[Surgical management of a recurrent iris stromal cyst]. / Prise en charge chirurgicale d'un kyste du stroma irien récidivant.

INTRODUCTION: Cysts of the iris stroma may be congenital or acquired. They are rare tumors of the anterior segment. We describe the case of a 51-year-old patient presenting with a recurrent iris stromal cyst. OBSERVATION: The patient presented emergently for sudden recurrence of an iris stromal cyst with decreased visual acuity. He had already undergone needle aspiration and argon laser photocoagulation of the cyst 1 year previously. A Ultrasound BioMicroscopy (UBM) examination was performed to rule out any malignant tumor of the iris or ciliary body. Surgical treatment consisted of complete removal of the external layer of the cyst with Implantable Contact Lens (ICL) forceps after marsurpialization with scissors. The postoperative course was uneventful. CONCLUSION: Cysts of the iris stroma are rare benign tumors that pose problems due to their extension into the anterior chamber and recurrence.

Expression and localization of extracellular matrix-degrading proteinases and their inhibitors in the bovine mammary gland during development, function, and involution.

In degrading the extracellular matrix, matrix metalloproteinases (MMP) and the plasminogen activator (PA) system may play a critical role in extensive remodeling that occurs in the bovine mammary gland during development, lactation, and involution. Therefore, the aim of our study was to investigate the mRNA expression of MMP-1, MMP-2, MMP-14, MMP-19, tissue inhibitor of metalloproteinases (TIMP)-1, TIMP-2, urokinase-type PA, tissue-type PA, urokinase-type PA receptor, and PA inhibitor-1 by quantitative PCR and to localize with immunohistochemistry MMP-1, MMP-2, MMP-14, and TIMP-2 proteins in the bovine mammary gland during pubertal mammogenesis, lactogenesis, galactopoiesis, and involution. Expression of mRNA for each of the studied factors was relatively lower during galactopoiesis and early involution but was markedly increased during mammogenesis and late involution, 2 stages in which tissue remodeling is especially pronounced. The localization of proteins for MMP-1, MMP-14, and TIMP-2 showed a similar trend with strong staining intensity in cytoplasm of mammary duct and alveolar epithelial cells during pubertal mammogenesis and late involution. Interestingly, MMP-2 protein was localized only in the cytoplasm of endothelial cells during late involution. Our study demonstrated clearly that expression of extracellular matrix-degrading proteinases coincides with a concomitant expression of their inhibitors. High expression levels of MMP, TIMP, and PA family members seem to be a typical feature of the nonlactating mammary gland.

Regulation of progesterone and prostaglandin F2alpha production in the CL.

After the luteinizing hormone (LH) surge, the cells that remain from the ovulated follicle undergo a process of differentiation termed luteinization. Two key features of the cells after luteinization are the capacity for tremendous production of progesterone [10(16) molecules of progesterone per (min/(g of CL))] and the capacity to undergo regression or death of the cells at the appropriate time. There are two steroidogenic cell types, the small and large luteal cells that are regulated by different mechanisms. In small luteal cells, production of progesterone is stimulated by LH through the protein kinase A (PKA) pathway. The large luteal cells of ruminants produce large quantities of progesterone that is independent of LH stimulation. Although luteotrophins clearly regulate luteal function, much of luteal progesterone production in some species appears to be constitutive, consistent with the autonomous aspects of the large luteal cell. The key regulated step in luteal progesterone production appears to be regulation of transport of cholesterol to the inner mitochondrial membrane apparently mediated by the steroidogenic acute regulatory protein (StAR). In addition, our recent research indicates that PKA is tonically active in large luteal cells and this may be responsible for the high, relatively autonomous nature of luteal progesterone production. Regression of the corpus luteum (CL) in many species is initiated by prostaglandin (PG) F2alpha secreted from the uterus. Luteal cells also have the capacity for production of PGF2alpha. Luteal PGF2alpha production can be regulated by a variety of substances including inhibition by progesterone and stimulation by cytokines. We have also characterized a positive feedback pathway in ruminant and porcine CL in which small amounts of uterine PGF(2alpha) stimulate intraluteal production of PGF2alpha due to induction of the cycloxygenase-2 (Cox-2) enzyme in large luteal cells. This positive feedback pathway is only present in CL that has acquired the capacity for luteal regression ( approximately day 7 in cow, approximately day 13 in pig). Regulation by protein kinase C (PKC) of transcriptional factors interacting with an E-box in the 5' flanking region of the Cox-2 gene is the critical regulatory element involved in this positive feedback pathway. Thus, luteinization in some species appears to change specific gene transcription such that progesterone production becomes relatively independent of acute luteotrophic regulation and intraluteal PGF2alpha synthesis is induced by the second messenger pathways that are activated by PGF2alpha.

Interobserver agreement in the staging of rectal cancer using endoscopic ultrasonography.

BACKGROUND AND STUDY AIMS: In rectal tumors invasion of the rectal fat and perirectal lymph nodes are generally regarded as independent prognostic factors in most prospective series. There are no studies in the literature concerning interobserver agreement on the staging of rectal cancer by endorectal ultrasonography (EUS). The aim of the present study was to assess interobserver agreement using EUS in the TN staging of rectal cancer. PATIENTS AND METHODS: Thirty-seven patients with rectal cancer were investigated at two centers using EUS as part of the pretherapeutic staging (Olympus EUM-3 or EUM-20). All examinations were videotaped and reviewed six months later by four independent observers who assessed the stage of the tumor (from uT1 to uT4) and lymphatic invasion on a blinded basis. When the tumor was assessed as uT3, the observers specified the degree of involvement of the rectal fat (in millimeters). Interobserver agreement was estimated using the kappa coefficient (k) and the intraclass correlation coefficient (ICC). Agreement was classed as poor (k < 0.40), fair to good (0.40 < or = k < 0.75) or excellent (k < or = 0.75). RESULTS: Agreement was fair for uT1 tumors (k = 0.40) and poor for uT2 tumors (k = 0.20). Agreement was good (k = 0.58; CI 0.51 to 0.65) for uT3 tumors; there was a significant interobserver correlation for the exact measure of the extent of rectal fat (ICC = 0.65). The agreement was also good (k = 0.54, CI 0.47 to 0.61) for metastatic lymph nodes. CONCLUSION: As in the case of esophageal cancer, interobserver agreement on the staging of uT2 tumors is poor with EUS. The evaluation of rectal tumors with a poor prognosis shows good interobserver agreement.

Labeled granulocyte scanning for the diagnosis of infected necrosis in acute pancreatitis: what kind of labeling should be used?

Clinical and laboratory data or imaging results cannot provide a positive diagnosis of septic complications of pancreatic and peripancreatic necrosis in patients with acute pancreatitis. Confirmation can be obtained only after percutaneous computed tomography (CT)-guided aspiration of the necrotic tissues or fluid collection; although the important role of 99Tc(m)-HMPAO-labeled granulocyte scintigraphy has been recently emphasized. The aim of this study was to determine the sensitivity and specificity of 99m-technetium-hexamethylpropyleneamine oxime (99Tc(m)-HMPAO)- or 111In-oxine-labeled granulocyte scintigraphy for the diagnosis of infection in pancreatic or peripancreatic necrosis to define the ideal label for diagnosis. Thirty-six scintigraphic examinations were performed in 34 consecutive patients (mean age, 58 +/- 2 years) 20 +/- 2 days after the onset of acute pancreatitis (Balthazar classes A-C, n = 7; classes D and E, n = 29). The scintigraphic study included scintigraphic tomography and static acquisition 1 and 3 h, respectively, after reinjection of the autologous 99Tc(m)-labeled granulocytes and static images 3-4 and 24 h after the simultaneous reinjection of 111In-oxine-labeled autologous granulocytes. The diagnosis of infected pancreatic or peripancreatic necrosis was confirmed with percutaneous CT-guided aspiration (14 positive aspirates among 20 performed) and sterile necrosis after negative aspiration (6 negative aspirates) or after a 6 +/- 1-month follow-up free of clinical or biological signs of ongoing sepsis. The sensitivity and specificity were 86 and 73%, respectively, for scintigraphic tomography, 100 and 55% for 3-h 111In images, 93 and 68% for 3-4-h 111In images, and 100 and 64% for 24-h 111In images. The fall in splenic activity between the 3-4 and the 24-h 111In images was 26 +/- 3% in patients with septic pancreatic and peripancreatic necrosis (n = 14) and 16 +/- 3% in those with sterile necrosis (n = 22) (p < 0.01). Labeled granulocyte scintigraphy was thus shown to be an effective tool for the diagnosis of infection in pancreatic and/or peripancreatic necrosis due to acute pancreatitis, especially when the scintiscans are performed early after injection of 99Tc(m) or when the fall in splenic activity over the 24 h following reinjection of 111In is measured in particularly difficult cases. These promising preliminary results should be confirmed by a prospective study.

Anismus and biofeedback: who benefits?

BACKGROUND: Biofeedback is the main treatment for dyschezia in patients with anismus, but retraining may fail because of the frequent association of pelvirectal disorders with anismus. We set out to identify indices of biofeedback failure in the treatment of anismus. PATIENTS AND METHODS: From May 1990 to May 1993, 27 patients (20 women and seven men; median age 46 years) with anismus in which dyschezia was not improved by laxative agents were enrolled in a biofeedback retraining programme. All patients underwent proctologic examination, anal manometry and defecography. Anismus was defined as an increase in anal pressure during attempted defecation in conjunction with an impairment of rectal emptying as assessed using an objective test (barium paste expulsion). Associated disorders were encountered frequently. These included abnormal perineal descent (22 cases), large rectocoele (12 cases), high-grade rectal prolapse (six cases), abnormally high anal canal pressures at rest (seven cases) and abnormal rectal response to inflation (20 cases). Anismus was the sole abnormality in 12 patients when perineal descent, low-grade prolapse and abnormal rectal sensations were not taken into account. RESULTS: Biofeedback retraining did not suppress dyschezia in 13 out of 27 patients. Neither associated disorders (rectocoele, rectal prolapse, abnormal perineal descent, anal pressure and abnormalities of rectal sensation) nor a relevant past history (hysterectomy, laxative abuse, use of antidepressive agents) were encountered more frequently in these 13 patients than in the other 14. The duration of symptoms before treatment was significantly longer in the group unresponsive to biofeedback retraining (81 +/- 61 compared with 33 +/- 34 months for the responsive group, P < 0.01), but the total duration of symptoms and the number of retraining sessions attended did not differ significantly between the two groups. CONCLUSIONS: (1) Extensive examination (defecography and manometry) before biofeedback retraining of anismus is not mandatory because the failure of retraining (48%) is not related to the presence of associated pelvirectal disorders. (2) A long past history of dyschezia seems to provide an index of the failure of biofeedback retraining.

Serum increase and liver overexpression of carbohydrate 19.9 antigen in patients with genetic haemochromatosis.

CA 19.9 antigen is mainly secreted by biliary and pancreatic duct cells. Its metabolism could be modified in genetic haemochromatosis by iron accumulation within these cells. Therefore, CA 19.9 was assayed in the serum samples of 84 patients with genetic haemochromatosis before and after iron depletion and immunolocalised in the liver of 24 untreated genetic haemochromatosis cases. The study showed that serum CA 19.9 (N < 37 IU/l) was increased (SD) before treatment (41.2 (34)) when compared with after the venesection period (16 (12)), and correlated, before treatment, with the amount of iron excess, transaminases, fibrosis, and biliary iron deposits. Hepatic CA 19.9 was located within the cytoplasm of bile duct and cholangiolar cells. In conclusion, this study shows that a mild, reversible, and non-specific increase in serum CA 19.9 is common in genetic haemochromatosis patients and shows that this increase is related to iron excess, directly or through associated liver damage. The unexplained finding of a mild increase in serum CA 19.9 should lead, in a patient with no diagnosis, to the search for liver iron overload, and, in a patient with untreated genetic haemochromatosis, not to further diagnostic procedures unless this finding persists after completion of the venesection treatment.

[Pericarditis during inflammatory bowel diseases. Extra-intestinal or iatrogenic complication?]. / Péricardite au cours des maladies inflammatoires intestinales. Complication extra-intestinale ou iatrogène?

Acute pericarditis is rarely associated with inflammatory bowel disease. In such cases, when usual aetiologies have been excluded, pericarditis can be considered to be either an extraintestinal manifestation of inflammatory bowel disease or due to an adverse drug effect. We report a case of acute pericarditis in a 17-year old patient with ulcerative colitis treated with mesalazine for 15 days. Mesalazine was discontinued with a prompt and spontaneous resolution of the symptoms. Extensive investigations revealed no known cause for his pericarditis. Eight days and 75 days after the diagnosis, a lymphoblastic transformation test in the presence of mesalazine was performed and was positive for concentration greater than or equal to 10 micrograms/mL; this test was negative in 3 control patients treated with mesalazine without adverse drug effect. This observation together with the rare documented cases allows to consider the possibility that pericarditis may be caused by an adverse drug reaction in these patients.