Duodeno-jejunal junction dyssynergia： Description of a novel syndrome

AIM： To investigate the hypothesis that duodeno-jejunal dyssynergia existed at the duodeno-jejunal junction.
METHODS： Of 112 patients who complained of epigastric distension and discomfort after meals, we encountered nine patients in whom the duodeno-jejunal junction did not open on duodenal contraction. Seven healthy volunteers were included in the study. A condom which was inserted into the ist duodenum was filled up to 10 mL with saline in increments of 2 mL and pressure response to duodenal distension was recorded from the duodenum, duodeno-jejunal junction and the jejunum.
RESULTS： In healthy volunteers, duodenal distension with 2 and 4 mL did not produce pressure changes, while 6 and up to 10 mL distension effected significant duodenal pressure increase, duodeno-jejunal junction pressure decrease but no jejunal pressure change. In patients, resting pressure and duodeno-jejunal junction and jejunal pressure response to 2 and 4 mL duodenal distension were similar to those of healthy volunteers. Six and up to 10 mL 1^st duodenal distension produced significant duodenal and duodeno-jejunal junction pressure increase and no jejunal pressure change.
CONCLUSION： Duodeno-jejunal junction failed to open on duodenal contraction, a condition we call ＇duodenojejunal junction dyssynergia syndrome＇ which probably leads to stagnation of chyme in the duodenum and explains patients＇ manifestations.     

Manic-depressive psychosis as prevalent manifestation of multiple sclerosis

INTRODUCTION: Manic-depressive psychosis (MDP) and multiple sclerosis (MS) coexistence is unusual but well-proven. OBSERVATIONS: We report two cases observed in two women aged 30 and 31, who were followed up for neurological episodes associated with concomitant or deferred manic or depressive fits. Brain magnetic resonance imaging revealed multiple zones of high intensity signals in the white matter. Biological balance was normal. The diagnosis of multiple sclerosis (MS) was established. Given to treat acute episodes, high-dose corticosteroids enabled regression of the psychological fits. Similarly, long-term treatment in one patient enabled significant regression of fits, which became less frequent and less severe. DISCUSSION/CONCLUSION: The MDP-MS association may be due to local MS-related brain damage or to common genetic susceptibility. The positive effect of corticosteroids against psychological fits is another finding favouring an organic cause of these disorders.     

Inguinal canal dilatation: a novel technique for the repair of failed testicular descent despite hormonal treatment

Treatment of the undescended testicle (UT) after it failed to descend on hormonal therapy is surgical. Spermatic cord elongation may impair testicular function, particularly in cases in which cord integuments or veins have to be divided to provide an extra cord length. A factor that might impede testicular descent is presence of a narrowed or obliterated inguinal canal. We investigated the hypothesis that dilatation of a narrowed or obliterated inguinal canal might assist spontaneous testicular descent. Twenty-six boys (age 3.6 +/- 0.8 years) with unilateral UT and failed hormonal treatment, whose UT was located at deep inguinal ring, were included in the study. Through an inguinal incision, the inguinal canal was dilated, spermatic cord adhesions divided, hernial sac, if present, excised, and skin closed. Testicular descent into the scrotum occurred in 22 patients within 4.2 +/- 1.3 months. The remaining four patients were reoperated on by Fowler-Stephens orchiopexy after 14 months. A technique is presented for the treatment of the UT after failure to respond to hormonal treatment. It consisted of clearing the testicular pathway of any adhesions and dilating the narrowed inguinal canal. The technique is simple, easy, and does not interfere with the testicle or spermatic cord.     

Hepatic histopathologic condition does not correlate with laboratory abnormalities in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count)

OBJECTIVE: Our objective was to categorize the histologic findings in the liver in patients with HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) and to correlate these findings with the severity of clinical laboratory abnormalities. STUDY DESIGN: Eleven patients with laboratory criteria for HELLP syndrome who required cesarean delivery underwent needle biopsy of the liver under direct visualization. RESULTS: Eight patients had periportal hemorrhage, and six had fibrin deposition. Fatty infiltration was seen in four, one with large-droplet fat, three with microvesicular fat. There was no statistically significant correlation between the severity of the histologic findings of periportal hemorrhage and fibrin deposition and the clinical laboratory findings. Fatty infiltration did not correlate with the severity of the HELLP syndrome's histologic condition, but, in contrast, did correlate with thrombocytopenia and aminotransferase elevations. CONCLUSIONS: Laboratory abnormalities do not accurately reflect the severity of the underlying histopathologic condition in HELLP syndrome. We propose that all patients with HELLP syndrome, regardless of the degree of their laboratory abnormalities, be treated aggressively, primarily with delivery.