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Gitelman syndrome is a rare inherited tubulopathy, characterized by hypomagnesemia, hypokalemia, metabolic alkalosis, hypocalciuria and hyperreninemic hyperaldosteronism. The clinical spectrum is wide and includes: cramps, myalgias, muscle weakness, until episodes of carpo-podalic spasm, tetania, rhabdomyolysis and paralysis. Some cases have been described in literature underlining the association of this condition with chondrocalcinosis, as a typical example of hypomagnesemia-induced crystal deposition disease. The therapy of Gitelman syndrome consists on the administration of defective electrolytes, although not always effective. We describe two cases of Gitelman syndrome associated with chondrocalcinosis showing the wide range of presentation of this clinical condition.

Aldosterone is the major mineralocorticoid hormone produced by the zona glomerulosa of the adrenal cortex. Aldosterone secretion is mainly regulated by the renin-angiotensin system, and to a minor extent by serum concentration of potassium, sodium, adrenocorticotropic hormone. and dopamine. This hormone, as well as other adrenal corticosteroids, exert many of its physiological actions through modulation of gene expression. It binds cytosolic receptors that translocate to the nucleus in a ligand-dependent manner and induces transcription of specific genes that encode for proteins involved in the cardiovascular homeostasis. Such proteins act regulating vascular tone, sympathetic nervous system activity, and hydroelectrolyte transport in epithelial tissues. Classical aldosterone target tissues are kidney, colon, sweat and salivary glands. Apart from the genomic effects, which imply a direct action on DNA, rapid non-genomic actions of aldosterone have been recently described in both epithelial and non-epithelial tissues and structures such as heart, vasculature, and kidney. At these sites aldosterone contributes to the development of cardiac fibrosis, myocardial hypertrophy, heart failure and arrhythmias; other deleterious effects exerted by aldosterone include vascular remodeling, endothelial dysfunction, perivascular inflammation, renal fibrosis, and progressive renal failure. Finally, recent evidence has focused on the possible implications of aldosterone excess on metabolic alterations, as described in patients with primary aldosteronism. On these premises lies the pathogenetic role of aldosterone in the development of cardiovascular diseases and the rationale for the use of mineralocorticoid receptor antagonists in the primary and secondary prevention of the complications related to these diseases.

The objective of the study was to evaluate the significance of the determination of antithyroid antibodies in hyperthyroid patients. Two-hundred-fifteen untreated Graves' hyperthyroid patients (active toxic diffuse goiter-TDG), 54 Plummer's hyperthyroid patients (focal hyperthyroidism) and 46 subjects with other forms of hyperthyroidism were studied. Serum levels of T4, T3, TSH, TSH receptor antibody (TRAb), microsomal antibody (TMAb), and thyroglobulin antibody (TGAb) were evaluated before starting treatment, at regular intervals during therapy, and during the follow-up period after therapy was withdrawn. The antibodies were positive in all patients with active and non-active TGD but positive in only two patients (3.7%) with focal hyperthyroidism. During the treatment interval, TRAb, TMAb and TGAb serum levels fell with a nadir in the 7th month of therapy. In particular, TRAb fell to normal levels in all patients who had basal levels less than 500 U/l (97.7% of the cases) while TMAb and TGAb remained positive. Relapses, following the completion of therapy, occurred in 20.4% after one year and in 33% after two years. Relapses were always linked to a new increase in TRAb. In conclusion, TRAb can be useful in the determination of early disease and in diagnosing remission. It did not appear useful as a prognostic indicator for relapse in individual patients.

Natural history of partial thyroidectomy for thyroid disease has been studied in a population of 1196 consecutive cases surgically treated from 1977 to 1982. Follow-up analysis on this population (from six to eleven years) was carried out for appearance of recurrence. Generally, the recurrence incidence was small (only 9.9% of total population) but high frequency was observed for Graves' disease (46%) and lymphocytic chronic thyroiditis (21%). The substitutive/suppressive therapy administration did not influence recurrence of disease. Our results suggest that suppressive therapy does not modify the natural course of non cancerous thyroid pathology residual to partial thyroidectomy.