Acute abdomen secondary to ascaris lumbricoides infestation of the small bowel.

Ascariasis is a helminthic infection commonly found in tropical climates. It often propagates in communities of low socioeconomic status secondary to contamination of the soil and water supply with human feces. We present a case report of a 42-year-old Asian-Indian female presenting with a long-standing history of severe recurrent postprandial epigastric pain, requiring multiple hospital admissions. Ultrasound, computed tomography (CT), and nuclear biliary scan were negative. She underwent esophagogastroduodenoscopy that suggested ischemia. Magnetic resonance angiography (MRA) and mesenteric angiography were inconclusive. As conservative treatment had been unsuccessful, a small bowel series was performed. The radiographs demonstrated characteristic findings of Ascaris lumbricoides infestation. Although the prevalence, diagnosis, and subsequent treatment of an acute abdomen secondary to Ascaris lumbricoides infestation is commonly seen in developing countries, clinicians in developed countries may not consider this entity when faced with a patient with similar symptoms. We frequently care for immigrants from developing countries and our own citizens who visit the countries where ascariasis is endemic. Therefore, heightened awareness of Ascaris lumbricoides infection (ALI) presenting as an acute abdomen is necessary. The diagnosis requires an experienced radiologist and knowledge by the clinician of treatment options and of when a surgeon should be involved.

The effects of 17 alpha-methyltestosterone on myocardial function in vitro.

Testosterone analogs have been used as performance enhancers by athletes for more than 40 yr. We asked whether the anabolic steroid 17 alpha-methyl-4-androstene-17-ol-3-one (17 alpha-MT) would affect intrinsic contractile function of the heart. Male Sprague-Dawley rats, 125-150 g, were treated with 17 alpha-MT either parenterally or orally for up to 8 wk. Intrinsic contractile function of the hearts was assessed utilizing both the isolated working heart and isovolumic perfused heart preparations. Isolated working hearts from 17 alpha-MT-treated rats had a 45% decrease in heart work attributable largely to a similarly decreased stroke volume. Isovolumic perfused hearts from treated animals had elevated left ventricular systolic and diastolic pressures at similar interventricular volumes compared to controls. Rates of ventricular pressure development (+dP/dT) or relaxation (-dP/dT) were unchanged as a result of the treatment. However, static elastance was reduced in potassium-arrested hearts from the 17 alpha-MT treatment (63% increase in interventricular pressure), consistent with a limitation being imposed on stroke volume by a decreased myocardial compliance. Hydroxyproline content of the hearts was not altered by 17 alpha-MT treatment suggesting that increased stiffness was not a consequence of collagen proliferation. Treatment of the steroid rats with beta-aminopropionitrile, a compound that inhibits lysyl oxidase, restored the left ventricular volume-pressure relationship (elastance curve) to that of control hearts. Thus, chronic treatment with anabolic steroids appears to reduce left ventricular compliance, possibly related to an enhanced activity of lysyl oxidase, and results in increased crosslink formation between collagen strands in the extracellular matrix.

The effect of clenbuterol and recombinant erythropoietin on tumor growth and the anemia caused by the Walker 256 carcinosarcoma.

In patients with advanced cancer, anemia is a common complication indicative of a poor prognosis. Attempts to alleviate this have met with mixed success and interventions including erythropoietin often fail to elicit an appropriate response. We have used rats implanted with the Walker 256 carcinosarcoma as a model of non-responsive anemia. This study demonstrates that the provision of recombinant erythropoietin in the presence of clenbuterol, a beta2 agonist, attenuates both the cancer induced anemia and the growth of the tumor in this model. We hypothesize that this treatment relieves the tumor induced inhibition of hematopoiesis, which allows for not only an increase in hematocrit but an increased immunosurveillance resulting in tumor suppression.