Presence Of Perivascular Infiltrates Research Articles

Perivascular infiltration reflects subclinical lymph node metastasis in invasive lobular carcinoma.

Invasive lobular carcinoma (ILC) is characterized by discohesive cells due to irreversible loss of E-cadherin expression and multiple satellites, where individual cell migration is evident without disturbance of the stroma. Neoplastic cells sometimes infiltrate the surrounding vessel in satellites. Here, we aimed to clarify the specific role of perivascular infiltration (PVI) and ameboid migration, characterized by nondisturbance of the background stromal structure, in ILCs. A total of 139 cases with ILC and 122 cases with invasive breast carcinoma of no special type (IBC-NST) were evaluated retrospectively. PVI was significantly more common in ILC than in IBC-NST (50% [70 of 139 cases] vs. 9% [11 of 122 cases], p < 0.001). ILC cases with PVI showed a larger pathological tumour size than clinical tumour size (p < 0.01), a higher frequency of pathological node status pN2-pN3 when limited to clinically node-negative cases (p < 0.01) and lower circularity of tumour morphology on imaging (p < 0.01) than ILC cases without PVI. In the pathological evaluation, the intensity and occupancy of tumour cells expressing phospho-myosin light chain 2, which is a hallmark of ameboid migration, were significantly higher in ILC cases with PVI than in those without PVI at the tumour margins (p < 0.05). ILC with PVI is associated with irregular, poorly defined tumour margins and lymph node metastasis without adenopathy, which is difficult to assess using imaging. PVI may be caused by ameboid migration, as shown by the positive expression of phospho-myosin light chain 2. The presence of PVI may be a predictor for clinically node-negative pN2-pN3 in ILC patients.

Right ethmoid eosinophilic angiocentric fibrosis with orbital extension

IntroductionEosinophilic angiocentric fibrosis (EAF) is a slowly progressive, benign disease involving the mucosa of the upper airways or, more rarely, the orbit. It belongs to the spectrum of IgG4-related disease. Case reportThe authors report the case of a 61-year-old man who presented with orbital involvement (visual loss, pain, proptosis, and eyelid oedema), headache and nasal obstruction. Imaging revealed a right ethmoido-orbital mass infiltrating the periorbital fat and enveloping the optic nerve. Histological examination concluded on a diagnosis of EAF in the presence of perivascular infiltration by inflammatory cells, predominantly eosinophils, and zones of “onion skin” fibrosis. Immunohistochemistry attributed these lesions to IgG4-related disease. Initial treatment with corticosteroids followed by dapsone failed to control the disease and resulted in severe steroid dependence. Surgical ethmoidectomy with resection of the lamina papyracea was performed to allow displacement of the eyeball into the nasal cavity in the event of another episode. DiscussionThe combination of surgery and rituximab achieved lasting pain relief with no recurrence of exophthalmos.

Mitochondrial complex III deficiency in a case of HCV related noninflammatory myopathy

Sirs: Muscle involvement in the course of Hepatitis C Virus (HCV) infection has mainly been reported as a myositis secondary to an immunologically mediated reaction or to a direct effect of viral infection. Myositis was confirmed in these cases by the presence of perivascular infiltration of inflammatory cells in the muscle biopsy [1, 2]. However, lack of evidence for viral multiplication in muscle [3, 4] suggested a virus-triggered immune-mediated mechanism, rather than direct infection and in situ replication. On the other hand, several cases of HCV associated myopathy lacked signs of inflammation in the muscle biopsy [2, 5] suggesting other pathogenic mechanisms. A 60-year-old woman was admitted in April 2002 with a 3 year history of slowly progressive bilateral eyelid ptosis, diplopia, generalized weakness, severe distal upper limb weakness and respiratory distress after minimal exercise. Neurological examination disclosed mild neck and proximal upper limb weakness, bilateral ptosis and diplopia both in horizontal and upward gaze. Ptosis increased after sustained upward gaze. A mild impairment in the upward gaze was present mainly on the left side. Her family history was unremarkable. The patient had a post-transfusion HCV infection detected by chance ten years before the appearance of ptosis, and not treated with immunotherapy because of the benign course. Neoplastic, autoimmune, thyroidal, and rheumatologic diseases were excluded by appropriate tests. Repetitive stimulation (right ulnar nerveabductor digiti minimi muscle and facial nerve-nasalis muscle) did not show a decremental response. Acetylcholine receptor antibodies were absent. Ptosis did not improve after edrophonium chloride intravenous injection. Chest computed tomography (CT), spirometry, electrocardiography and echocardiography, brain and orbit, CT and magnetic resonance imaging were normal. Immunoglobulin G and immunoglobulin M cryoglobulins were detected (cryocrit value: 2 %). Electroneurography was completely normal. Automatic interference pattern analysis was consistent with a myopathic dysfunction. The patient had an abnormal turns/amplitude ratio demonstrated by scores below the sexand age-specific reference range in frontal muscle, left biceps brachii and quadriceps. The same muscles showed rapid recruitment of short duration and low amplitude motor unit potentials. Fibrillations and fasciculations were absent. A biopsy taken from the left deltoid muscle revealed moderate fiber atrophy, marked variation of fiber size with round or angular shape, type 2 myofiber predominance with increased nuclear centralization. Perivascular inflammation, necrosis, and ragged red fibers were absent. Mitochondrial enzyme activities showed decreased decylbenzoquinol cytochrome c reductase activity (complex III deficiency) (51.1 nmol/min mg, normal values: 70–150) while citrate synthase activity was normal (153 nmol/min mg, normal value: 80–210). Mitochondrial complex I, II IV and V activities were normal. The ultrastructural study showed increased subsarcolemmal accumulation of glycogen, and mitochondria with altered shape and concentric cristae. To verify these findings a LETTER TO THE EDITORS

Chronic Pruritic Papular Dermatitis in Adult Men: A Variant of Prurigo

Chronic recurrent pruritic papular eruptions in which a specific diagnosis cannot be established becomes a baffling experience to the dermatologist. We have met adult male patients with chronic recurrent pruritic papular eruptions, but their clinicopathological features are not described in English language textbooks. Our purpose was to study the clinical and histological features of this entity and review the various existing taxonomy. We conducted a study of 20 patients over a six year period by taking histories, performing skin biopsies, screening patch tests, and doing immunofluoresence studies. The eruptions occurred exclusively in male adults and had a predilection for the trunk and proximal extremities. The lesions were characterized by severely pruritic, nonfollicular, monomorphic, erythematous urticarial papules. There was no evidence of atopic diathesis or history of insect bite. Most patients had normal levels of serum eosinophils and IgE. The predominant histopathologic finding was a presence of perivascular infiltration of mononuclear cells with eosinophils. The patients followed a chronic course of at least six months with waxing and waning; systemic corticosteroids were the only effective treatment. Finally, all other pruritic erythematous papular dermatoses were ruled out. These cases comprise a distinct entity that has previously been mentioned in a few reports. Clear definition of this entity with an appropriate designation is in order to avoid confusion among dermatologists, and we propose the disease name "chronic papular dermatitis in adult men" as a variant of prurigo.