Even with the improvement in lifestyle interventions, a better control of cardiovascular (CV) risk factors, and improvements in CV outcomes, cardiovascular disease (CVD) still persists as the leading cause of morbidity and mortality in Portugal and Europe. Atherogenic dyslipidaemias, namely hypercholesterolaemia, have a crucial and causal role in the development of atherosclerotic CVD. The clinical approach of a patient with dyslipidaemia involves a watchful diagnosis, sustained in lipid and lipoprotein laboratory procedures, which must be harmonized and standardized. Standardization of lipid test results and reports, incorporating the total CV risk and the respective target and goals of treatment approach, guarantees that clinical guidelines and good clinical practices are followed and respected, increasing the reliability of lipid disorders screening, producing more accurate diagnoses and CV risk stratification, and improving the CV prevention and the achievement the desirable treatment goals.

Enquadramento: O baixo peso ao nascer é um fator de risco para a morbi-mortalidade neonatal, e um indicador geral do nível de saúde de uma população. Associa-se a baixos níveis de desenvolvimento socioeconómico, características maternas e de assistência materno-infantil.Objetivos: Analisar a influência das variáveis sociodemográficas, obstétricas e de assistência pré-natal ao baixo peso ao nascer.Participantes: 1846 puérperas, em que 161 apresentam recém-nascidos de baixo peso ao nascer.Métodos: Estudo transversal, descritivo correlacional e prospetivo com uma amostra não probabilística intencional. Foi utilizado um questionário aplicado entre Março de 2010 e Maio de 2012, em 26 instituições de saúde públicas portuguesas.Resultados: O baixo peso ao nascer, foi associado a: idade gestacional ≥41semanas (p<0,001), idade materna de risco*número gestações de risco (p=0,021); baixa escolaridade*rendimentos ≤1000€ (p=0,036), baixa escolaridade*desemprego (p=0,044), número filhos de risco*idade gestacional de termo (p<0,001), patologias na gravidez*idade gestacional de termo (p<0,001), patologias prévias*idade gestacional de termo(p<0,001), e com erro de 10% à baixa escolaridade (p=0,074) e não planeamento da gravidez (p=0,089). A prevalência de BPN foi de 8,7%.

A 71-year-old woman was referred to the endocrinology clinic to investigate postmenopausal hirsutism with 10 years of evolution. She had history of regular menses and menopause with 50 years old. Physical examination showed a male pattern facies, deepening of the voice, androgenic alopecia and hirsutism with a score of 23 according to the modified Ferriman-Gallwey scale. Testosterone and androstenedione were increased. Transvaginal ultrasound, abdominal and pelvic CT showed uterine fibroids with no pathological findings in the adrenals or ovaries. Since she had postmenopausal vaginal bleeding, uterine fibroids and suspicion of an ovarian source for her hyperandrogenism, total hysterectomy and bilateral oophorectomy were performed. Histopathological diagnosis was a Leydig cell tumour located in left ovary and endometrial carcinoma. Improvement of hirsutism was started to notice 1 month after the surgery and she was referred to the oncology clinic for adjuvant treatment.

Pituitary gigantism is extremely rare, resulting from excessive secretion of growth hormone (GH) before fusion of epiphysial growth plates. We report a case of a 13-year-old boy, who presented with increased statural growth and headaches since the age of 10 years. On physical examination, his height was 180.7 cm (+3.3 SD) and Tanner stage V. Investigation revealed increased levels of serum age-adjusted and sex-adjusted insulin-like growth factor 1 (IGF-1) and failure of GH suppression during an oral glucose tolerance test (OGTT). MRI of the sellar region revealed a pituitary macroadenoma. He underwent transsphenoidal surgery and histopathological evaluation revealed mammosomatotropic adenoma. Three months after surgery, IGF-1 normalised, nadir GH during OGTT was less than 1 ng/mL and no residual tumour was found on the MRI. Genetic testing identified a mutation in the AIP gene. This case emphasises the importance of early diagnosis of gigantism, as treatment delay increases long-term morbidity.

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