Vascular lesions of the breast

Vascular lesions of the breast comprise a heterogeneous group that includes a variety of benign, atypical, and malignant lesions. The presentation of these lesions ranges from those that are microscopic and discovered incidentally, to large tumors that may extensively involve the breast parenchyma and skin. In addition, some non-vascular breast lesions have features that may mimic those of vascular lesions and need to be distinguished from them in order to avoid an erroneous diagnosis. In this review, we discuss the spectrum of vascular lesions of the breast with particular emphasis on those lesions of greatest clinical importance, angiosarcoma and atypical vascular lesions. We also discuss lesions that may be mistaken for vascular lesions.     

Rare benign lesions of the breast

In this review a wide-range of uncommon benign breast lesions, which can present as a breast mass, are described and discussed. The entities are loosely grouped into five sections; developmental lesions, in which all components of the normal breast are present, epithelial lesions, stromal lesions, lesions associated with luminal secretion and, finally, a group of soft tissue lesions, which although not specific to the breast can present in the breast. We have attempted to address the common diagnostic pitfalls associated with the lesions described.     

Rare benign lesions of the breast

In this review a wide-range of uncommon benign breast lesions, which can present as a breast mass, are described and discussed. The entities are loosely grouped into five sections; developmental lesions, in which all components of the normal breast are present, epithelial lesions, stromal lesions, lesions associated with luminal secretion and, finally, a group of soft tissue lesions, which although not specific to the breast can present in the breast. We have attempted to address the common diagnostic pitfalls associated with the lesions described.     

Role of the fornix in the septal syndrome

Rats were tested for their reactivity to a puff of air, loud noise, and touch on the back following fornix and septal lesions. Septal lesions produced the expected hyperreactivity. Large fornix lesions 9 days prior to the septal lesion, or fornix lesions within 10 min of the septal lesions, blocked the hyperreactivity expected from the septal lesions. Partial fornix lesions partially suppressed the hyperreactivity. The data indicate that intact septohippocampal connections are necessary for the appearance of hyperreactivity following a septal lesion.     

Deeply infiltrating endometriosis: pathogenetic implications of the anatomical distribution

BACKGROUND: To investigate whether knowledge of the anatomical distribution of histologically proven deeply infiltrating endometriosis (DIE) lesions contributes to understanding the pathogenesis. METHODS: Observational study between June 1992 and December 2004 (retrospective study between 1992 and 2000; prospective study between 2001 and 2004). Continuous series of 426 patients suffering from pelvic pain who underwent complete surgical exeresis of DIE. DIE lesions were classified according to four different possibilities: (i) Firstly, DIE lesions were classified as located in the anterior or posterior pelvic compartment. (ii) Secondly, DIE were classified as left, median and right. (iii) Thirdly, DIE lesions were classified as pelvic or abdominal. (iv) Fourthly, DIE lesions that could present in a right and/or left location were classified as unilateral or bilateral. RESULTS: These 426 patients presented 759 histologically proven DIE lesions: bladder (48 lesions; 6.3%); uterosacral (USL) (400 lesions; 52.7%); vagina (123 lesions; 16.2%); ureter (16 lesions; 2.1%) and intestine (172, 22.7%). DIE lesions are significantly more often located in the pelvis (n=730 lesions) than in the abdomen (n=29 lesions) (P<0.0001). Pelvic DIE lesions are significantly more often located in the posterior compartment of the pelvis [682 DIE lesions (93.4%) versus 48 DIE lesions (6.6%); P<0.0001]. Pelvic DIE lesions are significantly more frequently located on the left side. For patients with unilateral pelvic DIE lesions, the anatomical distribution is significantly different in the three groups: left (172 lesions; 32.0%), median (284 lesions; 52.8%) and right (82 lesions; 15.2%) (P<0.0001). For patients with lateral lesions, left DIE lesions (172 lesions; 67.8%) were found significantly more frequently than right DIE lesions (82 lesions; 32.2%) (P<0.0001). A similar predisposition was observed when we included patients with bilateral pelvic DIE lesions (P=0.0031). The same significantly asymmetric distribution is observed for total (pelvic and abdominal) DIE lesions. CONCLUSIONS: Our results demonstrate that distribution of DIE lesions is asymmetric. It is possible that this is related to the anatomical difference between the left and right hemipelvis and to the flow of peritoneal fluid. These findings support the hypothesis that retrograde menstruation of regurgitated endometrial cells is implicated in the pathogenesis of DIE.     

Different types of segmental sclerosing glomerular lesions in six experimental models of proteinuria

From 133 to 615 glomeruli were examined in sections of kidneys from each of 60 animals, representing six rodent models of proteinuria. Particular attention was paid to the position of segmental lesions. Lewis rats given sheep anti-rat glomerular basement membrane antibodies had lesions almost exclusively at the glomerulo-tubular junction. Wistar rats on a diet of 24 per cent casein or with subtotal nephrectomy and a diet of 24 per cent soya had lesions mainly at the hilum. Wistar rats given bovine serum albumin had global lesions but virtually no segmental lesions. Wistar rats given puromycin aminonucleoside had lesions at the glomerulo-tubular junction and global mesangial abnormalities shortly after the treatment but later developed segmental lesions at all parts of the glomerulus. Untreated BUF/Mna rats had lesions at the glomerulo-tubular junction early in life but later had lesions at all parts of the glomerulus. Untreated NZB/NZW hybrid mice had various types of glomerulonephritis and also had lesions at the glomerulo-tubular junction. These findings showed that (1) segmental lesions at the glomerulo-tubular junction, or glomerular tip, occur in experimental animals, a fact not previously reported, and these tip changes are a common feature in several different models of proteinuria; (2) hilar segmental lesions are seen in conditions with hyperfiltration of protein; and (3) segmental lesions at various parts of the glomerulus are seen in some models of proteinuria and probably indicate late effects of random toxic damage to the glomerulus. Thus, there are at least three different types of segmental glomerular lesions in experimental animals--tip, hilar, and random--with different morphology and pathogenesis. It is likely that these findings can be extended to human renal diseases with segmental glomerular lesions. This will help to clarify the controversial and unsatisfactory term focal segmental glomerulosclerosis.     

Medial septal lesions mimic effects of both selective dorsal and ventral hippocampal lesions

Electrolytic medial septal (MS) lesions, which depleted acetylcholinesterase staining in both dorsal and ventral hippocampus, produced a constellation of behaviors, combining aspects of both selective dorsal and ventral hippocampal lesion effects. MS lesions impaired spatial working memory on the T maze, thus resembling the effects of dorsal hippocampal lesions. In addition, MS lesions reduced anxiety during successive alleys (a modified form of the elevated plus-maze), social interaction, and hyponeophagia tests. MS lesions also reduced postshock freezing. These effects more closely resemble those of ventral hippocampal lesions. Therefore, the effects of electrolytic MS lesions derive from the resulting combined deafferentation of dorsal and ventral hippocampal regions, suggesting that previously reported effects of cytotoxic dorsal hippocampal lesions are unlikely to be due to a demyelination of fibers of passage coursing through the septal pole.     

The spectrum of apocrine lesions of the breast

Apocrine change is seen in a wide spectrum of breast lesions, ranging from microscopic cysts to invasive carcinoma. This article reviews the range of apocrine lesions and discusses the clinical significance of these lesions. Although apocrine change in many cases does not present any diagnostic difficulty, apocrine proliferations demonstrating cytologic atypia can be particularly challenging. The histologic criteria that have been proposed to foster reproducibility in categorizing such lesions are reviewed. This review attempts to clarify the terminology that has been applied to a range of benign lesions, including sclerosing adenosis and complex sclerosing lesions, containing foci of apocrine change. Malignant apocrine lesions, including both in situ and invasive carcinoma, are also discussed.     

Pregnancy-associated breast disease: radiologic features and diagnostic dilemmas

In this paper, we evaluate the radiological features of pregnancy-associated breast lesions and discuss the difficulties in diagnosis by imaging. We selected patients who were diagnosed with pregnancy-associated breast lesions during the previous 5 years. All patients complained of palpable lesions in the breast and underwent ultrasonographic (US) examination, the first choice for examination of pregnancy-related breast lesions. Any suspicious lesions found by the US were recommended for a US-guided core biopsy, US-guided fine needle aspiration (FNA), or surgery. Various breast lesions were detected during pregnancy and lactation, including breast cancer, mastitis and abscesses, lactating adenoma, galactoceles, lobular hyperplasia, and fibroadenomas. The imaging features of pregnancy-associated breast lesions did not differ from the features of non-pregnancy-associated breast lesions; however, some pregnancy-associated benign lesions had suspicious sonographic features. A US-guided core biopsy was necessary for differentiating benign from malignant. In patients with breast cancer, the cancer was often advanced at the time of diagnosis. In conclusion, various pregnancy-related breast lesions were detected and the imaging of these lesions had variable findings. Breast ultrasound could be an excellent imaging modality for diagnosis and differentiation between benign and malignant lesions. However, when the imaging results are suspicious, a biopsy should be performed to obtain a pathologic diagnosis.     

Morphogenesis of hypertensive vascular lesions.

Accelerated hypertension is a convenient model for studying the pathomechanism of hypertensive vascular lesions. It has not been settled, however, whether such lesions are really equivalent to those developing slowly in the course of experimental hypertensive vascular disease. In the present study, early vascular lesions of accelerated hypertension have been compared with those of hypertensive vascular disease by using two complementary techniques: small-molecule plasma-protein label (Ferrlecit) and a macromolecular tracer protein (horse ferritin). Two kinds of vascular lesions have been distinguished. Non-destructive vascular lesions exhibit necrotic smooth-muscle cells with intracellular deposition of Ferrlecit-labelled plasma proteins and intact basement-membrane barrier to the macromolecular tracer. Destructive vascular lesions, in turn, are characterized by the breakdown of the basement-membrane barrier to the macromolecular tracer. Incipient destructive lesions are identified as dissecting microaneurysms initiated by small ruptures of the basement membrane framework. Both non-destructive vascular lesions and incipient destructive vascular lesions end in confluent medial destruction that precedes the formation of fibrinoid necrosis. The localization and morphology of vascular lesions is identical both in hypertensive vascular disease and in accelerated hypertension. Circumstantial evidence strongly suggests that non-destructive vascular lesions are caused by arterial contraction. Nevertheless, the possibility that non-destructive lesions are but abortive forms of destructive ones cannot be excluded.     

多排螺旋CT对胃肠道内可疑异位胰腺病灶的影像学诊断

目的:探讨多层螺旋CT诊断胃肠道内异位胰腺的价值及对误诊病变进行分析。方法:对18例术前64排螺旋CT诊断为异位胰腺并获得病理结果的病例进行分组回顾分析。结果:收集到18例患者共19处病灶。诊断正确组有10例患者11处病灶,其中7处位于胃黏膜,3处位于十二指肠,1处位于回肠。以上病灶中5处可见“中央脐凹征”。诊断错误组有8例患者共8处病灶,3处位于胃黏膜或粘膜下,4处位于十二指肠内,1处位于食管下段内,病理结果提示8处病灶中3处为炎性病灶,2处为肿瘤病灶（胃肠间质瘤及神经内分泌肿瘤）,1处为胃底腺异位,1处为胃粘膜脱垂,1处为Peutz-Jeghers息肉;其中胃底腺异位及间质瘤的影像表现上均有类似“中央脐凹征”表现。结论:通过64排多层螺旋CT扫描并收集到的病例中:（1）诊断正确组中大多数病灶位于胃及十二指肠;（2）诊断错误组中部分病灶表现为类似“中央脐凹征”,可能是导致误诊的原因之一;（3）误诊病例中炎性病变占比较大,认为胃肠道炎性病变需作为异位胰腺的鉴别诊断之一。     

Time-dependent fornix influence on increased light aversion induced by septal lesions

Rats were tested for aversion to light both preoperatively and following various combinations of septal and fornix lesions. Septal lesions alone induced a sustained increased aversion to light. Fornix lesions alone had little effect on the preoperative aversion level. Fornix lesions prior to, simultaneously with, or up to 12 hr following septal lesions were successful in preventing the increase in light aversion expected after the septal lesions. Fornix lesions 24 hr or later following the septal lesions had no effect on the increased light aversion. Results suggest that intact septohippocampal connections are necessary for the initial establishment of an increased light aversion following septal lesions, but not for the continued maintenance of an already present increased light aversion.     

Prevalence and Risk Factors of Gallbladder Polypoid Lesions in a Healthy Population

PurposeTo determine the prevalence of and investigate the risk factors for gallbladder (GB) polypoid lesions in a healthy population.ResultsThe prevalence of GB polypoid lesions was identified as 9.96%. On multivariate analysis, chronic hepatitis B infection (CHB) and the presence of metabolic syndrome (MS) were risk factors for GB polypoid lesions. CHB and MS were also significant independent risk factors for multiple GB polypoid lesions when compared with solitary GB polypoid lesions. In addition, gastric Helicobacter pylori infection and MS were significant risk factors for GB polypoid lesions with stones when compared with GB polypoid lesions without stones.ConclusionThe prevalence of GB polypoid lesions in a healthy Korean population was 9.96%. Patients with CHB and MS need to be carefully examined for such lesions.     

E-cadherin reactivity of 95 noninvasive ductal and lobular lesions of the breast. Implications for the interpretation of problematic lesions

Studies suggest that E-cadherin is useful to classify epithelial breast lesions as ductal or lobular, but extensive experience with this antibody is lacking. We studied reactivity of lesions with classic and indeterminate morphologic features. We reviewed 95 lesions and divided them into unanimous and nonunanimous diagnosis groups; the unanimous group served as benchmark lesions to which E-cadherin reactivity could be standardized and compared. All 37 ductal lesions in the unanimous group had strong, diffuse E-cadherin reactivity. Two of 22 classic lobular carcinoma in situ (LCIS) lesions had sparse E-cadherin-reactive lobular cells within a few terminal duct lobular units. Neither displayed transition from nonreactive to reactive cells. Of 36 lesions in the nonunanimous group, 19 had insufficient morphologic features for definitive classification. Only 6 of 19 were E-cadherin reactive, including several minimally proliferative lesions. The other 17 lesions in the nonunanimous group had LCIS and ductal carcinoma in situ (DCIS) features. All had no E-cadherin, or strong membrane reactivity of constituent cells in varying proportions, without a transition between reactive and nonreactive cells. Results suggest that the majority of morphologically nondiagnostic atypical lesions are lobular, including those associated with DCIS. E-cadherin seems to be absent in most lobular lesions.     

Subtotal lesions of the amygdala: the rostral central nucleus in passive avoidance and ulceration.

Rats received small bilateral electrolytic or ibotenate lesions of the rostral part of the amygdaloid central (rACE) or lateral (rAL) nuclei, or caudal part of the basolateral nuclei (cBL), or electrolytic lesions of the dorsal hippocampus (HIPP). All groups were tested in a drinking passive avoidance (PA) task that appears less sensitive to deficits in acquisition/retention or activity/spatial perception than are many other PA tasks, and more specifically sensitive to deficits in generation of fear. Consistent with this interpretation, performance in the task was facilitated, not deficient, in the HIPP group. Electrolytic lesions of rAL produced a mild deficit in PA, but ibotenate lesions did not, and neither did the more caudal lesions of the cBL groups. Ibotenate lesions of rACE did produce a deficit in PA, consistent with views of a role of this part of the amygdala in fear. Electrolytic lesions of rACE produced a very profound PA deficit and also blocked the rapid development of gastric erosions by water-restraint stress, effects that were not found with ibotenate lesions in this location. This suggests a particular contribution of fibers passing through rACE to some of the more marked effects of electrolytic lesions of rostrodorsal portions of the amygdala.     

Early gastric cancer: 52 cases of combined experience of two south Australian teaching hospitals

Fifty-two patients with early gastric cancer are described. At presentation, the average age was 60 years and the male:female ratio was 3:2. The patients had presenting symptoms indistinguishable from those due to benign peptic ulcer disease. Endoscopic examination with multiple biopsies was the most accurate means of diagnosis, with an overall 93% detection rate. The tumours were located predominantly along the lesser curve (75%) and in the antrum (64%), with ulcerated or depressed lesions most common and flat lesions least common. Approximately 58% of lesions were of intestinal type, submucosal invasion was seen in 45% and lymph node metastases had occurred in 7% of cases. Lesser curve and antral lesions were more likely to be ulcerated. Ulcerated lesions were on average, the same size as non-ulcerated lesions. Body lesions were larger than antral lesions and lesions which had spread to the submucosa were larger than mucosal lesions. Diffuse-type lesions were more likely to be ulcerated than intestinal-type lesions and dysplasia was more commonly associated with intestinal-type lesions than with diffuse or mixed-type lesions. The crude 5-year survival rate was 80%, but only one death was associated with a recurrence of gastric cancer.     

Indeterminate diagnosis in fine-needle aspiration of the pancreas: reasons and clinical implications

An indeterminate diagnosis made on fine-needle aspiration (FNA) samples of the pancreatic lesions can cause dilemmas in clinical management. We retrospectively analyzed FNA features of such lesions in 65 consecutive pancreatic FNAs from 56 lesions to learn more about the sources of uncertainty and their clinical implications. A definitive diagnosis based on follow-up information was available in 50 lesions. Radiologically, 39% of the lesions showed a cystic component, and 25% of the lesions were ill-defined. Cytologically, contributing factors included scant atypical cells, coexistence of gastrointestinal epithelium, pancreatitis, poor cellular preservation, and interpretation error. Repeat sampling, as requested by clinicians prior to treatment, was performed in 33 (66%) of the 50 lesions, leading to a definitive pathologic diagnosis in 20 (61%) lesions. Seventeen lesions were eventually resected, of which a definitive preoperative diagnosis was attempted in 12 lesions via repeat sampling and was successful in seven. We concluded that indeterminate cytologic diagnosis of a pancreatic lesion often needs to be pursued for optimal management. Although intrinsic natures of a lesion such as cystic component may contribute to insufficient sampling, diagnostic certainty can be improved by proper specimen handling, interpretation, and clinical and/or radiographic correlation.     

Histopathogenesis of intestinal metaplasia: minute lesions of intestinal metaplasia in ulcerated stomachs.

Minute lesions of intestinal metaplasia composed of a few metaplastic tubules were observed in the gastric mucosa during routine histological examination of gastrectomy specimens. The histological findings indicated that these lesions might be an initial stage of more advanced intestinal metaplasia. Accordingly, more than 18,000 serial sections in 10 stomachs with chronic ulcers were examined to clarify the histopathogenesis of the intestinal metaplasia. It was concluded from the three dimensional reconstruction of minute intestinal metaplasia lesions that these lesions originated during the regenerative process of healing of gastric erosions. The lesions were roughly globoid with a depression on the surface. It is thought that with continuous formation and healing of gastric erosions, more extensive intestinal metaplasia lesions would be formed by an increase in size and confluence of these focal minute intestinal metaplasia lesions.     

Stage-specific remodeling of atherosclerotic lesions upon cholesterol lowering in LDL receptor knockout mice

Reducing the concentration of circulating lipids leads to decreased cardiovascular morbidity and mortality, but the dynamic remodeling that established atherosclerotic lesions undergo upon lipid lowering is poorly understood. Early or advanced lesions in the aortic root were induced by feeding LDL receptor knockout mice a high-fat, high-cholesterol Western-type diet for 5 or 9 weeks, respectively. In the first week after switching to a chow diet, plasma total cholesterol levels dropped 70%, but both early and advanced lesions increased in size. Early lesions grew because of an increase in smooth muscle cells; advanced lesions had an enlargement of absolute macrophage area. From 1 to 3 weeks after the diet switch, plasma total cholesterol levels were completely normalized, but the size of early lesions remained stable; however, advanced lesions became smaller due to a reduction of the absolute macrophage area. From 3 to 6 weeks, both early and advanced lesions progressed further, as a result of expansion of the absolute collagen and necrotic core area. In contrast, early lesions became proinflammatory, as evidenced by the increased infiltration of neutrophils and increased oxidative stress, probably caused by the activation of mast cells in the adventitia. Thus, the severity of atherosclerotic lesions affects their dynamic response to lipid lowering, indicating the importance of establishing stage-specific therapeutic protocols for the treatment of atherosclerosis.