Lanreotide Reduces Liver Growth In Patients With Autosomal Dominant Polycystic Liver and Kidney Disease

Aerts, R; Kievit, Wietske; D’Agnolo, Hedwig M. A.; Blijdorp, Charles J.; Casteleijn, Niek F.; Dekker, Shosha E.I.; Fijter, Johan W. de; Gastel, Maatje D A van; Gevers, Tom J.G.; Laarschot, Liyanne F. M. van de; Lantinga, Marten A.; Losekoot, Monique; Meijer, Esther; Messchendorp, A. Lianne; Neijenhuis, Myrte K.; Pena, Michelle J; Peters, Dorien J.M.; Salih, Mahdi; Soonawala, Darius; Spithoven, Edwin M.; Visser, Folkert W.; Wetzels, Jack F.M.; Zietse, Robert; Gansevoort, Ron T.; Drenth, Joost P.H.

doi:10.1053/j.gastro.2019.04.018

Cited by 47 publications

(66 citation statements)

References 32 publications

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“…Of these, four included ADPKD patients alone25–28 and the remaining two included patients with PLD and ADPKD, but provided a subset of data for ADPKD patients when measuring renal function and TKV 23 24. A further three publications were included as they were secondary analyses of previous studies,29–31 all of which were investigating the change in TLV for a subset of patients with PLD in a post-hoc analysis. Excluding patient numbers from secondary analysis, a total of 592 patients were included.…”

Section: Resultsmentioning

confidence: 99%

“…Notable bias was detected in blinding for several studies. In ALADIN 2013 (and Pisani et al 30), physicians and staff were not blinded to patient allocation groups, and DIPAK-1 (and van Aerts et al 29) was an open-label study: therefore, both had a high risk of bias for blinding of participants. All studies except Ruggenentti et al 28 reported that TKV and TLV measurements were performed by blinded personnel.…”

Section: Resultsmentioning

confidence: 99%

“…All studies except Ruggenentti et al 28 reported that TKV and TLV measurements were performed by blinded personnel. DIPAK-1 and the subsequent secondary analysis by van Aerts et al 29 did not report final TKV and TLV (although they did report absolute and percentage changes and changes from baseline in TKV and TLV), resulting in a high risk of bias for selective reporting. Visual inspection of funnel plots did not reveal significant publication bias (online supplementary figure 1A-C).…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, several studies have commented that the benefits of somatostatin treatment may persist after treatment cessation. Indeed, Pisani et al reported that a residual volume reduction remained up to 5 years after treatment had ended and van Aerts et al reported TLV improvement throughout the 4-month washout period (long after the 28-day half-life of lanreotide) 29 30. These results suggest that somatostatin analogue treatment could confer a long-term benefit on TLV in patients with PLD.…”

Section: Discussionmentioning

confidence: 96%

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Long-acting somatostatin analogue treatments in autosomal dominant polycystic kidney disease and polycystic liver disease: a systematic review and meta-analysis

2020

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ObjectivesA number of randomised control trials (RCTs) investigating the effects of long-acting somatostatin analogues in autosomal dominant polycystic kidney disease (ADPKD) and polycystic liver disease (PLD) have been recently reported. We sought to evaluate all available RCTs investigating the efficacy of somatostatin analogues treatment in ADPKD and PLD.Data sourcesElectronic databases; Pubmed, Clincaltrials.gov and Cochrane Central Register of Controlled TrialsEligibility criteria for selecting studiesRCTs and randomised cross-over trials comparing the effects of somatostatin analogue treatment with controls in patients with ADPKD or PLD.Data extraction and synthesisData extraction and bias assessments were performed by two independent reviewers between January and May 2019. Outcomes assessed included estimated glomerular filtration rate (eGFR), total kidney volume (TKV), total liver volume (TLV), progression to end stage renal failure (ESRF) and adverse effects. Data were pooled using a random-effects model and reported as relative risk or mean difference with 95% CIs.ResultsMeta-analysis was performed of six RCTs or randomised cross-over trials and three secondary analyses. A total of 592 patients were included. Compared with controls, somatostatin analogue treatment significantly reduced TLV (mean difference −0.15 L, 95% CI −0.26 to −0.03, p=0.01). There was no significant effect on TKV (mean difference −0.19 L, 95% CI −0.50 to 0.12, p=0.23) or eGFR (mean difference 0.27 mL/min/1.73 m2, 95% CI −2.03 to 2.57, p=0.82). There was no effect on progression to ESRF. Somatostatin analogues were associated with known adverse effects such as gastrointestinal symptoms.ConclusionsThe available RCT data show improvement in TLV with somatostatin analogue treatment. There was no benefit to TKV or eGFR in patients with ADPKD, while being associated with various side effects. Further studies are needed to assess potential benefit in reducing cyst burden in patients with PLD.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 96%

See 2 more Smart Citations

Long-acting somatostatin analogue treatments in autosomal dominant polycystic kidney disease and polycystic liver disease: a systematic review and meta-analysis

2020

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“…These studies did not observe any beneficial effect on the estimated glomerular filtration rate (eGFR) decline, but one trial documented that fewer patients progressed from chronic kidney disease stage 4 to stage 5 [27]. Similarly, lanreotide reduced both hepatic and renal cyst growth in ADPLD and ADPKD patients in several large studies [3,[28][29][30]. As total kidney volume (TKV) predicts disease progression in ADPKD, it was assumed that preventing renal cyst growth would also prevent eGFR decline [31].…”

Section: Somatostatin Analoguesmentioning

confidence: 99%

New insights into targeting hepatic cystogenesis in autosomal dominant polycystic liver and kidney disease

Barten

Bernts

Drenth

et al. 2020

Expert Opinion on Therapeutic Targets

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Introduction: Polycystic liver disease (PLD) is a rare disease defined by the growth of hepatic cysts and occurs either isolated or as an extrarenal manifestation of polycystic kidney disease. While surgery has been the mainstay in treatment of symptomatic PLD, recently discovered regulatory mechanisms affecting hepatic cystogenesis provide potential new therapies to reduce hepatic cyst burden. Areas covered: This review summarizes intracellular pathways and therapeutic targets involved in hepatic cystogenesis. While drugs that target cAMP, mTOR and bile acids were evaluated in clinical trials, investigation in autophagy, Wnt and miRNA signaling pathways are still in the pre-clinical phase. Recent epidemiological data present female hormones as a promising therapeutic target. Additionally, therapeutic advances in renal cystogenesis are reviewed for their potential application in treatment of hepatic cysts. Expert opinion: Further elucidation of the pathophysiology of hepatic cystogenesis is needed to provide additional targets and improve the efficacy of current treatments. The most promising therapeutic target in PLD is the female hormone pathway, given the increased severity in women and the harmful effects of exogenous estrogens. In addition, combining current pharmaceutical and surgical therapies can lead to improved outcomes. Lastly, the rarity of PLD creates the need to share expertise internationally.

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Cystic diseases of the liver and biliary tract

Buxbaum¹,

Lu²

2022

Yamada's Textbook of Gastroenterology

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Lanreotide Reduces Liver Growth In Patients With Autosomal Dominant Polycystic Liver and Kidney Disease

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Cited by 47 publications

References 32 publications

Long-acting somatostatin analogue treatments in autosomal dominant polycystic kidney disease and polycystic liver disease: a systematic review and meta-analysis

Long-acting somatostatin analogue treatments in autosomal dominant polycystic kidney disease and polycystic liver disease: a systematic review and meta-analysis

New insights into targeting hepatic cystogenesis in autosomal dominant polycystic liver and kidney disease

Cystic diseases of the liver and biliary tract

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