PubMed · 14397107
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V M SITENKO. 1955. [Diagnostic errors in endarteritis obliterans].. https://pubmed.ncbi.nlm.nih.gov/14397107/
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Idiopathic arterial calcification in infancy is usually fatal with death in early life and diagnosis at post mortem. This report describes a unique, late presentation with hypertension and cardiac failure in a child aged 33 months, found to have widespread arterial calcification at radiological imaging. The calcium-phosphate axis was normal and there was no other demonstrable cause for calcification. Additionally, the histological features of arterial calcification at renal biopsy paralleled the findings in infants with this disorder. The late presentation in this case is unusual and has not been previously reported. Ultrasound and CT are sensitive for calcification, and the disease should be suspected in children presenting with cardiac or respiratory manifestations and features of arterial calcification, where no metabolic cause is established.
Individuals exhibiting precursor symptoms of diabetes mellitus or reaching diagnostic thresholds for diabetes are at increased risk of death due to cardiovascular disease (CVD). Moreover, patients with diabetes alone, as well as those who have diabetes paired with established CVD, remain undertreated for cardiovascular risk factors. The clear correlation between these disease processes has led many to speculate that they share common pathogenetic processes. Recent research has made it increasingly evident that the core metabolic defects that mark diabetes, including impaired glucose tolerance, insulin resistance, and proinflammatory and prothrombotic states, lead to endothelial dysfunction and accelerate atherogenesis. Moreover, increases in sympathetic tone with diabetes are associated with changes in cardiac and vascular function that lead to hypertension, left ventricular dysfunction, and cardiac autonomic neuropathy; such changes set the stage for arrhythmia, silent infarction, and sudden death. Furthermore, diabetes-related changes in metabolic and autonomic functioning, as well as increases in inflammatory and thrombotic signaling, compromise the ability of myocardial and vascular tissue to remodel after injury and to recover and sustain functionality. Because potentiation of atherogenesis and cardiac dysfunction occurs in the presence of early diabetic symptoms as well as in the established disease, early implementation of strategies to reduce cardiovascular risk factors and to slow diabetes progression may help to improve long-term outcomes for at-risk individuals. Such interventions may include well-established treatments for hypertension and dyslipidemia, diet improvements, weight loss, and exercise as well as novel pharmacologic interventions aimed at newly identified therapeutic targets.
Peripheral arterial disease is common, but the diagnosis frequently is overlooked because of subtle physical findings and lack of classic symptoms. Screening based on the ankle brachial index using Doppler ultrasonography may be more useful than physical examination alone. Noninvasive modalities to locate lesions include magnetic resonance angiography, duplex scanning, and hemodynamic localization. Major risk factors for peripheral arterial disease are cigarette smoking, diabetes mellitus, older age (older than 40 years), hypertension, hyperlipidemia, and hyperhomocystinemia. Nonsurgical therapy for intermittent claudication involves risk-factor modification, exercise, and pharmacologic therapy. Based on available evidence, a supervised exercise program is the most effective treatment. All patients with peripheral arterial disease should undergo aggressive control of blood pressure, sugar intake, and lipid levels. All available strategies to help patients quit smoking, such as counseling and nicotine replacement, should be used. Effective drug therapies for peripheral arterial disease include aspirin (with or without dipyridamole), clopidogrel, cilostazol, and pentoxifylline.