ABSTRACT
Introduction: The cystic duct connects the gallbladder to the extra hepatic bile duct. In its endoluminal surface are the mucosal folds which are characteristic of the duct. Aim:-The aim was to study the length and mid-length diameter of the cystic duct and the mucosal folds of its endoluminal surface with respect to their number, location, and orientation. Subjects and Methods: This study was carried out in the Anatomy Department of Parul Institute of Medical Sciences and Research, Vadodara, on 40 specimens of 10% formalin fixed human cystic ducts, from 2015 to 2018, after obtaining permission from the Institutional Ethics Committee. The cystic duct was isolated and its lumen was exposed by an incision parallel to its length to study the folds. Results: The length of the cystic duct was between 0.4 to 4.2 cm, and the diameter was between 0.2-0.6cm. The mucosal folds were present in 38(95%) specimens and were absent in two (5%). The maximum number of mucosal folds present in a specimen was eleven. In the 25 (62. 5%) specimens they spanned the entire length and in 13(32.5%) they were present only in the proximal part. Their disposition was either oblique, transverse interdigitating, combination type or saccular. Conclusion: It gives insight into the internal morphology of the cystic duct. Various types of mucosal folds have been described, the knowledge of which will be important to the laparoscopic surgeons during various interventional approaches undertaken in this region.
ABSTRACT
Objective: Gaucher disease in India has been reported only in a few case reports from India. The aim of the study was to assess the response to enzyme replacement therapy in Indian patients with Gaucher disease. Design: Retrospective analysis of patients receiving CHO-derived recombinant macrophage-targetted glucocorebrosidase. Setting: Five centers from India with experience in treating lysosomal storage disorders. Patients: The diagnosis of Gaucher disease was confirmed by low glucocerebrosidase levels, though it was first made on splenectomy in 8 and on bone marrow examination in 9 patients. Twenty five of 52 patients diagnosed with Gaucher disease (17 Type I, 8 mild Type III) received treatment for >6 months. Indications for treatment included symptomatic anemia, thrombocytopenia, organomegaly, bone disease or mild neurological symptoms leading to impairment of quality of life. Patients with significant neurological involvement were excluded. The drug infusions were given intravenously every 15 days. Main Outcome measures: Hemoglobin, platelet counts, liver and spleen volumes and growth parameters. Results: 22 of the 25 children who survived were analyzed. After 6 months of treatment, the mean (range) increase in hemoglobin was 1.5 (-3.4 to 6.1) g/dL (P=0.01) and in platelet count was 32 x 109/L (-98.5 x 109 to 145.5 x109) /L (P=0.02). The mean (range) increase in weight was 3 kg (-5.6 to 10.5) (P=0.04) and in height was 7.1 cm (0 to 26.5) (P=0.0003). Liver size decreased by a mean (range) of 38.5% (- 5.5 to 86.7) (P=0.0003) and the spleen size by 34.8% (0 to 91.7) (P=0.004). All patients had improvement in bone pains and in 2 patients, neurological symptoms improved with others remaining static. Conclusions: This is the first reported cohort of patients in India reporting our experience with imiglucerase enzyme replacement therapy for treatment of Gaucher Disease in India.
ABSTRACT
Plasma fibrinogen levels were estimated in 56 patients of stroke, admitted in the hospital within 24 hours of symptoms. The levels were found to be raised significantly (531.73 +/- 74 mg%) compared to those of the age and sex matched control group (445.78 +/- 92.28 mg%). When the levels in stroke group with one risk factor were compared to those of individuals with comparable control group with same risk factor, a significant difference was observed in hypertensive, smokers, alcoholics and atherosclerotic stroke groups, which indicates that the observed rise is related to phenomenon of stroke rather than the associated risk factors. However, the rise observed in hypertensive stroke group (554.26 +/- 47.08 mg%) is significantly more (p. less than 0.01) than that occurring for nonhypertensive stroke group (497.82 +/- 93.12 mg%) indicating that the presence of hypertension does contribute to the rise.