Metformin therapy in pregnancy [Zastosowanie metforminy w ciazy].

Gestational diabetes mellitus (GDM), i.e. a carbohydrate metabolism disorder at pregnancy, is one of the most common metabolic complications that occur during this period. Pancreatic b-cell dysfunction and insulin resistance during pregnancy are considered the main causes of the condition. It is currently estimated that GDM is confirmed in 1-25% of patients. Diagnosis and appropriate management allow to reduce the risk of complications in newborns and the perinatal mortality rate and also improve the prognosis for mother and offspring. Metformin is taken by many patients before pregnancy due to both previously diagnosed type 2 diabetes and in the treatment of prediabetes, obesity and polycystic ovary syndrome (PCOS) as part of therapy for insulin resistance. The use of metformin in pregnancy has been controversial for many years, particularly in terms of the safety of continuation of drug therapy. Available scientific data indicate both benefits and possible drug-related adverse effects in offspring of metformin-treated patients. This problem is related not only to patients with type 2 diabetes, but also to those with PCOS who are at increased risk of miscarriage, preterm delivery and the diagnosis of GDM in subsequent stages of pregnancy. Conclusive and uniform recommendations for the use of metformin at each stage of pregnancy have not been established yet due to the doubts about the mechanisms of action of the drug, particularly at the cellular level. This review paper presents the current state of knowledge on the use of metformin during pregnancy.

[Endocrine abnormalities in patients with chronic renal failure - part I]. / Zaburzenia endokrynologiczne u chorych z przewlekla niewydolnoscia nerek - czesc I.

The kidney plays an important role in synthesis, metabolism and elimination of a plethora of hormones. In subjects with chronic renal failure, particularly at its later stages, these adaptive responses are impaired and some of these alterations are of clinical relevance. Endocrine disturbances which are the most characteristic for chronic renal failure include: secondary and tertiary hyperparathyroidism, hypothalamic-pituitary-thyroid axis dysfunction and impaired growth. The pathogenesis of these complications is complex and multifactorial. This review discusses the most important changes in the function of the parathyroid glands, thyroid and the growth hormone-insulin-like growth factor 1 axis in the light of recent developments in this field. This article also tries to give insights into diagnosis and putative therapeutic strategies.

[Endocrine abnormalities in patients with chronic renal failure - part II]. / Zaburzenia endokrynologiczne u chorych z przewlekla niewydolnoscia nerek - czesc II.

The kidneys play a crucial role in maintaining homeostasis of fluids and electrolytes, acid-base balance, and volume regulation. In subjects with chronic renal failure, particularly at its later stages, these adaptive responses are impaired and some of these alterations are of clinical relevance. The ways in which chronic renal failure affects function of endocrine organs include impaired secretion of kidney-derived hormones, altered peripheral hormone metabolism, disturbed binding to carrier proteins, accumulation of hormone inhibitors, as well as abnormal target organ responsiveness. Apart from secondary hyperparathyroidism, thyroid dysfunction and impaired growth, reviewed in our previous study, endocrine disturbances that most frequently affect this group of patients include: abnormal functioning of the hypothalamic-pituitary-adrenal and hypothalamicpituitary- gonadal axes, bone loss and gynecomastia. The clinical picture and laboratory findings of these endocrine disturbances depend on the treatment strategy.

Eplerenone mimics features of the alternative activation in macrophages obtained from patients with heart failure and healthy volunteers.

Alternative activation of macrophages plays protective role in cardiac remodelling in heart failure and the activity of mineralocorticoid receptor may determine the phenotype of these cells. We examined the influence of eplerenone, aldosterone, and IL-4 on descriptors of alternative activation in blood monocytes collected from 19 patients with heart-failure and 20 healthy volunteers. "Heart failure" macrophages in comparison with "healthy" macrophages had increased mineralocorticoid activity, NO and reactive oxygen species production, expression of iNOS mRNA and protein, but decreased expression of arginase I and mannose receptor proteins, and activity of MnSOD and CuZnSOD. Aldosterone increased mineralocorticoid activity, NO and reactive oxygen species production, iNOS mRNA and protein expression, MnSOD and CuZnSOD activity. Eplerenone attenuated the effects of aldosterone on all but MnSOD and CuZnSOD variables. Eplerenone alone increased the production of NO, MnSOD and CuZnSOD activity, arginase I gene and protein expression, and mannose receptor gene and protein expression, but decreased mineralocorticoid activity only in "heart failure" macrophages. The latter suggests altered function of mineralocorticoid receptor in heart failure. Increased mineralocorticoid activity accounts for increased NO production, iNOS gene and protein expression but does not explain the increased basal reactive oxygen species production and decreased markers of alternative activation in "heart failure" macrophages. In the lack of change in basal mineralocorticoid activity, eplerenone increases markers of alternative activation in a mineralocorticoid receptor-independent manner. Because of changes in iNOS and NO variable, eplerenone induced qualitatively different activation of macrophages from that obtained with IL-4.

[Hypoaldosteronism]. / Hipoaldosteronizm.

Hypoaldosteronism is a clinical condition characterized by a deficiency of aldosterone or its impaired action at the tissue level. The disorder may result from disturbances in renal renin production and secretion, conversion of angiotensin I to angiotensin II, adrenal aldosterone synthesis and secretion, or from abnormal responsiveness of the target tissues to aldosterone. Hypoaldosteronism has a wide spectrum of clinical manifestations, ranging from asymptomatic hyperkalemia to life-threatening depletion of fluid volumes. Although the disease, if unrecognized and untreated, seems to be associated with increased morbidity and mortality compared to the normal population, it was surprisingly rarely reviewed in the literature. The aim of this paper is to summarize the present state of knowledge on the etiology, clinical presentation, diagnosis and treatment of various forms of hypoaldosteronism.

[Endocrine abnormalities in HIV-infected patients]. / Zaburzenia endokrynologiczne u osób zakazonych HIV.

HIV infection is associated with a number of adverse consequences, including endocrine disorders. The endocrine changes associated with HIV infection have been studied in depth and, as the results of so far carried out studies suggest, their aetiology is usually multifactoral. Their pathogenesis includes direct infection of endocrine glands by HIV or opportunistic organisms, infiltration by neoplasms and adverse effects of drugs. Endocrine problems that most frequently affect this group of patients include: hypogonadism, adrenal insufficiency, thyroid disorders, impaired growth hormone release, lipodystrophy and bone loss. They may develop in both the early as well as late stages of the infection, ranging from subclinical disturbances to overt endocrine symptoms. The purpose of this paper is to review the aetiology, clinical manifestations, diagnosis and treatment of HIV-associated endocrine disturbances with a special emphasis on the most recent literature.