonary edema after ingesting hydrochlorothiazide 12.5 mg for the first time. DISCUSSION: This is the fifteenth reported case of noncardiogenic pulmonary edema induced by hydrochlorothiazide. The investigations by previous authors seemed to rule out an immunologic mechanism; thus, the pathogenesis of the reaction is unknown. Most of the reactions have occurred in women. CONCLUSIONS: Noncardiogenic pulmonary edema appears to be an idiosyncratic reaction that occurs with some specificity with the thiazide diuretics. Clinicians should be aware of this potential, serious adverse reaction that occurs without warning.

Reassessment of circadian profile of blood pressure and heart rate in diabetic patients with autonomic neuropathy.

Previous studies have shown that the normal circadian blood pressure fall is absent in patients with diabetic autonomic neuropathy, while the reported rise in blood pressure during the night in the same patients is controversial. This study analyzed the circadian profile in 19 diabetic patients with established autonomic neuropathy. Twenty-four hour ambulatory systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate were recorded every 20 minutes during the day and every 60 minutes at night in 29 patients, 19 with diabetic autonomic neuropathy and 10 nondiabetic hypertensive patients as controls. Twelve diabetic patients with autonomic neuropathy with unknown hypertension were found to have hypertension based on 24 hour ambulatory blood pressure monitoring. Repeated measured analysis of variance (ANOVA) and trend analysis indicated that the linear systolic blood pressure increased from night to morning to afternoon while mean arterial pressure and diastolic blood pressure increased from night to morning but decreased from morning to afternoon. In practice, the early morning rise in systolic blood pressure in diabetic neuropathy is not different from that in normal or hypertensive patients and requires appropriate treatment. The absence of the nocturnal rise in the blood pressure revealed a subgroup of patients with diabetic neuropathy which demonstrated no fatal cardiovascular or renal events over 18 to 24 months of follow-up.

Unravelling the conundrums of the diabetic heart diagnosed in 1876: prelude to genetics.

During the past two decades epidemiological, clinical and laboratory studies have confirmed the existence of the diabetic heart in some patients with diabetes mellitus. The diagnosis was made in patients in whom other known etiological factors, such as coronary artery disease, alcoholism or hypertensive cardiovascular disease, were ruled out. The newer concept of the diabetic hypertensive heart is clinically based on a higher incidence of congestive heart failure caused by extensive myocardial involvement. In patients with hypertension and hypertension associated with diabetes, the intramyocardial arterioles present medial hypertrophy and a diminished lumen, increased periarteriolar fibrosis, accumulation of fibrillar collagen and patent extramural coronary arteries. Such confirmatory findings have been previously seen in experimental animals and in patients with diabetes and no hypertension. In the genetically diabetic rat, diabetes may be prevented by neonatal thymectomy, suggesting the existence of an autoimmune deficiency syndrome. Furthermore, conversion of Ala 776 into Thr 776 on the polyprotein by a point mutation results in loss of diabetogenicity. Abnormalities in systole and diastole related to lowering of CK-M and CK-B mRNA levels are normalized following insulin therapy. Identification of the genetic factors in the diabetic heart may lead to the identification of its pathogenic mechanisms.