ABSTRACT
Systemic sclerosis (SSc) is a protean disorder in which prognosis and treatment are tailored on the basis of organ involvement. Among SSc lung manifestations, interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH) or the combination of both, are the first cause of SSc mortality and impact heavily on patient quality of life. ILD may begin early in disease and usually progresses slowly. However, approximately 10% of patients with ILD may reach terminal respiratory insufficiency. PAH may be an early or late complication of SSc in which increased blood pressure in pulmonary arteries leads to right heart failure. Current treatments provide some benefit, but both SSc-ILD and PAH still represent an enormous unmet need of more efficacious therapeutic strategies.
Subject(s)
Hypertension, Pulmonary/etiology , Lung Diseases, Interstitial/etiology , Quality of Life , Scleroderma, Systemic/complications , Blood Pressure , Disease Progression , Health Services Needs and Demand , Humans , Hypertension, Pulmonary/physiopathology , Hypertension, Pulmonary/therapy , Lung Diseases, Interstitial/physiopathology , Lung Diseases, Interstitial/therapy , Prognosis , Scleroderma, Systemic/mortality , Scleroderma, Systemic/therapyABSTRACT
Pulmonary arterial hypertension (PAH) is a rare but potentially fatal complication of human immunodeficiency virus (HIV). It may occur in HIV-1 or 2 infection, irrespective of the route of transmission or the degree of immunosuppression. The improved survival of patients infected with HIV in the era of highly active antiretroviral therapy (HAART) justifies systematic screening for PAH according to an algorithm in patients with unexplained dyspnea. In all cases, right heart catheterization must be performed to establish the definitive diagnosis of pulmonary hypertension. The prevalence of PAH is about 0.5% in patients with HIV infection. A beneficial effect of HAART on the course of HIV-related PAH has not been clearly established. In contrast, PAH-specific therapies such as epoprostenol and bosentan have been demonstrated to be efficacious for short- and long-term outcomes in this context. Notably, some patients pulmonary hemodynamics and functional class normalized or near normalized with these treatments. Other PAH-specific therapies remain to be evaluated. The advent of HAART associated with the development of PAH-specific therapies has improved the prognosis of patients HIV-related PAH, with a survival rate of about 70% at 3 years.
Subject(s)
HIV Infections/complications , HIV-1/physiology , Hypertension, Pulmonary/etiology , Diagnostic Techniques, Cardiovascular , Diagnostic Techniques, Respiratory System , HIV Infections/diagnosis , HIV Infections/epidemiology , HIV Infections/therapy , Humans , Hypertension, Pulmonary/diagnosis , Hypertension, Pulmonary/epidemiology , Hypertension, Pulmonary/therapy , Models, BiologicalABSTRACT
The aim of this study was to characterize the time course of maximal oxygen consumption VO2(max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in VO2(max) tends to asymptote. On a total of 26 subjects who participated in one of three bedrest campaigns without countermeasures, lasting 14, 42 and 90 days, respectively, VO2(max) maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After all periods of HDT, VO2max, Qmax, and QaO2max were significantly lower than before. The VO2max decreased less than qmax after the two shortest bedrests, but its per cent decay was about 10% larger than that of Qmax after 90-day bedrest. The VO2max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max declines after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the VO2max, Qmax, and QaO2max decay during bedrest were less if the bedrest duration were longer, with the exception of that of VO2max in the longest bedrest. The asymptotic VO2max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the VO2max decrease were identified, which we postulate were related to cardiovascular deconditioning and to impairment of peripheral gas exchanges due to a possible muscle function deterioration.
Subject(s)
Bed Rest , Oxygen Consumption/physiology , Physical Endurance/physiology , Physical Exertion/physiology , Rest/physiology , Adaptation, Physiological/physiology , Adult , Exercise Test , Humans , Kinetics , MaleABSTRACT
A liquid chromatographic (LC) method was evaluated for the determination of free and total carbohydrates in soluble coffee. Samples are solubilized in water for free carbohydrates or hydrolyzed with 1.00N hydrochloric acid for total carbohydrates. An aliquot of the sample solution is analyzed on a pellicular anion-exchange polystyrene-divinylbenzene column using pure water as the mobile phase. Carbohydrates are quantitated by a pulsed amperometric detector. All major carbohydrates found in soluble coffee are determined in a single run. The technique allowed the detection of fraudulent addition of coffee husks or parchments as well as cereals or caramelized sugar for the 63 commercial products analyzed. High levels of free mannitol, free fructose, free glucose, sucrose, total glucose, and total xylose are a good indication of adulteration. Data were compared with those obtained from separate enzymatic determinations and from a different LC procedure. A close agreement among the methods was observed. However, the original method was superior in precision and was the only procedure that enabled the quantitation of all major carbohydrates. The technique is, therefore, a very powerful tool for routine analysis and for purity assessment of soluble coffee.
