13 research outputs found

    Musta maksa

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    Teema : elinsiirrot

    Postoperative serum CA19-9, YKL-40, CRP and IL-6 in combination with CEA as prognostic markers for recurrence and survival in colorectal cancer

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    Background In colorectal cancer (CRC) patients, guidelines only recommend measurement of preoperative carcinoembryonic antigen (CEA), although postoperative CEA may be more informative. However, the sensitivity of both preoperative and postoperative CEA in identifying relapse is limited. We studied whether CA19-9, YKL-40, C-reactive protein (CRP) and interleukin (IL)-6 add prognostic information combined with postoperative CEA. Material and methods This post-hoc analysis included 147 radically resected stage II (n = 38), III (n = 91) and IV (n = 18) CRC patients treated with adjuvant 5-fluorouracil (5-FU)-based therapy in the phase III LIPSYT study (ISRCTN98405441). We collected postoperative blood samples a median of 48 days after surgery. We analysed relapses, sensitivity, positive predictive value (PPV) and disease-free (DFS) and overall survival (OS) by bootstrap, Kaplan-Meier and adjusted Cox-models in the elevated vs. normal biomarker groups. Results Elevated postoperative CEA associated with impaired DFS (HR 7.23; CI(95%)3.85-13.58), impaired OS (HR 7.16; CI(95%)3.76-13.63), and more relapses (HR 7.9; CI(95%)3.4-18.2); but sensitivity for CEA in finding relapses was only 31% (CI(95%)21-48%). Normal CEA combined with an elevated YKL-40 or elevated CRP showed more relapses (HR for YKL-40 2.13 [CI(95%)1.10-4.13], HR for CRP 3.14 [CI(95%)1.21-8.16]), impaired DFS (HR 2.18 [CI(95%)1.12-4.24] or 3.23 [CI(95%)1.34-7.82]), and impaired OS (2.33 [CI(95%)1.24-4.40] or 2.68 [CI(95%)1.12-6.44]). Elevated CEA combined with a concomitantly elevated CA19-9, YKL-40, CRP or IL-6 showed a respective PPV of 100, 90, 100, and 100%. Conclusion In radically operated stage II to IV CRC patients who received adjuvant 5-FU-based chemotherapy, a postoperatively elevated CEA alone or in combination with CA19-9, YKL-40, CRP, or IL-6, or a normal CEA combined with an elevated YKL-40 or with an elevated CRP, may indicate patients at high risk of relapse.Peer reviewe

    Transient Changes in Serum CEA, CA19-9, CRP, YKL-40, and IL-6 during Adjuvant Chemotherapy and Survival of Patients with Colorectal Cancer

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    Serum carcinoembryonic antigen (CEA) is frequently monitored to detect colorectal cancer (CRC) recurrence after surgery. The clinical significance of transiently increased CEA during adjuvant chemotherapy is poorly understood. Serum CEA, CA19-9, CRP, YKL-40, and IL-6 were measured before, during, and after adjuvant 5-fluorouracil-based chemotherapy in the randomised LIPSYT study population. The biomarker kinetic patterns were classified into three groups: no increase, a transient increase (≥10% increase followed by a decrease), and a persistent increase during the adjuvant treatment, and the associations of these patterns with disease free-survival (DFS) and overall survival (OS) were investigated by using Cox regression analyses. The findings were validated in two single-centre cohorts that received modern adjuvant chemotherapy. A transient increase in CEA occurred in about a half of the patients during chemotherapy, in all the cohorts. The patients with a transient increase had a roughly similar DFS and OS to the patients with no increase, and a more favourable survival compared to the patients with a persistent increase. In the LIPSYT cohort, the hazard ratio was 0.21 for DFS (CI95% 0.07–0.66) and 0.24 for OS (CI95% 0.08–0.76). Transient increases in CA19-9 and YKL-40 tended to be associated with a favourable survival. A transient increase in CEA during adjuvant chemotherapy is associated with a favourable survival when compared with a persistent increase

    Lead Time and Prognostic Role of Serum CEA, CA19-9, IL-6, CRP, and YKL-40 after Adjuvant Chemotherapy in Colorectal Cancer

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    Simple Summary Colorectal cancer is the third most common cancer worldwide. Recurrence risk after curative intent surgery combined with adjuvant chemotherapy is substantial. Unlike many other cancers, curative metastasectomy is possible upon recurrence, which raises the question of personalized surveillance strategies according to individual risk factors. We studied whether elevated biomarkers, such as gold standard CEA and experimental CA19-9, IL-6, CRP, and YKL-40 after adjuvant therapy, are associated with disease-free and/or overall survival, and whether the diagnostic time from the elevated biomarker to the diagnosis of metastases can be prolonged by combining these biomarkers. We show that elevated post-adjuvant CEA, IL-6, and CRP are associated with impaired survival and that elevated IL-6 finds recurrences in patients with normal CEA. Lead time is shorter with CEA than with experimental biomarkers. Our findings thus may impact the follow-up strategies after curative intent treatment aiming at finding operable relapses. These biomarkers are readily available and feasible in clinical practice. In colorectal cancer (CRC), 20-50% of patients relapse after curative-intent surgery with or without adjuvant therapy. We investigated the lead times and prognostic value of post-adjuvant (8 months from randomisation to adjuvant treatment) serum CEA, CA19-9, IL-6, CRP, and YKL-40. We included 147 radically resected stage II-IV CRC treated with 24 weeks of adjuvant 5-fluorouracil-based chemotherapy in the phase III LIPSYT-study (ISRCTN98405441). All 147 were included in lead time analysis, but 12 relapsing during adjuvant therapy were excluded from post-adjuvant analysis. Elevated post-adjuvant CEA, IL-6, and CRP were associated with impaired disease-free survival (DFS) with hazard ratio (HR) 5.21 (95% confidence interval 2.32-11.69); 3.72 (1.99-6.95); 2.58 (1.18-5.61), respectively, and elevated IL-6 and CRP with impaired overall survival (OS) HR 3.06 (1.64-5.73); 3.41 (1.55-7.49), respectively. Elevated post-adjuvant IL-6 in CEA-normal patients identified a subgroup with impaired DFS. HR 3.12 (1.38-7.04) and OS, HR 3.20 (1.39-7.37). The lead times between the elevated biomarker and radiological relapse were 7.8 months for CEA and 10.0-53.1 months for CA19-9, IL-6, CRP, and YKL-40, and the lead time for the five combined was 27.3 months. Elevated post-adjuvant CEA, IL-6, and CRP were associated with impaired DFS. The lead time was shortest for CEA.Peer reviewe

    Evaluation of prognosis and treatment response in colorectal cancer with focus on biomarkers

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    Jag skickar referatet via e-postJag skickar referatet via e-pos

    Behandling av pilonidalsinus med hjälp av radial-laser teknik(FilaC™): Första finländska erfarenheterna

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    Bakgrund Pilonidalsinus är en sjukdom som drabbar 26/100 000 människor varje år. Etiologin bakom pilonidalsinus är inte fullständigt klar, men anses idag vara en förvärvad inflammatorisk process orsakad av hår i analfåran. Behandlingen av pilonidalsinus är kirurgisk, men det finns inte ännu någon behandlingsform som visat sig överlägsen andra. Nyligen har en behandling med laser introducerats. Syftet med denna studie är att undersöka hur bra behandlingen med laser har fungerat i Finland. Metoder: I denna retrospektiva registerstudie samlades data in från Helsingfors och Nylands sjukvårdsdistrikts (HUS) patientdatasystem. De 86 patienter som deltog i studien opererades för pilonidalsinus under 2017–2019 med den nya lasertekniken. Alla patienterna kontrollerades efter två månader av en kirurg. Även senare kontakter till vårdenheten gällande operationen beaktades i studien. Resultat: Uppföljningstiden i studien var i medeltal 14 månader. Vid kontrollen efter två månader hade ingreppet gett önskat resultat för 86% av patienterna, varav 3% fick återfall under uppföljningstiden. De flesta ingreppen utfördes dagkirurgiskt under lokalbedövning. Mediansjukledigheten efter ingreppet var 12 dagar. Totalt 17% av patienterna behövde en ny operation. I de fall där tecken på infektion av pilonidalsinusen förekom under ingreppsdagen var endast 53% av ingreppen framgångsrika. Slutsats: Laserbehandling för pilonialsinus är ett bra alternativ även i framtiden, speciellt för mindre komplicerade fall. Det är en minimalt invasiv teknik som möjliggör snabb återhämtning och ger goda resultat

    Can carcinoembryonic antigen replace computed tomography in response evaluation of metastatic colorectal cancer?

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    <p><b>Introduction:</b> Response Evaluation Criteria in Solid Tumours (RECISTs 1.1) define computed tomography (CT) as the gold standard in response evaluation of patients with metastatic colorectal cancer (mCRC) who are undergoing chemotherapy. The aim of this study was to evaluate whether carcinoembryonic antigen (CEA), which is cheaper and easier to perform, can replace repeated CT.</p> <p><b>Material and methods:</b> The study included 66 patients with non-resectable mCRC participating in a phase I–II study. CEA values were determined, and CT images were taken every 2 months. CT images were externally and retrospectively reviewed according to the RECIST 1.1 criteria. Different cut-off values for CEA change in percent (DeltaCEA%) compared with baseline or nadir value underwent testing to find patients with disease control (that is stable disease, partial or complete response) at 2, 4, 6 and 8 months, in order to identify those who could have continued with chemotherapy based on CEA values alone. CT verification is needed in progressive disease (PD), and therefore identifying PD patients was our secondary endpoint.</p> <p><b>Results:</b> The results showed that by using a cut-off value of 0 for DeltaCEA%, disease control was seen in all patients at all measuring points (negative predictive value (NPV) = 1.0). Secondarily, increasing CEA was able to identify all PD patients (sensitivity (Se) = 1.0) and in 50–74% of the patients increasing CEA provided a lead time to PD on upcoming CT. It was possible to replace CT with CEA in all patients with decreasing CEA, meaning that 23–47% of CT scans could have been avoided at any given time point.</p> <p><b>Conclusion:</b> When the CEA level at a certain measuring point is the same or lower than CEA at baseline or at nadir (the measuring point with the lowest CEA value) during treatment, CEA can replace CT.</p

    Neutrophil gelatinase-associated lipocalin does not originate from the kidney during reperfusion in clinical renal transplantation

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    Background: Acute Kidney Injury (AKI) is a common clinical complication. Plasma/serum neutrophil gelatinase-associated lipocalin (NGAL) has been proposed as a rapid marker of AKI. However, NGAL is not kidney-specific. It exists in three isoforms (monomeric, homo-dimeric and hetero-dimeric). Only the monomeric isoform is produced by renal tubular cells and plasma NGAL levels are confounded by the release of all NGAL isoforms from neutrophils. Our aim was to investigate whether NGAL is released into blood from injured renal tubules. Methods: Kidney transplantation (n = 28) served as a clinical model of renal ischaemic injury. We used ELISA to measure NGAL concentrations at 2 minutes after kidney graft reperfusion in simultaneously taken samples of renal arterial and renal venous blood. Trans-renal gradients (venous-arterial) of NGAL were calculated. We performed Western blotting to distinguish between renal and non-renal NGAL isoforms. Liver-type fatty acid binding protein (LFABP) and heart-type fatty acid binding protein (HFABP) served as positive controls of proximal and distal tubular damage. Results: Significant renal release of LFABP [trans-renal gradient 8.4 (1.7-30.0) ng/ml, p = 0.005] and HFABP [trans-renal gradient 3.7 (1.1-5.0) ng/ml, p = 0.003] at 2 minutes after renal graft reperfusion indicated proximal and distal tubular damage. NGAL concentrations were comparable in renal venous and renal arterial blood. Thus, there was no trans-renal gradient of NGAL. Western blotting revealed that the renal NGAL isoform represented only 6% of the total NGAL in renal venous blood. Conclusions: Ischaemic proximal and distal tubular damage occurs in kidney transplantation without concomitant NGAL washout from the kidney graft into blood. Plasma/serum NGAL levels are confounded by the release of NGAL from neutrophils. Present results do not support the interpretation that increase in plasma NGAL is caused by release from the renal tubules.Peer reviewe
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