25550116
Noninvasive estimation of clinically asymptomatic pulmonary hypertension in idiopathic pulmonary fibrosis.
OBJECTIVES
To determine the prevalence of pulmonary hypertension in patients with idiopathic pulmonary fibrosis (IPF) by noninvasive methods.


PATIENTS AND METHODS
Twenty seven patients with IPF attending the Chest Clinic over a period of one-and-a-half-years underwent echocardiography for evidence of pulmonary hypertension, which was defined as pulmonary artery systolic pressure > or = 40 mmHg by Doppler echocardiography, or pulmonary acceleration time < or = 100 milliseconds or two-dimensional echocardiographic findings of right ventricular hypertrophy or overload.


RESULTS
Two patients with clinical evidence of pulmonary hypertension were excluded from analysis. Their mean age (n = 25) was 53.8 years. The mean duration of symptoms before presentation was 2.1 years. Pulmonary hypertension was diagnosed by echocardiography in nine of the 25 patients (36%). There was a statistically significant difference between the duration of illness, arterial oxygen tension (PaO2) levels and forced vital capacity in patients with pulmonary hypertension than in those without pulmonary hypertension. Logistic regression analysis showed a significant association between the duration of illness, decreasing forced vital capacity and hypoxemia with the development of pulmonary hypertension.


CONCLUSIONS
Echocardiography detects pulmonary hypertension in clinically asymptomatic individuals, and should be used routinely for the diagnosis of pulmonary hypertension in patients with IPF.
26068481
Efficacy and safety of iodopovidone pleurodesis through tube thoracostomy.
OBJECTIVE
To evaluate the efficacy and safety of iodopovidone as an agent for pleurodesis through tube thoracostomy in patients with recurrent pleural effusions and pneumothorax.


METHODS
This was a prospective study in which pleurodesis was performed with a solution of 20 mL 10% iodopovidone and 80 mL normal saline solution infused through a tube thoracostomy and left in the pleural cavity for 4 h.


RESULTS
A total of 64 patients (34 men) with a mean (+/-SD) age of 47.1 +/- 15.4 years were included. There were 37 cases of pleural effusion and 27 of pneumothorax. A complete response (neither reaccumulation of fluid nor recurrence of pneumothorax) was obtained in 32 (86.5%) patients with pleural effusion and 25 (92.6%) patients with pneumothorax. A second procedure (i.e. repeated pleurodesis) was attempted successfully in four patients in the pleural effusion group. All patients experienced chest pain to a varying degree as recorded on a Visual Analogue Scale (median 50.5, range 10-95). Seven patients developed fever and one immunocompromised patient developed empyema following the procedure. There were no recurrences at a median follow up of 5 months (range 3-15 months) in the pleural effusion group, and 13 months (range 6-24 months) in the pneumothorax group.


CONCLUSIONS
Iodopovidone can be used as an effective and safe agent for (chemical) pleurodesis (through tube thoracostomy), which is inexpensive and readily available.
22528299
Pulmonary hypertension as a presenting manifestation of allergic bronchopulmonary aspergillosis.
The case of a 46-year-old lady who presented with respiratory failure and pulmonary hypertension in the absence of clinical signs of asthma or bronchiectasis, and in whom a diagnosis of allergic bronchopulmonary aspergilloma [ABPA] was made subsequently on the basis of radiological and laboratory investigations is reported. Symptomatic and objective improvement was seen with corticosteroid therapy. To the best of the authors' knowledge, such an occurrence has not been reported previously. This case highlights the importance of keeping a high index of suspicion while investigating a patient with pulmonary hypertension in whom the aetiology is not apparent on initial evaluation. Identification of the disease, in its early-stage, can prevent progression to bronchiectasis and fibrotic lung disease, and thus, patients can be saved from the morbidity related to end-stage disease.
45999589
Noninvasive ventilation in acute heart failure.
33491888
Noninvasive ventilation in ARDS caused by Mycobacterium tuberculosis: report of three cases and review of literature
3038618
Is the mortality higher in the pulmonary vs the extrapulmonary ARDS? A meta analysis.
BACKGROUND AND AIM
ARDS can occur from the following two pathogenetic pathways: a direct pulmonary injury (ARDSp); and an indirect injury (ARDSexp). The predisposing clinical factor can influence the pathogenesis and clinical outcome of ARDS. This metaanalysis was aimed at evaluating whether there is any difference in mortality between the two groups.


METHODS
We searched the MEDLINE, EMBASE, and CINAHL databases for relevant studies published from 1987 to 2007, and included studies that have reported mortality in the two groups of ARDS. We calculated the odds ratio (OR) and 95% confidence interval (CI) to assess mortality in patients with ARDSp vs patients with ARDSexp and pooled the results using three different statistical models.


RESULTS
Our search yielded 34 studies. In all, the studies involved 4,311 patients with 2,330 patients in the ARDSp group and 1,981 patients in the ARDSexp group. The OR of mortality in ARDSp group compared to the ARDSexp group was 1.11 (95% CI, 0.88 to 1.39), as determined by the random-effects model; 1.04 (95% CI, 0.92 to 1.18), as determined by the fixed-effects model; and 1.04 (95% CI, 0.92 to 1.18), as determined by the exact method, indicating that mortality is similar in the two groups. The mortality was no different whether the studies were classified as prospective (OR, 1.15; 95% CI, 0.87 to 1.51) or retrospective (OR, 1.01; 95% CI, 0.61 to 1.69); small (OR, 1.11; 95% CI, 0.77 to 1.60) or large (OR, 1.1; 95% CI, 0.82 to 1.49); or observational (OR, 1.10; 95% CI, 0.82 to 1.49) or interventional (OR, 0.97; 95% CI, 0.79 to 1.19). There was methodological and statistical heterogeneity (I(2), 50.9%; 95% CI, 21.3 to 66.2%; chi(2) statistic, 67.22; p = 0.0004).


CONCLUSIONS
The results of this study suggest that there is no difference in mortality between these two groups. Further studies should focus on specific etiologies within the subgroups rather than focusing on the broader division of ARDSp and ARDSexp.
22856684
Prediction of hypertension in chronic hemodialysis patients.
BACKGROUND
There are no universally accepted criteria for the diagnosis of hypertension in hemodialysis (HD) patients. We sought to determine the clinical performance of predialysis and postdialysis systolic and diastolic blood pressure values (BPs) in diagnosing hypertension or assessing its control.


METHODS
Seventy patients [77% African American, 46% females, mean age 59 +/- 17 (SD) years, 34% diabetics] on chronic HD underwent a single 44-hour interdialytic ambulatory blood pressure monitoring (ABPM) and concomitant recording of BP by conventional syphygmomanometer in the HD unit for two weeks. Hypertension was defined as systolic BP (SBP) > or =135 mm Hg or diastolic BP (DBP) > or =85 mm Hg on an average 44-hour ABPM.


RESULTS
Average ABP was 144 +/- 22/81 +/- 11 mm Hg. Seventy-three percent of the patients had systolic hypertension; 40% had diastolic hypertension, and 24% were normotensive or had well-controlled BP. Area under the curve of receiver operating characteristic (ROC) curves exceeded 80% for all BPs, but the thresholds for best sensitivity and specificity were markedly different for predialysis and postdialysis BPs. A two-week averaged predialysis BP of > 150/85 mm Hg or a postdialysis BP of > 130/75 mm Hg had at least 80% sensitivity in diagnosing hypertension. Specificity of at least 80% was achieved if predialysis BP of > 160/90 mm Hg or postdialysis BP of > 140/80 mm Hg was used. There was poor agreement between HD unit BP and ABP values.


CONCLUSIONS
HD unit BP values can be used to identify the presence or absence of hypertension, although prediction of ambulatory BPs from HD unit BP values cannot be made reliably in individual patients.
5428839
Blood pressure components and the risk for end-stage renal disease and death in chronic kidney disease.
BACKGROUND AND OBJECTIVES
Mean arterial pressure has been used in clinical trials in nephrology to randomly assign and treat patients, yet the pulsatile component of BP is recognized to influence outcomes in older people. I examined the unique contributions of systolic (SBP) and diastolic BP (DBP) on the risk for ESRD and death in patients with chronic kidney disease (CKD).


DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS
A single-center, prospective cohort study was conducted of 218 veterans with CKD (22% black, 4% women, mean age 68 yr, clinic BP 154.1 +/- 25.1/85.2 +/- 13.9 mmHg, 48% with diabetes).


RESULTS
During follow-up of up to 7 yr, 63 patients had ESRD and 102 patients died. Compared with those with controlled SBP (<130 mmHg), patients with moderate control (130 to 149 mmHg) had hazard ratio of 3.87 and those with poor control hazard ratio of 9.09 for ESRD. DBP had no direct ability to predict ESRD. For all-cause mortality, a J-shaped relationship was seen for SBP and an inverse relationship was seen for DBP. Considered jointly in the Cox model, a higher SBP and lower DBP improved the prediction of all-cause mortality compared with either BP component alone. The presence of J curve was especially pronounced in patients with advanced CKD, absence of clinical proteinuria, or age >65 yr.


CONCLUSIONS
In older patients with CKD, SBP predicts ESRD and a higher SBP and lower DBP predicts all-cause mortality. Lower BP of <110/70 mmHg is a marker of higher mortality in older individuals with advanced CKD.
5643940
Individualizing decision-making--resurrecting the doctor-patient relationship in the anemia debate.
Among patients with chronic kidney disease (CKD), erythropoiesis-stimulating agents (ESAs) are approved for avoiding transfusions, a risk that increases when hemoglobin (Hgb) falls to <10 g/dl. Transfusions increase sensitization, prolong the waiting time to and the likelihood of transplantation, and when transplantation is performed worsen graft survival. Accordingly, the risk of transfusion among those expecting transplantation is comparable to that of cardiovascular events. Nonetheless, targeting Hgb to >13 g/dl is associated with increased cardiovascular events. Paradoxically, if this level is achieved mortality is lower. The anemia paradox--higher cardiovascular events when targeting higher Hgb but lower events when patients achieve these targets--appears to be at least partially attributable to a hyporesponse to ESAs. Whether it is the ESAs or conditions that lead to the increased ESA dose that provokes morbidity cannot be answered definitively at present. The lowest ESA dose to achieve the desired level of anemia correction appears to be a safer strategy. In acute illnesses, reducing the dose of ESAs or stopping it altogether may aggravate anemia, but this may be permissible. The rate of rise in Hgb>1 g/dl in any 2-week period is associated with an increase in blood pressure (BP) and poor outcomes. Accordingly, while initiating and maintaining ESA therapy, monitoring BP at home twice daily is warranted. The clinical decision-making process in managing anemia should consider the risks of transfusion; kidney transplant potential; presence of cancer; and the risks of stroke, heart failure, and possibly death. Above all, clinical decision-making should incorporate patient preference.
23599085
A pilot randomized controlled trial of renal protection with pioglitazone in diabetic nephropathy.
BACKGROUND
Diabetic nephropathy progresses relentlessly to end-stage renal disease (ESRD). Animal experiments have found that peroxisome proliferator activated receptor-gamma (PPAR-gamma)-based therapy can have a glucose independent effect on renal protection. We hypothesized that PPAR-gamma-based antidiabetic therapy would result in greater reduction in proteinuria compared to sulfonylurea-based therapy.


METHODS
In 44 patients with overt diabetic nephropathy, an open-label, blinded end point trial was conducted in which subjects were randomized to either pioglitazone or glipizide to achieve similar glucose control. Proteinuria was assessed by two collections of 24-hour urine samples each month for 4 months.


RESULTS
The glipizide group had an adjusted mean increase in proteinuria of 6.1% (95% CI -11.7%, 23.8%), whereas the pioglitazone group had a reduction of 7.2% (95% CI -24.9%, 10.6%). The adjusted reduction with pioglitazone of 13.2% (95% CI -38.4%, 11.9%) was not statistically significant (P= 0.294). Baseline proteinuria, diastolic ambulatory blood pressure, and serum albumin concentration were independent predictors of reduction in proteinuria. The frequency and patterns of adverse events were similar in the two groups.


CONCLUSION
In patients with advanced diabetic nephropathy, we found no reduction in proteinuria over 4 months. These data are useful to design larger studies with longer duration of follow-up to demonstrate renal protection of PPAR-gamma agonists.
9892105
Evidence for multiple inducible cytochrome P450 isozymes in SENCAR mouse skin by pyridine.
Pyridine, an amphipathic solvent, is widely used in industry and is also a constituent of tobacco and its smoke. Since, in addition to inhalation and ingestion, pyridine is also readily absorbed through skin, we assessed the effect of skin application of pyridine on monooxygenase activities and cytochrome P450 (CYP) isozymes and CYP mRNA levels in the skin of SENCAR mice. Compared to controls, a single topical application of pyridine (30 or 50 mg/100 g body weight) resulted in induction of cutaneous 7-ethoxyresorufin O-deethylase, 7-pentoxyresorufin O-depentylase, and erythromycin N-demethylase activities. Pyridine treatment also resulted in an increase in reactivity with monoclonal antibodies directed against CYP 1A1, 2B1 and 3A. In Northern blot analysis, treatment of pyridine also showed a significant increase in mRNA for Cyp1a-1 in the skin. These data indicate that murine skin contains multiple inducible CYP isozymes, and that pyridine results in the induction of at least three families of CYP in murine skin.