Cutaneous and systemic vasculitis: cellular players and pathogenetic aspects.

Vascular wall damage, inflammatory cell recruitment and subsequent structural remodelling define a vasculitic process. Histopathological classification of vasculitis is based on the caliber of the vessel involved and on the prevalent type of inflammatory cells (neutrophils in acute forms, lymphocytic for chronic, histiocytic for granulomatous). A large amount of information is emerging from the literature on the complex pathophysiology of the cellular components of vessel wall. For instance, endothelial cells not only have the task to cover the inner surface of the vascular system but they also play an active role in tuning the immunological response in a very sophisticated way. Neutrophils are not only terminally differentiated cells sacrificed for a valuable cause. Cellular types of the perivascular microenvironment play roles one time not expected. The spread of the inflammatory process into the vascular wall is not necessarily inside-out. These and other selected concepts will be discussed in this paper.

Pathophysiology of subcutaneous fat.

Adipocytes are the most representative cells of the adipose tissue. For a long time adipocytes have been defined as no more than "fat guys", passively occupying large body regions, often with undesirable cosmetic effects. The apparent structural uniformity of adipose tissue contrasts with the functional complexity that may be documented at different anatomical sites. A growing body of scientific evidence is telling us that adipose tissue is a very sophisticated organ regulating both energy storage and metabolic management of our body, as well as the main branches of immune system. The adipose tissue is strictly linked with our brain and regulates other organ systems. Adipose tissue paracrine activity regulates turnover, regeneration homeostasis of epidermis, dermis and cutaneous appendages. Adipokines, molecules produced by adipocytes play an important role in many skin disease other than in systemic diseases. This review will focus on the pathophysiology of the adipose tissue with special emphasis on recent scientific acquisitions. Improving our knowledge on fat tissue is necessary to develop interesting new perspectives and therapeutic strategies for both systemic and cutaneous diseases.

Lack of CD 29 (beta1 integrin) and CD 54 (ICAM-1) adhesion molecules in intravascular lymphomatosis.

Intravascular Lymphomatosis (IL) is a rare and usually aggressive form of non-Hodgkin's lymphoma characterized by the growth of neoplastic cells within vascular lumina that usually presents with skin or central nervous system (CNS) involvement. The mechanism(s) for the selective intravascular growth of this neoplasm remain(s) unexplained. We now report clinical and immunohistologic data on surgical material from 6 cases of IL; in 4 of 6 cases, autopsies were performed. Our IL cases shared the following features: (1) B-cell lineage; (2) lack of skin involvement at presentation; (3) aggressive behavior; and (4) lack of extravascular lymphomatous masses; in addition, 1 case had an associated gastric low-grade MALT lymphoma. We studied by immunohistochemistry formalin-fixed, paraffin-embedded sections with monoclonal antibodies to molecules known to be involved in lymphocyte and endothelial adhesion phenomena, that is, CD29 (beta1 integrin subunit), CD43 (leukosialin), CD44 (H-CAM), CD54 (ICAM-1), embryonal N-CAM (e-NCAM), and EMA (episialin). In all cases, the surfaces of IL aggregates reacted for CD44 but were consistently negative for CD29; also absent was CD54. Conversely, the integrity of the endothelial cells was underscored by their even reactivity for CD29, CD44, and CD54. Given that CD29 is currently regarded as critical for lymphocyte trafficking in general and for transvascular migration in particular, and CD54 is also involved in transvascular lymphocyte migration, we conclude that their consistent absence in IL may contribute to its intravascular and disseminated distribution pattern. The rather frequent association of IL with various conventional lymphomas is known; yet, one of our cases appears to be the first report of IL associated with a low-grade MALT lymphoma.

Role of esophageal brushing cytology in monitoring patients treated with sclerotherapy for esophageal varices.

Recent reports claim that there might be a relationship between sclerotherapy for esophageal varices and cancer of the esophagus. The discovery of a squamous cell cancer of the lower esophagus in a patient treated three years previously with sclerotherapy led us to set up a follow-up protocol. In order to assess this relationship and to monitor the evolution of such lesions, 68 patients treated with sclerotherapy with polidocanol because of esophageal varices were examined endoscopically at six-month intervals, and brushing samples were taken. The ages of the patients ranged between 35 and 81 years, and all had portal hypertension due to cirrhosis; 10 patients with the same disease but without bleeding varices were also examined. The interval between sclerotherapy and the first cytologic follow-up examination averaged 34 months, while the interval to the last follow-up examination averaged 40 months. One patient was examined four times (1.4%), 10 three times (14.7%), 39 twice (57.4%) and 18 only once (26.5%). Two cases were interpreted as nuclear hyperplasia associated with inflammation and were found to have regressed at a subsequent examination; all the other cases were reported as negative although sometimes associated with inflammation. None of the controls showed any abnormalities. While the occurrence of esophageal cancer after sclerotherapy might be associated with other risk factors, such as alcohol intake and smoking, esophageal brushing cytology can successfully monitor these patients and detect early stages of neoplasia.

[Gastric leiomyoblastoma. Two case reports]. / Il leiomioblastoma gastrico. Descrizione di due casi clinici.

Two cases of gastric leiomyoblastoma (one of which of exceptional size, measuring more than 40 cm) observed respectively in 1992 at the Surgery Division of USSL 45 at Asola (MN) and in 1990 at the Second Surgery Division of USSL 47 in Mantova are reported. In the first case anaemia revealed the tumor whereas in the second case the patient suffering from a pain in the abdomen was admitted to hospital. These two tumors raise interest for their rarity and for their uncertain biological evolution. They generally develop very slowly and tend to remain intramural. The most frequently attacked seats are the antum-pyloric region and the stomach body. The main symptoms are epigastric pain, nausea, vomiting, weight loss, sideropenic anaemia, epigastric palpable mass. The diagnostic iter includes radiologic examination (digestive tube X-ray, echography, TAC, arteriography), gastroscopy and laparoscopy. In most cases surgical resection is not completely destroying, except for those cases in which the tumor measures more than 5 cm and total or subtotal gastrectomy is performed.

T-cell receptor gamma-delta positive lymphocytes in synovial membrane.

The distribution of T-lymphocytes expressing CD3 and T-cell receptor gamma-delta (T gamma/delta) has been examined by immunocytochemistry in the synovial membrane of eight patients with inflammatory arthritis (six rheumatoid arthritis, two spondyloarthritis) and eight with non-inflammatory arthritis (four osteoarthritis, four post-traumatic arthritis). T gamma/delta cells were present in eight out of eight inflammatory arthritis synovial membranes, but in only one out of eight non-inflammatory membranes (P less than 0.005). The mean T gamma/delta percentage (of total T-cells) in inflammatory arthritis was 14% (range 7-25%). T gamma/delta cells were found mainly in the transitional area of the synovial membrane with a scattered distribution as single cells or couplets. No relation was found between the presence and percentage of T gamma/delta cells and disease duration or steroid treatment.

The morphogenesis of human hepatocellular carcinoma.

In both cirrhotic and non cirrhotic livers, hepatic carcinogenesis appears as a multistep process commonly starting from hyperplastic nodules and reaching HCC via a continuous spectrum of lesions. Minute HCC without a background of hyperplastic lesions have also been identified in cirrhotic livers. These observations suggest that the morphological progression of carcinogenesis in the human liver can develop through two different main pathways.