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The relationship between allergic diseases and cancer is a very controversial topic, widely discussed in the last decades. Many studies have demonstrated inverse association between allergy and cancer, but others have reached neutral conclusions or have indicated a positive role of allergy in the development of cancer. However, either inhibiting or favoring, many cells and molecules relevant in the allergic process play a role in tumorigenesis. On the one hand, activated immune cells, like classically activated macrophages "M1", activated dendritic cells, IL-33 and amphiregulin stimulated Innate Lymphoid Cells (ILC2), Th1, IFN-γ producing T CD8+ and B lymphocytes have inhibitory effects on tumorigenesis and tumor progression. On the other hand, tolerogenic immune cells, like alternatively activated macrophages "M2" (M2a, M2b and M2c), tolerogenic dendritic cells, ILC3, T regulatory and B regulatory lymphocytes, while inhibiting allergic sensitization and response, appear to favour carcinogenesis. Furthermore, M2 subtypes macrophages (M2a, M2b), IL-25 stimulated ILC2 and Th2 lymphocytes have a role both in inducing allergic reactions and in favouring cancer progression. In addition, mast cells, pivotal cells in allergy, have a different effect of tumorigenesis based on their location - they can promote cancer progression or inhibit it. Finally, eosinophils have shown a prevalent tumoricidal function mediated by α-defensins, TNF-α, granzymes A and IL-18. Better understanding the role of various cells on carcinogenesis can help in developing new strategies (diagnostic, therapeutic and of follow up) against tumor.

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Mast cells are abundant in the heart, among myocardial fibers, around coronary arteries, within arterial intima and intramural vessels, and in atherosclerotic plaques. Their mediators can be released during anaphylaxis and be responsible for acute coronary syndrome. This condition has been described as Kounis syndrome (KS). We report three cases of acute myocardial ischemia, which fulfill the definition for KS. In Cases 1 and 2, the association of intense chest pain with acute urticaria after an allergenic contact (wasp sting and betalactam antibiotic administration, respectively) was suspected to be an attack of angina related to an allergic reaction. No signs of an allergic reaction were observed in Case 3, but only the history of a wasp sting suggested its relationship to loss of consciousness and heart ischemia when hypersensitivity to venom was ascertained. These cases strongly recommend measurement of anaphylactic biomarkers, such as tryptase, during acute coronary syndromes to detect the possible involvement of an allergic reaction. Conversely, measurement of cardiac biomarkers during anaphylaxis, even without obvious signs of myocardial ischemia, might identify patients at risk of myocardial injury.

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Although measurement of chemiluminescence has become a widespread tool in the study of phagocytosis of peripheral neutrophils, several problems linked to spontaneous fluctuation in chemiluminescence and the number of variables involved have occasionally either limited its usefulness for clinical and experimental purposes or compelled operators to take particular care when using the technique. In the present paper, sources of variability are investigated and most of the parameters involved are thoroughly analysed and step-by-step normalised. A stochastic calibration procedure for validation of the method is applied and a monofunctional test protocol for quantitative evaluation of plasma opsonizing activity in whole blood chemiluminescence is suggested. With regard to the goal of proposing a reverse monofunctional test, we discuss the reasons why further studies aimed at standardised evaluation of the cellular components are needed.

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Previous studies showed increased growth hormone (GH) plasma levels in patients with severe heart failure. It has been hypothesized that the activation of adenohypophysis determines the enhanced release of GH. The present study was designed to verify whether impaired hepatic function, due to biventricular cardiac failure and hepatic stasis, by reducing synthesis and release of insulin-like growth factor-1 (IGF-1), may affect the negative feedback mechanism of the IGF-1 on GH secretion. We studied 20 normotensive, non diabetic patients without primitive liver disease; 10 patients in NYHA functional class IV with clinical signs of biventricular cardiac impairment and hepatic stasis (Group A); 10 patients in NYHA functional class III with prevalent left ventricular dysfunction (Group B). Blood samples for radioimmunologic determination of GH, IGF-1, atrial natriuretic factor (ANF), proteins, albumin plasma levels and transaminase plasma levels measurements, were collected 24 hours before hemodynamic study. Group A patients had clinical and hemodynamic signs of hepatic stasis with impaired liver function (SGOT 68 +/- 5.5 U/l; SGPT 89 +/- 4.3 U/1; proteins 4.56 +/- 0.4 g/dl with albumin/globulin ratio < 1; albumin plasma levels 2.8 +/- 0.7 g/dl). The parameters were normal in Group B (SGOT 16 +/- 3.7 U/l;SGPT 13 +/- 1.9 U/l; proteins 7.5 +/- 0.7 g/dl with albumin/globulin ratio > or = 1.5;albumin plasma levels 4.2 +/- 1.2 g/dl). ANF values, over normal range in both groups, were significantly higher in Group A (157.9 +/- 43.9 vs 65.6 +/- 14.6 fmol/ml.p < 0.0001). In Group A GH values were increased (4.9 +/- 4.5 vs 0.12 +/- 0.04 ng/ml); on the contrary IGF-1 values were lower (187.9 +/- 98.2 vs 260.4 +/- 141.4 ng/ml, p < 0.01). The comparison between IGF-1 and albumin plasma levels showed a high correlation either in Group A (r = 0.88, p < 0.001;) or in Group B (r = 0.81, p < 0.001). Our findings allow to hypothesize that the reduced hepatic synthesis and release of IGF-1 may be responsible for the lack of trophic action of GH on cardiac myocytes in patients with biventricular heart failure and hepatic stasis.

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PURPOSE: To evaluate the presence of central nervous system degeneration in patients with low-tension glaucoma using magnetic resonance imaging. METHOD: Ten patients with low-tension glaucoma and ten age-matched control subjects underwent magnetic resonance imaging. Cortical atrophy and cerebral infarcts were graded from "0" (normal) to "3," which was done subjectively by two neuroradiologists independently in a masked fashion. Midsagittal corpus callosum section was evaluated by measuring the thickness and cross-sectional area. RESULTS: There was a significantly greater extent of cerebral infarcts in the patients with low-tension glaucoma (P = 0.02). The thickness of the body (P = 0.03) and genu (P = 0.04) of the corpus callosum were thinner in the patients with low-tension glaucoma. The corpus callosum cross-sectional area was smaller in the low-tension glaucoma group (P = 0.04). There were no significant differences in the other parameters in this study. CONCLUSION: This study suggests a greater extent of cerebral infarcts and corpus callosum atrophy in patients with low-tension glaucoma. This may imply a greater degree of neuronal degeneration, possibly on an ischemic basis in low-tension glaucoma.

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31 patients with successful kidney grafts were studied. Ep, Ht, Hb and T lymphocytes were determined. Native and grafted kidneys were studied by ultrasonography. After KT, 45% of patients had PTE and in 71% of these a spontaneous regression was observed. Mean serum Ep activity in patients with and without PTE was significantly higher than in healthy controls. Different erythroid colony growth sensibility and responsiveness to higher serum Ep (PTE and non-PTE patients) may be due to T3 cell interaction with BFU-E.

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HLA Class I soluble antigen serum levels have been evaluated in 178 subjects who were positive for human immunodeficiency virus (HIV) and in 66 HIV-negative controls. The serum levels of HIV p24 antigen, interleukin 2 receptor (IL 2r), CD8 soluble antigen (CD 8ag), B2-microglobulin (B2-m), and neopterin (Npt), as well as the number of CD4+ and CD8+ T cells were also evaluated. Results show that mean HLA class I serum levels of HIV-positive subjects: (1) are significantly higher than controls (p less than 0.001); (2) increase with disease progression (67.7 RU/ml, 103.4 RU/ml, and 169.6 RU/ml for subjects belonging to groups II, II, and IV of the Centers for Disease Control [CDC] classification, respectively); (3) correlate with HIV p24 antigen, IL2r, and CD 8 soluble antigen levels. Present data show that elevated levels of HLA class I soluble antigens, correlating with disease stage, are found in sera of HIV-positive subjects. Circulating HLA class I molecules, interfering with some immune functions, might contribute to the pathogenesis of the immune deficiency of HIV-positive subjects.

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The authors present a case of Henoch-Schönlein purpura in a young soldier (19 years old) which they consider important for its etiology and the length of its oligoanuric phase. The syndrome followed a Salmonella hirschfeldii infection, and a protracted oligoanuric phase was followed by nephrotic syndrome and selective glomerular proteinuria which lasted for 1 year. The young man recovered after the eradication of the Salmonella. It seems possible that there was an overall anomalous regulation of the 'lymphoid system of the mucosa', perhaps dependent on a genetic predisposition.

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Microangiopathy is one of the most frequent diseases in diabetic patients. A diabetic man with a kidney transplant and with severe and progressive vasculopathy with early necrosis of the fingers and toes was submitted to three prostacyclin (PGI2) intravenous infusions (5 ng/kg/min for forty-eight hours) during a period of two months. Three months after the last infusion, radiographs of the hands and feet showed a marked reduction in the extent of the vascular calcifications and healing of the ischemic-necrotic areas. The authors discuss the immediate and later effects of PGI2 infusion in a case of diabetic vascular disease.

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Nine patients undergoing regular dialytic treatment (RDT) for more than 60 months (mean 125 +/- 33 months) showed clinical and radiological evidence of non-infective destructive spondyloarthropathy (DSA). The cervical spine was the skeletal segment most affected (100% of cases). Three patients were found also to be suffering from discal and bone alterations of the dorsal column, and in two other patients the vertebral bodies L4-L5 were changed. Typical radiological pictures showed a narrowing of intervertebral spaces with the destruction or sclerosis of adjacent subchondral bones, erosions of vertebral body plates and cavitations. CT studies of the altered spines confirmed discal lesions and osteolytic areas with bone condensation at each level. Ligamentous lesions resulting in severe disorders of spinal statics were discovered during autopsy of three patients. Histological study of disc and peridiscal ligaments indicated the presence of large amyloid deposits containing beta-2-microglobulin (B2-m). It is possible that the minor biocompatibility of the cuprophan membrane of dialyzers is the most significant factor responsible for the hyperproduction of B2-m and thus of the osteo-articular deposition of a new type of amyloidosis.

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The effect of acute reduction of intraocular pressure (IOP) through oral administration of glycerol was assessed in 15 eyes of 15 patients with ocular hypertension by means of automated perimetry, Farnsworth-Munsell 100 hue testing, measurement of spatial contrast sensitivity with a laser interferometer and automated optic disc analysis. There was no significant relation between the absolute or relative change in IOP and the corresponding changes in any of the visual field or optic disc indices studied. The colour vision score increased significantly as the IOP decreased (p = 0.03). There was a significant reduction in the logarithm of spatial contrast sensitivity at grating sizes of 3 (p = 0.007) and 7.5 (p = 0.05) cycles per degree as the IOP decreased.

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The accumulation of amyloid in the bone and joint system has recently been recognized as a peculiar disease in patients undergoing long-term hemodialysis (5 years at least), especially in those who use cuprophan membranes. The pathology of amyloidosis is characterized by deposits of amyloid (beta 2-microglobulin mainly) in the bone, in the synovia, and in pericapsular soft tissues. The skeleton of 46 long-term hemodialysis patients (19 males and 27 females) was studied by X-ray: bone and joint abnormalities due to amyloid deposition were observed in 45% of cases. The shoulder, hip, and wrist were the most frequently involved joints. Destructive spondyloarthropathy was present in 15% of cases. The radiographic patterns of AOD are generally divided into axial and peripheral lesions. In the appendicular skeleton abnormalities include: well-defined lytic areas (geodes), pathologic fractures, marginal erosions, and periarticular soft tissue swelling. Destructive spondyloarthropathy is frequently present in the cervical spine (85% of our cases), and is characterized by narrowing of the intervertebral space, marginal erosion, and subchondral bone sclerosis of the vertebral body.

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Serum erythropoietin (Epo) activity, hemoglobin (Hb), and hematocrit (Ht) were determined in 21 cross-country skiers during the training season. The Epo levels were not significantly reduced in the skiers relative to the normal population (P less than 0.01 and P less than 0.001, respectively). In 11 athletes Epo, Ht, urinary gamma-glutamyltransferase, N-acetyl-beta-glucosaminidase, and microalbuminuria were determined before and after a 50-km ski race at 1600 m above sea level. A significant increase of these variables (except for Ht) was found after the competition (P less than 0.001). It is concluded that while the reductions in Hb and Ht, which are typical of several endurance exercises, are not accompanied by a renal hypoxia sufficient to stimulate Epo overproduction, the renal hypoxia reached during the strenuous exercise of the race at altitude may be effective in determining blood increases in Epo.

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A highly polymorphic DNA probe (3'HVR) with genetic linkage to the locus of autosomal dominant polycystic kidney disease was used for screening. Families with subjects at risk were from the Po river delta region (Northern Italy), where the disease accounts for 24% of the demands for dialysis. 3'HVR alleles were investigated in white blood cell DNA from 142 members of 18 families. The genomic marker was found informative in 88% of cases. Two recombinations between the marker and the disease locus were observed in 79 meioses. In 42 of the subjects at risk the results of DNA analysis and renal ultrasonography were compared. In 36 subjects the tests confirmed each other (18 were positive). In the other six subjects (all under 20 years of age and four under 10) only DNA analysis could diagnose the inheritance of cystic disease in the absence of demonstrable cysts. The findings indicate that in the population of the Po river delta the presymptomatic detection of adult polycystic kidney disease by 3'HVR linkage analysis is feasible in 88% of cases with approximately 95% reliability.

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