Tuberculous aortoarteritis is a distinct entity. Despite the still wide prevalence of active tuberculosis in developing countries, tuberculous aortoarteritis appears to be rare. The vessel is often involved by a direct extension of the disease from adjacent tuberculous tissue. Occasionally it may result from blood-borne seedlings from an active distant focus. True and false aneurysms are the common manifestations. Stenosing and/or constricting types of lesions and perivascular fibrosis have been encountered by us. The probable pathogenesis is discussed with illustrative cases.
This report presents the clinical features of 78 cases of the chronic Budd-Chiari syndrome encountered over a period of 13 years. The diagnosis of hepatic venous outflow obstruction was confirmed by venographic studies in all cases. In 20 patients there was hepatic vein occlusion without inferior vena caval (IVC) obstruction (Group A). In 17 patients there was constriction of the IVC above the drainage site of the right hepatic vein which was patent (Group B). In 13 patients there was short segmental obstruction of the hepatic segment of the IVC along with blockage of the hepatic venous orifices (Group C). In 28 patients there was hepatic venous obstruction with long segment involvement of the IVC extending to varying lengths of the infrahepatic segment (Group D). Of particular interest are the operative findings in 12 of 17 patients of Group B of hour glass constriction of the IVC, which can be labelled as 'coarctation of the IVC'. Dorsal cavoatrial bypass using a polytetra fluoroethylene graft has proved useful in Group B. Interesting histopathological findings of the liver in some of the cases are also described; The possible aetiology of the Group B cases is discussed.
Extra- and intrasplenic arterial aneurysms have occasionally been encountered in cases of portal hypertension both with and without cirrhosis. The exact pathogenesis is speculative; however, it is postulated that hyperkinetic splenic circulation, probably related to hepatic arterial insufficiency or hypoplasia, constitutes the primary pathogenic mechanism. Other factors such as splenomegaly and hormonal influence may be contributory.
Menorrhagia during the reproductive years may be caused by an imbalance in the metabolism of local endometrial prostaglandins [1]. A micronized purified flavonoid fraction (MPFF; Daflon 500, Serdia, India) containing 90% of diosmin and 10% of flavonoids expressed as hesperidin has been shown to suppress prostaglandins E 2 , F 2a , thromboxane A 2 , and prostacycline; reduce capillary hyperfragility; and increase lymphatic drainage [2]. This study examines the efficacy of MPFF in preventing ovulatory menorrhagia and dysmenorrhoea due to dysfunctional uterine bleeding.In the absence of an institutional review board, the authors approved the study protocol. Consecutive outpatients aged between 20 and 45 years who had a history of untreated menorrhagia over the three previous cycles were identified. Following a detailed examination that included transvaginal ultrasonography, hysteroscopy, and endometrial biopsy, those with ovulatory cycles but no evidence of pregnancy, pelvic pathology, coagulation disorder, hypothyroidism, or hepatic or renal disease, and who were not taking steroids or using an intrauterine contraceptive device, were selected for the study.After obtaining informed consent, MPFF was prescribed at a dose of 1000 mg/day (2 tablets of 500 mg) 5 days prior to the expected onset of menstruation (preventive phase) and up to the end of bleeding (treatment phase) for three consecutive cycles. The women were trained to use a pictorial blood assessment chart (PBAC) [3] and were followed up for three cycles.The 36 patients studied had a mean (S.D.) age of 33.3 (7.1) years, with a clinical history of menorrhagia for 11.7 (14.4) months. The effect of treatment on the variables studied is shown as mean change from baseline in Table 1 and as the proportion of patients showing improvement on 0020-7292/$ -see front matter D
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