***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Symptoms in polycystic liver disease ( PLD ) are thought to be caused by compression of organs and structures by the enlarged liver . Aim The aim of this article is to assess the impact of liver volume on symptoms and quality of life ( QoL ) in PLD . Methods We included PLD patients from two prospect i ve studies that used the PLD- question naire ( PLD-Q ) for symptom assessment .  QoL was assessed through SF-36 , summarized in a physical ( PCS ) and mental ( MCS ) component score . Liver volume was correlated with PLD-Q total scores . Patients were classified based on height-corrected liver volume in mild ( < 1600 ml ) , moderate ( 1600–3200 ml ) , and severe ( > 3200 ml ) disease . PLD-Q and QoL ( PCS and MCS ) scores were compared across disease stages . Results We included 82 of 131 patients from the original studies ( disease stages ; mild n = 26 , moderate n = 33 , and severe n = 23 ) . Patients with larger liver volume reported higher symptom burden ( r = 0.516 , p < 0.001 ) . Symptom scores increased with disease progression , except for abdominal pain ( p = 0.088 ) . PCS decreased with advancing disease ( p < 0.001 ) , in contrast to MCS ( p = 0.055 ) . Moderate ( p = 0.007 ) and severe ( p < 0.001 ) PLD patients had lower PCS scores than the general population . Conclusion PLD with larger liver volume is more likely to be symptomatic and is associated with lower BACKGROUND & AIMS Therapy for polycystic liver is invasive , expensive , and has disappointing long-term results . Treatment with somatostatin analogues slowed kidney growth in patients with polycystic kidney disease ( PKD ) and reduced liver and kidney volume in a PKD rodent model . We evaluated the effects of lanreotide , a somatostatin analogue , in patients with polycystic liver because of autosomal-dominant ( AD ) PKD or autosomal-dominant polycystic liver disease ( PCLD ) . METHODS We performed a r and omized , double-blind , placebo-controlled trial in 2 tertiary referral centers . Patients with polycystic liver ( n = 54 ) were r and omly assigned to groups given lanreotide ( 120 mg ) or placebo , administered every 28 days for 24 weeks . The primary end point was the difference in total liver volume , measured by computerized tomography at weeks 0 and 24 . Analyses were performed on an intention-to-treat basis . RESULTS Baseline characteristics were comparable for both groups , except that more patients with ADPKD were assigned to the placebo group ( P = .03 ) . The mean liver volume decreased 2.9 % , from 4606 mL ( 95 % confidence interval ( CI ) : 547 - 8665 ) to 4471 mL ( 95 % CI : 542 - 8401 mL ) , in patients given lanreotide . In the placebo group , the mean liver volume increased 1.6 % , from 4689 mL ( 95 % CI : 613 - 8765 mL ) to 4895 mL ( 95 % CI : 739 - 9053 mL ) ( P < .01 ) . Post hoc stratification for patients with ADPKD or PCLD revealed similar changes in liver volume , with statistically significant differences in patients given lanreotide ( P < .01 for both diseases ) . CONCLUSIONS In patients with polycystic liver , 6 months of treatment with lanreotide reduces liver volume There are no proven , effective therapies for polycystic kidney disease ( PKD ) or polycystic liver disease ( PLD ) . We enrolled 42 patients with severe PLD result ing from autosomal dominant PKD ( ADPKD ) or autosomal dominant PLD ( ADPLD ) in a r and omized , double-blind , placebo-controlled trial of octreotide , a long-acting somatostatin analogue . We r and omly assigned 42 patients in a 2:1 ratio to octreotide LAR depot ( up to 40 mg every 28+/-5 days ) or placebo for 1 year . The primary end point was percent change in liver volume from baseline to 1 year , measured by MRI . Secondary end points were changes in total kidney volume , GFR , quality of life , safety , vital signs , and clinical laboratory tests .  Thirty-four patients had ADPKD , and eight had ADPLD .  Liver volume decreased by 4.95%+/-6.77 % in the octreotide group but remained practically unchanged ( + 0.92%+/-8.33 % ) in the placebo group ( P=0.048 ) . Among patients with ADPKD , total kidney volume remained practically unchanged ( + 0.25%+/-7.53 % ) in the octreotide group but increased by 8.61%+/-10.07 % in the placebo group ( P=0.045 ) . Changes in GFR were similar in both groups . Octreotide was well tolerated ; treated individuals reported an improved perception of bodily pain and physical activity . In summary , octreotide slowed the progressive increase in liver volume and total kidney volume , improved health perception among  patients with PLD , and had an acceptable side effect profile BACKGROUND The course of autosomal dominant polycystic kidney disease ( ADPKD ) is often associated with pain , hypertension , and kidney failure . Pre clinical studies indicated that vasopressin V(2)-receptor antagonists inhibit cyst growth and slow the decline of kidney function . METHODS In this phase 3 , multicenter , double-blind , placebo-controlled , 3-year trial , we r and omly assigned 1445 patients , 18 to 50 years of age , who had ADPKD with a total kidney volume of 750 ml or more and an estimated creatinine clearance of 60 ml per minute or more , in a 2:1 ratio to receive tolvaptan , a V(2)-receptor antagonist , at the highest of three twice-daily dose regimens that the patient found tolerable , or placebo . The primary outcome was the annual rate of change in the total kidney volume . Sequential secondary end points included a composite of time to clinical progression ( defined as worsening kidney function , kidney pain , hypertension , and albuminuria ) and rate of kidney-function decline . RESULTS Over a 3-year period , the increase in total kidney volume in the tolvaptan group was 2.8 % per year ( 95 % confidence interval [ CI ] , 2.5 to 3.1 ) , versus 5.5 % per year in the placebo group ( 95 % CI , 5.1 to 6.0 ; P<0.001 ) . The composite end point favored tolvaptan over placebo ( 44 vs. 50 events per 100 follow-up-years , P=0.01 ) , with lower rates of worsening kidney function ( 2 vs. 5 events per 100 person-years of follow-up , P<0.001 ) and kidney pain ( 5 vs. 7 events per 100 person-years of follow-up , P=0.007 ) . Tolvaptan was associated with a slower decline in kidney function ( reciprocal of the serum creatinine level , -2.61 [ mg per milliliter](-1 ) per year vs. -3.81 [ mg per milliliter](-1 ) per year ; P<0.001 ) . There were fewer ADPKD-related adverse events in the tolvaptan group but more events related to aquaresis ( excretion of electrolyte-free water ) and hepatic adverse events unrelated to ADPKD , contributing to a higher discontinuation rate ( 23 % , vs. 14 % in the placebo group ) . CONCLUSIONS Tolvaptan , as compared with placebo , slowed the increase in total kidney volume and the decline in kidney function over a 3-year period in patients with ADPKD but was associated with a higher discontinuation rate , owing to adverse events . ( Funded by Otsuka Pharmaceuticals and Otsuka Pharmaceutical Development and Commercialization ; TEMPO 3:4 Clinical Trials.gov number , NCT00428948 . ) BACKGROUND AND OBJECTIVES No medical treatment is available for polycystic liver disease , a frequent manifestation of autosomal-dominant polycystic kidney disease ( ADPKD ) . In a prospect i ve , r and omized , double-blind , crossover study , 6 months of octreotide ( 40 mg every 28 days ) therapy limited kidney volume growth more effectively than placebo in 12 patients with ADPKD . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS In this secondary , post hoc analysis of the above study , octreotide-induced  changes in liver volumes compared with placebo and the relationship between concomitant changes in liver and kidney volumes were evaluated . Those analyzing liver and kidney volumes were blinded to treatment . RESULTS Liver volumes significantly decreased from 1595 + /- 478 ml to 1524 + /- 453 ml with octreotide whereas they did not appreciably change with placebo .  Changes in liver volumes were significantly different between the two treatment periods ( -71 + /- 57 ml versus + 14 + /- 85 ml ) .  Octreotide-induced liver volume reduction was fully explained by a reduction in parenchyma volume from 1506 + /- 431 ml to 1432 + /- 403 ml . Changes in liver volumes were significantly correlated with concomitant changes in kidney volumes ( r = 0.67 ) during octreotide but not during placebo treatment . Liver and kidney volume changes significantly differed with both treatments ( octreotide : -71 + /- 57 ml versus + 71 + /- 107 ; placebo : + 14 + /- 85 ml versus + 162 + /- 114 ) , but net reductions in liver ( -85 + /- 103 ml ) and kidney ( -91 + /- 125 ml ) volume growth on octreotide versus placebo were similar . CONCLUSIONS Octreotide therapy reduces liver volumes in patients with ADPKD and is safe Background In a previous trial involving patients with early autosomal dominant polycystic kidney disease ( ADPKD ; estimated creatinine clearance , ≥60 ml per minute ) , the vasopressin V2‐receptor antagonist tolvaptan slowed the growth in total kidney volume and the decline in the estimated glomerular filtration rate ( GFR ) but also caused more elevations in aminotransferase and bilirubin levels . The efficacy and safety of tolvaptan in patients with later‐stage ADPKD are unknown . Methods We conducted a phase 3 , r and omized withdrawal , multicenter , placebo‐controlled , double‐blind trial . After an 8‐week prer and omization period that included sequential placebo and tolvaptan run‐in phases , during which each patient 's ability to take tolvaptan without dose‐limiting side effects was assessed , 1370 patients with ADPKD who were either 18 to 55 years of age with an estimated GFR of 25 to 65 ml per minute per 1.73 m2 of body‐surface area or 56 to 65 years of age with an estimated GFR of 25 to 44 ml per minute per 1.73 m2 were r and omly assigned in a 1:1 ratio to receive tolvaptan or placebo for 12 months . The primary end point was the change in the estimated GFR from baseline to follow‐up , with adjustment for the exact duration that each patient participated ( interpolated to 1 year ) . Safety assessment s were conducted monthly . Results The change from baseline in the estimated GFR was ‐2.34 ml per minute per 1.73 m2 ( 95 % confidence interval [ CI ] , ‐2.81 to ‐1.87 ) in the tolvaptan group , as compared with ‐3.61 ml per minute per 1.73 m2 ( 95 % CI , ‐4.08 to ‐3.14 ) in the placebo group ( difference , 1.27 ml per minute per 1.73 m2 ; 95 % CI , 0.86 to 1.68 ; P<0.001 ) . Elevations in the alanine aminotransferase level ( to > 3 times the upper limit of the normal range ) occurred in 38 of 681 patients ( 5.6 % ) in the tolvaptan group and in 8 of 685 ( 1.2 % ) in the placebo group . Elevations in the aminotransferase level were reversible after stopping tolvaptan . No elevations in the bilirubin level of more than twice the upper limit of the normal range were detected . Conclusions Tolvaptan result ed in a slower decline than placebo in the estimated GFR over a 1‐year period in patients with later‐stage ADPKD . ( Funded by Otsuka Pharmaceuticals and Otsuka Pharmaceutical Development and Commercialization ; REPRISE Clinical Trials.gov number , NCT02160145 . BACKGROUND & 
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There was no effect on progression to ESRF  .
Somatostatin analogues were associated with known adverse effects such as gastrointestinal symptoms .
Conclusions The 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 .