[Scarlet fever with multisystem organ failure and hypertrophic gastritis]. / Scarlatine compliquée d'une défaillance multiviscérale avec gastrite hypertrophique.

Scarlet fever is a rare disease in adult patients. We report a patient in whom scarlet fever was associated with hypertrophic gastritis and multiple organ failure. A 62-year-old woman presented with septic shock and multiple organ failure. Bacteriological survey was negative. Abdominal tomodensitometry showed an hypertrophic gastritis. Histological analysis demonstrated a non specific gastritis without any tumoral sign. Cefotaxime and amoxicillin led to improvement and hypertrophic gastritis progressively resolved. A sandpaper rash over the body with finger desquamation, elevation of antistreptolysin O and a recent contact with an infected grandson led to the diagnosis of scarlet fever. Due to antibiotic prescription, scarlet fever is now uncommon. Although classical, ENT or gastroenteritis presentations may be puzzling for the diagnosis of scarlet fever. As 150 years ago, diagnosis of scarlet fever is still a clinical challenge.

Different pathological phenotypes of autoimmune gastritis induced by neonatal thymectomy between BALB/c and (BALB/c x DBA/2) F1 mice: role of eosinophils in hypertrophic autoimmune gastritis.

BACKGROUND: A unique pathological feature of murine autoimmune gastritis (AIG) is its pronounced mucosal hypertrophy, which is different from human type A chronic atrophic gastritis with pernicious anemia. The aim of this study was to clarify the mechanism of gastric hypertrophy in murine AIG, especially in relation to inflammatory cells infiltrating the gastric mucosa. METHODS: Neonatally thymectomized (NTx) BALB/c and (BALB/c x DBA/2) F1 mice with gastritis were examined histologically and serologically. The T-helper (Th1/Th2) immune balance in the spleen was evaluated by intracellular cytokine staining for interferon-gamma and a flow-cytometric beads array for several cytokines. Additionally, NTx AIG BALB/c mice were orally administered an H(2)-blocker to decrease eosinophils. RESULTS: NTx AIG BALB/c mice exhibited gastritis without stomach hypertrophy at 2 months of age, and developed gastritis with mucous gland hypertrophy accompanied by eosinophil infiltration at 6 months of age. In contrast, NTx AIG (BALB/c x DBA/2) F1 mice displayed gastritis with neither stomach hypertrophy nor eosinophil infiltration even at the age of 6 months. Upregulation of interleukin-4 and granulocyte-macrophage colony-stimulating factor in the spleen was observed in BALB/c mice but not in (BALB/c x DBA/2) F1 mice. Additionally, some NTx AIG BALB/c mice did not show gastric hypertrophy or eosinophil infiltration owing to the administration of an H(2)-blocker. CONCLUSIONS: There are two different pathological phenotypes of murine AIG, chronic gastritis and hypertrophic gastritis, in NTx AIG BALB/c mice. Furthermore, eosinophil infiltration and the Th2 immune response might play a key role in the phenotypic shift from chronic gastritis to hypertrophic gastritis in these mice.

[Immunoglobulin rearrangement in the differential diagnosis of primary gastric lymphoma]. / Reordenamiento de inmunoglobulinas en el diagnóstico diferencial del linfoma gástrico primario.

BACKGROUND: The traditional methods to distinguish Chronic Follicular Gastritis and Primary Gastric Lymphoma do not allow an adequate definitive diagnosis in a significant number of cases. The molecular Biology diagnostic methods are based on the rearrangement of immunoglobulin genes. The polymerase chain reaction (PCR) specifically amplifies this rearrangement and allows molecular analysis of minimal tissue samples obtained with endoscopical biopsies. AIM: To test the usefulness of this PCR method in the differential diagnosis between Chronic Follicular Gastritis and Primary Gastric Lymphoma. MATERIAL AND METHODS: We analyzed the endoscopical biopsies of six Chronic Follicular Gastritis cases and eight surgically treated Primary Gastric Lymphoma cases, six with the correct diagnosis in the endoscopical biopsies and two with a diagnosis of Chronic Follicular Gastritis. RESULTS: A policlonal immunoglobulin rearrangement was found in the six cases with Chronic Follicular Gastritis. A monoclonal arrangement was found in 5 of 6 biopsies with the diagnosis of Primary Gastric Lymphoma. The same monoclonal rearrangement was observed in the two biopsies incorrectly diagnosed as Chronic Follicular Gastritis. CONCLUSIONS: PCR analysis of immunoglobulin rearrangement is a useful method in the differential diagnosis between Chronic Follicular Gastritis and Primary Gastric Lymphoma.

Hypertrophic lymphocytic gastritis with a gastric carcinoma.

Lymphocytic gastritis is a recently described gastric inflammation, characterized by an increased intraepithelial lymphocytic infiltrate mainly composed of T-lymphocytes. Endoscopically it correlates mainly with diffuse varioliform gastritis. Ménétrier's disease is a hypertrophic gastropathy with enlarged gastric folds. The histological picture is that of foveolar hyperplasia and glandular cysts of the mucosa. A few small series of lymphocytic gastritis with microscopic and endoscopic features of Ménétrier's disease have been published previously. We describe a similar case associated with a gastric adenocarcinoma.

Spontaneous remission of hypertrophic lymphocytic gastritis associated with hypoproteinemia.

A 54-year-old woman came to our office because of pretibial edema. She had no gastrointestinal symptoms. Laboratory tests revealed severe hypoproteinemia. Upper gastrointestinal endoscopy demonstrated enlarged gastric folds and multiple aphthoid nodules on the body and the fornix of the stomach. The biopsy specimen revealed a large number of CD8 positive intraepithelial T-lymphocytes infiltrating the gastric mucosa. Both serum total protein and the gastric lesions improved eight months after her first visit without any therapy for peptic ulcer or eradication of Helicobacter pylori. The data suggest that spontaneous remission may occur in lymphocytic gastritis without any gastrointestinal symptoms.

Transient protein-losing hypertrophic gastropathy associated with Mycoplasma pneumoniae infection in childhood.

A 3-year-old boy with transient protein loss due to hypertrophic gastropathy is described. Serologic evidence of concomitant Mycoplasma pneumoniae infection was present. Although sometimes associated with infections, protein-losing hypertrophic gastropathy has not been reported previously in association with Mycoplasma pneumoniae infection.

Hypertrophic gastropathy with gastric adenocarcinoma: Menetrier's disease and lymphocytic gastritis?

Lymphocytic gastritis is a form of gastric inflammation characterised by a pronounced increase in lymphocytes in gastric surface and foveolar epithelium. Lymphocytic gastritis is often associated with endoscopic evidence of 'varioliform gastritis'. Lymphocytic gastritis has recently been reported to be associated with other forms of hypertrophic gastropathies. We present a case of hypertrophic gastropathy with gastric adenocarcinoma, with both Menetrier's disease and lymphocyte gastritis. Immunohistochemical studies showed that the intraepithelial lymphocytes were predominantly alpha/beta T cells as in the normal stomach and not gamma/delta T cells as in coeliac sprue. This case together with the six recently published cases suggests that Menetrier's disease and lymphocytic gastritis may be part of the same disease spectrum.

[The potentials of low-intensity laser radiation in treating precancerous diseases of the stomach]. / Vozmozhnosti nizkoénergeticheskogo lazernogo izlucheniia v lechenii predopukholevykh zabolevanii zheludka.

The beneficial effect of low-energy laser radiation on the natural course of disease, morphologic characteristics of gastric mucosa and key elements of systemic hemostasis was observed in 98 patients with precancer of the stomach (gastric ulcer and chronic atrophic-hyperplastic gastritis with epithelial dysplasia). A correlation between clinical response and normalization of morphologic appearance and homeostasis makes the above-mentioned treatment modality promising and worth further development.

Increased tight junction width in two children with Ménétrier's disease.

Protein-losing enteropathy (PLE) and edema are usually the most prominent clinical features in children with Ménétrier's disease. However, the changes in gastrointestinal mucosa that can cause PLE have not been described yet in children. We studied by electron microscopy the mucosa of the gastric fundus, which is the site where macroscopic changes are most prominent, in two children with Ménétrier's disease. We found that tight junction width was increased to 10.5 +/- 0.94 nm (mean +/- 1 SD) in one child and to 9.7 +/- 0.7 in the other. Tight junction width returned to normal when PLE and edema subsided. These ultrastructural changes were similar to those described in adults with the disease, although the clinical course of Ménétrier's disease is very different in adults and in children. Both patients showed evidence of cytomegalovirus (CMV) infection, as indicated by increasing IgG antibodies against the virus or recovery of the virus in the urine. Although Helicobacter pylori was found in the antral mucosa of one patient, the clinical course of the disease was not related to this microorganism. We conclude that increased tight junction width plays a role in PLE seen in Ménétrier's disease in children and that CMV, rather than Helicobacter pylori, is associated with the disease.

Effects of experimental gastroduodenal reflux on density of mast cells and plasmocytes in the fundic mucosa of the rat.

IgA-, IgM-, IgG- and IgE-positive plasmocytes and mast cells were counted in the fundic mucosa of two groups of rats which underwent gastroenteroanastomosis or sham operation 12 months previously. Experimentally induced duodenogastric reflux constitutes a model for biliary gastritis which is characterized by a decrease in the IgA plasmocyte count along with an increase in IgG and IgE plasmocytes and, especially, an increase in mast cells. It is suggested that this allergic-type reaction is responsible for the hyperplasia of gastric crypts seen in biliary gastritis.