Radiation induces<Emphasis Type="Italic"> p53</Emphasis>-dependent cell apoptosis in bladder cancer cells with wild-type-<Emphasis Type="Italic">p53</Emphasis> but not in<Emphasis Type="Italic"> p53</Emphasis>-mutated bladder cancer cells

Purpose. It has been reported in several studies that the absence in cancer cells of the p53 tumor suppressor gene, mutations of which are frequently found in bladder cancer, increases their resistance to ionizing radiation. Other studies, however, suggest that mutations of the p53 gene could increase the radiosensitivity of cancer cells, although the evidence is still inconclusive. In the present study, we investigated the relationship between p53 status and radiation response in five different bladder cancer cell lines. Materials and Methods. Five different human bladder cancer cell lines (KK47: with wt-p53, RT4: with wt-p53, T24: with mutated p53, 5637: with mutated p53, UM-UC-3: with mutated p53) were used in the study. Cells were irradiated with 0, 2, 4, 6 or 8 Gy, then trypsinized and re-plated for clonogenic survival assay, quantitative RT-PCR assay, flow-cytometry analysis and TUNEL assay. Results. The clonogenic assay demonstrated that KK47 and RT4 had significantly higher radiosensitivity than other cell lines. Quantitative RT-PCR analysis showed that radiation induced increased expression of p53, Bax, and p21 mRNA in KK47 and RT4. After irradiation, G1 cell-cycle arrest was observed in KK47 and RT4 under flow cytometry analysis, while T24, 5637, and UM-UC-3 showed an increase in the proportion of G2 cells. Increased cell apoptosis was also observed under TUNEL assay in KK47 and RT4, but not in other cell lines. Conclusions: It was demonstrated that ionizing radiation induces p53-dependent cell apoptosis in bladder cancer cells with wt-p53 but not in those with mutated p53.     

<Emphasis Type="Italic">WT1</Emphasis> and <Emphasis Type="Italic">NPHS2</Emphasis> mutations in Korean children with steroid-resistant nephrotic syndrome

Although several genetic causes of steroid-resistant nephrotic syndrome (SRNS) have been identified, occurrence of these genetic abnormalities appears to be influenced by race. Seventy Korean children (39 girls, 31 boys) with SRNS underwent analysis for mutations of WT1 and NPHS2. Although NPHS2 mutations were not present in any of the patients, two different intronic mutations of WT1, IVS9+4 C>T and IVS9+5 G>A, were detected in four patients (three girls, one boy). Among the four patients with mutation, two girls with a karyotype of 46,XY had complete XY gonadal dysgenesis, one girl with a karyotype of 46,XX had normal genitalia, and one boy with a karyotype of 46,XY had hypospadia. A kidney biopsy conducted in three of the four patients revealed focal segmental glomerulosclerosis. The incidence of WT1 mutations observed in this study was similar to that of previous reports. However, the incidence of NPHS2 mutations seems to be very rare in Korean children. Genetic diagnosis of WT1 mutations should be recommended for children with SRNS, especially in cases involving a female phenotype or males with genital anomalies.     

No evidence for genotype/phenotype correlation in<Emphasis Type="Italic"> NPHS1</Emphasis> and<Emphasis Type="Italic"> NPHS2</Emphasis> mutations

Primary steroid-resistant nephrotic syndrome (SRNS) is characterized by childhood onset of proteinuria and progression to end-stage renal disease. In 26% of cases it is caused by recessive mutations in NPHS2 (podocin). Congenital nephrotic syndrome (CNS) is caused by mutations in NPHS1 (nephrin) or NPHS2. In three families mutations in NPHS1 and NPHS2 had been reported to occur together, and these tri-allelic mutations were implicated in genotype/phenotype correlations. To further test the hypothesis of tri-allelism, we examined a group of 62 unrelated patients for NPHS1 mutations, who were previously shown to have NPHS2 mutations; 15 of 62 patients had CNS. In addition, 12 CNS patients without NPHS2 mutation were examined for NPHS1 mutations. Mutational analysis yielded three different groups. (1) In 48 patients with two recessive NPHS2 mutations (11 with CNS), no NPHS1 mutation was detected, except for 1 patient, who had one NPHS1 mutation only. This patient was indistinguishable clinically and did not have CNS. (2) In 14 patients with one NPHS2 mutation only (4 with CNS), we detected two additional recessive NPHS1 mutations in the 4 patients with CNS. They all carried the R229Q variant of NPHS2. The CNS phenotype may be sufficiently explained by the presence of two NPHS1 mutations. (3) In 12 patients without NPHS2 mutation (all with CNS), we detected two recessive NPHS1 mutations in 11 patients, explaining their CNS phenotype. We report ten novel mutations in the nephrin gene. Our data do not suggest any genotype/phenotype correlation in the 5 patients with mutations in both the NPHS1 and the NPHS2 genes.Members of the Study Group of the Arbeitsgemeinschaft für Pädiatrische Nephrologie (APN) participating in this study: J. Thaarup (Aalborg, Denmark); P. Henning (Adelaide, Australia); I. Attrach (Aleppo, Syria); A. Bakkaloglu (Ankara, Turkey); C. Rudin (Basel, Switzerland); R. Bogdanovic (Belgrade, Yugoslavia); S. Briese, J. Gellermann, T. Lennert, U. Querfeld, Sacherer, M. Schürmann, and M. Zimmering (Berlin, Germany); C. Roth, C. Schröter, and B. Utsch (Bonn, Germany); Matthes (Bremen, Germany); A. Heilmann and G. Kalvoda (Dresden, Germany); F. Wegner (Düren, Germany); V. Schumacher (Düsseldorf, Germany); Bär, B. Bosch, M. Kamm, S.M. Karle, K. Nüsken, C. Plank, W. Rascher, and B. Zimmermann (Erlangen, Germany); K. E. Bonzel, M. Bald, P. Hoyer, and U. Vester (Essen, Germany); U. Neyer (Feldkirch, Austria); Rippel (Frankfurt, Germany); M. Brandis, A. Fuchshuber, K. Häffner, A. Kirchhoff, and M. Pohl (Freiburg, Germany); J. Steiss (Giessen, Germany); J.P. Haas (Greifswald, Germany); L. Patzer (Halle, Germany); M. Kemper, H. Altrogge, D.E. Müller-Wiefel, U. Peters, and K. Timmermann (Hamburg, Germany); J.H.H. Ehrich, H. Haller, and C. Strehlau (Hannover, Germany); M. Daschner, S. Hessing, Janssen, D. Kiepe, S. Köpf, O. Mehls, and B. Tönshoff (Heidelberg, Germany); F. Prüfer and L.B. Zimmerhackl (Innsbruck, Austria); U. John, J. Misselwitz, G. Rönnefarth, and J. Seidel (Jena, Germany); D. Blowey and J. Scheinman (Kansas City, Mo., USA); B. Beck, K. Frankenbusch, B. Hoppe, C. Licht, D. Michalk, T. Ronda, and L. Stapenhorst (Cologne, Germany); D. Drozdz and A. Pogan (Krakau, Poland); Froster, E. Vogel and S. Wygoda (Leipzig, Germany); R. Hettenger (Los Angeles, Calif., USA); H. Schriewer and H.-P. Weber (Lüdenscheid, Germany); R. Beetz (Mainz, Germany); M. Konrad (Marburg, Germany); H. Fehrenbach (Memmingen, Germany); M. Griebel and B. Klare (München, Germany); M. Bulla, S. Fründ, E. Kuwertz-Bröking, A. Schulze-Everding and Yelbuz (Münster, Germany); L. Monnens (Nijmegen, The Netherlands); J. Janda and T. Seemann (Prag, Czech Republic); G. Adomssent, G. Krüger, Lorenzen, J. Muscheites, H.-J. Stolpe and M. Wigger (Rostock, Germany); W. Sperl (Salzburg, Austria); R. Egger (Schaffhausen, Switzerland); V. Tasic (Skopje, Macedonia); M. Bald and H.-E. Leichter (Stuttgart); O. Amon (Tübingen, Germany); T. Arbeiter, C. Aufricht and K. Müller (Vienna, Austria); D. Bockenhauer and N. Siegel (New Haven, Conn., USA); and T. Neuhaus and A. Staub (Zürich, Switzerland)     

Intratumoral Heterogeneity in Microsatellite Alterations in <Emphasis Type="Italic">BRCA1</Emphasis> and <Emphasis Type="Italic">PTEN</Emphasis> Regions in Sporadic Colorectal Cancer

Background: Chromosome regions 17q21 (BRCA1) and 10q23 (PTEN) have been found deleted in colorectal cancer.Methods: We studied the frequency of loss of heterozygosity (LOH) in these 2 regions in 214 patients with only 1 sample per tumor and in 100 patients with several samples per tumor. Three microsatellite markers of each region were used for the LOH test. The polymerase chain reaction product was electrophoresed in 8% polyacrylamide gels, and band intensity was shown by silver staining.Results: The proportions of LOH in the two regions were 38.4% for 17q21 and 30.8% for 10q23 in the group of 214 and were 47.7% for 17q21 and 34.7% for 10q23 in the group of 110434_2003_Article_876. We found a high correlation between the LOH in both regions (P < .001), where 81% of LOH in 10q23 region was matched by concomitant LOH in 17q21. In the group of tumors with several samples (group of 100), 39% and 68% did not present LOH in the 17q21 and 10q23 regions, respectively, in all of their tumor samples. However, in the 20 patients with LOH in both regions in the group of 100 (several samples per tumor), all samples with LOH in 10q23 also had LOH in 17q21, whereas not all samples with LOH in 17q21 had LOH in 10q23.Conclusions: These results show that colorectal cancer is highly heterogeneous, at least for these tumors markers, and suggest a sequential acquisition pattern of these anomalies during tumor growth, in which changes in 17q21 could occur before those in 10q23.     

<Emphasis Type="Italic">PIK3CA</Emphasis>, <Emphasis Type="Italic">KRAS</Emphasis>, and <Emphasis Type="Italic">BRAF</Emphasis> mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/C) of the pancreas

Background and aims Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-α (PIK3CA) gene in various human tumors. Three hot-spot mutations in the exons 9 and 20 have been proven to activate the Akt signalling pathway. The Raf/MEK/ERK (mitogen-activated protein kinase) signal transduction is an important mediator of a number of cellular fates including growth, proliferation, and survival. The BRAF gene is activated by oncogenic RAS, leading to cooperative effects in cells responding to growth factor signals. Here we evaluate the mutational status of PIK3CA, KRAS, and BRAF in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMNC) of the pancreas. Materials and methods Exons 1, 4, 5, 6, 7, 9, 12, 18, and 20 of PIK3CA, exons 1 of KRAS, and exons 5, 11, and 15 of BRAF were analyzed in 36 IPMN/IPMC and two mucinous cystadenoma specimens by direct genomic DNA sequencing. Results We identified four somatic missense mutations of PIK3CA within the 36 IPMN/IPMC specimens (11%). One of the four mutations, H1047R, has been previously reported to be a hot-spot mutation. Furthermore, we found 17 (47%) KRAS mutations in exon 1 and one missense mutation (2.7%) in exon 15 of BRAF. Conclusion This data is the first report of PIK3CA mutation in pancreatic cancer and it appears to be the first oncogene to be mutated in IPMN/IPMC but not in conventional ductal adenocarcinoma of the pancreas. Our data provide evidence that PIK3CA and BRAF contribute to the tumorigenesis of IPMN/IPMC, but at a lower frequency than KRAS. German Society of Surgery, Surgical Forum 2008, Best Abstracts This work was supported by the National Cancer Institute (NCI) Temin Award CA95434 and the NCI R01 CA109525 (GHS).     

Acute glomerulonephritis in three siblings and suspected <Emphasis Type="Italic">emm</Emphasis>49-type <Emphasis Type="Italic">Streptococcus pyogenes</Emphasis> infection

Three siblings with poststreptococcal acute glomerulonephritis are presented. Streptococcal infection, impetigo, and pharyngitis preceded the acute glomerulonephritis. In one patient, emm49-type Streptococcus pyogenes was isolated, a strain which has not been reported as nephritogenic in Japan.     

Mutational analysis of <Emphasis Type="Italic">NPHS2</Emphasis> and <Emphasis Type="Italic">WT1</Emphasis> in frequently relapsing and steroid-dependent nephrotic syndrome

Idiopathic nephrotic syndrome is a common pediatric kidney disease, 80% of all cases are steroid sensitive (SSNS). A significant proportion of children with SSNS will have a frequently relapsing or steroid-dependent course (FRNS/SDNS) that is associated with significant treatment-related morbidity. Mutations in NPHS2 account for more than 28% of all cases of steroid-resistant nephrotic syndrome (SRNS) and dominant mutations in WT1 for 5%; while mutations are absent from children with uncomplicated SSNS. Since FRNS/SDNS is phenotypically positioned within a spectrum between SSNS and SRNS, we hypothesized that heterozygous mutations of NPHS2 may be causing FRNS/SDNS. Mutational analysis of NPHS2 and WT1 was carried out in a single-center cohort of 20 children with FRNS/SDNS, ten children with uncomplicated SSNS (control), and 22 children with SRNS (control). Renal biopsy findings were available in 15/20 children with FRNS/SDNS and revealed IgM nephropathy, MCNS, and FSGS in six, five, and four children, respectively. Children with FRNS/SDNS were significantly younger at first presentation than those with SSNS and SRNS (median age: 3.0 years in FRNS/SDNS patients, 7.0 years in SSNS patients, and 5.0 in SRNS patients; p < 0.001). No NPHS2 or WT1 mutations were found in patients with FRNS/SDNS and uncomplicated SSNS. The hypothesis that FRNS/SDNS may be associated with heterozygous mutations in NPHS2 or WT1 was not confirmed.     

Role of glycemic elements of <Emphasis Type="Italic">Cynodon dactylon</Emphasis> and <Emphasis Type="Italic">Musa paradisiaca</Emphasis> in diabetes management

The study defined the scientific evaluation of glycemic elements of extracts of Cynodon dactylon and Musa paradisiaca. A dose of 500 mg/kg body weight (bw) of C. dactylon produced maximum falls of 23.2% and 22.8% in blood glucose levels of normoglycemic rats during studies of fasting blood glucose and glucose tolerance, respectively, whereas the same dose of M. paradisiaca produced a rise of 34.9% and 18.4%. In diabetic rats during glucose tolerance tests, a fall of 27.8% and a rise of 17.5% were observed with the same dose of C. dactylon and M. paradisiaca, respectively. Laser-induced breakdown spectroscopy used for detection of glycemic elements present in both the extracts indicated that C. dactylon was rich in magnesium (Mg), whereas M. paradisiaca was rich in potassium (K) and sodium (Na), comparatively, suggesting thereby the defined roles of these elements in diabetes management.     

Polymorphisms in <Emphasis Type="Italic">ALOX12</Emphasis>, but not <Emphasis Type="Italic">ALOX15</Emphasis>, Are Significantly Associated With BMD in Postmenopausal Women

The murine arachidonate 15-lipoxygenase gene (Alox15) has recently been identified as a negative regulator of peak bone mineral density (BMD). The human ALOX15 gene shares significant sequence homology with the murine Alox15 gene; however, the human arachidonate 12-lipoxygenase gene (ALOX12) is functionally more similar to the mouse gene. Multiple single-nucleotide polymorphisms (SNPs) in the human ALOX15 and ALOX12 genes have previously been reported to be significantly associated with BMD in humans. On the basis of these data, we carried out our own investigation of the human ALOX15 and ALOX12 genes and their relationship with hip and spine BMD parameters. The study population consisted of 779 postmenopausal women with a mean (± standard deviation) age of 62.5 ± 5.9 years at BMD measurement and was recruited from a single large general practice in Chingford, northeast London. Three SNPs from ALOX15 and five from ALOX12 were analyzed. None of the SNPs that we analyzed in ALOX15 were significantly associated with any of the BMD parameters or fracture data. However, we found that three SNPs from ALOX12, all previously associated with spine BMD in women, were significantly associated with spine and various hip BMD parameters in our cohort (P = 0.029–0.049). In conclusion, we found no association between polymorphism in ALOX15 and BMD phenotypes but were able to replicate previous findings that genetic variation in ALOX12 seems to play a role in determining bone structure in Caucasian women.     

<Emphasis Type="Italic">Candida</Emphasis> in Acute Pancreatitis

Purpose A Candida infection of the pancreas, which previously was considered extremely unusual, has been increasingly reported in recent years. The present study was conducted with the aim of performing a cohort analysis of our patients with acute pancreatitis to find out the incidence, sites, and species of Candida involvement; and to evaluate the risk factors, severity, and course of illness of such patients. Methods A total of 335 patients with acute pancreatitis were investigated for a possible Candida infection of the pancreas from January 2000 to May 2003. The clinical records of all those patients who were positive for Candida spp. isolation from pancreatic tissue were analyzed. The clinical records of 32 more cases, randomly selected from the patients who were investigated for candidal pancreatitis but were negative for Candida spp., were also analyzed in order to compare their findings with those patients with a true Candida infection of the pancreas. Results A true or possible Candida infection was observed in 41 (12.2%) of those 335 patients and Candida tropicalis was the most common isolate (43.9%). Candida spp. were isolated from pancreatic necrotic tissue in 22 (6.6%) patients (true infection). A possible Candida infection (positive drain fluid effluents at least twice, without any Candida isolation from pre/per operative samples from pancreas) was seen in 19 (5.7%) patients. Candida was also isolated exclusively from the blood in another 19 patients with a clinical diagnosis of acute pancreatitis. A risk factor analysis showed that patients with severe injury to the pancreas, on prophylactic fluconazole, and after surgical intervention were significantly more prone to develop a Candida infection. Patients with a Candida superinfection also had a significantly increased hospital stay and higher mortality. Conclusion This study thus emphasizes the important role of Candida infection in patients with acute pancreatitis and demonstrates the need for early attention.     

Absence of mutations in the <Emphasis Type="Italic">HOXA11</Emphasis> and <Emphasis Type="Italic">HOXD11</Emphasis> genes in children with congenital renal malformations

Experimental studies have shown that homeobox genes are essential for the development of the kidney and urinary tract. Hoxa11/Hoxd11 double mutant mice demonstrate renal agenesis or hypoplasia. Since, to our knowledge, these genes have never been examined for alterations in humans with congenital anomalies of the kidney and urinary tract (CAKUT), we investigated whether mutations of HOXA11/HOXD11 genes are associated with non-syndromal congenital renal parenchymal malformations. DNA samples from 26 unrelated children with unilateral renal agenesis (URA), 20 with renal hypodysplasia (RHD) and 13 with multicystic dysplastic kidney (MCDK) were included in the study. Exons 1 and 2 of the HOXA11/HOXD11 genes were amplified individually by polymerase chain reaction (PCR) using 12 unique oligonucleotide primers. Single-strand conformation polymorphism (SSCP) analysis of overlapping polymerase chain reaction products was performed. SSCP analysis revealed no variant band shifts in the samples of the amplified segments of the 59 patients, suggesting lack of either mutation or polymorphisms. Our findings do not support the hypothesis that mutations in the HOXA11/HOXD11 coding regions are involved in the pathogenesis of human non-syndromal congenital renal parenchymal malformations. Further studies are necessary, since other genes known to affect nephrogenesis, as well as genetic and environmental factors, may be involved.     

<Emphasis Type="Italic">NPHS2</Emphasis> mutation associated with recurrence of proteinuria after transplantation

Mutations in the NPHS2 gene encoding podocin are associated with steroid-resistant nephrotic syndrome (SRNS) in childhood. Patients usually present with focal segmental glomerulosclerosis (FSGS). It is unclear to what extent SRNS due to NPHS2 mutations predisposes to recurrence of proteinuria/FSGS after renal transplantation (RTx). A 4-year-old girl with infantile SRNS was started on peritoneal dialysis because of end-stage renal disease due to FSGS. Mutational screening of the patient and her parents revealed a novel single nucleotide deletion in exon 8 of the NHPS2 gene (948delT), for which the patient was homozygous and her parents confirmed heterozygous asymptomatic carriers. At the age of 4.5 years the patient received a renal graft from her mother. On day 7 after RTx, the patient developed progressive proteinuria (urine protein/creatinine ratio 2.4 g/g), which responded within 1 week to prednisone pulse therapy, an increased cyclosporin A dosage, and ramipril therapy. The patient has maintained stable graft function and no further recurrence of proteinuria has been observed. In conclusion, patients with SRNS due to NPHS2 mutations are not protected from recurrence of proteinuria after RTx. The quick response to increased immunosuppression in our patient suggests an immune-mediated pathomechanism for recurrence of proteinuria.     

Reduction in oxalate-induced renal tubular epithelial cell injury by an extract from <Emphasis Type="Italic">Quercus salicina</Emphasis> Blume/<Emphasis Type="Italic">Quercus stenophylla</Emphasis> Makino

Urocalun, a herbal medicine prepared from an extract of Quercus salicina Blume/Quercus stenophylla Makino (QS extract), has been clinically used for the treatment of urolithiasis in Japan since 1969. In the present study, the effects of QS extract on oxalate-induced cell injury and NADPH-induced superoxide anion (O(2) (-)) production in the injured cells were investigated. Oxalate-induced cell injury was assessed by mitochondrial reduction of 3-(4,5-dimethyl-2-thiazol)-2,5-diphenyltetrazolium bromide and leakage of lactate dehydrogenase into the extracellular fluid. When NRK-52E cells were injured by exposure to oxalate for 24 h, QS extract prevented the injury in a dose-dependent manner. In addition, QS extract suppressed the increase in NADPH-induced O(2) (-) production, or NADPH oxidase activity, in the homogenate of cells injured by oxalate exposure. These findings suggest that the reduction in oxalate-induced O(2) (-) production contributes to the cytoprotective effect of QS extract.     

Type B aortic dissection associated with <Emphasis Type="Italic">Salmonella</Emphasis> infection

A 59-year-old man with a long history of hypertension and diabetes was admitted to our hospital with acute type B aortic dissection 14 days after the sudden onset of back pain. The dissecting descending thoracic aorta was enlarged to 5.2 cm in diameter, and laboratory tests showed an elevated white blood cell count (15 530/mm³) and an increased C-reactive protein level (19.2 mg/dl). Computed tomography performed 2 days after admission revealed rapid growth of the aortic dissection. Blood cultures obtained upon admission were positive for Salmonella. Impending rupture of the aortic dissection complicated by Salmonella infection was strongly suspected, and the patient underwent emergency surgery consisting of debridement and prosthetic graft placement covered by an omental flap. In this case, it is believed that insidious Salmonella aortitis caused acute type B aortic dissection.     

A novel mutation of<Emphasis Type="Italic"> NPHS2</Emphasis> identified in a Chinese family

Since the identification of the NPHS2 gene, which encodes podocin, several groups from European, Middle Eastern, and North American countries have reported NPHS2 mutations in families with steroid-resistant nephrotic syndrome (SRNS) or focal segmental glomerulosclerosis (FSGS). Families with SRNS have also been reported in China with a population of more than 1.3 billion. However, to our knowledge, there is no mutational analysis of the NPHS2 gene in familial SRNS or FSGS in China. We identified a novel mutation of NPHS2 (467_468insT and 503G>A) in a Chinese family with autosomal recessive SRNS using polymerase chain reaction, denaturing high-performance liquid chromatography, and DNA sequencing techniques. The results demonstrate that there is also NPHS2 mutation in Chinese familial SRNS. Therefore, Chinese SRNS patients with a familial history of NS should also be screened for possible mutations of NPHS2. We also detected clearly decreased staining with a specific podocin C-terminal antibody (P35) and negative staining with a specific podocin N-terminal antibody (P21). These results were contrary to those predicted from the mutated sites. Further studies are needed to explore the mechanism and impact of the mutant gene on the expression and localization of the relevant protein.     

Pulmonary <Emphasis Type="Italic">Paragonimus westermani</Emphasis> with false-positive fluorodeoxyglucose positron emission tomography mimicking primary lung cancer

We report the case of a 66-year-old woman with pulmonary Paragoniumus westermani showing false-positive fluorodeoxyglucose positron emission tomograpy (FDG-PET). Based on chest computed tomography and FDG-PET findings, we could not rule out the possibility of primary lung cancer. She underwent right middle and lower lobectomies as a primary lung cancer. As a possibility in the differential diagnosis of a pulmonary nodule with FDG-PET positive findings, paragonimiasis should be considered, although it is rarely seen.     

Atypical <Emphasis Type="Italic">Mycobacterium</Emphasis> infections of the upper extremity

Background: We encountered five patients with atypical Mycobacterium infections in the upper extremity, and examined their outcomes. Patients and methods: Two patients were male and three were female. The average patient age was 67 (range, 63–75) years. A wide synovectomy was performed to diagnose all cases followed by a therapeutic regimen of Rifampicin, Isoniazid, and Ethambutol. Results: The causative atypical organism was Mycobacterium marinum in three cases and Mycobacterium intracellulare in two cases. In one patient, inflammation recurred or did not disappear, and, therefore, three debridements were necessary. The average duration of antimicrobial therapy was 12 (range, 5–24) months. The average follow-up period was 26 (range, 5–66) months, and resolution had been achieved in all cases at the time of follow-up evaluation. Conclusion: Surgical debridement and appropriate mycobacterial culture or PCR method are critical to enable diagnosis and appropriate management.