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Hypertensive crises (i.e., blood pressure > 180/120 mmHg) are common issues in the emergency department. This term is used to indicate both emergencies and urgencies, characterized by presence and absence of target organ damage, respectively. A wide range of therapeutic options are available. The aim of this article is to review current knowledge and treatment trends in the literature to provide clinicians with diagnostic and therapeutic tools.

At present, a correct and thorough risk evaluation represents the best prognostic and therapeutic approach for hypertensive patients. Recent European and American guidelines recommend a global stratification of the cardiovascular risk of hypertensive patients, based on the evaluation of risk factors, organ damage, and the clinical conditions associated with hypertension. A similar approach uses numerical risk scores that transform the percentage risk, calculated from large populations, into absolute values. These scores have been calculated by different research groups and scientific organizations with the aim of better defining the real risk of a given population over time. Many of these risk scores have been conceived by American and European scientific groups on the basis of the epidemiology of different risk variables in the respective populations; in general, north American hypertensives are exposed to a higher cardiovascular risk compared to Europeans and some European countries have a higher risk than others. The present review underlines the pivotal role of a correct risk evaluation of hypertension as reported in the guidelines. We briefly analyze the principal studies on risk scores: we compare the advantages and disadvantages of the different scores, as well as the similarities and differences, in order to demonstrate not only their utility, but also the possible equivalence of the different parameters considered.

This report describes a clinical case with rare association: dexamethasone-suppressible hyperaldosteronism (DSH) and hyperprolactinemia. Previous studies reported that endogenous dopaminergic activity would be increased in both primary aldosteronism and in hyperprolactinemic syndromes. By manipulating dopamine tone with metoclopramide, bromocriptine, ACTH and amineptine, the aldosterone and prolactin responsiveness was evaluated. Our results showed a lack of dopamine inhibiting aldosterone secretion, despite dopaminergic tone is known to be increased in hyperprolactinemia. Thus it seems unlikely that dopaminergic control of aldosterone secretion could be account for this type of hyperaldosteronism associated to hyperprolactinemia, where the suggestion is that ACTH represents the principal regulator of aldosterone secretion.

Thirty patients (20 adults and 10 children) suffering from nutritional anaemias were treated with folinic acid for 15 days per os at a dosage of 4-8 mg daily. For each patient routine laboratory tests, folic acid assays in the serum and in the erythrocytes have carried out and the clinical parameters have been recorded at the beginning and at the end of the treatment. The results showed statistically significant increase in the number of red cells per cmm, in folic acid content both in the serum and in the erythrocytes; at the same time a decrease of mean corpuscular haemoglobin concentration (MCHC) and mean corpuscular haemoglobin (MCH) was observed.

The liver plays a dominant role in the metabolism of the thyroidal hormones; it is here that the 5' deiodase acts to convert part of T4 to T3. There are eight further circulating iodothyronines: the rT3, mainly derived from T4, appears to be the major inhibitor of T4 and T3. Thus, if rT3 increases, the metabolic effects of T3 and T4 can be quite different. In the course of some chronic systemic diseases (e.g. hepatic cirrhosis) rT3 increases simultaneously with the decrease of T3 levels. Therefore we can describe particular alterations of the thyroidal pattern typical of chronic liver diseases: low T3 syndrome, low T3 and T4 syndrome, high T4 syndrome, mixed forms. T3 and T4 diminish due to inefficient hepatic deiodination and defective hepatocellular uptake. Inefficient hepatic deiodination and defective hepatocellular uptake. T4 levels decrease, most likely because of an inefficient production of thyroid binding globulin, or the action of a peripheral binding inhibitor. During acute liver diseases and primitive biliary cirrhosis, we can observe an increase of T4 and TBG together with an increase of the acute phase proteins. Such complex hormonal mechanisms are not influenced by TSH, which appears normal or inhibited, as the TRH stimulus test is normal. The explication can be found in an enhanced conversion of T4 to T3 in the pituitary gland. The biological and clinical significance of these mechanisms might be that of creating a "protective" state for an organism in a catabolic state by reducing the circulating T3. A relationship has been found between circulating thyroidal hormones levels, particularly the T3, rT3 and rT3/T3 ratio, and the state of hepatic functional insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

A previously healthy 62 years old man was admitted for weight loss, weakness and pigmentation of skin with increased tumor markers and altered hepatic tests. The final diagnosis was Systemic Lupus Erythematosus, despite clinical appearance. High doses of glucocorticoids were used and a sudden improving of the disease was obtained.