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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary hypertension (PH) occurs frequently in parenchymal lung disease and is usually correlated with increased mortality. Thus, the treatment of PH in patients with lung disease has been an active area of interest. Secondary pulmonary hypertension (SPH), whether from parenchymal lung disease or other etiologies, is more common than primary pulmonary hypertension (PPH). In 2002, two new medications, oral bosentan and subcutaneous treprostinil, were released for the treatment of pulmonary arterial hypertension (PAH). These new agents are not restricted to use in PPH, as they are approved for use in PAH in general. It is reasonable to consider the use of these medications in select patients with SPH caused by parenchymal lung disease, although these groups have not yet been studied in clinical trials. The initial hemodynamic evaluation of SPH patients, the potential use of these new medications in the context of standard care, and the assessment of response to therapy are discussed in this update. A relevant case report is used to illustrate use of these new agents in SPH, and ongoing clinical trials are reviewed. The available treatment options for patients with SPH are rapidly improving.
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PMID:Advances in the treatment of secondary pulmonary hypertension. 1257 94

Pulmonary hypertension secondary to pulmonary venoocclusive disease (PVOD) is increasingly recognized (Wagenvoort, Chest 69:82-86, [20]; Scully et al., N Engl J Med 308:823-834, [21]). The clinical presentation is usually progressive pulmonary hypertension. It should be kept in mind when there is pulmonary arterial hypertension, pulmonary edema, and a normal pulmonary artery wedge pressure. Importance of diagnosing this condition is to protect patient from fatal pulmonary edema when using prostacyclins that are effective for treatment of primary pulmonary hypertension. Herein, we present multidetector computed tomography findings of PVOD in a pregnant woman that presented with pulmonary hypertension.
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PMID:PVOD suggested by MDCT and clinical findings in a pregnant woman. 1770 57

Morphological and morphometric studies have shown that secondary pulmonary hypertension is characterized by more pronounced pathological changes in the pulmonary arterial branches in severe chronic obstructive lung disease (COLD) than in idiopathic fibrosing alveolitis. Secondary pulmonary hypertension does develop in atopic bronchial asthma. Moreover, there are more significant pathological changes in the pulmonary arteries than in the bronchial ones. In severe COLD, the development of emphysema affects that of pulmonary arterial hypertension.
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PMID:[Morphofunctional characteristics of pulmonary and bronchial arteries in bronchial asthma, chronic obstructive lung disease, idiopathic fibrosing alveolitis]. 1836 6

Secondary pulmonary hypertension (PH) is emerging as one of the leading causes of mortality and morbidity in patients with hemolytic anemias such as sickle cell disease (SCD) and thalassemia. Impaired nitric oxide (NO) bioavailability represents the central feature of endothelial dysfunction, and is a major factor in the pathophysiology of PH. Inactivation of NO correlates with hemolytic rate and is associated with the erythrocyte release of cell-free hemoglobin, which consumes NO directly, and the simultaneous release of the arginine-metabolizing enzyme arginase, which limits bioavailability of the NO synthase substrate arginine during the process of intravascular hemolysis. Rapid consumption of NO is accelerated by oxygen radicals that exists in both SCD and thalassemia. A dysregulation of arginine metabolism contributes to endothelial dysfunction and PH in SCD, and is strongly associated with prospective patient mortality. The central mechanism responsible for this metabolic disorder is enhanced arginine turnover, occurring secondary to enhanced plasma arginase activity. This is consistent with a growing appreciation of the role of excessive arginase activity in human diseases, including asthma and pulmonary arterial hypertension. New treatments aimed at improving arginine and NO bioavailability through arginase inhibition, suppression of hemolytic rate, oral arginine supplementation, or use of NO donors represent potential therapeutic strategies for this common pulmonary complication of hemolytic disorders.
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PMID:Nitric oxide and arginine dysregulation: a novel pathway to pulmonary hypertension in hemolytic disorders. 1899 48