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Robert Krysiak

Publications and source records attributed to Robert Krysiak.

At least 19 recordsLinked to original sources
PubMed2006

Rapid, real-time detection of acute HIV infection in patients in Africa.

BACKGROUND: We conducted a prospective study to evaluate methods of detecting clients with sexually transmitted diseases (STDs) who were acutely coinfected with human immunodeficiency virus (HIV) in Lilongwe, Malawi. METHODS: After informed consent was obtained, all clients with acute STDs were offered voluntary HIV counseling and testing by 2 rapid antibody tests. Samples from rapid test-negative or -discordant subjects were pooled (50 : 5 : 1) and tested for HIV RNA. Western blots were performed on all rapid test-discordant specimens with detectable HIV RNA. A subset of specimens received p24 antigen testing with standard and/or ultrasensitive methods. Patients with possible acute HIV infection were followed to confirm seroconversion. RESULTS: A total of 1450 clients (34% female and 66% male) agreed to testing, of whom 588 (40.55%) had established HIV infection and 21 (1.45%) had acute infection. Discordant rapid antibody tests identified 7 of 21 (33.3% sensitivity), standard p24 antigen identified 12 of 16 (75% sensitivity), and ultrasensitive p24 antigen identified 15 of 17 (88% sensitivity) acute cases. By definition, the sensitivity of the RNA assay was 100%. CONCLUSIONS: Real-time pooled RNA testing for the detection of acute HIV infection is feasible in resource-limited settings. However, parallel rapid testing and p24 antigen testing are technologically simpler and together may detect approximately 90% of acute cases.

Acute Disease↗
PubMed2006

Effects of short-term fenofibrate treatment on circulating markers of inflammation and hemostasis in patients with impaired glucose tolerance.

CONTEXT: Apart from lowering lipid levels, peroxisome proliferator-activated receptor (PPAR) alpha activators (fibrates) produce many other favorable effects that may contribute to their clinical effectiveness in dyslipidemic and diabetic patients. OBJECTIVE: The objective of this study was to compare the impact of a short-term treatment with fenofibrate and the American Heart Association (AHA) step 1 diet on systemic inflammation, hemostasis, and monocyte secretory function in relationship with their metabolic actions. DESIGN, SETTING, PARTICIPANTS, AND INTERVENTIONS: This was a prospective, randomized, placebo-controlled trial involving the group of 91 ambulatory patients with impaired glucose tolerance (IGT) (diagnosed on the basis of the American Diabetes Association criteria), randomly divided into three groups, simultaneously treated for 30 d with the AHA step 1 diet (n = 30), micronized fenofibrate (267 mg/d, n = 31), or placebo (n = 30). The control group included 34 age-, sex-, and weight-matched subjects with normal glucose tolerance. Eighty-six (95%) patients and all control subjects completed the study. MAIN OUTCOME MEASURES: Plasma markers of inflammation and hemostasis and monocyte release of proinflammatory cytokines were measured. RESULTS: Compared with subjects with normal glucose tolerance, IGT patients exhibited higher plasma levels/activities of fibrinogen, factor VII, plasminogen activator inhibitor-1, high-sensitivity C-reactive protein, and oxidized low-density lipoproteins. Lipopolysaccharide-activated monocytes from IGT patients released significantly more TNF-alpha, IL-1beta, IL-6, and monocyte chemoattractant protein-1 in comparison with monocytes from control subjects. Thirty-day treatment with fenofibrate but not with the AHA step 1 diet: 1) improved lipid/lipoprotein profile and glucose metabolism, and 2) reversed or alleviated all the above-mentioned abnormalities. The favorable effects of fenofibrate on plasma high-sensitivity C-reactive protein and on monocyte release of TNF-alpha, IL-1beta, IL-6, and monocyte chemoattractant protein-1 did not correlate with its action on plasma lipids but was related to the improvement in insulin sensitivity and weakly to free fatty acid-lowering action. CONCLUSIONS: Our study is the first to show that relatively small disturbances in glucose metabolism are associated with marked and multidirectional abnormalities in plasma markers of inflammation and hemostasis and in monocyte secretory function. Moreover, fenofibrate may exhibit early pleiotropic effects in patients with IGT.

Adult↗
PubMed2006

[Thyroid hormone resistance syndrome].

Resistance to thyroid hormones (RTH) is an inherited syndrome characterised by reduced target tissue responsiveness to these hormones. In the recent years, it has become clear that RTH is probably much more common than is generally recognised, and is often misdiagnosed and inaccurately treated. Subjects suffering from RTH have raised serum thyroid hormone levels and raised or inappropriately normal thyrotropin levels. Two major forms of a clinical presentation of this disorder are asymptomatic or slightly symptomatic subjects with generalised resistance and patients with thyrotoxic features suggesting predominant pituitary resistance. Surprisingly, these various clinical situations are determined by the same genetic defect. In this paper, aetiology, symptoms, clinical classification, diagnosis and treatment of RTH are reviewed with putting special emphasis on the results of recently published studies.

Diagnosis, Differential↗
PubMed2006

[Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency].

Congenital adrenal hyperplasia is a general term applied to a group of several inherited enzymatic defects of cortisol biosynthesis. The most frequent cause of this disease is by far 21-hydroxylase deficiency which is considered one of the commonest metabolic disorders. The degree to which the activity of this enzyme is diminished correlates with the severity of congenital adrenal hyperplasia and therefore the clinical presentation of 21-hydroxylase deficiency has a wide spectrum of clinical and laboratory abnomalities. The recent developments have improved prenatal diagnosis and treatment of affected females to minimise genital virilisation. Despite progress made in its recognition and treatment, diagnosis and management of 21-hydroxylase deficiency is still the subject of many debates and controversies. In this paper, aetiology, symptoms, diagnosis and treatment of 21-hydroxylase deficiency in various groups are reviewed with putting special emphasis on the results of recently published studies.

Adrenal Hyperplasia, Congenital↗
PubMed2006

[Normoaldosterone spironolactone sensitive hypertension].

We report the case of normoaldosterone spironolactone sensitive hypertension. Patients suffering from this recently identified form of arterial hypertension exhibit clinical symptoms resembling the symptoms of primary aldosteronism. The described disturbances may be misdiagnosed as essential hypertension because plasma aldosterone levels and aldosterone/renin ratio in patients are within the normal ranges. In the described state of the examined female, detection of the disease and implementation of spironolactone treatment not only normalised arterial blood pressure but also allowed to avoid unnecessary administration of many antihypertensive agents.

Aged↗
PubMed2006

[Precocious puberty].

Precocious puberty is usually defined as the appearance of secondary sexual development before the age of 8 years in girls and 9 years in boys. Precocious puberty is a heterogenous condition generally divided into central and peripheral forms driven respectively by hypothalamic-pituitary axis or by excessive production of sex steroids. Taking into account the risk associated with the underlying disorder as well as the impact of precocious puberty on stature growth and development of reproductive and mental functions, this condition has important consequences for affected children and their families. In this paper, the pathophysiology, clinical presentation, laboratory and radiological features, and treatment of the disorders leading to precocious puberty are reviewed. Particular attention is devoted to the results of the recently published studies.

Child↗
PubMed2006

[Postparum thyroiditis].

Postpartum thyroiditis is one of the most common endocrinological disorders annually affecting millions of women world-wide. It is is defined as a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery. A thyrotoxic phase of postpartum thyroiditis may be brief and unnoticed before a more long-lasting (permanent in up to 30%) hypothyroid phase occurs. The disease, found in approximately 5-10% of mothers in the general population, is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. Women suffering from other autoimmune conditions, or having a previous or family history of thyroid disease are at increased risk of its development. In this paper we present an overview of the pathogenesis, clinical aspects, diagnosis, and treatment options for postpartum thyroiditis with putting special emphasis on the results of recently published studies.

Diagnosis, Differential↗
PubMed2006

[Incidentaloma--one of the greatest challenges of modern endocrinology].

Technological advance of the recent years has contributed to the development of the situation during which clinically inapparent masses are discovered in endocrine organs by high-resolution radiological imaging procedures that have been performed for other reasons. Most of these lesions, frequently referred to as incidentalomas, are clinically insignificant benign and hormonally inactive adenomas that neither pose a risk to a patient's health nor warrant the risks of further diagnosis and treatment. One of the greatest challenges of modern endocrinology is to distinguish the vast majority of clinically insignificant changes from other masses requiring further management such as hormone-secreting tumours and malignant lesions. Over the years a myriad of the diagnostic and therapeutic approaches has been recommended and presently there are still no uniform guidelines. The purpose of his article is to give an overview on the recent advances in diagnosis and management of pituitary and adrenal incidentalomas. We provide the reader with practical recommendations and underline areas in which further studies are required.

Adrenal Gland Neoplasms↗
PubMed2005

Amitriptyline and nortriptyline inhibit interleukin-1 release by rat mixed glial and microglial cell cultures.

Pro-inflammatory cytokines, such as interleukin (IL)-1beta and tumour necrosis factor (TNF)-alpha have been suggested to be involved in the pathophysiology of depression and in the mechanism of action of antidepressant drugs. Until now the effect of antidepressants on cytokines has been examined only in plasma, blood mononuclear cells and spleen, which reflect the activity of peripheral cytokine network. The aim of this study was to evaluate the effect of amitriptyline and its metabolite nortriptyline on the release of IL-1beta and TNF-alpha by lipopolysaccharide (LPS)-activated rat mixed glial and microglial cell cultures. LPS stimulated the release of both cytokines. The exposure of mixed glial culture to amitriptyline and nortriptyline led to a decrease in both IL-1beta and TNF-alpha release. Moreover, amitriptyline reduced LPS-stimulated IL-1beta release by microglial cultures. Although amitriptyline reduced secretion of both cytokines, the drug did not affect IL-1beta and TNF-alpha mRNAs in mixed cell cultures. Our study has shown for the first time that amitriptyline and nortriptyline administered at concentrations which may be achieved in plasma and brain structures during treatment, inhibit the secretion of IL-1beta and TNF-alpha in rat mixed glial and microglial cell cultures. The obtained results support the previous observations that antidepressants are able to reduce peripheral release of pro-inflammatory cytokines and suggest that the cytokine network may be involved in the central mechanism of action of amitriptyline and nortriptyline.

Amitriptyline↗
PubMed2005

Effect of monthly atorvastatin and fenofibrate treatment on monocyte chemoattractant protein-1 release in patients with primary mixed dyslipidemia.

The aim of this study was to compare the effect of 30-day treatment with atorvastatin and fenofibrate on monocyte release and plasma levels of monocyte chemoattractant protein-1 (MCP-1). We studied 52 atherosclerotic patients with primary mixed dyslipidemia and 16 age-, sex-, and weight-matched control subjects with asymptomatic atherosclerosis. Dyslipidemic patients enrolled into the study were randomly divided into three groups, simultaneously treated with atorvastatin (20 mg/d, n = 18), fenofibrate (267 mg/d, n = 16), or placebo (n = 18). Plasma lipid-profile and content of MCP-1, and monocyte release of this chemokine were measured at baseline and after 30 days of therapy. Compared with the control subjects, dyslipidemic patients exhibited the increased plasma levels and monocyte MCP-1 release. Atorvastatin and fenofibrate not only improved lipid profile but also decreased monocyte secretion of this chemokine. Moreover, hypolipemic agents slightly reduced its plasma levels. MCP-1-lowering effect of atorvastatin and fenofibrate did not correlate with the lipid-lowering potential of these agents. Our results suggest that atorvastatin and fenofibrate produce their antiinflammatory effect partially via inhibiting monocyte release of MCP-1. The treatment-induced reduction in its secretion may contribute to the clinical effectiveness of statins and fibrates in the therapy for atherosclerosis and other chronic fibroproliferative diseases.

Adult↗
PubMed2005

Monocyte release of tumor necrosis factor-alpha and interleukin-1beta in primary type IIa and IIb dyslipidemic patients treated with statins or fibrates.

Both 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) as well as peroxisome proliferator-activated receptor (PPAR)alpha activators (fibrates) proved to be effective in the primary and secondary prevention of cardiovascular diseases. The benefits of hypolipemic therapy in cardiovascular diseases cannot be explained only by the lipid-lowering potential of these agents. The aim of this study was to clarify the effect of hypolipemic agents on proinflammatory cytokine release from human monocytes in relationship with their action on plasma levels of sensitive systemic marker of low-grade vascular inflammation. Plasma lipid and high-sensitivity C-reactive protein (hsCRP) levels, and the release of tumor necrosis factor-alpha (TNFalpha) and interleukin-1beta from monocytes were assessed at baseline and 30 and 90 days following randomization of IIa dyslipidemic patients into fluvastatin or simvastatin groups and randomization of type IIb dyslipidemic patients to the micronized form of either ciprofibrate or fenofibrate. Lipopolysaccharide-stimulated monocytes from dyslipidemic patients released significantly more TNFalpha (types IIa and IIb dyslipidemias) and interleukin-1beta (type IIa dyslipidemia) in comparison with monocytes in 59 age-, sex-, and weight-matched control subjects. Their baseline hsCRP levels were also higher. Both statins and fibrates reduced the release of TNFalpha and interleukin-1beta, and lowered plasma hsCRP levels. The effects of hypolipemic agents on cytokine release and plasma hsCRP were unrelated to their lipid-lowering action. Our results have demonstrated that type IIa and IIb dyslipidemic patients exhibit the abnormal pattern of TNFalpha and interleukin-1beta production by activated monocytes. Both HMG-CoA reductase inhibitors and PPARalpha activators normalize monocytic secretion of these cytokines, and this action may partially contribute to the systemic antiinflammatory effect of hypolipemic agents. The statin- and fibrate-induced suppression of proinflammatory cytokine release from monocytes seems to play a role in their beneficial effect on the incidence of cardiovascular events.

Adult↗
PubMed2005

[Anabolic therapy in osteoporosis--part 1].

Osteoporosis is one of the most important problems in developed societies. Unfortunately, all drugs available nowadays on the market exhibit antiresorptive action bringing only moderate benefits to patients suffering from this disease. For the last few years, the number of studies on the suggested use of anabolic therapy in the treatment of osteoporosis has been growing up. In the present study we describe in details sodium fluoride, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins), growth hormone, insulin-like growth factor I, and parathormone and its analogues, describing their mechanism of action and adverse effects. We also show the results of experimental studies and clinical trials in which the mentioned drugs were used. On the basis of available results we are trying to establish the exact position of anabolic agents in pharmacotherapy of osteoporosis.

Human Growth Hormone↗
PubMed2005

[Recent insights into the role of aldosterone in physiology, pathology and therapy].

Recently, it has become clear that the action of aldosterone is far more complicated than it was previously thought. Beyond regulating sodium and volume homeostasis by its epithelial action, the hormone exhibits its effects in other organs, such as the heart, blood vessels and central nervous system. Some of these actions, so called non-genomic effects, are not related to the aldosterone-induced stimulation of classical mineralocorticoid receptors. In this paper we discuss the progress made in understanding the physiological function of aldosterone and the role of its excess in the etiology of cardiovascular disorders. In the second part of this article, we provide an overview of the clinically-proven benefits of a new selective aldosterone-receptor antagonist, eplerenone.

Aldosterone↗
PubMed2005

[A rare association of postpartum thyroiditis and ulcerative colitis].

It is well known that chronic thyroiditis is frequently associated with other autoimmune disorders, but its association with inflammatory bowel diseases has rarely been described. We report a case of a 26-year-old woman, seven months after delivery, who developed a moderate attack of ulcerative colitis. Laboratory analysis, ultrasonography, anti-thyroid antibodies and cytological examination of fine needle aspiration biopsy led us to diagnose postpartum thyroiditis. The patient also presented erythema nodosum, anti-parietal cell and anti-intrinsic factor antibodies and a family history of autoimmune disorders. This case illustrates the need for clinical awareness of concomitant postpartum thyroiditis and ulcerative colitis and suggests that in patients with inflammatory bowel diseases thyroid function test should be carried

Adult↗
PubMed2005

[Gonadotropin-releasing hormone analogs].

Pituitary-gonadal axis activity depends on pulsative hypothalamic gonadotropin-releasing hormone (GnRH) secretion. Two groups of GnRH analogs, agonists and antagonists, are presently used for the treatment of clinical conditions in which modulation or interference with sex hormone production is beneficial. They are administered in assisted reproductive technologies to prevent premature luteinizing hormone surges during controlled ovarian stimulation. Due to an inhibitory effect on the growth of hormone-dependent tumors, GnRH analogs are used in the treatment of some cancers. In the present study we discuss in details both these applications. Moreover, we review the potential role of these agents in pharmacotherapy of endometriosis, uterine myomas and central precocious puberty. Based on the available literature we try to show their exact place in the medical therapy of gynecological disorders.

Endometriosis↗
PubMed2005

[Anabolic therapy of osteoporosis].

Osteoporosis is one of the most important problems in developed societies. Unfortunately, all drugs available nowadays on the market exhibit antiresorptive action bringing only moderate benefits to patients suffering from this disease. For the last few years, the number of studies on the suggested use of anabolic therapy in the treatment of osteoporosis has been growing up. In the present study we describe in details sodium fluoride, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins), growth hormone, insulin-like growth factor I, and parathormone and its analogues, describing their mechanism of action and adverse effects. We also show the results of experimental studies and clinical trials in which the mentioned drugs were used. On the basis of available results we are trying to establish the exact position of anabolic agents in pharmacotherapy of osteoporosis.

Anabolic Agents↗
PubMed2005

[Verapamil-induced hyperprolactinemia--a case report].

In many cases hyperprolactinemia can be caused by taking medications. Occasionally, verapamil-treated patients experience a slight asymptomatic increase in serum prolactin level. In this article we report the case of 42-year woman with manifest verapamil-induced hyperprolactinemia whose clinical symptoms suggested the occurrence of prolactinoma. A marked increase in prolactin levels and the preserved reactivity of this hormone in dynamic tests suggested that the patient exhibited "hypersensitivity" to verapamil. In the described state of the examined female detection of the disease, verapamil withdrawal and temporary bromocriptine administration have led to a full normalization of patient's clinical status.

Adult↗