Extrapelvic endometriosis: diagnosis and treatment.

BACKGROUND: Young women with nondescript abdominal pain can be difficult to diagnose. Although extrapelvic endometriosis is infrequent, we have treated 7 patients over the past 3 years with endometriosis in the abdominal wall, inguinal canal, or surgical incisions as the etiology of their symptoms. PATIENTS AND METHODS: We reviewed the medical records of patients whose final pathology report confirmed a diagnosis of extrapelvic endometriosis. Seven women who were treated at the University of Rochester Strong Memorial Hospital from May 1, 1991 through April 30, 1994 were identified. RESULTS: All patients were premenopausal with no history of pelvic endometriosis. In 4 patients, symptoms were cyclical. Surgical excision was initially curative in 5 patients. Two women required reexcision. The diagnosis of endometriosis was established at exploration by gross appearance and by frozen section. CONCLUSIONS: Endometriosis should be included in the differential diagnosis of a symptomatic mass in a celiotomy scar, the abdominal wall, or the inguinal canal. Principles of management include obtaining an accurate diagnosis and performing an adequate excision to prevent recurrence.

Chondroid chordoma. Case report and literature review.

A case of the chondroid variant of chordoma is presented. The differentiating features of this entity are discussed on a clinical and histopathologic basis. A review of the topic of chordoma is also provided.

The relation of hypercholesterolemic fatty streaks to intimal permeability changes shown by Evans blue.

The aortic localization of diet-induced fatty streaks in relation to focal increases in intimal permeability was evaluated in cynomoglus monkeys. Animals fed a hypercholesterolemic diet and studied at 10, 15, and 100 days had increasing intensity of Evans blue dye uptake. The overlap of fatty streaks with areas of dye intake increased as the areas of dye uptake enlarged, but all hypercholesterolemic groups showed some fatty streaks not topographically related to areas of dye uptake or flow instability. Because the upper thoracic aorta tended to show more advanced fatty streak formation dissociated from evident permeability change or hydraulic instability, it is suggested that mechanical factors associated with the geometric configuration of the descending thoracic aorta may have a significant role in the localization of some hypercholesterolemic fatty streaks.

The CLUE test. A multiparameter coagulation and fibrinolysis screening test using the platelet aggregometer.

Optical density measurements of plasma clot formation and lysis were recorded using a platelet aggregometer and strip chart recorder. It was discovered that, by adding standard solutions of ellagic acid-activated partial thromboplastin, urokinase, and CaCl2, and monitoring the reaction via the recorder, characteristic curves would be generated by normal human plasma. The curve segments were labeled Tc (clotting time), which correlated with the activated partial thromboplastin time, Fc (maximum optical density change), which paralleled fibrinogen concentration, and Tl (lysis time), which corresponded generally to plasminogen levels. Deviations from normal curve segments, observed in disseminated intravascular coagulation, hypo- and hyperfibrinogenemia, factor VIII deficiency, severe hepatocellular disease, juvenile rheumatoid arthritis, and neonates (normally low in plasminogen), indicated abnormalities which were substantiated by standard procedures. This new test, given the acronym "CLUE" for clotting and lysis, urokinase enzyme activated, appears to be sensitive, inexpensive and easily performed on a sample of 0.2 ml. of plasma in only 15 minutes.

Myocardial injury from transthoracic defibrillator countershock.

Myocardial damage resulting from transthoracic administration of direct current with cardiac defilbrillators present in clinical use was studied in 66 dogs. Electrodes were applied to the thoracic skin. All direct current discharges were delivered via a commercially available defilbrillator. Most of the animals received ten consecutive discharges with a dial setting of 400 watt-seconds. Animals were killed from 3 to 14 days after receiving the discharges. Myocarial necrosis was produced in most of the animals. The lesions were characterized by sharply localized areas of muscle necrosis that progressed to fibrous scars. Mineralization of damaged muscle and florid proliferation of large mononuclear cells were striking features of the lesions.

Utilization of long-chain free fatty acids by human platelets.

There was a rapid net uptake of free fatty acid (FFA) by human platelets when long-chain FFA, bound to human serum albumin, were incubated with platelet suspensions. Results from experiments in which both palmitate and albumin were labeled indicated that the fatty acid dissociated from the protein during uptake. Much of the FFA taken up by the platelet in short-term incubations remained in unesterified form, i.e., it was recovered as platelet FFA. As the incubation continued, increasing amounts of FFA were oxidized to CO(2) and incorporated into platelet lipid esters, particularly lecithin. Essentially all of the fatty acid that was incorporated into the platelet FFA fraction was released rapidly from the cells when they were exposed to a medium containing FFA-free albumin. The magnitude of uptake into the platelet FFA fraction was similiar at 0 degrees and 37 degrees C. Likewise, the rate and magnitude of FFA release from the platelet were similar at 0 degrees and 37 degrees C. Therefore, it is likely that both FFA uptake and FFA release occur by energy-independent mechanisms. The major effect of increasing the FFA concentration of the incubation medium was increased fatty acid uptake into the platelet FFA fraction. Similar results occurred when platelets were incubated in human plasma containing increasing amounts of added palmitate. At a given extracellular FFA concentration, considerably more of the saturated fatty acids, palmitate and stearate, were taken up as platelet FFA than either oleate or linoleate.

Effects of triiodothyronine-induced hypermetabolism on factor 8 and fibrinogen in man.

Triiodothyronine (liothyronine sodium) (400-500 mug/day for 14 days) was given to six normal subjects. Factor VIII (antihemophilic globulin) activity increased from 109 to 167% (P < 0.05); fibrinogen increased from 344 to 581 mg/100 ml (P < 0.01). To test whether the increases in factor VIII activity and fibrinogen were mediated by beta adrenergic receptors, propranolol (20 mg every 6 hr) was given orally to four other normal subjects in addition to triiodothyronine for 14 days. Factor VIII increased from 100 to 161%; fibrinogen increased from 374 to 564% (P < 0.01). Factor VIII activity did not change in a severe classical hemophiliac made hypermetabolic with triiodothyronine, but it increased from 39 to 82% in a patient with von Willebrand's disease. Triiodothyronine-induced hypermetabolism increased the incorporation of selenomethionine-(75)Se into plasma fibrinogen. These results suggest that the increases in clotting factor activity during triiodothyronine-induced hypermetabolism reflect an effect of increased protein synthesis rather than enhanced stimulation of beta adrenergic receptors.

Toxic effects of glucagon-induced acute lipid mobilization in geese.

The toxic effects associated with rapid lipid mobilization and a high plasma free fatty acid (FFA) concentration produced by glucagon were evaluated. Glucagon (0.5 mg/kg of body wt) was injected intravenously into nonfasting geese. The geese developed rapid respirations and high plasma FFA levels within 15 min after the glucagon injection; three of eleven died. Control geese, injected with saline, did not exhibit toxic signs. Peak FFA concentrations developed 15 min after glucagon and high levels persisted for over 90 min. Geese injected with glucagon frequently developed electrocardiographic abnormalities that included supraventricular tachycardia, premature ventricular contractions, and signs of myocardial ischemia. Light and electron microscopy revealed acute myocardial degeneration and fatty infiltration of the liver. The increase in plasma FFA concentrations and toxic effects were not prevented by pretreatment with nicotinic acid or propranolol.