Prevalence of adrenal masses in Japanese patients with type 2 diabetes mellitus

<p>Abstract</p> <p>Introduction</p> <p>To date, there have been no reports on the prevalence of adrenal masses in type 2 diabetic patients. The present study aimed to evaluate the prevalence of adrenal incidentaloma in type 2 diabetic patients in Japan.</p> <p>Subjects</p> <p>We retrospectively evaluated the presence of adrenal masses using abdominal CT scans in 304 type 2 diabetic patients. In those with adrenal masses, we examined the hormone production capacity of the adrenal mass.</p> <p>Results</p> <p>Fourteen patients (4.6%) had an adrenal mass. Hormonal analysis identified one case as having subclinical Cushing's syndrome, two with primary aldosteronism. Eleven cases had non-functioning masses.</p> <p>Discussion</p> <p>The reported prevalence of adrenal incidentaloma in normal subjects is 0.6-4.0% in abdominal CT scan series. Our results show a relatively high prevalence of adrenal tumors in diabetic patients. On the other hand, the frequency of functional adenoma in diabetic patients is 21.4%, which is similar to that of normal subjects.</p> <p>Conclusion</p> <p>Although further studies are needed to evaluate the prevalence of adrenal tumors in diabetic patients, our data suggest that evaluation of the presence of adrenal masses may be needed in patients with type 2 diabetes mellitus.</p

Type 1 Diabetes Mellitus Associated with Pegylated Interferon-α Plus Ribavirin Treatment for Chronic Hepatitis C: Case Report and Literature Review

Combined pegylated interferon (PEG-IFN)+ribavirin (RBV) therapy has been used as a primary treatment for chronic hepatitis C. However, IFN-induced autoimmune disease, including type 1 diabetes mellitus, has been highlighted as one of the problems with this therapy. Here we report the case of a patient who developed type 1 diabetes mellitus during combined PEG-IFN+RBV therapy for hepatitis C but who showed no exacerbation of diabetes despite continued use of IFN. A 63-year-old man with chronic hepatitis C and a nonresponder to previous IFNα treatments, was admitted to our hospital because of excessive thirst, polydipsia, and polyuria 24 weeks after the start of PEG-IFNα+RBV therapy. High levels of blood glucose and glycosylated hemoglobin and low levels of C-peptide and immunoreactive insulin were observed. The serum antiglutamic acid decarboxylase antibody titer was 27,700 U/mL. We diagnosed IFN-induced type 1 diabetes mellitus; however PEG-IFNα+RBV therapy was continued for 48 weeks. Serum HCV remains negative five years after this treatment. Intensive insulin therapy was started immediately after the diagnosis of type 1 diabetes. Although the patient initially required 22 U/day of insulin, the dosage could be gradually reduced after completion of PEG-IFNα+RBV therapy and blood glucose remained well controlled. Prediction of onset of type 1 diabetes mellitus on the basis of baseline measurement of pancreas-associated autoantibodies is difficult. Therefore, it would be advisable to consider the possibility of onset of type 1 diabetes mellitus in all patients receiving IFN+RBV therapy

Heparanase expression in B16 melanoma cells and peripheral blood neutrophils before and after extravasation detected by novel anti-mouse heparanase monoclonal antibodies.

Degradation of extracellular matrix is associated with extravasation of metastatic tumor cells and inflammatory cells. Heparanase, the heparan sulfate-specific endo-beta-glucuronidase, is a key enzyme for the matrix degradation, yet its involvement in extravasation and invasion during pathological processes was not fully clarified in vivo. In the present study, we examined heparanase expression in mouse experimental models, lung metastasis of melanoma and skin infiltration of neutrophils. Sixteen novel monoclonal antibodies specific for mouse heparanase were established by enzyme-linked immunosorbent assay with a recombinant mouse proheparanase, immunocytochemical staining of B16F10 melanoma cells cultured in vitro, and immunoprecipitation of the lysate of heparanase transfectant cells. Heparanase expression in metastatic nodules of B16F10 melanoma cells and in neutrophils localized in the inflamed skin was immunohistochemically detected using a monoclonal antibody RIO-1 that recognized the C-terminus of mouse heparanase. Homogeneous and strong heparanase staining was observed in 46% of the lung micrometastases of B16F10 melanoma cells. The staining was intensely positive on the invasive front of larger established metastasis nodules, but it was weak or heterogeneous inside the nodules. Heparanase expression in skin-infiltrating neutrophils was examined after inducing local inflammation with croton oil. The monoclonal antibody stained a significant portion of neutrophils inside and along the blood vessels, whereas it did not stain dermal neutrophils located distant from the vasculatures. The present study strongly suggests that both melanoma cells and neutrophils transiently express heparanase before and during the invasive process in vivo

Heparanase expression in B16 melanoma cells and peripheral blood neutrophils before and after extravasation detected by novel anti-mouse heparanase monoclonal antibodies.

Degradation of extracellular matrix is associated with extravasation of metastatic tumor cells and inflammatory cells. Heparanase, the heparan sulfate-specific endo-beta-glucuronidase, is a key enzyme for the matrix degradation, yet its involvement in extravasation and invasion during pathological processes was not fully clarified in vivo. In the present study, we examined heparanase expression in mouse experimental models, lung metastasis of melanoma and skin infiltration of neutrophils. Sixteen novel monoclonal antibodies specific for mouse heparanase were established by enzyme-linked immunosorbent assay with a recombinant mouse proheparanase, immunocytochemical staining of B16F10 melanoma cells cultured in vitro, and immunoprecipitation of the lysate of heparanase transfectant cells. Heparanase expression in metastatic nodules of B16F10 melanoma cells and in neutrophils localized in the inflamed skin was immunohistochemically detected using a monoclonal antibody RIO-1 that recognized the C-terminus of mouse heparanase. Homogeneous and strong heparanase staining was observed in 46% of the lung micrometastases of B16F10 melanoma cells. The staining was intensely positive on the invasive front of larger established metastasis nodules, but it was weak or heterogeneous inside the nodules. Heparanase expression in skin-infiltrating neutrophils was examined after inducing local inflammation with croton oil. The monoclonal antibody stained a significant portion of neutrophils inside and along the blood vessels, whereas it did not stain dermal neutrophils located distant from the vasculatures. The present study strongly suggests that both melanoma cells and neutrophils transiently express heparanase before and during the invasive process in vivo