Follow-up investigation in patients with anorexia nervosa

Sixty-three female patients with anorexia nervosa were assessed for outcome, on average 27.5 months after treatment. The treatment program, in a general adolescent medical service, is multidisciplinary, stressing appropriate weight gain in conjunction with various therapeutic modalities. Half the group required at least one hospitalization; the remainder received treatment as outpatients. Mean weight of the patients was 41.8 kg at first contact, 46.2 kg at conclusion of treatment, and 52.2 kg at follow-up. Average height at the time of follow-up was in the 38th percentile. Average weight was in the 15th percentile at first contact, and in the 29th percentile at follow-up. Current weight is 8% below ideal. Ninety-three percent of the patients had amenorrhea at diagnosis, and 9.5% at follow-up. Vomiting declined from 59% of patients to 16%. Vomiting was significantly associated with poor outcome. The majority function successfully, academically and vocationally. Most continue to restrict diet, and 79% consider themselves overweight. Forty percent report chronic feelings of depression, and 22% have unsatisfactory social relationships. The data suggest no difference in outcome between those receiving psychotherapy (65%) and those who did not (35%). Type and duration of therapy were also not associated with long-range improvement.     

Are vasopressin peripheral V1 receptors involved in the development of malignant hypertension and stroke in SHR-SPs?

Summary— The aim of this study was to determine whether activation of vasopressin (AVP) peripheral V₁ receptors is involved in the development of malignant hypertension, stroke, and end-organ damage in stroke-prone spontaneously hypertensive rats (SHR-SPs). For this purpose, young salt-loaded SHR-SPs were treated orally daily from their 5th to 34th week of age, by a selective AVP V₁ receptor antagonist, SR 49059, used in a dose (30 mg/kg) that achieved complete peripheral V₁ receptor blockade. Untreated SHR-SPs served as controls. SR 49059 slightly and transiently (8th to 10th week of age) limited the rise in blood pressure, but thereafter systolic blood pressure values were similar in the two groups of SHR-SPs. Stroke-related mortality was not significantly different in SR 49059-treated and in control animals (65% vs 65% at 30 weeks, 65% vs 83% at 34 weeks). SR 49059 did not prevent the increases in fluid intake, diuresis and proteinuria seen in controls. Histological examination of the brain, kidneys and heart revealed that the development of fibrinoid necrosis and arterial thickening was not prevented by SR 49059, nor was that of malignant nephroangiosclerosis and of myocardial infarction and fibrosis. These data strongly suggest that AVP peripheral V₁ receptor activation is not involved in the pathological processes that develop in SHR-SPs.     

Intrahepatic amebic abscesses: indications for and results of percutaneous catheter drainage

Medical therapy is standard for intrahepatic amebic abscess and generally is effective. However, we have encountered a group of patients in whom percutaneous aspiration and drainage was indicated due to uncertainty of diagnosis or clinical deterioration of the patient. Twenty such patients underwent percutaneous drainage with ultrasound or CT guidance, and each patient was cured (appropriate antibiotics were administered concomitantly). The specific indications for intervention were to differentiate pyogenic from amebic abscess, pain and imminent rupture, poor response to medical therapy, false-negative results of serologic tests, noncompliance with medical treatment, left lobe abscess, and pregnancy. Diagnosis of amebiasis from examination of the fluid was seldom possible, while findings from core biopsy of the wall of the abscess led to diagnosis in three cases. Recurrence necessitating redrainage occurred in three patients; in each, catheters were removed the same day drainage was performed. There were three minor complications. Differences from percutaneous management of pyogenic abscesses included more rapid removal of catheters (four days), more frequent use of US guidance, and more common use of the prone angled approach to avoid pleural contamination. Catheter drainage may be curative and may expedite care for problematic amebic liver abscesses in selected cases.     

The Mechanism of Enhanced Streptokinase-Induced Clot Lysis following In-vitro Factor-XIII Inactivation

S ummary . Factor-XIII (fibrin stabilizing factor, FSF) activity in human plasma may be inhibited in vitro by a variety of sulphydryl inhibitors and by several derivatives of glycine. Incorporation of small amounts (40 units) of streptokinase (SK) into a clot formed from plasma after in vitro inactivation of Factor XIII, resulted in marked shortening of clot lysis times compared to controls without Factor-XIII inactivation.
Enhancement of SK-induced clot lysis by the sulphydryl inhibitors is in part related to Factor-XIII inactivation. Further acceleration of lysis is noted with concentrations greater than the minimal amount necessary for complete Factor-XIII inhibition. At higher concentrations, clotting is delayed and ultimately completely inhibited. These reagents also produce marked changes on the thromboelastogram consistent with a weakened clot structure. No evidence to suggest increased plasminogen-plasmin conversion, enhanced plasmin activity or inhibition of anti-plasmin by sulphydryl inhibitors could be found.
Glycine ethyl ester (GEE) incorporation results in marked enhancement of SK-induced plasma clot lysis in vitro and pronounced changes on the thromboelastogram. The enhanced clot lysis is related to Factor-XIII inhibition. No further acceleration of clot lysis was obtained once Factor-XIII activity was completely inhibited. GEE alone shows an additional effect of inhibiting anti-plasmin activity.
Thus enhanced SK-induced clot lysis following in vitro inhibition of Factor-XIII activity with sulphydryl inhibitors and derivatives of glycine is considered to be due to the greater ease with which plasmin may act on a weakened clot. GEE, in addition to promoting the formation of a weaker clot, inhibits anti-plasmin activity, and so further increases the relative effectiveness of streptokinase.