Growth of the fetal gall bladder in normal pregnancies.

Our objective was to obtain dimensions of the fetal gall bladder as a basis, for further studies and to establish normative data to assess deviations in growth. The study group included 183 normal pregnant women from 13 to 40 weeks' gestation. Routine biometric measurements were obtained on all fetuses, including biparietal diameter, head and abdominal circumferences and measurements of the long bones and the two diameters of the fetal gull bladder. The gall bladder area and circumference were calculated for each gestational age.A linear growth function was observed across the gestational age and a first-degree correlation was found to exist between gestational age and both the longitudinal (r = 0.77067; p < 0.00001; y = -0.41060 + 0.0907 x gestational age) and transverse (r = 0.602; p < 0.00001; y = 0.58567 + 0.01925 x gestational age) diameters of the fetal gall bladder. A significant correlation was also found between gull bladder area and gestational age (r = 0.6878; p < 0.00001), biparietal diameter (r = 0.72768; p < 0.00001), abdominal circumference (r = 0.71363; p < 0.00001) and femoral length (r = 0.72190; p < 0.00001). In addition, a significant correlation was found between gall bladder circumference and gestational age (r = 0.76181; p < 0.00001), biparietal diameter (r = 0.80039; p < 0.00001), abdominal circumference (r = 0.78030; p < 0.00001) and femoral length (r = 0.79694; p < 0.00001).These results provide normative data of the fetal gall bladder in various dimensions and across gestational age. In addition, the data offer the potential for prenatal diagnosis of additional lesions in the extrahepatic biliary duct system.     

Papillary adenoma of the gall bladder: ultrasonic demonstration.

A papillary adenoma of the gall bladder was demonstrated by gray scale echography. The pathology of the tumor was described and the ultrasonic characteristics which distinguish it from a calculus were discussed.     

Ultrasonic parameters and relationship between compressive strength, microstructure of gall bladder stones.

Patients with symptomatic stones are at a great risk for complications and these complications are a major cause of morbidity. The gall bladder stones may have a complex structure and variable composition. In the present investigation stones have been grouped into three categories namely cholesterol, bilirubinate and mixed, and a correlation between the surface structure, ultrasonic parameters and compressive strength is estimated. A double-probe through-transmission technique was used for the ultrasonic parameters study, a universal testing instrument for hardness and a scanning electron microscope (SEM) for microstructure study. Gall bladder stones of mixed type with higher ultrasonic velocity, less attenuation and higher crushing strength were found to be more difficult to break in comparison to other types of stones. SEM of mixed type stones showed rough surface as compared to bilirubinate and cholesterol stones. The results obtained as well as the relationship might be useful in the design of a focussed ultrasonic 0lithotripter.     

Chenodeoxycholic acid therapy for gallstones: effectiveness, toxicity and influence on bile acid metabolism.

Chenodeoxycholic acid (1 g daily) was administered to 10 patients with gallstones and three patients with biliary stricture and recurrent cholangitis. Four gallstone patients showed diminution or disappearance of stones including one patient whose stone was in the common bile duct. The patients with recurrent cholangitis showed marked improvement in symptoms during treatment. Serum bile acid levels were significantly elevated in 8 gallstone patients during treatment. Liver biopsy in eight gallstone patients during treatment revealed minor changes in five. Lithocholic acid and bile acid sulphates were found in only small amounts in the bile of patients during treatment. No significant trend in biliary lipid composition during treatment was observed. There was no overall trend in the group of patients whose stones disappeared or diminished. Changes in biliary bile acid composition and in bile acid pool sizes were variable following treatment and could not be correlated with the clinical results of treatment. A further trial of chenodeoxycholic acid is recommended in patients with stones in the biliary tree and recurrent cholangitis who are not amenable to surgical treatment.     

Current therapy and drug pipeline for the treatment of patients with acromegaly

Introduction  Acromegaly is a multisystem disease resulting from chronic exposure to supraphysiological levels of growth hormone (GH), and is associated with significant morbidity and excess mortality. The etiology is almost exclusively an underlying pituitary adenoma. Current therapeutic interventions include surgery, radiotherapy, and medical therapy. Results  Despite surgery, around 50% of patients fail to achieve the biochemical targets shown to correlate with normalization of mortality rates. Radiotherapy is efficacious in controlling tumor growth and GH secretion; still, achievement of biochemical targets may take up to a decade and a number of safety issues have been raised with this treatment modality. Medical therapy, therefore, has an important role as adjuvant therapy in patients who fail to achieve control with surgery, or while awaiting the effects of radiotherapy to be realized. Furthermore, medical therapy is increasingly being used as primary therapy. Current medical therapies include dopaminergic agonists, somatostatin analogs, and GH receptor (GHR) antagonists. Dopaminergic agonists achieve biochemical targets in up to 30% of patients, and somatostatin analogs in around 60%. The currently available GHR antagonist pegvisomant effectively controls insulin-like growth factor-I levels in over 90% of patients; however, it has no effect on the tumor itself and has considerable financial implications. Research into optimizing the somatostatin and dopaminergic systems has led to promising advances in agonist development. Moieties with selectivity for various combinations of somatostatin receptor subtype receptors have been examined, along with molecules that additionally show high affinity for the dopaminergic D2 receptor. Of the molecules studied in vitro, only pasireotide (SOM230) and BIM-23A760 are currently undergoing further development. Other innovations to improve convenience of currently available drugs are also being investigated. Conclusion  Significant advances in under standing of the somatostatin and dopaminergic system have aided drug development. This may lead to new clinically available therapies enabling control of acromegaly in a larger proportion of patients, and at an earlier stage in their disease management.     

Cholesterosis of the gall bladder and atherogenic dyslipidemia: etiology, pathogenesis, clinical symptoms, diagnosis and treatment

AIM: To detect specific morphological signs of hepatic lesion in patients with cholesterosis of the gall bladder and atherogenic dyslipidemia in the presence of steatohepatitis. MATERIAL AND METHODS: Atherogenic dyslipidemia was detected in 150 patients with steatohepatitis. Ultrasound investigation diagnosed cholesterosis of the gall bladder in 51.3% patients. The protocol included the following examinations: analysis of the disease history, physical examination, laboratory, device and morphological tests. Thirty patients received therapy with ursodesoxycholic acid medicine for 3 months. RESULTS: Basic clinical symptoms of gall bladder cholesterosis (GBC) and its risk factors are defined. The biochemical blood test registered elevated levels of transaminase, alkaline phosphatase and bilirubin. All the patients had an atherogenic type of dyslipidemia. According to USI, a focal-reticular form of GBC prevailed. Histologic examination of the liver detected the following alterations: fat infiltration, portal and intralobular infiltration, hydropic dystrophy, binuclear hepatocytes, lobular hepatitis, fibrosis of the portal tracts, periductular fibrosis, ductual proliferation, ductual epithelium detachment. Histologically, the walls of the gall bladder contain foam cells in the mucous and submucous layer. The same changes were seen in the wall of the hepatic artery as well as cholesterol polyps, epithelial destruction. Ursosan treatment resulted in a significant lowering of total cholesterol. CONCLUSION: GBC seems to be a chain of successive conditions: lipid disbolism at the level of hepatocyte, development of steatosis, steatohepatitis, fibrosis, involvement of all anatomo-morphological structures of the liver including the biliary tract, GBC.     

膀胱过度活动症(OAB)治疗近况

膀胱过度活动症(overactive bladder，OAB)是常规的排尿功能障碍的临床症状，也是目前国内外研究的热点之一。OAB的异名很多，但有神经异常原因者，常称逼尿肌反射亢进(detrusor hyperflexia)。根据国际尿控协会将OAB定义为逼尿肌无意识收缩，前提是没有感染或其他明显的病理改变，表现为尿急，伴有／也可不会急迫性尿失禁，并且经常有尿频和夜尿症状。     

Improvement in the ultrasonic evaluation of the gall bladder by using the left lateral decubitus position.

The authors discuss the value of routinely using the left lateral decubitus position for ultrasound evaluation of the gall bladder. This technique often affords improved visualization, clarifies abnormalities suspected in the supine position, and in some cases demonstrates a gall bladder that cannot be seen in the supine position.     

Assessment of experts' approach to insulin therapy and development of a simulator for diabetes insulin adjustment.

OBJECTIVE--To develop a computer program (Macintosh) to predict changes in blood glucose after changes in insulin dose, timing, and regimen. RESEARCH DESIGN AND METHODS--We established program parameters (apparent insulin action profiles; different for insulin-dependent and non-insulin-dependent diabetes mellitus) to match predictions by five diabetes specialists at our hospital of blood glucose changes after insulin-dose adjustment in 22 hypothetical patient cases. We compared the action profiles, which represent the blood glucose changes predicted by the experts with glucose-clamp studies of insulin action. We tested the program's performance in 22 different hypothetical cases against the responses of 15 specialists from outside our hospital. RESULTS--The specialists, when predicting effects of insulin dose adjustment, integrate numerous processes (insulin action, diet, sequential blood glucose interactions). They could not specify algorithms for determining these individual factors, but they could easily predict the overall effect in the context of patient cases. The computer program's insulin-action profiles simulate this "composite" approach. The developed program incorporates multiple insulin regimens, which may be changed during the stimulation, and adjusts predicted responses according to the patient's estimated sensitivity to insulin. Its predicted change in 172 blood glucose levels (22 cases) correlated well with the corresponding means of the outside specialists (r = 0.83, P = 0.0001). Comparing this correlation with that of individual specialists ranked the program third. CONCLUSIONS--A computer program can simulate specialists' "composite" approach (not based purely on conscious application of physiological data) to insulin adjustment.     

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of pancreozymin-cholecystokinin on immunoreactive somatostatin release were studied in the isolated perfused dog pancreas. Gastrin at a concentration of 65 ng/ml and the octapeptide of pancreozymin-cholecystokinin at a concentration of 25 ng/ml produced a prompt, but transient statistically significant, twofold rise in mean somatostatin concentration. Secretion at a concentration of 0.3 U/ml and gastric inhibitory polypeptide concentration of 58 ng/ml produced a prompt two- to threefold rise in mean somatostatin release, which persisted throughout the perfusion period. With all four polypeptides the pattern of the somatostatin response resembled that of insulin. It appears that pancreatic somatostatin release is stimulated by gastrointestinal hormones that influence the secretion of insulin and glucagon.