Increase in basal cell carcinoma incidence steepest in individuals with high socioeconomic status: results of a cancer registry study in the Netherlands

Background  Development of both basal cell carcinoma (BCC) and cutaneous malignant melanoma (MM) is associated with acute and intermittent sun exposure. In contrast to MM, the association between socioeconomic status (SES) and BCC is not well documented.
Objectives  To investigate the incidence of BCC according to SES, stratifying by age and tumour localization in a large population-based cohort. To assess changes over time in the distribution of the patients with BCC across the SES categories.
Methods  All patients with a histologically confirmed first primary BCC ( n  = 27 027) diagnosed between 1988 and 2005 in the Southeast of the Netherlands were stratified by sex, age (25–44, 45–64 and ≥ 65 years), period of diagnosis, SES category (based on income and value of housing) and localization of the BCC. Age-standardized BCC incidence rates were calculated for the year 2004 by SES category and localization. Ordinal regression was used to assess changes over time in the proportion of patients with BCC by sex, age and SES.
Results  For men in all age groups higher BCC incidence in the highest SES category was observed, which remained significant after stratification for tumour localization. For women a consistent relationship was found only in younger women (< 65 years) for truncal BCCs, which occurred more frequently in high SES groups. Between 1990 and 2004, the proportion of BCC patients with high SES increased (+6%) and the proportion with low SES decreased (−7%).
Conclusions  High SES is associated with increased incidence of BCC among men. Our data suggest that BCC is changing from a disease of the poor to a disease of the rich.     

Evidence for spirochetal origin of circumscribed scleroderma (morphea)

Acrodermatitis chronica atrophicans (ACA) and morphea are clinically distinct skin diseases with some common features and possible coexistence. We found antibodies to Borrelia burgdorferi in eight of fifteen patients with morphea. Six of them had IgG antibodies and two both IgG and IgM antibodies. Four of the eight seropositive and five of the seven seronegative patients had been treated with high dose penicillin previously. Spirochetal organisms could be cultured in Barbour-Stoenner-Kelly's medium from a skin biopsy of one seropositive untreated patient. Spirochetes were recovered from histological sections in three of eight, two seropositive and one seronegative morphea and in one of three erythema chronicum migrans patients by an avidin-biotin immunoperoxidase method. The similar clinical picture of ACA and morphea, the response to penicillin therapy in both entities, the presence of antispirochetal antibodies, the isolation of spirochetes in culture and the detection of spirochetal organisms on histological sections suggest a close relationship among these diseases. We conclude that morphea may represent a Borrelia infection. The correlation to ACA is discussed.     

Promoter polymorphisms of the genes encoding tumor necrosis factor-alpha and interleukin-1beta are associated with different subtypes of psoriasis characterized by early and late disease onset

The psoriatic inflammatory process is characterized by an overexpression of pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin-1beta compared with a relative deficiency of anti-inflammatory factors such as interleukin-10 and the interleukin-1 receptor antagonist (interleukin-1Ra). Gene polymorphisms that affect cytokine production may contribute to the disease-associated cytokine imbalance and influence susceptibility to psoriasis. Here, we investigated the relationship between polymorphisms in the genes encoding for tumor necrosis factor-alpha (G-238A, G-308A), interleukin-1beta (C-511T, T+3953C), and interleukin-1Ra (intron 2), and cytokine production in peripheral blood mononuclear cells of healthy donors, and analyzed the distribution of these polymorphisms in patients with psoriasis vulgaris (n = 231) and healthy controls (n = 345). Carriage of tumor necrosis factor A-238 allele 2 (-238*A) was associated with increased production of tumor necrosis factor-alpha in response to lipopolysaccharide in vitro, and with early onset disease (< 40 y), especially in male patients with psoriasis [32% vs 7% in male controls; odds ratio = 6.78, 95% confidence interval = (3.18-15.15), p(adjusted) = 2 x 10(-7)]. Carriage of the interleukin-1B-511*1 (-511*C) homozygous genotype was associated with increased production of interleukin-1Ra in response to lipopolysaccharide and interleukin-10, and with late onset psoriasis [> or = 40 y; 61% vs 44% in controls; odds ratio = 2.04, 95% confidence interval = (1.19-3.53), p(adjusted) = 0.0419]. These findings indicate that gene polymorphisms associated with altered cytokine responses in vitro may modify age of onset of psoriasis. They also provide further evidence that patients with early and late onset psoriasis differ in their genetic background.     

Prediction of clinical outcomes in Crohn’s disease by using confocal laser endomicroscopy: results from a prospective multicenter study

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In Acute Myocardial Infarction Liver Parameters Are Associated With Stenosis Diameter

Detection of high-risk subjects in acute myocardial infarction (AMI) by noninvasive means would reduce the need for intracardiac catheterization and associated complications. Liver enzymes are associated with cardiovascular disease risk. A potential predictive value for liver serum markers for the severity of stenosis in AMI was analyzed.Patients with AMI undergoing percutaneous coronary intervention (PCI; n = 437) were retrospectively evaluated. Minimal lumen diameter (MLD) and percent stenosis diameter (SD) were determined from quantitative coronary angiography. Patients were classified according to the severity of stenosis (SD ≥ 50%, n = 357; SD < 50%, n = 80). Routine heart and liver parameters were associated with SD using random forests (RF). A prediction model (M10) was developed based on parameter importance analysis in RF.Age, alkaline phosphatase (AP), aspartate aminotransferase (AST), and MLD differed significantly between SD ≥ 50 and SD < 50. Age, AST, alanine aminotransferase (ALT), and troponin correlated significantly with SD, whereas MLD correlated inversely with SD. M10 (age, BMI, AP, AST, ALT, gamma-glutamyltransferase, creatinine, troponin) reached an AUC of 69.7% (CI 63.8–75.5%, P < 0.0001).Routine liver parameters are associated with SD in AMI. A small set of noninvasively determined parameters can identify SD in AMI, and might avoid unnecessary coronary angiography in patients with low risk. The model can be accessed via http://stenosis.heiderlab.de.     

The endophytic fungus Piriformospora indica reprograms barley to salt-stress tolerance, disease resistance, and higher yield

Disease resistance strategies are powerful approaches to sustainable agriculture because they reduce chemical input into the environment. Recently, Piriformospora indica, a plant-root-colonizing basidiomycete fungus, has been discovered in the Indian Thar desert and was shown to provide strong growth-promoting activity during its symbiosis with a broad spectrum of plants. Here, we report on the potential of P. indica to induce resistance to fungal diseases and tolerance to salt stress in the monocotyledonous plant barley. The beneficial effect on the defense status is detected in distal leaves, demonstrating a systemic induction of resistance by a root-endophytic fungus. The systemically altered "defense readiness" is associated with an elevated antioxidative capacity due to an activation of the glutathione-ascorbate cycle and results in an overall increase in grain yield. Because P. indica can be easily propagated in the absence of a host plant, we conclude that the fungus could be exploited to increase disease resistance and yield in crop plants.     

Neonatal purpura fulminans due to homozygous protein C or protein S deficiencies

Homozygous protein C deficiency or homozygous protein S deficiency are rare genetic diseases with catastrophic and fatal purpura fulminans-like or thrombotic complications occurring during the neonatal period. These diseases can now be successfully treated. Purpura fulminans is at least in part a cutaneous manifestation of the syndrome of systemic DIC. It is characterized by microvascular thrombosis in the dermis followed by perivascular hemorrhage, necrosis, and minimal inflammation. Laboratory findings are consistent with DIC. Although the pathogenesis is not fully understood, the DIC in purpura fulminans appears to involve the skin selectively. The development of purpura fulminans from homozygous protein C or protein S deficiencies can be separated into the two distinct phases. The first phase is the time period when the initial reversible lesions develop and grow. This reversible progression can be halted and reversed with the administration of protein C or protein S. The second phase is the irreversible stage in which the lesion continues to develop into a necrotic lesion, whether or not treated with protein C. This irreversible lesion will ultimately develop into a large full-thickness necrotic injury of the skin. It is very similar to the lesions seen in idiopathic purpura fulminans, warfarin-induced skin necrosis, and acute infectious purpura fulminans. Unfortunately, our current understanding of the mechanism or mechanisms of the induction and propagation of the purpura fulminans-like lesions in homozygous protein C or protein S deficiencies is minimal, since it has never been studied. We can only speculate on the mechanism based on laboratory data and comparison with the little that is known about the other similar types of lesions.