Unilateral male breast masses: cancer risk and their evaluation and management.

Breast cancer is an uncommon cause of breast enlargement in the adult male. Overall, it accounts for <1 per cent of all male cancers. Although most male breast carcinomas are clinically apparent, distinguishing early breast cancer from gynecomastia, the most common cause of male breast enlargement, is considered a difficult task. To overcome this difficulty, many surgeons proceed directly to surgery as their initial diagnostic test. Although appropriate in some cases, the infrequent occurrence of male breast cancer and the diagnostic accuracy of mammography and fine-needle aspiration cytology suggest a modification of our present management. The aim of this study was to assess the incidence of breast cancer in men with unilateral breast masses and to propose a treatment algorithm for unilateral male breast masses. The medical records of 36 male patients who underwent subcutaneous mastectomy for a unilateral breast mass at the Buffalo Veterans Administration Medical Center between 1989 and 1996 were retrospectively reviewed. Data was collected on a standard data form. The median age was 63-years-old (range, 22-82). Gynecomastia was diagnosed in 30 patients (83%), lipoma in 4 patients (11%), invasive breast cancer in 1 patient (3%), and melanoma in situ in 1 patient (3%). Of the 30 patients with gynecomastia, 60% (18 patients) gave a history of a medical condition or use of medications known to cause gynecomastia, compared with 16 per cent (1 of 6) of the patients without gynecomastia (P = 0.08). Half of the patients with gynecomastia presented with an asymptomatic mass compared with 67 per cent of the patients without gynecomastia (P = not significant). The median duration of symptoms for patients with gynecomastia was 3 months. Men with unilateral breast masses have a low incidence of breast cancer. A male patient with a palpable unilateral breast mass consistent with gynecomastia on the basis of historical, physical and mammographic findings does not require surgical biopsy unless other clinical indications prevail. Lack of symptoms (pain) related to the mass is probably not helpful in deciphering gynecomastia from breast cancer.

Effect of allopurinol on venous endothelial dysfunction after resuscitated hemorrhagic shock.

BACKGROUND: Blood flow deficits contribute to organ dysfunction in patients resuscitated from hemorrhage. AIM: To determine the contribution of xanthine oxidase mediated reperfusion injury to venous endothelial function after resuscitated hemorrhagic shock. METHODS: Rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment animals received a 50mg/kg bolus and a 25mg/kg/h infusion of the xanthine oxidase inhibitor allopurinol (allo) after shock but before resuscitation with shed blood and an equal volume of Ringer's lactate. A similarly resuscitated group (Std) and a non-hemorrhage group (No HS) served as control. Endothelial function was quantified at baseline, 30 min (R30) and 90 min (R90) post resuscitation as a change in mesenteric vessel diameter after topical application of acetylcholine (Ach), an endothelial dependent vasodilator. RESULTS: Resuscitation restored cardiac output and blood pressure in both hemorrhage groups. First order venules (V1) demonstrated a 39% and a 36% reduction in ability to dilate to Ach at R30 and R90 after resuscitation with shed blood and Ringer's lactate (Std). Second order venules (V2) demonstrated a 20% and a 25% reduction in ability to dilate to Ach at R30 and R90 after resuscitation with shed blood and Ringer's lactate (Std). Addition of allopurinol to standard resuscitation attenuated this response resulting in the preservation of endothelial dependent venous vasodilation. CONCLUSIONS: These data suggest that xanthine oxidase mediated ischemia-reperfusion injury contributes to venous endothelial dysfunction in the mesenteric microcirculation after resuscitated hemorrhagic shock. Endothelial function can be preserved by the addition of the xanthine oxidase inhibitor allopurinol to standard resuscitation lending support for its inclusion as an adjunct to resuscitation after hemorrhagic shock.

Justification for visceral angiography prior to pancreaticoduodenectomy.

The hepatic arterial anatomy is aberrant in almost 50 per cent of all individuals. The most common anomalies include the right hepatic artery arising from the superior mesenteric artery (25%) and the left hepatic artery arising from the left gastric artery (25%). Anomalies of the common hepatic artery, usually a branch of the celiac artery, are rare. A replaced common hepatic artery originating from the superior mesenteric artery occurs in 2.5% of the entire population. Injury to hepatic blood supply is more common in the presence of aberrant arterial anatomy. Knowledge of aberrant arterial anatomy in patients about to undergo pancreaticoduodenectomy can lead to measures to preserve the vessels, and avoid fatal hepatic injury. We present a patient with a replaced common hepatic artery originating from the superior mesenteric artery successfully treated with a standard pancreaticoduodenectomy for pancreatic adenocarcinoma. The anomalous vessel was identified on visceral angiography, performed as part of the initial preoperative evaluation. At the time of laparotomy, the artery followed a course atypical for replaced hepatic arteries, lying medial to the common bile duct, and closely mimicking the gastroduodenal artery that would normally be divided during a Whipple procedure. This case emphasizes the importance of preoperative visceral angiography and the margin of safety it can provide when that knowledge is used in the operative strategy. Visceral angiography should be considered routine before pancreaticoduodenectomy, particularly in surgical residency training programs.

Xanthine oxidase inhibition after resuscitated hemorrhagic shock restores mesenteric blood flow without vasodilation.

To determine the contribution of xanthine oxidase-mediated reperfusion injury to the blood flow deficits seen in the intestinal microcirculation after resuscitated hemorrhagic shock, rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment animals received a 50 mg/kg bolus and a 25 mg/kg/h infusion of the xanthine oxidase inhibitor allopurinol after shock but before standard resuscitation with shed blood and an equal volume of Ringer's lactate. A similarly resuscitated group served as control. Blood flow and vessel diameters were measured in the neurovascularly intact terminal ileum using intravital microscopy and doppler velocimetry. Resuscitation restored cardiac output and blood pressure in both groups. Blood flow in first order arterioles 120 min postresuscitation was 41% of baseline in the standard resuscitation group and 77% of baseline in the allopurinol-treated group. A1 arteriolar diameter was not significantly different between the two groups, being 73 and 82% of baseline, respectively. These data suggest that xanthine oxidase-mediated ischemia-reperfusion injury contributes to blood flow deficits in the small intestinal microcirculation after resuscitated hemorrhagic shock and that the improvement in blood flow seen with allopurinol is not due to vasodilation within the microvasculature.

Heat shock protein 70 expression in native and heterotopically transplanted rat hearts.

Heat shock proteins (hsp) are intracellular proteins that are rapidly synthesized in response to a variety of stress factors. Recent studies in rats have shown that these proteins can elicit a lymphocyte response during cardiac allograft rejection. We studied the expression of the inducible (i) and constitutive (c) forms of hsp70 in rat cardiac allograft and isograft recipients to evaluate their utility as indicators of transplant rejection. Heterotopic transplantation of rat hearts was performed, using Lewis to Lewis isografts and ACI to Lewis allografts. Sham-operated rats were used as controls. Transplanted isograft, allograft, and native hearts of the transplant recipients and their livers and spleens were harvested at 5 days posttransplant and analyzed for hsp70 (i) and (c) expression by Western blots. Seven animals were studied in each group. Isografts at 3 and 60 days and allografts at 8 days were also studied. Quantification of band densities was carried out by laser densitometry. Physiological function of the native hearts of the transplant recipients was studied using Langendorff preparations. High levels of hsp70 (i) were noted in the transplanted and native hearts of the transplant recipients but not in their livers or spleens or in the hearts of the sham-operated control animals. Myocardial function of the native hearts of the transplant recipients was not significantly different from that of the controls. Significantly higher levels of hsp70 (c) were present in mild and severely rejecting allografts compared with controls and nonrejecting isografts. In the rat model of heterotopic cardiac transplantation, high levels of hsp70 (i) in the native hearts of the allograft and isograft recipients suggest a transplant-related, cardiac-specific stress process, not previously described. Heat shock protein 70 (c) expression is significantly increased during early and late allograft rejection and may serve as an indicator of transplant rejection.

Concanavalin A, ribose, and adenine resuscitate preserved rat hearts.

Preserved hearts may have cardiac dysfunction associated with inadequate myocardial high-energy phosphates. To resuscitate preserved hearts, hearts from male Wistar adult rats were preserved in 4.0 degrees C cold-modified Krebs-Henseleit buffer (pH 7.40) for 8 h, subjected to 30 min of reperfusion at 36.5 degrees C with the administration of concanavalin A (Con A; 40 mg/L), ribose (0.1 mM), and adenine (0.1 mM). In comparison with the normal control, the preserved group had a decrease in cardiac output (CO; p < 0.001), myocardial adenosine triphosphate (ATP; p < 0.001), and creatine phosphate (CP; p < 0.001), associated with an increase in myocardial Ca2+ (p < 0.01) and release of myocardial adenine nucleosides (ANs; p < 0.001). In comparison with the preserved group, the group reperfused with ribose and adenine had no improvement of these parameters (p > 0.05). The group reperfused with Con A had an increase in CO (p < 0.01) and myocardial CP (p < 0.01), associated with a decrease in myocardial Ca2+ (p < 0.05) and ANs release (p < 0.01), and no change in myocardial ATP. However, the group reperfused with Con A, ribose, and adenine achieved a significant increase in CO (p < 0.005), ATP (p < 0.005), CP (p < 0.005), and a decrease in myocardial Ca2+ (p < 0.01) and ANs release (p < 0.01). Data suggest that the combination of Con A, ribose, and adenine may resuscitate cold-preserved rat hearts.

Post-OKT3 induction therapy CD complex response predicts renal allograft rejection.

CD complex response to cessation of induction with OKT3 may be predictive of rejection. Twenty-seven patients receiving renal allografts and OKT3 induction immunosuppression were retrospectively analyzed for CD complex repopulation and allograft rejection. Flow cytometric monitoring was utilized in all patients. Responder status groups were identified based on CD complex repopulation, with fast responders demonstrating CD complex repopulation above the determined cohort mean. Slow responders had repopulation below this mean. Student's t test yielded P<0.01 (CD2), P<0.02 (CD3), and P<0.01 (CD8). Nonresponder patients were identified with repopulation below the mean, but flat compared with depletion. All nine fast responders lost their graft or were treated for rejection. No slow responder experienced graft loss or rejection episodes. One nonresponder was treated for rejection. CD complex activity following OKT3 cessation correlates with future rejection. Identification of responder status provides insight into propensity to reject, allowing individual tailoring of immunosuppression to patient response.

Primary adenocarcinoma, signet-ring, and transitional cell carcinoma of the bladder with penile metastasis.

This article reports a rare case of primary signet-ring cell carcinoma of the bladder with transitional cell and adenocarcinoma variants and metachronous metastases to the penis and lungs. This combination of lesions has not previously been reported. Together, they portend widespread dissemination and an early demise as is frequently the case with signet-ring cell carcinomas arising in other organs such as the breast and gastrointestinal tract. The optimal therapeutic intervention for this myriad of neoplasms with metastasis to the penis has yet to be ascertained because of the rarity of the lesions. Early diagnosis and an aggressive surgical approach appear to offer the best chance for quality survival and possible cure.

Xanthine oxidase inhibition prevents mesenteric blood flow deficits after resuscitated hemorrhagic shock by preserving endothelial function.

To determine the contribution of xanthine oxidase-mediated endothelial dysfunction to the blood flow deficits seen in the mesenteric circulation after resuscitated hemorrhagic shock, rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment animals received a 50 mg/kg bolus and a 25 mg/kg/hr infusion of the xanthine oxidase inhibitor allopurinol (allo) after shock but before resuscitation with shed blood and an equal volume of Ringer's lactate. A similarly resuscitated group (Std Res) and a nonhemorrhage group served as controls. Endothelial function was quantified at baseline, 30 min (R30), and 90 min (R90) postresuscitation as a change in mesenteric vessel diameter after topical application of acetylcholine (Ach), an endothelial-dependent vasodilator. Resuscitation restored cardiac output and blood pressure in both groups. First-order arteriolar blood flow (A1) remained depressed in the Std Res group but was restored to baseline in the group treated with allo. A1 arterioles demonstrated a 22 and a 27% reduction in ability to dilate to Ach at R30 and R90 after Std Res. V1 venules demonstrated a 39 and a 36% reduction in ability to dilate to Ach at R30 and R90 after Std Res. Endothelial-dependent vasodilation and blood flow were preserved in the group receiving Std Res plus allo. The preservation of endothelial function correlated with the restoration of microvascular blood flow postresuscitation. These data suggest that xanthine oxidase-mediated ischemia-reperfusion injury contributes to endothelial dysfunction and blood flow deficits in the mesenteric microcirculation after resuscitated hemorrhagic shock, the effect of which can be attenuated by the addition of the xanthine oxidase inhibitor allopurinol to standard resuscitation.

Beneficial effects of fluosol-polyethylene glycol cardioplegia on cold, preserved rabbit heart.

BACKGROUND: Because of its high oxygen-carrying capacity, especially at low temperatures, fluosol may enhance heart preservation. METHODS: Hearts of male New Zealand white rabbits (1.5-2.0 kg) were excised and flushed through the aorta with 0 degree C St. Thomas' Hospital solution, fluosol, or polyethylene glycol or fluosol-polyethylene glycol cardioplegic solution. Hearts were then stored for 12 hours at 0 degree C and reperfused with Krebs-Henseleit buffer at 36.5 degrees C for 60 minutes using a Langendorff system. RESULTS: Myocardial contractile function was significantly greater in the fluosol-polyethylene glycol cardioplegia-preserved group (p < 0.01) and polyethylene glycol-cardioplegia preserved group (p < 0.05) than in the St. Thomas' Hospital solution-preserved group. The myocardial high-energy phosphate content was significantly higher in the fluosol-polyethylene glycol-cardioplegia-preserved group (p < 0.01), with reduced release of lactate dehydrogenase (p < 0.01) in comparison with the St. Thomas' Hospital solution-preserved group. CONCLUSIONS: The addition of fluosol and polyethylene glycol to the cardioplegic solution may enhance long-term cold heart preservation.

Morgagni hernias: an uncommon cause of chest masses in adults.

Morgagni hernia is a congenital diaphragmatic hernia that occurs secondary to potential anterior medial defects in the diaphragm. Although the hernia usually is diagnosed incidentally, appearing as a mass on chest radiograph, symptoms of bowel obstruction may occur. Surgical repair is required in all cases and may be performed with either the abdominal or transthoracic approach.

Cardiac papillary fibroelastomas: rationale for excision.

We experienced a case of papillary fibroelastoma of the left ventricular outflow tract in a patient with severe valvular heart disease that was detected only by transesophageal echocardiography. Preoperative detection of this lesion altered the surgical procedure to include resection of the mass through the aortic valve annulus along with repair/replacement of the valves. The literature documents sufficient morbidity/mortality to support excision of these lesions regardless of symptoms or location.

A complication of T-fasteners in percutaneous endoscopic gastrostomy (PEG) placement.

Two patients with sinus tracts from retained T-fasteners following PEG tube placement are reported. Both patients had the PEG tubes subsequently removed and presented with purulent discharge and granulations near well-healed gastrostomy sites. The management of this complication and a possible method of prevention are discussed.

Etiology of diverticular disease with classic illustrations.

Diverticulosis is a common colonic disorder and often is found incidentally on colonic endoscopy and contrast enema radiographs. Theories relating to the etiology of the pathologic processes are commonly quoted, although the actual anatomic features are rarely seen during colonoscopic examinations. Here we show classic illustrations that support the widely held theories regarding the etiologies of diverticular diseases.

Calcified ball thrombus in the left atrium.

We experienced a case of calcified ball thrombus that was fixed to the atrial septum in the left atrium. This patient had no symptoms and no cardiac dysfunction. the thrombus was detected during preoperative work-up of a retroperitoneal tumor. The process of fixation to the atrial septum and calcification is unclear.

Pathologic aspects of polytetrafluoroethylene sutures in human heart.

BACKGROUND: Polytetrafluoroethylene (PTFE) sutures have been widely used as a mitral chord substitute. We present the cases of 4 patients who underwent mitral valve repair with chordal replacement by PTFE sutures and these required another operation. This gave us the chance to examine the PTFE sutures. METHODS: Structural analysis of the PTFE sutures was performed 26 to 378 days postoperatively. The specimens were examined grossly, microscopically, and by scanning or transmission electron microscopy or both. RESULTS: The PTFE suture in 1 patient was found to be completely covered with endothelial cells 154 days postoperatively. There was no calcification, and the flexibility and pliability of the PTFE sutures was preserved. Even though the PTFE sutures seemed uncovered on visual inspection, there was a thin lining of collagen and fibrin on the surface. Endothelial cells were seen in areas that looked clear in one specimen 26 days postoperatively. CONCLUSIONS: We think that the new layer of collagen could be promising in terms of durability and that the endothelial layer wil resemble normal tissue in its anticoagulant properties.

Consistent hepatic metastasis of human colorectal cancer in severe combined immunodeficient mice.

A major stumbling block in the study of human colorectal cancer metastasis has been the lack of an effective in vivo model producing liver metastasis on a consistent basis. In this study surgical specimens of colorectal carcinoma were implanted in scid mice and studied for engraftment, growth, and the capacity to produce hepatic metastases. Human colorectal cancers would engraft and propagate in the subcutis and intraperitoneally. Sporadic metastasis to the liver occurred in 3 of 54 (6%) animals with cancer implanted subcutaneously. Liver metastasis occurred in 24 of 25 (96%) mice with cancer implanted in the gonad fat pad. Tumor growth to extremely large volumes subcutaneously did not enhance metastatic potential, and neither did longer term growth in the subcutaneous space. Tumor placed in the gonad fat required no special manipulation and in most cases a single piece of solid tumor was implanted. In situ hybridization confirmed the persistence of the human tissue in these metastasizing tumors. Our model will allow for the study of the processes involved in metastasis of solid tumors, characterization of differences between the primary tumor and the metastatic one, and evaluation of possible therapeutic modalities.

Laparoscopic cholecystectomy in patients with ventriculoperitoneal (VP) shunts.

Increased intracranial pressure is often relieved by a ventriculoperitoneal shunt. The shunt has a one-way valve which can withstand pressures of 300 mmHg and prevent reflux of intraabdominal fluid. We have utilized laparoscopy for cholecystectomy in four patients with VP shunts. In all patients the peritoneal cavity was free of adhesions. When CO2 insufflation pressure was as high as 10-15 mmHg cerebrospinal fluid was still noted to flow from the end of the shunts. In three patients the entire procedure was performed laparoscopically. In the fourth patient the procedure was converted to an open cholecystectomy because of extensive inflammation surrounding a gangrenous gallbladder. Postoperatively the shunts remained intact and functional. There were no central nervous system sequelae. None of the shunts became infected. Elective laparoscopic cholecystectomy in patients with VP shunts can be done safely without a need for clamping or other manipulation of the shunt.

Allopurinol plus standard resuscitation preserves hepatic blood flow and function following hemorrhagic shock.

To determine the contribution of ischemia-reperfusion injury (IRI) to the blood flow deficit and hepatocellular dysfunction seen after resuscitation from hemorrhagic shock, the xanthine oxidase inhibitor allopurinol was given to rats as a 50 mg/kg bolus after shock but before resuscitation and continued as a 25 mg/kg/h infusion. Resuscitation with shed blood and lactated Ringer's restored cardiac output and blood pressure in both groups. Control animals demonstrated a reduction in total hepatic and effective hepatic blood flow to 59% and 43% of baseline values, respectively. Allopurinol resulted in a return to baseline values of both variables. Allopurinol treatment resulted in a 350% increase in xanthine, a 630% increase in hypoxanthine, and a 70% reduction in uric acid concentrations. These data suggest that IRI contributes to the organ dysfunction and blood flow deficits seen after resuscitated hemorrhagic shock the effect of which can be attenuated by the addition of the xanthine oxidase inhibitor allopurinol to standard resuscitation.

Human villous adenomas engrafted into scid mice survive for prolonged period without malignant transformation.

Human villous adenomas are thought to represent premalignancies that subsequently give rise to colorectal adenocarcinomas. Currently there is no in vivo model in which to study the dedifferentiation and malignant transformation of these tumors. We establish here that human villous adenomas can be successfully engrafted into severe combined immunodeficient (scid) mice. Furthermore, these xenografts remain viable for up to 18 mo after either a subcutaneous or intraperitoneal inoculation of the human tissue. Tumors grew slowly and secreted a clear mucinous fluid. Examination of the tumors histologically at 1, 4, and 12 mo after implantation revealed that the villous polypoid structure was maintained and islands of atypical cells were observed within pockets of mucin surrounding the adenomatous tissue. No gross or histologic evidence of malignancy was detected throughout the 20-mo observation period. The human identity of the cells in the graft was confirmed by DNA in situ hybridization with a human-specific probe. We conclude that the human-scid xenograft described here represents a viable animal model with which to study the potential malignant dedifferentiation of villous adenomas over a prolonged period of time and to evaluate the possible contribution of selected oncogenic vectors on the malignant transformation of these adenomas.