Suppurative thyroiditis caused by Salmonella enteritidis

Ropne zapalenie tarczycy jest rzadką chorobą, której przebieg może być początkowo przyczyną błędnej diagnozy. Jednocześnie właściwa diagnoza jest niezbędna w celu wdrożenia właściwego leczenia. W pracy przedstawiono przypadek 82-letniego mężczyzny chorego na cukrzycę typu 2 i z wywiadem kortykosteroidoterapii. Pacjent zgłosił się do lekarza z powodu dysfagii i odynofagii, którym towarzyszyła gorączka, dreszcze, ból gardła i ból prawego ucha. Na podstawie obrazu klinicznego, badań radiologicznych, cytologii komórek tarczycy, posiewu krwi i aspiratu tarczycy rozpoznano ropne zapalenie tarczycy w przebiegu zakażenia Salmonella enteritidis. Chorego skutecznie wyleczono, stosując antybiotyki i drenaż chirurgiczny. (Endokrynol Pol 2011; 62 (5): 466–470)Bacterial thyroiditis is a rare disease, and one of which the clinical symptoms and signs are frequently misleading. On the other hand, prompt diagnosis is crucial for successful treatment. We report the case of an 82 year-old man with diabetes mellitus type 2 and a history of steroid treatment who presented with severe odynophagia and dysphagia associated with fever, chills, sore throat and right ear pain. Based on the clinical picture, radiological studies, thyroid cytology, blood and thyroid aspirate culture, suppurative thyroiditis caused by Salmonella enteritidis was diagnosed. The patient was successfully treated with antibiotics and surgical drainage. (Pol J Endocrinol 2011; 62 (5): 466–470

Loss of the Orphan Nuclear Receptor SHP Is More Pronounced in Fibrolamellar Carcinoma than in Typical Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) remains a major problem in oncology. The molecular mechanisms which underlie its pathogenesis are poorly understood. Recently the Small Heterodimer Partner (SHP), an orphan nuclear receptor, was suggested to be involved as a tumor suppressor in hepatocellular carcinoma development. To date, there are no such studies regarding fibrolamellar carcinoma, a less common variant of HCC, which usually affects young people and displays distinct morphological features. The aim of our project was to evaluate the SHP levels in typical and fibrolamellar hepatocellular carcinoma with respect to the levels of one of the cell cycle regulators, cyclin D1. We assessed the immunoreactivity levels of SHP and cyclin D1 in 48 typical hepatocellular carcinomas, 9 tumors representing the fibrolamellar variant, 29 non malignant liver tissues and 7 macroregenerative nodules. We detected significantly lower SHP immunoreactivity in hepatocellular carcinoma when compared to non malignant liver tissue. Moreover, we found that SHP immunoreactivity is reduced in fibrolamellar carcinoma when compared to typical hepatocellular carcinoma. We also found that SHP is more commonly lost in HCC which arises in the liver with steatosis. The comparison between the cyclin D1 and SHP expression revealed the negative correlation between these proteins in the high grade HCC. Our results indicate that the impact of loss of SHP protein may be even more pronounced in fibrolamellar carcinoma than in a typical form of HCC. Further investigation of mechanisms through which the loss of SHP function may influence HCC formation may provide important information in order to design more effective HCC therapy

The Blocking on the Cathepsin B and Fibronectin Accumulation in Kidney Glomeruli of Diabetic Rats

Hyperglycemia results in the activation of tissue angiotensin II. Angiotensin II stimulates the synthesis of ECM proteins and causes a decrease activity of proteolytic enzymes. The aim of this study was to assess the impact of multilevel blocking of the RAAS, cathepsin B activity, and fibronectin accumulation in the glomerular in the rats diabetes model. Sixty male Wistar rats were initially included. Diabetes was induced by intravenous administration of streptozotocin. The animals were randomized to six groups of ten rats in group. Rats in the four groups were treated with inhibitors of the RAAS: enalapril (EN), losartan (LOS), enalapril plus losartan (EN + LOS), and spironolactone (SPIR); another group received dihydralazine (DIH) and the diabetic rats (DM) did not receive any drug. After six weeks, we evaluated blood pressure, 24 h urine collection, and blood for biochemical parameters and kidneys. In this study, fluorometric, ELISA, and immunohistochemical methods were used. Administration of EN + LOS increased activity of cathepsin B in homogenates of glomeruli compared to DM. Losartan treatment resulted in reduction of the ratio kidney weight/body weight compared to untreated diabetic rats. SPIR resulted in the increase activity of cathepsin B in the homogenate of glomeruli. The values of cathepsin B in the plasma of rats in all studied groups were similar and showed no tendency

The cyclin D1 expression in hepatocellular carcinoma.

<p>A- the immunoreactivity of cyclin D1 in HCC tumor; B- the cyclin D1 immunoreactivity in fibrolamellar carcinoma; scale bar 5 µm; C- Spearman's rank graph showing a negative correlation between the SHP and cyclin D1 immunoreactivity in G3 hepatocellular carcinoma.</p

Clinicopathological characteristic of patients with results of the immunostaining.

<p>Abbreviations: Ca cm maximal tumor size in cm; Inflamm inflammation; G tumor grade; S stage; N normal; C cirrhosis; R HCC recurrence;</p><p>*data not available; n/a not applicable.</p

SHP immunoreactivity in normal liver.

<p>A, B – immunohistochemical staining of the normal hepatic lobule; C, D- immunofluorescence staining showing exclusively nuclear (C) or cytoplasmic (D) SHP localization in different lobules; scale bar: A 100 µm; B 20 µm; C,D 25 µm. E- result of the SHP immunohistochemistry preceded with (lower image) or without (upper image) anti-SHP blocking antibody; F- Western blot analysis of three liver (LV1–LV3) lysates, the SHP protein present in a single band; G- Result of the RT-PCR study showing the SHP mRNA in the normal liver; GAPDH mRNA was used as a control.</p

SHP immunoreactivity in macroregenerative nodules.

<p>Note uniform staining of all hepatocytes; scale bar A-100 µm, B-50 µm.</p