Retroperitoneal fibrosis after treatment with atenolol.

Doherty, C C; McGeown, Mary G.; Donaldson, R. A.

doi:10.1136/bmj.2.6154.1786-b

Cited by 26 publications

(10 citation statements)

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“…This finding is consistent with IBMX serving to mainitain a higher intracellular cANMP content throtugh its inhibition of phosphodiesterase, and further clemiioni- The finding that the ,8-blocker l-propranolol can block the effect of 8-agonists on collagen production not only supports the conclusion that the f8-adrenergic receptor-adenylate cyclase system regulates collagen production, but also may have important pharmacological consequences for the regulation of collagen production in the body. All of the 3-blocking agents that have been used clinically, including propranolol, practolol, metoprolol, timolol, and atenolol, have been reported to cause fibrosis (21)(22)(23)(24)(25)(26). Since the concentration of propranolol used in these experiments was similar to that which is effective in vivo (27) …”

Section: Discussionmentioning

confidence: 83%

Regulation of Collagen Production by the β-Adrenergic System

Berg¹,

Moss²,

Baum³

et al. 1981

J. Clin. Invest.

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A B S T R A C T The suppression of collagen production by increasing the cyclic (c)AMP content ofcultured cells was examined vis-a-vis the f3-adrenergic system. Cultured human fetal lung fibroblasts incubated for 6 h with the f-agonists isoproterenol or epinephrine produced -30% less collagen per cell than in the absence of the hormones. To demonstrate that the ,B-agonists were operating by their interaction with the ,8-receptor to stimulate adenylate cyclase to increase the intracellular content of cAMP, d-and l-isoproterenol were incubated separately with the cultured cells. Only l-isoproterenol increased intracellular cAMP and decreased collagen production. While 20 nM l-isoproterenol was effective, the d-isomer was ineffective even at 2,M. An increase in cAMP from 40 to 73 pmol/mg protein was effective in suppressing collagen production; increasing the cAMP content to much higher levels had little additional effect on collagen production. 3-Isobutyl-l-methylxanthine, an analog of theophylline that inhibits phosphodiesterase, potentiated the effect of isoproterenol in suppressing collagen production. Further support for the concept that isoproterenol suppressed collagen production by acting through the ,8-receptor was provided by the finding that only the i-isomer of propranolol, a ,8-blocker, was effective in blocking both the increase in intracellular cAMP and the suppression of collagen production caused by isoproterenol. These results demonstrate that collagen production in human fibroblasts can be regulated by the 18-adrenergic system and indicate that when the cAMP content is increased beyond a threshold value, collagen production is suppressed. Since collagen production is sensitive to the small changes of Received for publication 29 May 1980 and in revised form 26 November 1980. in cultured cells, the results point to a possibly important mechanism for the regulation of collagen production in the body. INTRODUCTION Collagen is the major extracellular protein in connective tissues and is present to varying extents in all organs of the body (1-3). In most organs, fibroblasts are the major collagen-producing cells. Normally, fibroblasts from tissues such as skin and lung rigidly control the quantity of collagen they produce at 2-4% of their total protein production (4-6). It is known, however, that collagen production by fibroblasts can be influenced by numerous environmental factors, including hormones, metabolites, and pharmacologic agents (7-10). In addition, recent studies have shown that prostaglandins and cholera toxin dramatically elevate fibroblast cyclic AMP content and suppress collagen production in fibroblasts (11).In vivo, the cyclic AMP content of cells is controlled, in part, by the 1-adrenergic system (12). Since collagen production by fibroblasts has been shown to be inversely correlated with the cyclic AMP Serum Co., Denver, Colo.), penicillin 100 U/ml, streptomycin 100,ug/ml (both from Grand Island Biological, Grand Island, N. Y.), and 0.06% glutamine as previously described (6,...

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Section: Discussionmentioning

confidence: 83%

Regulation of Collagen Production by the β-Adrenergic System

Berg¹,

Moss²,

Baum³

et al. 1981

J. Clin. Invest.

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“…After excluding duplicates and screening for eligibility of 424 initial hits in our electronic search, 31 full‐text articles were retrieved for scrutiny (Figure 2). This resulted in 18 case reports for inclusion in this study 10–27 . No additional cases were identified in the manual searches through references.…”

Section: Resultsmentioning

confidence: 99%

Retroperitoneal fibrosis and β‐blocking agents: Is there an association?

Kharagjitsing

Eekeren

Puijenbroek

et al. 2021

Brit J Clinical Pharma

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Aims Retroperitoneal fibrosis (RPF) is a rare chronic fibro‐inflammatory disorder that may be secondary to certain drugs, including β‐blocking agents (BBAs). However, their causative role is unclear. We aimed to investigate this association. Methods Disproportionality analysis was carried out on cases from 1985 to 4 October 2020 in VigiBase, the World Health Organization pharmacovigilance database. The Bayesian‐based IC025 metric and reporting odds ratio were used in order to assess the adverse event signal. We also analysed all published case reports from the literature regarding BBA‐associated RPF to assess the value of suggested supportive clinical evidence. Results In total, 1599 individual case safety reports of RPF were reported to VigiBase, of which 132 (32%) concerned 16 different single BBA. For 12 of these agents (75%), reporting of RPF was disproportionate, indicating a potential safety signal. Line listing analysis of individual case safety reports showed no consistent time interval from start of BBA to RPF diagnosis (range 0.7–264 mo). Dechallenge was negative or unknown in the majority of cases (74%). In 18 published cases from the literature, time from start of BBA to RPF diagnosis varied widely (range 3–156 mo). BBA were discontinued 6 months before (n = 1) or at the time of RPF diagnosis (n = 17). Most patients (84%) also received RPF specific treatment. Follow‐up duration was short (median 5 mo [range 1–24 mo]) and in most cases (83%) relevant follow‐up data were lacking. Conclusion Although disproportionality analysis indicated a potential safety signal for RPF associated with BBAs, clinical evidence did not support a cause‐and‐effect relationship.

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“…The association between beta-blockers and RPF is currently not well established. Various cases were published in the 70s-80s (28)(29)(30). Some authors suggested that beta-blockers were probably being used to treat hypertension associated with RPF rather than to induce directly RPF (31).…”

Section: Discussionmentioning

confidence: 99%