Willard A. Burns

Fibrosarcoma occurring at the site of a plastic vascular graft.

A sarcoma, arising in association with a prosthetic arterial graft, was surgically excised. The patient, a 31‐year‐old man, sustained a soft tissue injury to the thigh 10 years previously. A lacerated superficial femoral artery was repaired with a woven teflon‐dacron graft. A large tumor surrounded, but did not invade, the graft. The tumor posed diagnostic difficulties and was thought to be either an angiosarcoma or a fibrosarcoma. Electron microscopy, performed retrospectively, showed the tumor to be probably a fibrosarcoma. The relationship of the tumor to the graft and similar experimentally induced tumors are discussed.

THE SEVERITY OF COPPER DEFICIENCY CAN BE AMELIORATED BY DEFEROXAMINE

The present study was undertaken in order to determine whether hepatic iron overload plays a role in the exacerbation of copper deficiency. Weanling male Sprague-Dawley rats were fed a copper-deficient (0.6 microgram Cu/g) diet containing 62% fructose for 5 weeks. Some of the copper-deficient rats were injected daily with deferoxamine (DFX), an iron chelator that has been widely used to reduce iron overload. DFX reduced hepatic iron concentrations, which in turn ameliorated the pathology of copper deficiency when compared with nontreated copper-deficient animals. It is suggested that hepatic iron overload in a reduced environment plays a major role in the exacerbation of copper deficiency. Once the concentration of hepatic iron is reduced, the severity of the deficiency should be improved.

Hepatic injury associated with nitrofurantoin therapy.

The clinical and biochemical findings on two patients who developed hepatic injury while taking nitrofurantoin are described. In both patients the main biochemical abnormality was elevation of serum transaminase values. Clinical and biochemical findings reverted to normal after with-drawal of medication. Nitrofurantoin was readministered to one patient, and hypertransaminasemia recurred. The light-microscopic and ultrastructural findings from hepatic biopsy specimens from both patients were those of a predominantly hepatocellular type of injury. Different pathogenic mechanisms are postulated for the hepatic injury in the two patients. Six previously reported cases are compared and contrasted with the present patients.

Low dietary iron prevents free radical formation and heart pathology of copper-deficient rats fed fructose.

Abstract Two studies were conducted to determine whether hepatic iron overload in rats fed fructose plays a role in the exacerbation of the signs associated with copper deficiency. When fed the adequate iron diet (50 μg Fe/g), copper-deficient rats fed either fructose or starch exhibited hepatic iron overload of similar magnitude. However, only livers of copper-deficient rats fed fructose exhibited the presence of high peaks associated with an iron compound detected by electron spin resonance. In addition, only copper-deficient rats fed fructose developed anemia, pancreatic atrophy, and heart hypertrophy with histopathologic changes, and they died prematurely of heart-related abnormalities. Lowering dietary iron from 50 μg/g to 30 μg/g was not sufficient to protect the animals against the pathologic consequences of copper deficiency. In contrast, the consumption of a fructose diet inadequate in both copper (0.6 μg/g) and iron (17 μg/g) resulted in the reduction of hepatic iron, which in turn caused the amelioration of the deficiency, compared with rats fed the adequate iron (50 μg/g) diet. None of these rats developed pancreatic atrophy, none exhibited myocardial lesions, and none died of the deficiency. Electron spin resonance spectra of their livers did not show the presence of free radicals. The data suggest that hepatic iron overload plays a role in the exacerbation of copper deficiency only when fructose diets are consumed.

Clinical conditions associated with columnar lined esophagus.

Three case reports are presented which illustrate clinical conditions which may arise in a patient with a columnar lined esophagus. Inflammation, ulceration, stricture and fistula formation are discussed, with emphasis on their clinical presentations and diagnoses by endoscopy and radiology. Of the 3 patients, 2 developed adenocarcinoma as a complication of the lesion. The possible malignant potentiality of this anomaly is stressed, and diligent search for a neoplastic focus in all such cases is urged.

Rheumatic heart disease in a patient with acquired immunodeficiency syndrome

Acute rheumatic heart disease (RHD) with Aschoff nodules and biventricular dilation was diagnosed at autopsy in a patient with acquired immunodeficiency syndrome who died of pneumonia due to Pneumocystis carinii. The relationship of acute RHD and human immunodeficiency virus-associated immune deficiency is discussed.

Effect of coenzyme Q10 supplementation on cardiac hypertrophy of male rats consuming a high-fructose, low-copper diet

Administration of coenzyme Q10 to humans and animals has a beneficial effect on a number of cardiac diseases. The purpose of the present study was to determine if coenzyme Q10 treatment could ameliorate cardiac abnormalities associated with the carbohydrate × copper interaction in rats. Weanling male rats were provided with a copper-deficient diet (0.6 μg Cu/g) containing either 62.7% starch (S−Cu) or fructose (F−Cu) for 5 wk. Half of the rats provided with the F−Cu diet were given daily oral supplements of 300 mg coenzyme Q10/kg body weight (F−Cu+Q). Heart hypertrophy, liver enlargement, or pancreatic atrophy were not affected by, nor was body growth or anemia improved by, supplementation with coenzyme Q10 when compared to rats fed only the F−Cu diet. Hearts from rats fed the F−Cu diet had severe inflammation, degeneration, fibrosis, and giant mitochondria with abnormal cristae. Hearts from F−Cu+Q rats had similar mitochondrial changes as the F−Cu rat hearts but without any apparent degenerative changes. None of the F−Cu+Q rats, but 30% of the F−Cu rats, died during the study as a result of heart rupture. These observations show that whereas coenzyme Q10 treatment did not prevent the cardiac hypertrophy of the carbohydrate × copper interaction, it did play a role in maintaining the integrity of the heart.

Leiomyoma of the ileum presenting as perforated viscus

SummaryA 50-year-old white male presented with an “acute abdomen” secondary to perforation of a leiomyoma. After operative treatment, the patient has had an uneventful course for the past year.