Ho letto su una rivista di medicina che la presenza di un particolare batterio, l' Helicobacter pylori, causa gastriti e alla lunga provoca atrofia gastrica,( una condizione, che puo evolvere in ulcera gastrica, in cui le ghiandole responsali della produzione di acido gastrico sono distrutte) e in alcune forme di tumore allo stomaco.
Questo articolo mi ha incuriosito in quanto sapevo mi era gia noto di virus capaci attraverso la loro attivita infettiva di danneggiare il dna delle cellule inducendo una trasfomazione in senso neoplastico ma non ignoravo di batteri capaci di fare altrettanto anche se con diversi meccanismi; quindi deciso di approfondire l'argomento.
Helicobacter pylori
Su pubmed ho impostato la ricerca helicobacter and gastric cancer.
In questi estratti sono destritti i meccanismi, con i quali l'Helicobacter provoca atrofia gastrica e la comparsa del tumori allo stomaco, e i geni coinvolti nella trasformazione neoplastica.
Patients infected with Helicobacter pylori, a stomach colonizing bacteria, have an increased risk of developing gastric malignancies, in particular gastric carcinomas. Aim : This review was aimed to analyze the relationship between gastric carcinoma and Helicobacter pylori infection and to rule out the possibility of preventive measures.
The risk for developing cancer includes environmental, host-genetic and bacterial factors, which induce physiologic and histologic changes in the stomach. There are two major pathways for the development of gastric cancer by helicobacter pylori: the indirect action on gastric epithelial cells through inflammation leading to gastric atrophy and intestinal metaplasia and the direct action through the induction of protein modulation and gene mutation.
Background and aims Helicobacter pylori infection of gastric mucosa causes gastritis and transient hypochlorhydria, which may provoke emergence of a mucosal precancer phenotype; H pylori strains containing a cag pathogenicity island (PAI) augment cancer risk. Acid secretion is mediated by the catalytic alpha subunit of parietal cell H,K-ATPase (HKalpha). In AGS gastric epithelial cells, H pylori induces nuclear factor-kappaB (NF-kappaB) binding to and repression of transfected HKalpha promoter activity. This study sought to identify bacterial genes involved in HKalpha repression and to assess their impact on acid secretion. Methods and results AGS cells transfected with an HKalpha promoter construct or human gastric body biopsies were infected with wild-type (wt) or isogenic mutant (IM) H pylori strains. AGS cell HKalpha promoter activity, and biopsy HKalpha mRNA, protein and H(+) secretory activity were measured by luminometry, reverse transcription-PCR, immunoblotting and extracellular acidification, respectively. Wt H pylori and DeltavacA, DeltaureA, Deltaslt and DeltaflaA IM strains repressed HKalpha promoter activity by approximately 50%, a DeltacagA IM strain repressed HKalpha by approximately 33%, and DeltacagE, DeltacagM and DeltacagL IM strains elicited no HKalpha repression. Wt H pylori-infected biopsies had markedly reduced HKalpha mRNA and protein compared with IM strain infections or mock-infected controls. Histamine-stimulated, SCH28080-sensitive biopsy acid secretion was significantly inhibited by wt but not by DeltacagL IM H pylori infection compared with vehicle-only controls. Conclusions It is concluded that H pylori cag PAI gene products CagE, CagM, CagL and, possibly, CagA are mechanistically involved in repression of HKalpha transcription. Further, acute H pylori infection of human gastric mucosa downregulates parietal cell H,K-ATPase expression, significantly inhibiting acid secretion.
fonte:
Abstract by
Helicobacter pylori and gastric cancer.
Ouakaa-Kchaou A, Elloumi H, Gargouri D, Kharrat J, Ghorbel A.
Gastric cancer can progress from a chronic inflammation of the gastric mucosa resulting from Helicobacter pylori infection that activates the inflammatory response of the host. Therefore, polymorphisms in genes involved in the inflammatory response, such as inducible nitric oxide synthase (NOS2), have been implicated in gastric carcinogenesis. The aim of this study was to evaluate the association of NOS2 polymorphisms Ser608Leu (rs2297518) in exon 16, -954G/C and -1173C/T, both in the promoter region, with gastric cancer and chronic gastritis and the association of cancer with risk factors such as smoking, alcohol intake and H. pylori infection.
We conducted a population-based case-control study in 474 Southeast Brazilian individuals (150 with gastric cancer, 160 with chronic gastritis, and 164 healthy individuals), in which we performed NOS2 genotyping by PCR-RFLP. RESULTS: SNP Ser608Leu was not associated with risk of chronic gastritis or gastric cancer. The polymorphic allele -1173T was not found in the studied population. However, the frequency of -954GC+CC genotypes was significantly higher
Abstract by BMC Gastroenterol. Gastric cancer is associated with NOS2 -954G/C polymorphism and environmental factors Jorge YC, Duarte MC, Silva AE.
Melanoma
Ho trovato una ricerca condotta dal dipartimento di scienze dermatologiche dell' Università di Firenze, in cui si studiano gli effetti dello stress nell' evoluzione del melanoma.
Stress as a possible mechanism in melanoma progression.
Sanzo M, Colucci R, Arunachalam M, Berti S, Moretti S.
Department of Dermatological Sciences, University of Florence, 50121 Florence, Italy.
The incidence of melanoma, the most aggressive type of cutaneous malignant tumor, is currently on the rise. Treatment in advanced stages is still unsuccessful compared with other malignant tumors, thus it is important to indentify the key mechanisms responsible for melanoma progression and metastasis. Genetic and molecular components, in particular, that are up- or downregulated in melanoma cells, affect the invasive potential of melanoma. Another possible important cofactor highlighted by recent studies is chronic stress, involving environmental and psychological factors, which can be an important cofactor in not only cancer progression in general but also in melanoma spreading. The negative effects of chronic stress have been evaluated epidemiologically in patients with breast and prostate cancer. In particular, the effects of stress mediators, namely, catecholamines have been studied on various human malignancies, including melanoma and have highlighted a significant increase of progression-related molecules. As such, this could be the starting point for a new approach in the treatment of advanced melanoma, in which the negative effects of stress are reduced or blocked.
Invece questo studio condotto dall'altra parte del mondo mette in relazione il fototipo e il colore di capelli col rischio di sviluppare un melanoma:
Effect of hair color and sun sensitivity on nevus counts in white children in Colorado.
Aalborg J, Morelli JG, Byers TE, Mokrohisky ST, Crane LA.
Department of Community and Behavioral Health, Colorado School of Public Health, University of Colorado Denver, Aurora, Colorado.
BACKGROUND: It has been widely reported that individuals with a light phenotype (ie, light hair color, light base skin color, and propensity to burn) have more nevi and are at greater risk for developing skin cancer. No studies have systematically investigated how phenotypic traits may interact in relation to nevus development. OBJECTIVE: We sought to systematically examine whether any combinations of phenotype are associated with a greater or lesser risk for nevus development in white children. METHODS: In the summer of 2007, 654 children were examined to determine full body nevus counts, skin color by colorimetry, and hair and eye color by comparison with charts. Interviews of parents were conducted to capture sun sensitivity, sun exposure, and sun protection practices. RESULTS: Among 9-year-old children with sun sensitivity rating type II (painful burn/light tan), those with light hair had lower nevus counts than did those with dark hair (P value for interaction = .03). This relationship was independent of eye color, presence of freckling, sex, usual daily sun exposure, sunburn in 2004 to 2007, sun protection index, and waterside vacation sun exposure. The difference in nevus counts was further determined to be specific to small nevi .
Fascite necrotizzante
Infine ho fatto un ricerca sulla fascite necrotizzante.
Necrotizing fasciitis (NF) is a necrotizing soft tissue infection that can cause rapid local tissue destruction, necrosis and life-threatening severe sepsis. Predisposing conditions for NF include diabetes, malignancy, alcohol abuse, and chronic liver and kidney diseases. NF is classified into two categories (types 1 and 2) based on causative microorganisms. The initial clinical picture of NF mimics that of cellulitis or erysipelas, including fever, pain, tenderness, swelling and erythema. The cardinal manifestations of NF are severe pain at onset out of proportion to local findings, hemorrhagic bullae and/or vital sign abnormality. In such cases, NF should be strongly suspected and immediate surgical intervention should be considered, along with broad-spectrum antimicrobials and general supportive measures, regardless of the findings of imaging tests.
Abstract
Shimizu T, Tokuda Y.
Rollins School of Public Health, Emory University, Georgia, Atlanta, USA.
Volevo sapere se si sono verificati casi di fascite necrotizzante in italia.
Ho trovato riportato un caso di fascite necrotizzante accertato presso l'università di Catania che pultroppo ha avuto un esito infausto.
Necrotizing fasciitis. Case report.
Università degli Studi di Catania, Dipartimento Scienze chirurgiche, trapianti d'Organo e Tecnologie avanzate, Unità Operativa Clinicizzata di Endocrinochirurgia P.O.U. S. Luigi-S. Currb, Italy.
Necrotizing fasciitis (NF) is an infection localized at the fascial structures (both the superficial and deep ones) layering the muscles though never affecting them. NF death rate is very high (20-40%). NF can be a post-surgery, traumatic or infective complication and its prognosis quoad vitam is fatal without a timely and correct therapy. A 57-year-old woman was got into observation due to her temperature, left thigh pain, erythema and tumefaction in the left groin-crural seat. She suffered from obesity, insulin-dependent mellitus diabetes and modest but chronic renal failure and ischaemic cardiopathy from previous Acute Myocardial Infarctions. It was then started a wide-spectrum antibiotics therapy. But after just six hours there took place a rapid development of the clinical picture with the appearance of haemorrhagic-content blisters and areas of cutaneous necrosis. The patient therefore underwent-under general anaestesia-multiple incisions in the groin-crural seat and on the ipsilateral thigh. The multiple biopsies carried out during the operation too underwent cultural and histomorphopathological analysis. The anatomic pathological study highlighted the presence of necrosis of the fascia, vascular thrombosis and myonecrosis. The cultural analysis of the tissue biopsies showed a polymicrobial infection. Both the pharmacological therapy and the surgical cleaning were carried out daily but without any improvement of the clinical picture. On the eighth day a worsening of the patient's general conditions took place, with a multiple organ failure determining the patient's exitus.
Qui invece sono riportati 11 casi di fascite necrotizzante osservati a Bologna dall' ottobre del 1995 al dicembre del 2001 e la terapia adotta per contrastare l'infezione (molto interessante).
Necrotizing fasciitis: a dramatic surgical emergency.
Catena F, La Donna M, Ansaloni L, Agrusti S, Taffurelli M.
Department of Emergency Surgery, Sant Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy.
OBJECTIVES: Necrotizing fasciitis is a challenging and potentially lethal disease; early diagnosis is of paramount importance and aggressive multidisciplinary treatment is mandatory. Overall mortality rates of 33-73% have been reported. The aim of this study was to report the experience with necrotizing fasciitis of an emergency surgery department. METHODS: From October 1995 to December 2001 we observed 11 cases of necrotizing fasciitis. The patients were five men and six women, with ages ranging from 33 to 80 years. RESULTS: Triggering aetiological factors were found in eight cases. In all patients a multidisciplinary approach was utilized. Every patient had a daily surgical debridement of the necrotic areas in the operating room. Polyantibiotic therapy was performed, and was changed according to culture results. After surgery, nine patients were submitted to hyperbaric oxygen therapy. Seven deaths (63.6%) were observed: two cases of pulmonary embolism and five cases of septic shock. Four patients survived; three had a complete recovery with progressive healing of the wounds, whereas one patient had severe impairment of the motility of the affected hand. The mean interval between the onset of symptoms and hospital admission was 5.4 days; for patients who ultimately died it was 7.3 days, whereas for patients who ultimately survived it was 2 days ; moreover these patients were significantly younger than those who died . CONCLUSION: The treatment for necrotizing fasciitis is a combination of surgical debridement, appropriate antibiotics and optimal oxygenation of the infected tissues. However, the mortality for this disease is quite high, and is related to late diagnosis and advanced age. Necrotizing fasciitis must be considered a true dramatic surgical emergency.
