Pleural fibrosis after practolol therapy.

Hall, Donna; Morrison, John; Edwards, F. Ronald

doi:10.1136/thx.33.6.822

Cited by 30 publications

(18 citation statements)

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“…They indicated that some beta-blockers cause not only peritoneal fibrosis but also pulmonary fibrosis, [16,17] suggesting that these medications damage both the mesothelium and pneumocytes [16,17]. Beta-blockers may inhibit mesothelial synthesis and release of surfactant, leading to damage of the peritoneal membrane.…”

Section: Discussionmentioning

confidence: 98%

Encapsulating peritoneal sclerosis: a single-center experience and review of the literature

et al. 2010

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Encapsulating peritoneal sclerosis (EPS) is a serious and often fatal complication of long-term PD with severe malnutrition and poor prognosis. It causes progressive obstruction and encapsulation of the bowel. This retrospective study reviews our experience and that reviewed in the literature concerning EPS. It refers to a total of 1966 patients treated with chronic PD between 1974 and 2008. Twenty one of them (1.1%) developed EPS, with the incidence increasing with the duration of PD. Mean age of our patients with EPS was 43, ranging from 18 to 71 years, 8 were men and 13 women with a mean body mass index (BMI) of 21.6 kg/m(2). Only one patient had Type II diabetes, 15 patients had glomerular disease, and six of these 15 had an autoimmune disease such as Wegener's granulomatosis and SLE. Thirteen patients developed EPS while on PD, 7 within 2 years after transfer to HD, and only one after renal transplantation. However, 7 patients had a previous renal transplant before returning to PD and subsequently developing EPS. Interestingly, we did not observe more episodes of EPS after transplantation. In the patients who developed EPS, the peritonitis rate over the period of observation was 1/15.6 pt-months and was due to Staphylococcus aureus, coagulase-negative staphylococcus, Pseudomonas and fungi. A history of peritonitis was not a prerequisite for developing EPS, since one patient had no episodes of peritonitis and 4 had just one previous episode. Fifteen patients presented with peritonitis within 4 months before the diagnosis of EPS with particularly virulent micro-organisms such as S. aureus, Candida, Pseudomonas, Corynebacterium, and Peptostreptococcus. Eleven patients were treated with hypertonic dextrose solutions (4.25 g/dl of dextrose) and seven with icodextrin, indirectly suggesting problems with ultrafiltration. Nine of 21 patients were on beta-blockers. The diagnosis of EPS was made either surgically or radiologically with signs of small bowel obstruction in combination with severe malnutrition. Eleven of our patients (52%) had evidence of small bowel obstruction and 14 patients required total parenteral nutrition (TPN). Tamoxifen (10-20 mg daily) was started in 6 patients, 4 of whom are alive and 2 deceased 3 and 5 years after EPS was diagnosed. Of the 12 patients who were not given tamoxifen, 2 are alive and 10 died. No side effects of tamoxifen were reported. Only 7 of our patients (33%) died during the first year after the diagnosis of EPS. Currently, 4 patients are on HD and 3 have had a renal transplant. Six patients of the fourteen who underwent surgery (42.8%) died within the first 6 months after operation and five died after an average of 6.6 years, mostly due to cardiovascular causes, three are still alive. As EPS becomes more prevalent with longer duration of PD, large multicenter prospective studies are needed to establish its incidence and identify risk factors, therapeutic approach, and prognosis.

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Section: Discussionmentioning

confidence: 98%

Encapsulating peritoneal sclerosis: a single-center experience and review of the literature

et al. 2010

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“…Others report an interstitial pneumonitis with fibrosis [9, 16]or a subacute interstitial pneumonitis [12]. Concomitant pleurisy [7, 17], or pleural fibrosis [18]have also been found. In some cases, pleuro-pulmonary involvement is seen in the context of drug-induced systemic lupus erythematosus [7, 10, 15, 19].…”

Section: Discussionmentioning

confidence: 99%

“…Although other reactions involving the lung parenchyma or the pleura are quite unusual [21], some cases of hypersensitivity pneumonitis have been attributed to almost all β-blockers: propranolol [2, 3, 4], acebutolol [5, 6, 7, 8], pindolol [9, 10], nadolol [11], atenolol [12], sotalol [13], celiprolol [14], betaxolol [15]. Indeed, one of these drugs, practolol, was withdrawn from therapeutic use because of pleuropulmonary adverse reactions, pericardial fibrosis and additional extrapulmonary problems [16, 17, 18]. Labetalol, a combined α- and β-blocker, has also been reported as a cause of drug-induced diffuse interstitial pulmonary fibrosis with lymphocytic and neutrophilic alveolitis in BAL [20].…”

Section: Discussionmentioning

confidence: 99%

“…It is a relatively novel agent that has been utilized in recent years in the treatment of hypertension, coronary artery disease and heart failure [1]. Although there are many reports of drug-induced pneumonitis caused by β-blockers [2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19]or by drugs with combined β- and α-blockade activity [20], no such reactions have been attributed to carvedilol up to now. This is the first report of pneumonitis caused by carvedilol.…”

Section: Introductionmentioning

confidence: 99%

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A Case of Drug-Induced Pneumonitis Caused by Carvedilol

et al. 2004

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“…In experimental animals [17], ␤-blockers inhibit surfactant release from type II pneumocytes. A change in surfactant production could damage serous membranes throughout the body: in fact, pleural fibrosis, pericarditis, and joint effusions have been documented in 25% of patients with SP due to practolol [18]. Moreover, ␤-blockers in PD patients induce a decrease in ultrafiltration, irrespective of SP [19].…”

Section: Etiology and Pathogenesismentioning

confidence: 99%

Fibrosis and Sclerosis: Different Disorders or Different Stages?

Garosi

Cappelletti

Paolo³

2006

Contributions to Nephrology

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Peritoneal sclerosis is very common in peritoneal dialysis (PD) patients. It can vary from the mild, clinically silent sclerosis always present after years of PD, to rare but dramatic and often fatal cases. In our opinion, peritoneal sclerosis is a single disorder, so its variable manifestations are different stages of one nosological entity: this opinion relies mainly on strong connections in pathophysiology. In our view, the frequency, pathology, animal models, etiology and pathogenesis often show a bimodal configuration with suggests that peritoneal sclerosis is actually two distinct nosological entities: simple sclerosis and sclerosing peritonitis. The former is very frequent, with minor anatomical alterations and low clinical impact; it is reproducible in animals by means of PD, and is clearly due to the poor biocompatibility of PD. The latter is rare, with radical anatomical alterations and high mortality; it can only be reproduced in animal models by means other than PD and seems to be due to factors both related and unrelated to PD.

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Pleural fibrosis after practolol therapy.

Cited by 30 publications

References 1 publication

Encapsulating peritoneal sclerosis: a single-center experience and review of the literature

Encapsulating peritoneal sclerosis: a single-center experience and review of the literature

A Case of Drug-Induced Pneumonitis Caused by Carvedilol

Fibrosis and Sclerosis: Different Disorders or Different Stages?

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