Transjugular intrahepatic portosystemic shunt for variceal hemorrhage due to recurrent of hereditary hemorrhagic telangiectasia in a liver transplant.

Hepatic involvement in hereditary hemorrhagic telangiectasia (HHT) consists of vascular malformations associated with arteriovenous (AV), arterioportal, and/or portovenous shunting. Most patients with HHT have liver involvement. Symptoms, although rare, consist of cardiac failure, pulmonary hypertension, portal hypertension, portosystemic encephalopathy, cholangitis, and atypical cirrhosis. Reported treatments for symptomatic AV malformations have been associated with substantial morbidity and mortality. This report describes a case of hepatic HHT that required liver transplantation after hepatic artery embolization. Recurrent vascular malformations developed in the transplant, resulting in portal hypertension and life-threatening variceal hemorrhage that was controlled with transjugular intrahepatic portosystemic shunt creation.

MDCT angiography of mesenteric bypass surgery for the treatment of chronic mesenteric ischemia.

OBJECTIVE: Chronic mesenteric ischemia (CMI) is a serious condition that requires surgical or endovascular intervention. Surgical revascularization for the treatment of CMI uses different operative techniques including endarterectomy, vessel reimplantation, and mesenteric bypass. A basic understanding of the operative techniques is essential for the adequate interpretation of imaging studies in patients who have undergone surgery for CMI. In this article, we review the different operative techniques used in the treatment of CMI, discuss the results of surgical intervention for CMI, and illustrate how MDCT angiography (MDCTA) can be used for follow-up and for the detection of early and late complications after surgery. CONCLUSION: MDCTA is a powerful tool for the postoperative evaluation of patients with CMI. Early detection of graft dysfunction is critical to prevent graft occlusion and the development of potentially fatal mesenteric ischemia. MDCTA can detect early and late complications after surgery and guide additional surgical or endovascular interventions.

Recognizing pitfalls in early and late migration of clip markers after imaging-guided directional vacuum-assisted biopsy.

Directional vacuum-assisted biopsy has become an irreplaceable tool in the management of suspicious mammographic lesions. Often, the entire lesion is removed and clips are used to localize the biopsy site. Postbiopsy mammograms are used to determine the adequacy of clip placement and the location of the clip. Clip displacement from the site of deployment is not an uncommon finding. Clips may migrate within the same quadrant where the lesion was located or to another quadrant of the breast. Clip migration may occur immediately after biopsy or may be seen on later follow-up mammograms. Clip migration can affect interpretation of mammographic findings and localization for future surgery. It should not be assumed that the clip is correctly located at the biopsy site on subsequent mammograms. It is essential to recognize the relationship of the clip to the targeted lesion to ensure accurate localization of lesions that require surgical excision.

Midaortic syndrome associated with fetal alcohol syndrome.

Midaortic syndrome (MAS) is an uncommon condition characterized by progressive narrowing of the abdominal aorta and its branches and impressive formation of collateral circulation. It affects children and young adults and presents predominantly as untreatable hypertension. Fetal alcohol syndrome (FAS) refers to a constellation of physical, behavioral, and cognitive abnormalities secondary to alcohol exposure in utero. The authors present an unusual association between a hypoplastic abdominal aorta and fetal alcohol syndrome. The patient discussed in this article presented with severe hypertension that was successfully treated with renal angioplasty.

Phase I and pharmacokinetics study of crotoxin (cytotoxic PLA(2), NSC-624244) in patients with advanced cancer.

A Phase I clinical trial was performed on patients with solid tumors refractory to conventional therapy. Crotoxin was administered i.m. for 30 consecutive days at doses ranging from 0.03 to 0.22 mg/m(2). Patients entered the study after providing a written informed consent. Although 26 patients were entered only 23 were evaluated. Reversible, nonlimiting neuromuscular toxicity evidenced as diplopia because of pareses of the external ocular muscles was present in 13 patients. It started at doses of 0.18 mg/m(2) and lasted from 2 to 6 h. These episodes did not require dose adjustment and disappeared in 1-3 weeks of treatment. Three patients experienced palpebral ptosis, nystagmus (grade 2), and anxiety (grade 2-3) at the dose-limiting toxicity of 0.22 mg/m(2). Also at dose-limiting toxicity, 1 patient showed nystagmus (grade 2) and anxiety (grade 3) without evidence of palpebral ptosis. Transient increases (grades 1-3) in the levels of creatinine kinase, aspartate aminotransferase, and alanine transaminase attributed to crotoxin myotoxicity were observed but returned to normal by the last week of treatment. At 0.21 mg/m(2) there was a case of grade-3 anaphylactic reaction on day 31, which required treatment. Hypersensitivity was regarded as an adverse drug-related reaction, and the patient was removed from the protocol. Two patients at different doses (0.12 mg/m(2) and 0.22 mg/m(2)) had sialorrhea. Four patients had asymptomatic transient increase in blood pressure (up to 20 mm Hg) 12 h after the first injection, which lasted 24 h. No treatment was required and toxicity did not reappear. Six patients experienced slight eosinophilia during the first 2 weeks. The maximum tolerated dose was set at 0.21 mg/m(2). Objective measurable partial responses (>50% reduction of tumor mass) were noted in 2 patients treated at 0.21 mg/m(2) and 1 at 0.12 mg/m(2). One patient (at 0.21 mg/m(2)) presented a complete response on day 110. Crotoxin pharmacokinetics showed rapid absorption from the injection site to blood (t(1/2 A) = 5.2 +/- 0.6 min). Plasma concentration reached a peak (C(max) = 0.79 +/- 0.1 ng/ml) at tau(max) = 19 +/- 3 min. The half-life of the distribution (alpha) phase is 22 +/- 2 min. Starting at 1.5 h after injection, the decrease in plasma concentration becomes slower, reaching 14 +/- 3 pg/ml 24 h after injection. The profile is dominated by the elimination (beta) phase with a half-life of 5.2 +/- 0.6 h. Consequently, 24 h after the injection ( approximately 5 half-life) 97% of the product was eliminated. The area under plasma concentration versus time curve was 0.19 +/- 0.05 microg/min/ml. Assuming availability (F) approximately 1, the clearance is C(L) = 26.3 +/- 7 ml/min, and the apparent volume of distribution is V(d) = 12 +/- 3 liter/kg. The recommended dose for a Phase II study is 0.18 mg/m(2).