Indifferentiated osteoclastic-type giant cell carcinoma

Initially described 40 years ago (Rosai), the undifferentiated osteoclastic-type giant cell carcinoma (IOGCC) is a variant of ductal adenocarcinoma and accounts for less than 1% of exocrine pancreatic tumors. Its extreme rarity, with consequent existence of few reports and clinical experience, leads to the arousal of doubts with regard to its histogenesis, types of approach and therapeutical attitudes. It is important to note that in Portugal no similar case is registered in medical literature. A 61 year old patient admitted to the Internal Medicine Ward 3 at Coimbra University Hospital presents with a volumous intra-abdominal mass in the left hypochondrium and microcytic anemia. During the investigation, a pancreatic neoplasm was identified, and the patient was submitted to surgical resection, the anatomo-pathological study of the tumor having revealed IOGCC. The particularities of the case, current available therapeutical options and its evolution are discussed, as well as a revision of the existing literature

Disfunção tiróidea e amiodarona

Although most patients remain clinically euthyroid, some develop amiodarone-induced hyperthyroidism (HPEAI) or hypothyroidism (HPOAI). The authors present a retrospective analysis of ten patients with amiodarone-induced thyroid dysfunction. Six patients were female and mean amiodarone intake was 17.7 months. HPOIA was more common (six patients). From all the patients with HPEAI, two had type 2, one had type 1, and one had type 3 hyperthyroidism. Symptoms suggestive of thyroid dysfunction occurred in five patients, most of them with HPOAI. In HPEAI, the most frequent symptom was exacerbation of arrhythmia (three patients). Discontinuation of amiodarone and treatment with levothyroxine was chosen in 83.3% of the HPOAI cases, while thyonamide treatment with corticosteroids and without amiodarone was the option in 75% of the HPEAI cases. There were three deaths, all in patients with HPEAI. HPEAI is potentially fatal. The clinical picture may be vague, so the thyroid monitoring is mandatory

Paraquat Intoxication – experience of an Internal Medicine ward for 18 years

Introduction: Paraquat is a contact herbicide commercially available since 1962. Paraquat intoxication (PI) is usually voluntary and highly lethal, since there is no effective antidote. Toxicity occurs through cyclic redox reactions, damaging mainly the kidneys and lungs. Aim, material and methods: featuring the clinical presentation, management and outcome of patients with PI over an 18 years period (from the 01st January 1993 to the 31st December 2010) through the retrospective analysis of clinical files and comparing the survivors and the deceased. Results: Thirty-one cases of Paraquat intoxication were included, with a male: female ratio 1:1. Age range from 13 to 80 years, mean age 42.4years (±18.7).All intoxications were voluntary and by oral route. There was statistical difference in the amount ingested (22.1 mL vs. 72.7 mL, p<0.0005). A non-significant trend to a longer delay until getting medical attention in the deceased group (1.6 h vs. 3.2 h, p=0.091). Statistical significance was found between mortality and leukocytosis, hypocapnea, hypoxemia, LDH, alkaline phosphatase and AST. There was no difference between groups according to treatment options, although hemocarboperfusion was used more often in the deceased group (53.9% vs. 66.7%, p=0.471) and corticosteroids in the survivor group (61.5% vs. 44.4%, p=0.350). Mortality rate was 58.1% (66.7% in the first 72 hours), due to respiratory insufficiency and multiple organ failure. Variable levels of pulmonary fibrosis occurred in 38.5% of the survivors. Discussion & Conclusion: Paraquat intoxication has a poor prognosis with limited efficiency of treatment approaches. The relation between Paraquat in the urine and the time elapsed after ingestion is the main determinant factor in the prognosis. In this study the presence of dyspnea, hypocapnea and hypoxemia was linked to a bad prognosis. There was no statistical difference between the available treatment options

Aberrant p15, p16, p53, and DAPK Gene Methylation in Myelomagenesis: Clinical and Prognostic Implications

BACKGROUND: Aberrant DNA methylation is considered a crucial mechanism in the pathogenesis of monoclonal gammopathies. We aimed to investigate the contribution of hypermethylation of 4 tumor suppressor genes to the multistep process of myelomagenesis. METHODS: The methylation status of p15, p16, p53, and DAPK genes was evaluated in bone marrow samples from 94 patients at diagnosis: monoclonal gammopathy of uncertain significance (MGUS) (n = 48), smoldering multiple myeloma (SMM) (n = 8) and symptomatic multiple myeloma (MM) (n = 38), and from 8 healthy controls by methylation-specific polymerase chain reaction analysis. RESULTS: Overall, 63% of patients with MM and 39% of patients with MGUS presented at least 1 hypermethylated gene (P < .05). No aberrant methylation was detected in normal bone marrow. The frequency of methylation for individual genes in patients with MGUS, SMM, and MM was p15, 15%, 50%, 21%; p16, 15%, 13%, 32%; p53, 2%, 12,5%, 5%, and DAPK, 19%, 25%, 39%, respectively (P < .05). No correlation was found between aberrant methylation and immunophenotypic markers, cytogenetic features, progression-free survival, and overall survival in patients with MM. CONCLUSIONS: The current study supports a relevant role for p15, p16, and DAPK hypermethylation in the genesis of the plasma cell neoplasm. DAPK hypermethylation also might be an important step in the progression from MGUS to MM.info:eu-repo/semantics/publishedVersio