Background: We evaluated the phenotype of sporadic gastric cancer based on HP status and binding of a tumor risk marker monoclonal, Adnab-9. Methods: We compared a familial GC kindred with an ...extremely aggressive phenotype to HP-positive (HP+) and -negative (HP−) sporadic gastric adenocarcinoma (GC) patients in the same community to determine if similar phenotypes exist. This might facilitate gene discovery to understand the pathogenesis of aggressive GC phenotypes, particularly with publications implicating immune-related gene-based signatures, and the development of techniques to gauge the stance of the innate immune system (InImS), such as the FERAD ratio (blood ferritin:fecal Adnab-9 binding OD-background binding). Resection specimens for the sporadic and familial group were stained for HP and examined for intestinal metaplasia (IM) and immunostaining for Adnab-9. Familial kindred specimens were also tested for the E-cadherin mutation and APC (adenomatous polyposis coli). Survival was evaluated. Results: Of 40 GC patients, 25% were HP+ with a greater proportion of intestinal metaplasia (IM) and gastric atrophy than the HP− group. The proband of the familial GC kindred, a 32-year-old mother with fatal GC, was survived by 13-year-old identical twins. Twin #1 was HP− with IM and Twin #2 was HP+. Both twins subsequently died of GC within two years. The twins did not have APC or E-cadherin mutations. The mean overall survival in the HP+ sporadic GC group was 2.47 ± 2.58 years and was 0.57 ± 0.60 years in the HP− group (p = 0.01). Survival in the kindred was 0.22 ± 0.24 years. Adnab-9 labeling was positive in fixed tissues of 50% of non-familial GC patients and in gastric tissue extract from Twin #2. The FERAD ratio was determined separately in six prospectively followed patient groups (n = 458) and was significantly lower in the gastric cancer patients (n = 10) and patients with stomach conditions predisposing them to GC (n = 214), compared to controls (n = 234 patients at increased risk for colorectal cancer but without cancer), suggesting a failure of the InImS. Conclusion: The HP+ sporadic GC group appears to proceed through a sequence of HP infection, IM and atrophy before cancer supervenes, and the HP− phenotype appear to omit this sequence. The familial cases may represent a subset with both features, but the natural history strongly resembles that of the HP− group. Two different paths of carcinogenesis may exist locally for sporadic GC. The InImS may also be implicated in prognosis. Identifying these patients will allow for treatment stratification and early diagnosis to improve GC survival.
Background: We evaluated the phenotype of sporadic gastric cancer based on HP status and binding of a tumor risk marker monoclonal, Adnab-9. Methods: We compared a familial GC kindred with an ...extremely aggressive phenotype to HP-positive (HP+) and -negative (HP−) sporadic gastric adenocarcinoma (GC) patients in the same community to determine if similar phenotypes exist. This might facilitate gene discovery to understand the pathogenesis of aggressive GC phenotypes, particularly with publications implicating immune-related gene-based signatures, and the development of techniques to gauge the stance of the innate immune system (InImS), such as the FERAD ratio (blood ferritin:fecal Adnab-9 binding OD-background binding). Resection specimens for the sporadic and familial group were stained for HP and examined for intestinal metaplasia (IM) and immunostaining for Adnab-9. Familial kindred specimens were also tested for the E-cadherin mutation and APC (adenomatous polyposis coli). Survival was evaluated. Results: Of 40 GC patients, 25% were HP+ with a greater proportion of intestinal metaplasia (IM) and gastric atrophy than the HP− group. The proband of the familial GC kindred, a 32-year-old mother with fatal GC, was survived by 13-year-old identical twins. Twin #1 was HP− with IM and Twin #2 was HP+. Both twins subsequently died of GC within two years. The twins did not have APC or E-cadherin mutations. The mean overall survival in the HP+ sporadic GC group was 2.47 ± 2.58 years and was 0.57 ± 0.60 years in the HP− group (p = 0.01). Survival in the kindred was 0.22 ± 0.24 years. Adnab-9 labeling was positive in fixed tissues of 50% of non-familial GC patients and in gastric tissue extract from Twin #2. The FERAD ratio was determined separately in six prospectively followed patient groups (n = 458) and was significantly lower in the gastric cancer patients (n = 10) and patients with stomach conditions predisposing them to GC (n = 214), compared to controls (n = 234 patients at increased risk for colorectal cancer but without cancer), suggesting a failure of the InImS. Conclusion: The HP+ sporadic GC group appears to proceed through a sequence of HP infection, IM and atrophy before cancer supervenes, and the HP− phenotype appear to omit this sequence. The familial cases may represent a subset with both features, but the natural history strongly resembles that of the HP− group. Two different paths of carcinogenesis may exist locally for sporadic GC. The InImS may also be implicated in prognosis. Identifying these patients will allow for treatment stratification and early diagnosis to improve GC survival.
Previous studies have established the value of magnetic resonance imaging (MRI) in detecting articular changes characteristic of osteoarthritis (OA) of the knee. We have observed some MRI features in ...OA of the knee presumably indicating synovial thickening. To determine whether these MR features represent chronic synovial inflammation, we studied the knees of nine patients at the mild end of the spectrum of OA of relatively short duration (89%: ≤4 yr), who were selected because MRI showed anatomical abnormalities compatible with synovial thickening. The painful knee was examined using conventional and weight-bearing radiographs, MRI, and arthroscopy. MR images suggestive of synovial thickening typically appeared in or near the intercondylar region of the knee, in the infrapatellar fat pad, or in the posterior joint margin. The site of an arthroscopic biopsy of the synovial membrane was guided by MRI to the area thought to represent synovial thickening for each patient knee. Pathological examination of these synovial membrane biopsies showed a mild chronic synovitis, and thus a correspondence with the synovial thickening detected by MRI. Our results suggest that MRI can be used to evaluate the extent of synovitis, observed as synovial thickening, in patients with early OA of the knee.
A case of adenosquamous carcinoma arising in the background of disseminated pelvic endometriosis presented as unilateral hydronephrosis and a polypoid intraluminal ureteral mass. This is the first ...case of a malignancy arising in endometriosis presenting as an obstructive ureteral mass. The patient had a history of total hysterectomy and bilateral salpingo-oophorectomy 5 years earlier because of an endometriotic cyst, and had since been under unopposed estrogen replacement therapy. An analysis of the case and related literature is presented. Possible pathogenic mechanisms are discussed.
Sphincter of Oddi dysfunction (SOD) is one of the causes of post‐cholecystectomy syndrome and biliary pain and is a challenge from both the diagnostic and therapeutic points of view. Sphincter of ...Oddi dysfunction is typically diagnosed months to years after cholecystectomy. Continued biliary type pain after cholecystectomy may occur in as many as 10–20% of patients. Ten percent or more of these patients may eventually be shown to have SOD. The syndrome is often associated with a variety of other gastrointestinal disorders thought to be caused by dysmotility. According to the Milwaukee classification, patients with biliary pain can be divided into three types. Type I patients show all the objective signs suggestive of a disturbed bile outflow (i.e. elevated liver function tests, dilated common bile duct and delayed contrast drainage during endoscopic retrograde cholangiopancreatography). Type II patients have biliary type pain along with one or two of the criteria from type I. Type III patients have biliary pain only, with no other abnormalities. The present paper will focus primarily on SOD syn‐drome, papillary stenosis and the diagnostic and therapeutic approaches, in particular endoscopic sphincterotomy.
Immunohistochemical localization of S‐100 protein α and β subunits in the cells of melanocytic nevi and malignant melanomas was studied by using monoclonal antibodies directed against each subunit. ...Although polyclonal anti‐S‐100 reactivities have been demonstrated uniformly in all nevus cells and melanoma cells, monoclonal anti‐S‐100α and anti‐S‐100β reactivities were either absent or rarely found in ordinary junctional nevi or junctional nests of ordinary compound nevi. However, in the junctional nests of dysplastic junctional nevi and junctional components of dysplastic compound nevi, monoclonal anti‐S‐100α reactivity become more frequent, whereas monoclonal anti‐S‐100β reactivity remains negative. In the superficial variety of melanomas such as superficial spreading melanoma and lentigo maligna melanoma, monoclonal anti‐S‐100β is nonreactive until vertical growth or invasiveness begins. Most nodular melanomas are positively stained with both monoclonal anti‐S‐100α and anti‐S‐100β. It is suggested that monoclonal anti‐S‐100α can be an indicator of active junctional nevus of melanocytic nevi and the reactivity with monoclonal anti‐S‐100β may be related to vertical progression of superficial spreading melanomas and lentigo maligna melanomas.
Etoposide-induced pulmonary toxicity Gurjal, Anagha; An, Teisa; Valdivieso, Manuel ...
Lung cancer (Amsterdam, Netherlands),
11/1999, Letnik:
26, Številka:
2
Journal Article
Recenzirano
After treatment with etoposide, two patients with lung cancer developed interstitial infiltrates and respiratory failure. Of the two, one patient responded rapidly to steroid therapy and developed ...recurrent symptoms on re-challenge with etoposide. Both patients had histopathologic findings consistent with drug-induced pulmonary toxicity. Etoposide-induced lung disease needs to be considered in patients who develop subacute dyspnea and interstitial infiltrates during treatment with this agent.
Sphincter of Oddi dysfunction (SOD) is one cause of post-cholecystectomy syndrome and biliary pain. It is a diagnostic and therapeutic challenge. The syndrome is often associated with a variety of ...other gastrointestinal dysmotility disorders. The Milwaukee classification divides patients with biliary pain into three categories. Biliary Type I patients show the entire objective signs of disturbed biliary outflow : elevated liver function tests dilated common bile duct (CBD) and delayed contrast drainage during ERCP. Biliary Type II patients have biliary pain along with one or two of the criteria from Biliary Type I. Biliary Type III patients have only biliary pain, with no other abnormalities. Recently the huge increase of cholecystectomy by Laparoscopy has increased the number of patients with post-cholecystectomy syndrome and possible Sphincter of Oddi dysfunction (SOD). We described eight patients with Biliary Type I SOD treated by endoscopic sphincterotomy (EST) and confirmed that Biliary Type I SOD is actually papillary stenosis. After seeing several patients with sickle cell disease, concomitant papillary stenosis, and common duct stones, we modified the definition of papillary stenosis to include patients with biliary stones. This paper will focus primarily on SOD syndrome, papillary stenosis, and the diagnostic and therapeutic approaches-in particular endoscopic sphincterotomy.
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