Disabling portosystemic encephalopathy in a non-cirrhotic patient: Successful endovascular treatment of a giant inferior mesenteric-caval shunt via the left internal iliac vein.

Hepatic encephalopathy is suspected in non-cirrhotic cases of encephalopathy because the symptoms are accompanied by hyperammonaemia. Some cases have been misdiagnosed as psychiatric diseases and consequently patients hospitalized in psychiatric institutions or geriatric facilities. Therefore, the importance of accurate diagnosis of this disease should be strongly emphasized. A 68-year-old female patient presented to the Emergency Room with confusion, lethargy, nausea and vomiting. Examination disclosed normal vital signs. Neurological examination revealed a minimally responsive woman without apparent focal deficits and normal reflexes. She had no history of hematologic disorders or alcohol abuse. Her brain TC did not demonstrate any intracranial abnormalities and electroencephalography did not reveal any subclinical epileptiform discharges. Her ammonia level was > 400 mg/dL (reference range < 75 mg/dL) while hepatitis viral markers were negative. The patient was started on lactulose, rifaximin and low-protein diet. On the basis of the doppler ultrasound and abdomen computed tomography angiography findings, the decision was made to attempt portal venography which confirmed the presence of a giant portal-systemic venous shunt. Therefore, mechanic obliteration of shunt by interventional radiology was performed. As a consequence, mesenteric venous blood returned to hepatopetally flow into the liver, metabolic detoxification of ammonia increased and hepatic encephalopathy subsided. It is crucial that physicians immediately recognize the presence of non-cirrhotic encephalopathy, in view of the potential therapeutic resolution after accurate diagnosis and appropriate treatments.

A male patient with acromegaly and breast cancer: treating acromegaly to control tumor progression.

BACKGROUND: Acromegaly is a rare disease associated with an increased risk of developing cancer. CASE PRESENTATION: We report the case of a 72-year-old man who was diagnosed with acromegaly (IGF-1 770 ng/ml) and breast cancer. Four years before he suffered from a colon-rectal cancer. Pituitary surgery and octreotide-LAR treatment failed to control acromegaly. Normalization of IGF-1 (97 ng/ml) was obtained with pegvisomant therapy. Four years after breast cancer surgery, 2 pulmonary metastases were detected at chest CT. The patient was started on anastrozole, but, contrary to medical advice, he stopped pegvisomant treatment (IGF-I 453 ng/ml). Four months later, chest CT revealed an increase in size of the metastatic lesion of the left lung. The patient was shifted from anastrozole to tamoxifen and was restarted on pegvisomant, with normalization of serum IGF-1 levels (90 ng/ml). Four months later, a reduction in size of the metastatic lesion of the left lung was detected by CT. Subsequent CT scans throughout a 24-month follow-up showed a further reduction in size and then a stabilization of the metastasis. CONCLUSIONS: This is the first report of a male patient with acromegaly and breast cancer. The clinical course of breast cancer was closely related to the metabolic control of acromegaly. The rapid progression of metastatic lesion was temporally related to stopping pegvisomant treatment and paralleled a rise in serum IGF-1 levels. Normalization of IGF-1 after re-starting pegvisomant impressively reduced the progression of metastatic breast lesions. Control of acromegaly is mandatory in acromegalic patients with cancer.

The effect of Greek herbal tea consumption on thyroid cancer: a case-control study.

BACKGROUND: Although in the last decade several studies have addressed the protective role of black and green tea on several diseases, including cancer, there are only few and controversial studies on the effect of tea on benign and malignant thyroid diseases. METHODS: An age and gender group matched case-control study conducted in Athens, Greece, was designed. 113 Greek patients with histologically confirmed thyroid cancer and 286 patients with benign thyroid diseases along with 138 healthy controls were interviewed with a pre-structured questionnaire in person by trained interviewers. RESULTS: An inverse association between chamomile tea consumption and benign/malignant thyroid diseases was found (P < 0.001). The odds of chamomile tea consumption, two to six times a week, after controlling for age, gender and BMI, were 0.30 (95% CI: 0.10-0.89) and 0.26 (95% CI: 0.12-0.5) for developing thyroid cancer and benign thyroid diseases, respectively when compared with not consumption. The duration of consumption was also inversely associated with the diseases. Thirty years of consumption significantly reduced the risk of thyroid cancer and benign thyroid diseases development by almost 80%. Similar, although weaker protective association, was found for sage and mountain tea. Adjustment for smoking, alcohol and coffee consumption did not alter the results. CONCLUSIONS: Our findings suggest for the first time that drinking herbal teas, especially chamomile, protects from thyroid cancer as well as other benign thyroid diseases.

Exposure to perfluorinated compounds: in vitro study on thyroid cells.

Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are widely used perfluorinated chemicals (PFCs). Previous studies detected PFOA and PFOS in human tissues including the thyroid gland. There are no studies on the in vitro effects of PFOA and PFOS on thyroid cells. Our study was aimed at evaluating the effect of the in vitro exposure to PFOA and PFOS on thyroid cell proliferation and viability. These objectives were investigated using Fisher rat thyroid line-5 (FRTL-5) cells. FRTL-5 cells cultured in the presence of PFOA and PFOS at concentrations up to 10(4) nM do not display changes in their viability and proliferation rate, while at a concentration of 10(5) nM of either PFCs, a significant inhibition of cell proliferation, mainly due to increased cell death, was found. PFOA and PFOS were detected in FRTL-5 cell pellets after 72 h of incubation with PFCs but not in control cultures. When FRTL-5 were incubated with PFCs then washed in PBS and re-cultured for 72 h without PFCs in the medium, no detectable concentrations of PFOA and PFOS were measured in the cell pellet. This indicates that PFOA and PFOS enter thyroid cells by a gradient-based passive diffusion mechanism. Future studies are required to evaluate the potential toxic effect resulting from prolonged in vivo exposure to even lower concentrations of PFCs.

Serum negative autoimmune thyroiditis displays a milder clinical picture compared with classic Hashimoto's thyroiditis.

BACKGROUND: Despite high sensitivity of current assays for autoantibodies to thyroperoxidase (TPO) and to thyroglobulin (Tg), some hypothyroid patients still present with negative tests for circulating anti-thyroid Abs. These patients usually referred to as having seronegative autoimmune thyroiditis (seronegative CAT) have not been characterized, and definite proof that their clinical phenotype is similar to that of patients with classic chronic autoimmune thyroiditis (CAT) is lacking. OBJECTIVE: To compare the clinical phenotype of seronegative CAT (SN-CAT) and CAT as diagnosed according to a raised serum level of TSH with negative and positive tests for anti-thyroid Abs respectively. METHODS: A case-control retrospective study enrolling 55 patients with SN-CAT and 110 patients with CAT was performed. Serum free triiodothyronine (FT3), free thyroxine (FT4), TSH, Tg Abs, and TPO Abs were measured in all patients. RESULTS: Patients with SN-CAT displayed significantly lower mean levels of TSH (6.6±3.4 vs 10.2±9.8 µU/ml; P=0.009), higher mean FT4 levels (1.1±0.2 vs 0.9±0.2 ng/dl; P=0.0002), and similar FT3 levels when compared with CAT patients. Mean thyroid volume was significantly greater in patients with CAT when compared with SN-CAT patients (11.2±6.5 vs 8.1±3.7 ml; P=0.001). Logistic regression demonstrated that FT4 (0.123 (0.019-0.775); (P=0.026)) and thyroid volume (1.243 (1.108-1.394); (P=0.0002)) were significantly and independently related to the diagnosis (CAT/SN-CAT). Patients with SN-CAT had a similar prevalence of thyroid nodules and female gender but a lower prevalence of overt hypothyroidism (5.4 vs 20.9%; P=0.012) as opposed to patients with CAT. CONCLUSIONS: These results suggest an autoimmune etiology of SN-CAT, which, however, seems to have a milder clinical course when compared with CAT.

Type I and type II interferons inhibit both basal and tumor necrosis factor-α-induced CXCL8 secretion in primary cultures of human thyrocytes.

Interferons (IFNs) and tumor necrosis factor-α (TNF-α) cooperate in activating several inflammation-related genes, which sustain chronic inflammation in autoimmune thyroid disease (AITD). Much is known about the positive signaling of IFNs to activate gene expression in AITD, while the mechanisms by which IFNs negatively regulate genes remain less studied. While IFNs inhibit CXCL8 secretion in several human cell types, their effects on thyroid cells were not evaluated. Our aim was to study the interplay between TNF-α and type I or type II IFNs on CXCL8 secretion by human thyroid cells. CXCL8 was measured in supernatants of primary cultures of thyroid cells basally and after a 24-h incubation with TNF-α. CXCL8 was detected in thyroid cell supernatants in basal conditions (96.2±23.5 pg/mL) being significantly increased (784.7±217.3 pg/mL; P<0.0001 vs. basal) by TNF-α. Twenty-four hour incubation with IFN-γ or IFN-ß or IFN-α dose dependently and significantly inhibited both basal and TNF-α-induced CXCL8 secretion. The degree of the inhibitory effect was IFN-γ>IFN-ß>IFN-α. This study demonstrates that type I and type II IFNs downregulate both basal and TNF-α-induced CXCL8 secretion by human thyrocytes, IFN-γ being the most powerful inhibitor. Future studies aimed at a better comprehension of the interplay between CXCL8 and thyroid diseases appear worthwhile.