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We recently documented an unexpectedly high prevalence of mitral valve prolapse, a connective tissue disorder, in sickle cell discase. To investigate this association, skin biopsies were analyzed from 32 sickle cell disease patients, 11 of whom had mitral prolapse. Total and type III collagen, collagen solubility, and uronic acid were not different between the patients with or without mitral prolapse (p > 0.05). Computerized morphometric quantitation of the volume fraction of elastic fibers was greater in sickle cell disease patients than in 10 normals (3.1 ± 0.1 mean ± SEM vs 2.0 ± 0.3%; p < 0.01) but less than in three patients with pseudoxanthoma elasticum (9.7 0.6%; p < 0.001). Desmosine radioimmunoassay (an index of elastic fibers) was greater in sickle cell disease patients with mitral prolapse than those without (239.3 ± 9.3 vs 171.7 ± 25.4 ng\u002Fmg wet weight; p < 0.02). Histopathologic grading showed a similar trend (p = 0.07). The combined probabilities of these three independent tests of elastic fiber quantity showed an increased elastic fiber concentration in mitral prolapse patients compared to those without mitral prolapse (p < 0.02). Thus, there is no evidence for a specific collagen defect; rather, sickle cell disease appears to be associated with a spectrum of elastic tissue disorders, a feature that could predispose to mitral valve prolapse.\u003C\u002Fjats:p>",{"EN":1411},"Mitral valve prolapse in sickle cell disease: Manifestation of a generalized connective tissue disorder",{"VOID":1413},"3985003",{"VOID":1415},"10.1002\u002Fajh.2830190102",[114],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fajh.2830190102",[1419,1438,1453,1468,1485,1510,1527],{"id":1420,"sortIndex":25,"researcher":24,"roles":1421,"affiliations":1422,"properties":1431},"6a6bffe3-b3f0-4e9d-8e44-58cad7b7ab46",[],[1423],{"id":1424,"sortIndex":25,"affiliation":1425,"properties":24},"eb41d826-6814-4c6a-a772-7fc7cf23263d",{"id":1424,"createTime":24,"updateTime":24,"relativeEntities":1426,"slug":24,"properties":1427,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1430,"statistic":24},[],{"title":1428},{"EN":1429},"Departments of Medicine, Harbor-UCLA Medical Center, UCLA School of Medicine, Torrance, California",[],{"orcid":1432,"title":1434,"openalex":1436},{"VOID":1433},"https:\u002F\u002Forcid.org\u002F0000-0002-1643-4124",{"EN":1435},"Scott M. 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An etiologic and pathogenic enigma, Arch Pathol Lab Med, 106, 369",{},{"id":24,"text":1651,"url":24,"identifiers":1652},"Frable WJ, 1969, Mucinous degeneration of the cardiac valves. The “floppy valve” syndrome, J Thorac Cardiovasc Surg, 58, 62, 10.1016\u002FS0022-5223(19)42629-9",{"doi":1653},"10.1016\u002FS0022-5223(19)42629-9",{"id":24,"text":1655,"url":24,"identifiers":1656},"Robbins SL, 1979, Pathologic Basis of Disease, 703",{},{"id":24,"text":1658,"url":24,"identifiers":1659},"10.1161\u002F01.CIR.64.1.121",{"doi":1658},{"id":24,"text":1661,"url":24,"identifiers":1662},"LippmanSM GinztonLE ThigpenT TanakaKR LaksMM: Mitral valve prolapse in sickle cell disease: Presumptive evidence for a linked connective tissue disorder.Arch Int Med 1985(in press).",{"doi":1663},"10.1001\u002Farchinte.1985.00360030067014",{"id":24,"text":1665,"url":24,"identifiers":1666},"10.1016\u002FS0002-9149(77)80100-8",{"doi":1665},{"id":24,"text":1668,"url":24,"identifiers":1669},"10.1016\u002F0002-9149(82)90027-3",{"doi":1668},{"id":24,"text":1671,"url":24,"identifiers":1672},"10.1056\u002FNEJM197605132942004",{"doi":1671},{"id":24,"text":1674,"url":24,"identifiers":1675},"10.1161\u002F01.CIR.53.3.464",{"doi":1674},{"id":24,"text":1677,"url":24,"identifiers":1678},"10.1016\u002F0003-2697(67)90160-1",{"doi":1677},{"id":24,"text":1680,"url":24,"identifiers":1681},"10.1016\u002FS0006-291X(76)80180-5",{"doi":1680},{"id":24,"text":1683,"url":24,"identifiers":1684},"Bittar T, 1962, A modified uronic acid carbazole reaction, Anal Biochem, 4, 330, 10.1016\u002F0003-2697(62)90095-7",{"doi":1685},"10.1016\u002F0003-2697(62)90095-7",{"id":24,"text":1687,"url":24,"identifiers":1688},"10.3109\u002F03008208009152362",{"doi":1687},{"id":24,"text":1690,"url":24,"identifiers":1691},"Uitto J, 1983, Elastic fibers in human skin: Quantitation of elastic fibers by computerized digital image analyses and determination of elastin by radioimmu noassay of desmosine, Lab Invest, 49, 499",{},{"id":24,"text":1693,"url":24,"identifiers":1694},"Dixon WJ, 1983, BMDP Statistical Software",{},{"id":24,"text":1696,"url":24,"identifiers":1697},"Fisher RA, 1932, Statistical Methods for Research Workers, 99",{},{"id":24,"text":1699,"url":24,"identifiers":1700},"Brown OR, 1975, Incidence of mitral valve prolapse in the asymptomatic normal (abstract), Circulation, 52, 11",{},{"id":24,"text":1702,"url":24,"identifiers":1703},"10.1378\u002Fchest.75.5.555",{"doi":1702},{"id":24,"text":1705,"url":24,"identifiers":1706},"Criley JM, 1979, Congenital Heart Disease in Adults, 213",{},{"id":24,"text":1708,"url":24,"identifiers":1709},"10.1136\u002Fhrt.38.7.718",{"doi":1708},{"id":24,"text":1711,"url":24,"identifiers":1712},"10.1016\u002F0002-9343(76)90568-4",{"doi":1711},{"id":24,"text":1714,"url":24,"identifiers":1715},"10.1016\u002F0002-9149(83)90208-4",{"doi":1714},{"id":24,"text":1717,"url":24,"identifiers":1718},"10.1136\u002Fbjo.60.1.31",{"doi":1717},{"id":24,"text":1720,"url":24,"identifiers":1721},"10.1111\u002F1523-1747.ep12546063",{"doi":1720},{"id":24,"text":1723,"url":24,"identifiers":1724},"Brown FR, 1982, Cutis laxa, Johns Hopkins Med J, 150, 148",{},{"id":24,"text":1726,"url":24,"identifiers":1727},"10.1146\u002Fannurev.bi.49.070180.004521",{"doi":1726},{"id":24,"text":1729,"url":24,"identifiers":1730},"10.1016\u002FS0140-6736(80)91382-3",{"doi":1729},{"id":24,"text":1732,"url":24,"identifiers":1733},"Davies MJ, 1981, Collagen synthesis in floppy mitral valve, Br Heart J, 45, 345",{},{"id":24,"text":1735,"url":24,"identifiers":1736},"Ryhanen L, 1983, Biochemistry and Physiology of the Skin, 433",{},{"id":24,"text":1738,"url":24,"identifiers":1739},"10.1073\u002Fpnas.75.3.1456",{"doi":1738},{"id":24,"text":1741,"url":24,"identifiers":1742},"10.1073\u002Fpnas.79.21.6627",{"doi":1741},{"id":24,"text":1744,"url":24,"identifiers":1745},"SandbergLB DavidsonJM:Elastin and its gene. Peptide Prot Rev 1984(in press).",{},{"id":1747,"createTime":1748,"updateTime":1748,"relativeEntities":1749,"slug":1750,"properties":1751,"entityType":109,"verifyStatus":110,"verifyTime":1748,"verifyNote":112,"languages":1762,"translateLanguages":24,"viewCount":25,"primaryUrl":1763,"fullTextUrl":24,"authors":1764,"publicationType":286,"publisherRelationship":2029,"citationCount":2075,"citationInfo":2076,"publishDate":2079,"publishYear":2077,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2080,"openAccess":24,"references":2081,"isForceReanalyzing":412},"afb60b77-8dd5-40c0-a102-2b98283df2ac","2025-02-10T18:54:28.845+00:00",[],"Blinatumomab-is-associated-with-favorable-outcomes-in-patients-with-B-cell-lineage-acute-lymphoblastic-leukemia-and-positive-measurable-residual-disease-at-a-threshold-of-10-sup-4-sup-and-higher",{"openalex":1752,"abstract":1754,"title":1756,"pm":1758,"doi":1760},{"VOID":1753},"W4283074795",{"EN":1755},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The presence of measurable residual disease (MRD) is the strongest predictor of relapse in acute lymphoblastic leukemia (ALL). We conducted a prospective, single‐arm, phase II study in adults with B‐cell ALL with MRD ≥1 × 10\u003Cjats:sup>−4\u003C\u002Fjats:sup> after ≥3 months from the start of frontline therapy or one month from any salvage therapy. Blinatumomab was administered at a standard dosing of 28 micrograms daily as a continuous infusion for up to five cycles and up to four additional maintenance cycles. Thirty‐seven patients with a median age of 43 years (range, 22–84 years) were treated. Twenty‐seven patients (73%) were treated in first complete remission (CR) and 10 patients (27%) in second CR and beyond. Eighteen patients (49%) had Philadelphia‐chromosome positive ALL and received concomitant tyrosine kinase inhibitor therapy. Twenty‐three patients (62%) had a baseline MRD ≥10\u003Cjats:sup>−3\u003C\u002Fjats:sup>. A median of three cycles (range, 1–9 cycles) were administered. Overall, 27 patients (73%) achieved MRD‐negative remission. With a median follow‐up of 31 months (range, 5–70 months), the estimated 3‐year relapse‐free survival (RFS) rate was 63% (95% confidence interval [CI], 43%–77%) and overall survival (OS) rate 67% (95% CI, 46%–81%). These rates were 51% (95% CI, 27%–70%) and 61% (95% CI, 36%–78%) in patients with baseline MRD ≥1 × 10\u003Cjats:sup>−3\u003C\u002Fjats:sup>, and 83% (95% CI, 45%–95%) and 77% (95% CI, 32%–95%) in patients with baseline MRD <10\u003Cjats:sup>−3\u003C\u002Fjats:sup> respectively. The rates of adverse events were consistent with previous studies of blinatumomab. In summary, blinatumomab induced MRD negativity in most patients and resulted in high rates of RFS and OS. This study is registered at \u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" xlink:href=\"http:\u002F\u002Fwww.clinicaltrials.gov\">www.clinicaltrials.gov\u003C\u002Fjats:ext-link> as #NCT02458014. 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\u002F>\u003Cjats:p>The combination of ponatinib, a third‐generation BCR::ABL1 tyrosine kinase inhibitor, with hyper‐CVAD chemotherapy resulted in high rates of complete molecular remissions and survival, without the need for stem cell transplantation (SCT) in most patients with Philadelphia chromosome(Ph)‐positive acute lymphocytic leukemia (ALL). Confirming these results in a large cohort of patients with longer follow‐up would establish this regimen as a new standard of care. Adults with newly diagnosed Ph‐positive ALL were treated with the hyper‐CVAD regimen. Ponatinib was added as 45 mg daily × 14 during induction, then 45 mg daily continuously (first 37 patients) or 30 mg daily continuously, with dose reduction to 15 mg daily upon achievement of a complete molecular response (CMR; absence of a detectable \u003Cjats:italic>BCR::ABL1\u003C\u002Fjats:italic> transcript by quantitative reverse transcription polymerase‐chain reaction at a sensitivity of 0.01%). Maintenance therapy consisted of daily ponatinib and vincristine‐prednisone monthly for 2 years, followed by daily ponatinib indefinitely. Twelve intrathecal injections of cytarabine alternating with methotrexate were given as central nervous system prophylaxis. The trial is registered on \u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" xlink:href=\"http:\u002F\u002Fclinicaltrials.gov\">clinicaltrials.gov\u003C\u002Fjats:ext-link> with the identifier NCT01424982. Eighty‐six patients were treated. Their median age was 46 years (range, 21–80). All 68 patients with active disease at the initiation of therapy achieved complete response (CR) The cumulative CMR rate was 86%. Twenty‐ patients (23%) underwent allogeneic SCT. With a median follow‐up of 80 months (range, 16–129 months), the estimated 6‐year event‐free survival rate was 65% and the overall survival rate was 75%. There was no difference in outcome by performance of allogeneic SCT in first CR. Common grade 3–5 adverse events included infection (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 80, 93%), increased liver transaminases (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 26, 31%) and total bilirubin (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 13, 15%), hypertension (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 15, 17%), pancreatitis (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 13, 15%), hemorrhage (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 12, 13%), and skin rash (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 9, 10%). Two ponatinib‐related deaths from myocardial infarction (3%; at months 2.6 and 4.3, respectively; both in CR) in the first 37 patients treated led to the ponatinib dose‐modifications mentioned earlier, with no further ponatinib‐related deaths observed. 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