När en man diagnostiseras med prostatacancer innebär det en psykisk påfrestning för mannen och hans kvinnliga partner. Reaktioner som chock, meningsförlust, ensamhet och ångest är vanligt förekommande. Syftet med denna litteraturstudie var att beskriva hur det vardagliga livet upplevs och påverkas hos par där mannen lever med diagnostiserad prostatacancer. Resultaten i studien baseras på tio vetenskapliga artiklar med fokus på parens erfarenheter av sjukdomen. Impotens, inkontinens och fatigue var symtom som drabbade mannen till följd av sjukdomen. Dessa förändringar inverkade på parets vardag och relation. Förändringarna var psykiskt påfrestande för parets hälsa och både mannens och kvinnans livskvalitet försämrades på grund av cancersjukdomen. Psykiska problem som depression, oro, ångest och skuld var dock mer förekommande hos kvinnan. Trots att paren var i stort behov av information upplevde de att hälso- och sjukvården inte uppmärksammade deras behov. Tydligare riktlinjer inom sjukvården för hur par som lever med prostatacancer ska bemötas efterlyses. På så sätt kan sjuksköterskan lättare tillgodose parets behov av information och stöd. Sjuksköterskan bör uppmärksamma och bemöta kvinnans individuella önskemål samt visa en öppenhet gentemot de sexuella problem som kan drabba paren. Mer forskning, speciellt i Skandinavien, efterlyses för att få en klarare bild över hur både en homosexuellt och heterosexuell relation påverkas av prostatacancer. / When a man is diagnosed with prostate cancer it implies a psychological strain for the man and his female partner where reactions such as shock, loss of meaning, loneliness and anxiety are common. The purpose of this literature review was to describe how everyday life is perceived and influenced in couples where the man has been diagnosed with prostate cancer. The results of the study are based on ten scientific articles focused on exploring couple’s experiences of the disease and how they are affected by the situation. Symptoms such as impotence, incontinence and fatigue were changes that affected the couple’s everyday life and their relationship. These changes were psychologically trying for the couple’s health and their quality of life decreased because of the cancer.  Psychological problems like depression, anxiety and guilt were more common for the woman. Despite the fact that the couples were in great need of information, they felt that health care providers were not attentive to these needs. Clearer guidelines are needed within the health-care system for how couples living with prostate cancer should be treated. The nurse would thereafter be better equipped to meet the couple’s needs for information and support. The nurse should highlight and approach women’s individual needs and show openness towards the sexual problems that can befall couples. More research is needed, particularly in Scandinavia, in order to get a clearer picture of how a homosexual and heterosexual relationship is affected by prostate cancer.

Prostate-specific antigen (PSA) testing has caused a steep increase in the incidence of prostate cancer, especially the incidence of localised low risk disease. In order to decrease the overdiagnosis accompanied by PSA testing, analysis of inherited genetic variants have been suggested as potential tools for clinical assessment of disease risk. With the aim of minimizing overtreatment and postpone side-effects of curative treatment for low risk prostate cancer, active surveillance, a treatment strategy with initial surveillance and deferred radical prostatectomy at the time of progression has evolved.  The aim of this thesis was to study the validity of PSA (paper I) and inherited genetic variants (paper II) for early diagnosis of prostate cancer, to assess the extent of PSA testing in Sweden (paper III), and to study the safety of deferred radical prostatectomy in localised low to intermediate risk prostate cancer (paper IV). The study designs were i) case-control studies nested within the Västerbotten intervention project (paper I and II), ii) observational study in the Cancer Register of Sweden (paper III), and iii) observational study in the NPCR Follow-up study (paper IV). PSA had a high validity in predicting a prostate cancer diagnosis with an area under the receiver operating characteristics (ROC) curve of 0.86 (95% CI, 0.84 to 0.88). A combined test, including PSA, the ratio of free to total PSA, and 33 single nucleotide polymorphisms (SNPs) in a genetic risk score, increased the area under curve to 0.87 (95% CI, 0.85 to 0.89). The estimated uptake of PSA testing among men aged 55 to 69 years increased from zero to 56% between 1997 and 2007 and there were large variations in the uptake of PSA testing between counties in Sweden. After a median follow-up time of eight years there was no significant difference in presence of any one or more adverse pathology features or prostate cancer specific mortality after primary compared to deferred radical prostatectomy in localised low to intermediate risk prostate cancer. Results from these studies indicate that PSA and the hitherto identified SNPs are not suitable biomarkers in single-test prostate cancer screening. It is possible to estimate the uptake of PSA testing on a population level. Initial surveillance and deferred radical prostatectomy represent a feasible treatment strategy in localised low to intermediate risk prostate cancer.

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) constitute a group of vasculitides characterized by neutrophil-rich necrotizing inflammation of small vessels and the presence of ANCA in the circulation. Dying neutrophils surrounding the walls of small vessels are a histological hallmark of AAV. Traditionally it has been assumed that these neutrophils die by necrosis, but neutrophil extracellular traps (NETs) have recently been visualized at the sites of vasculitic lesions. NETs were first described to be involved in capture and elimination of pathogens but dysregulated production and/or clearance of NETs are thought to contribute to vessel inflammation in AAV; directly by damaging endothelial cells and indirectly by acting as a link between the innate and adaptive immune system through the generation of pathogenic PR3-ANCA and MPO-ANCA that can activate neutrophils. ANCA can, however, be found in all individuals and are therefore suggested to belong to the repertoire of natural antibodies produced by innate-like B cells, implying that not all ANCA are pathogenic.  In paper I, we found neutrophils in patients to be more prone to undergo NETosis/necrosis spontaneously compared with neutrophils in healthy controls (HC), as well as that active patients possessed elevated levels of NETs in the circulation. Our results also suggest that ANCA during remission could contribute to the clearance of NETs as we observed an inverse relation between ANCA and NETs. In paper II, we observed neutrophils in patients to be more easily activated upon ANCA stimulation as they produced more ROS than neutrophils in HC. In paper III, we showed for the first time that cells of adaptive immunity (B and T cells) in addition to cells of innate immunity can release ET-like structures, in this case consisting of mitochondrial (mt) DNA. mtDNA can act as a damage-associated pattern molecule (DAMP) and promote inflammation, and increased levels of mtDNA has been observed in AAV. Our finding broadens our perspective of the possible roles of T and B cells in immunological responses, and should be further investigated in AAV. In paper IV, we observed reduced frequencies of MZ-like B cells, considered to be innate-like B cells that produce natural antibodies, and of the proposed regulatory B (Breg) cell populations CD24highCD27+ and CD25+CD27+ B cells in patients, particularly in those with active disease. We also observed the phenotypes of these different Breg cell populations to be different from the corresponding cells in HC. We hypothesize that the increased activation potential by neutrophils in AAV to produce ROS and undergo NETosis/necrosis contribute to the excessive inflammation as well as an increased antigen load of PR3 and MPO, and that this in combination with dysregulation of innate-like B cells and Breg cells could lead to break of tolerance to these antigens and production of pathogenic autoantibodies. ANCA can in turn activate neutrophils to release NETs, suggesting a vicious circle in disease development.

Abstract Elective urological patients’ medication usage at the time of admission Author: Nygren. J. Supervisor: Gillespie. U. Examiner: Nielsen. E. Department of Pharmaceutical Biosciences, division of pharmacokinetics and drug therapy. Faculty of pharmacy. Uppsala University, Sweden.   Background and Objective: Information about the patient’s current medication treatment before elective urologic surgery has been based upon a prefilled self-reported health declaration or a patient provided medication list. A new work procedure has recently been adopted where a pharmacist performs a medication reconciliation in order to increase the patient safety, receive deeper insight into the patients ongoing treatment and to reduce the physician’s workload. The objective of the study was to map out how well the patients could account for their medication usage at the time of admission and to identify discrepancies between the health declaration/patient’s medication list and the medication list after medication reconciliation. Design: The study population consisted of adult men and women scheduled for elective urological surgery.  A clinical pharmacist performed a medication reconciliation and stored appurtenant patient data and medication lists in anonymised forma. Data was then analysed by a student undertaking his degree project (MSc Clinical pharmacy). The population and discrepancies were divided into sub-groups and a t-test was performed to identify any statistical difference between selected sub-groups of the population. Setting: Urology department, Uppsala University Hospital Main outcome measures: The proportion of patients having at least one discrepancy were studied. Distribution of discrepancies per patient was compared between sub-groups; number of medications, age and county of residence. Results: At least one discrepancy (range 1-7) was observed in 51 (66%) out of the 77 patients included in the study. Patients using >5 medications at the time of admission had more discrepancies per patient than those using 0-5 medications (3.2 vs 1.0; p=5.6x10-6) and there was a trend towards Uppsala patients having more discrepancies per patient than those residing outside the region (2.4 vs 1.5; p=0.057). There was no significant difference observed between the age groups. Conclusion: The health declaration/medication list presented at the time of admission did not provide enough information to determine the patient’s complete medication usage.

Bladder dysfunction is seen as a public health problem with a strongly increasing incidence in older men. Despite this, the man's experience of bladder dysfunction is a topic that has not been researched in the empirical field as much as women’s experiences. Not highlighting the man's experience leads to suffering and constitutes an obstacle to equal care. The aim of this study was to illustrate the man's experience of living with bladder dysfunction. This study is intended to illustrate experiences, therefore it was well suited to make an integrative compilation of qualitative research – inspired by meta-synthesis. Nine qualitative articles that described the man's experiences were analysed schematically and resulted in three themes and six sub-themes. Experiences that were noticed in the man were the impact of the environment in bladder dysfunction which included environmental and health care responses. Emotional impact in bladder dysfunction, which highlighted the experiences that arose in connection with bladder dysfunction. The life adaptations in bladder dysfunction was an experience which described the changes the man made to achieve a normality in everyday life as well as changes to hide the condition. The man used a range of strategies to maintain normality in life and to keep his condition a secret from those around him. This is seen because of the stigmatization that emerged through this study. Healthcare failed to care for the man with bladder dysfunction and was seen as partially responsible for the stigmatization the man experienced.

Aim: To study the possibility of detecting lymph node metastasis in locally advanced urinary bladder cancer (UBC) treated with radical cystectomy (RC) by using preoperative positron emission tomography/computed tomography (PET/CT) and peroperative sentinel node biopsy (SNB) technique. We also investigate the clinical significance of macrophage traits expression by cancer cells, M2-macrophage infiltration (MI) in tumor stroma and the immunohistochemical expression of biomarkers in cancer cells in relation to clinicopathologic data. Patients and Methods: We studied prospectively 122 patients with UBC, pathological stage pT1–pT4 treated with RC and pelvic lymph node dissection (PLND) during 2005–2011 at the Department of Urology, Linköping University Hospital. In the first study, we compared the results of preoperative PET/CT and conventional CT with the findings of postoperative histopathological evaluation of lymph nodes (LNs). In the second study we investigated the value of SNB technique for detecting pathological LNs during RC in patients with UBC. W also examined the significance of the primary tumor location in the bladder in predicting the site of LN metastases, and the prognostic significance of lympho-vascular invasion (LVI) and lymph node metastasis density (LNMD) on survival. In the third study, we investigate the clinical significance of macrophage infiltration (MI) in tumor stroma and macrophage-traits expression by tumor cells. In the fourth study, we investigate the cell cycle suppression proteins p53, p21, pRb, p16, p14 ARF as well as tumors proliferative protein Ki67 and DNA repair protein ERCC1 expression in cancer cells. The results were compared with clinical and pathological characteristics and outcome. Results: Prior to RC, PET/CT was used to detect LN metastasis in 54 patients. PET/CT had 41% sensitivity, 86% specificity, 58% PPV, and 76% NPV, whereas the corresponding figures for conventional CT were 41%, 89%, 64%, and 77%. SNB was performed during RC in 103 patients. A median number of 29 (range 7–68) nodes per patient were examined. SNs were detected in 83 out of 103 patients (81%). The sensitivity and specificity for detecting metastatic disease by SNB varied among LN stations, with average values of 67% -90%. LNMD or ≥8% and LVI were significantly related to shorter survival. In 103 patients, MI was high in 33% of cases, while moderate and low infiltration occurred in 42% and 25% of tumors respectively. Patients with tumors containing high and moderate compared to low MI had low rate of LN metastases (P=0.06) and improved survival (P=0.06), although not at significant level. The expression of different tumor suppression proteins was altered in 47-91% of the patients. There were no significant association between cancer specific survival (CSS) and any of the studied biomarkers. In case of altered p14ARF, ERCC1 or p21, CSS was low in case of low p53 immunostaining but increased in case of p53 accumulation, although not at a significant level, indicating a possible protective effect of p53 accumulation in these cases. Conclusion: PET/ CT provided no improvement over conventional CT in detection and localization of regional LN metastases in bladder cancer. It is possible to detect the SN but the technique is not a reliable for perioperative localization of LN metastases; however, LVI and LNMD at a cut-off level of 8% had significant prognostic values. MI in the tumor microenvironment but not CD163 expression in tumor cells seems to be synergistic with the immune response against urinary bladder cancer. Our results further indicate that altered p53 might have protective effect on survival in case of altered p14ARF, p21, or ERCC1 indicating an interaction between these biomarkers.

Rectal cancer is one of the three most common malignancies in Sweden with an annual incidence of about 2000 cases. Current treatment consists of surgical resection of the rectum including the loco-regional lymph nodes in the mesorectum. In advanced cases, neoadjuvant chemo-radiotherapy (CRT) prior to the operative treatment reduces local recurrences and enables surgery. The neoadjuvant treatment can also eradicate the tumour completely, i.e. complete response. This research project was designed to investigate the effects of preoperative radiotherapy/ CRT and analyze methods to predict response to CRT. Study I investigated the expression of the FXYD-3 protein with immunohistochemistry in rectal cancer, with or without preoperative radiotherapy. The results from the total cohort showed that, strong FXYD-3 expression was correlated to infiltrative tumour growth (p = 0.02). In the radiotherapy group, strong FXYD-3 expression was related to an unfavourable prognosis (p = 0.02). Tumours with strong FXYD-3 expression had less tumour necrosis (p = 0.02) after radiotherapy. FXYD-3 expression in the primary tumour was increased compared to normal mucosa (p=0.008). We concluded that FXYD-3 expression was a prognostic factor in patients receiving preoperative radiotherapy for rectal cancer. Study II investigated FXYD-3 expression in tumours that developed local recurrences following surgery and compared this with expression in tumours that did not develop local recurrences. There was no difference in the expression of FXYD-3 between the group that developed local recurrences and the group that did not develop local recurrences. There was no difference in survival between those with strong or weak FXYD-3 expression. We concluded that this study could not confirm the findings from study 1 i.e. that FXYD-3 expression has prognostic significance in rectal cancer. Study III was a register-based study on the incidence and effects of complete response to neoadjuvant treatment. Eight per cent of the patients with adequate CRT to achieve complete response also had a complete histological response of the luminal tumor in the resected bowel. Sixteen per cent of that group had remaining lymph node metastases in the operative specimen. Chemotherapy together with radiotherapy doubled the chance of complete response in the luminal tumour. Patients with remaining lymph node metastases had a lower survival rate compared to those without. We concluded that residual nodal involvement after neoadjuvant treatment was an important factor for reduced survival after complete response in the luminal tumour. Study IV followed up the results from the previous study by re-evaluating magnetic resonance imaging (MRI)- images in patients with complete tumour response. Two experienced MRI radiologists performed blinded re-staging of post CRT MR- images from patients with complete response in the luminal tumour. One group with lymph node metastases and another one without were studied and the results compared with the pathology reports. The sensitivity, specificity, and positive and negative predicted values for correct staging of positive lymph nodes was 37%, 84%, 70% and 57%. The size of the largest lymph node (4.5 mm, p=0.04) seemed to indicate presence of a tumour positive lymph node. We concluded that MRI couldn’t correctly stage patients for lymph node metastases in patients with complete response to CRT in the luminal tumour.

This thesis focused on the acute management of patients with ST-segment elevation myocardial infarction (STEMI) in an effort to provide information that may improve outcome. The aim was to evaluate the efficacy and safety of bivalirudin versus unfractionated heparin (UFH) in STEMI patients during primary PCI. Furthermore, to provide pharmacodynamic data of novel ways of ticagrelor administration compared to standard tivcagrelor. Additionally, to identify subgroups of patients, such as women who may derive greater benefit from specific antithrombotic strategies due to their risk/benefit profile. Finally, to evaluate current formulas for estimation of renal function in the acute phase of STEMI. In Paper I, all STEMI patients in Sweden between 2008 and 2014, treated with primary PCI and UFH or bivalirudin were included in our analysis. Of the total population of 23 800 patients, 8 783 (36.9%) were included in the UFH group and 15 017 (63.1%) in the bivalirudin group. Concomitant GPI administration was 68.5% in the UFH arm compared to 3.5% in the bivalirudin arm (p<0.01).The adjusted incidence of 30-day mortality was not significant different between the two groups (UFH vs bivalirudin, adjusted HR 0.94; 95% CI 0.82 -1.07). The adjusted risk for 1-year mortality, 30-day and 1-year stent thrombosis and re-infarction did not differ significantly between the two groups. In contrast, patients treated with UFH had a significantly higher incidence of major in-hospital bleeding (adjusted OR 1.62; 95%CI 1.30 -2.03). In Paper II pharmacodynamic data of chewed or crushed ticagrelor compared to standard ticagrelor loading dose (LD) was assessed in 99 patients with stable angina. Platelet reactivity (PR) was assessed with VerifyNow before, 20 and 60 minutes after LD. High Residual platelet reactivity (HRPR) was defined as > 208 P2Y12 reaction units (PRU). Chewed ticagrelor tablets resulted in significantly lower PRU values compared to crushed or integral tablets at 20 and 60 minutes. Crushed ticagrelor LD resulted in significantly lower PRU values compared to integral tablets at 20 minutes whereas no difference was observed at 60 minutes. At 20 minutes, no patients had HRPR with chewed ticagrelor compared to 68% with integral and 30% with crushed ticagrelor LD (p<0.01). In Paper III we presented a pre-specified gender analysis of the ATLANTIC trial including 1 862 STEMI patients that were randomly assigned to pre-hospital versus in-hospital administration of 180mg ticagrelor. Women were older and had higher TIMI risk score. Women had a 3-fold higher risk for all-cause mortality compared to men (5.7% vs 1.9%, HR 3.13, 95% CI 1.78 – 5.51). However, after adjustment for baseline characteristics, the difference was lesser and no longer significant (HR 1.98, 95% CI 0.97 – 4.04). Female gender was not an independent predictor of risk for bleeding after multivariable adjustments (BARC type 3-5 HR 1.52, 95% CI 0.74-3.09). There was no interaction between gender and efficacy or safety of randomised treatment. In Paper IV, forty patients with PCI- treated STEMI were included between November 2011 and February 2013. We validated the performance of the Cockcroft-Gault (CG), the Modification of Diet in Renal Disease (MDRD-IDMS), the Chronic Kidney Disease Epidemiology (CKD-EPI) and the Grubb relative cystatin C (rGCystC) equations for estimation of GFR against measured GFR (mGFR) during the index hospitalisation for STEMI. MDRD-IDMS and CKD-EPI demonstrated a good performance to estimate GFR with accuracy within 30% (P30) 82.5% vs 82.5%, respectively. CKD was best classified by CKD-EPI (Kappa 0.83). CG showed the worst performance with the lowest P30. The rG-CystC equation had a marked bias of -17.8% and significantly underestimated mGFR (p=0.03). Conclusions – In STEMI patients treated with primary PCI, bivalirudin should be preferred in patient at high risk for bleeding. With crushed or chewed ticagrelor tablets a more rapid platelet inhibition may be achieved, compared with standard integral tablets. In STEMI patients, fast and potent platelet inhibition with chewed ticagrelor may reduce the risk of early stent thrombosis and patients treated with a less aggressive antithrombotic strategy, such as UFH or bivalirudin monotherapy, may derive a greater benefit. Although gender differences in adverse outcomes could mainly be explained by older age and clustering of comorbidities in women, a bleedreduction strategy in women with high risk characteristics is warranted in order to improve their outcome. Regardless the choice of antithrombotic strategy, dose adjustment of drugs cleared by kidneys based on GFR estimation is of crucial importance. MDRD and CKD-EPI should be the formulas used for estimation of GFR in STEMI patients

Background. Angiogenesis is essential for tumour growth. Vascular endothelial growth factor (VEGF) and its isoforms were investigated in relation to the clinical course in a large number of patients with renal cell carcinoma (RCC). Methods. RCC subtypes and behaviour were established by clinicopathological criteria and surveillance. VEGF expression was analysed in serum by enzyme-linked immuno-sorbent assay (ELISA) and in tumour tissue by reverse transcription polymerase chain reaction (RT-PCR), immunohistochemistry (IHC), and Western blot (WB). Results. Serum VEGF (S-VEGF) was increased in RCC compared to control group. S-VEGF correlated with tumour stage and grade and was associated with survival in men but not in women. S-VEGF correlated with blood platelet counts, which were inversely correlated to increasing age in women, and they were decreased in chronically medicated patients, particularly in men. In contrast to S-VEGF, platelet counts associated with survival only in patients free of medication and chronic diseases. RT-PCR showed a correlation between VEGF121/VEGF165 mRNA and between VEGF165/VEGF-R1 mRNA. There was no association between different VEGF mRNA isoforms and S-VEGF. Conventional renal cell carcinoma (CRCC) had higher VEGF165, VEGF121, and VEGF-R1 mRNA levels compared with papillary renal cell carcinoma (PRCC). IHC VEGF staining was strong in kidney cortex. Kidney tumour showed a considerable variation in cytoplasmatic VEGF expression, which correlated with tumour size. Although, there was no difference in VEGF expression between the RCC types, VEGF expression was associated with survival only in CRCC. WB showed a strong protein expression of both VEGF189 and VEGF165 in kidney cortex. In kidney tumour, expression of VEGF189 varied the most, VEGF165 less so, and VEGF121 was rarely detected. Both CRCC and PRCC expressed low levels of VEGF189 and VEGF165 compared with kidney cortex. Chromophobe renal cell carcinoma (ChRCC) expressed VEGF189 levels comparable to those from kidney cortex, while VEGF165 was lower. In PRCC and ChRCC, VEGF189 levels correlated inversely with advancing tumour stage, and in PRCC, VEGF165 levels correlated inversely with increasing tumour size. VEGF189 was an independent prognostic factor for survival in patients with PRCC. Conclusions. S-VEGF has a stronger association to progression in RCC than platelet count. CRCC showed high levels of VEGF mRNA isoforms and VEGF-R1 mRNA compared to PRCC. VEGF mRNA isoforms expression decreased with advancing stage. IHC demonstrated VEGF expression in cell cytoplasm related to tumour growth, particular in CRCC. Different VEGF isoform patterns were found in different RCC types. Protein VEGF189 expression was associated with tumour stage and was an independent prognostic factor in PRCC. Protein VEGF165 expression was generally low and had no prognostic value. The trend for decreasing levels of VEGF isoforms in advanced tumour stages may indicate that angiogenic activity is an early event in tumour growth induced by VEGF, but that during later tumour progression the role of VEGF is less clear.

Pyelonefrit är en inflammation i njurarna och undersökningen som främst används vid utredning är dimerkaptosuccinat (DMSA)-scintigrafi. Pyelonefrit drabbar framförallt barn och risk finns för njurparenkymskador. Syftet med studien var att utreda om DMSA-scintigrafi efter pyelonefrit hos barn är berättigad. Detta granskades genom att beräkna den generella risken för cancer, specifika riskökningen för njurparenkymcancer, antal upptäckta njurparenkymskador och eventuella könsskillnader. Vetenskapliga artiklar söktes upp via sökmotorn PRIMO. Metoden var retrospektiv med kvantitativ ansats där materialet bestod av svarsutlåtanden från DMSA-scintigrafier på barn 0-2 år med frågeställning njurparenkymskador efter pyelonefrit. Urvalet bestod av 91 barn; 52 flickor och 39 pojkar varav 16 stycken exkluderades. Av de studerade 75 barnen hade sex (8 %) njurparenkymskador, med medelålder på 9,2 månader, och det fanns ingen signifikant skillnad mellan kön och njurparenkymskada (p=0,246). Medelvärdet på given aktivitet gav en effektiv medeldos på 0,69 mSv. Den generella riskökningen vid en DMSA-scintigrafi blev 0,01-0,014 och 0,00019 för njurparenkymcancer. Trots att relativt få barn drabbas av njurparenkymskador, finns ändå risk att drabbas av komplikationer från skadan. Skadorna är därför viktiga att upptäcka. Riskökningen för cancerutveckling och njurparenkymcancer efter DMSA-scintigrafi är mycket låg. Nyttan (att upptäcka njurparenkymskadorna) överväger risken (strålningen), vilket gör DMSA-scintigrafin till en berättigad undersökningsmetod. / A dimercaptosuccinic acid (DMSA) scintigraphy is used to test for pyelonephritis, an inflammation of the kidneys with risk of renal scarring. Aiming to investigate if DMSA scan after pyelonephritis in children is justified, we calculated the general cancer risk, the specific increased renal cancer risk, the number of discovered renal scarring and potential differences between the sexes. The method was retrospective and quantitative and data was based on results from DMSA scans of children aged 0-2 years. From the original set of 91 children (52 girls, 39 boys), 16 were excluded. Of the remaining 75, six (8 %) had renal scarring; with an average age of 9,2 months, and there was no significant difference between sex and renal parenchymal damage (p=0,0246). The mean activity from a DMSA scan equaled an effective dose of 0.69 mSv, with general cancer versus renal cancer risk being 0.01-0.014 and 0.00019, respectively. Even though only a few children develop renal scarring, there is still a risk of complications. Renal scarring is therefore important to discover. The increased risk for cancer and renal cancer after a DMSA scan is low. The benefits (discovering renal scarring) are greater than the risk (radiation), making the DMSA scan justified.