Arthritis in children as a result of a previous infection caused by Yersinia enterocolitica and Yersinia pseudotuberculosisInfections caused by Yersinia enterocolitica and Yersinia pseudotuberculosis, often referred to as Yersiriiosis, are classified as diseases occurring in human and animals which originate from their reservoir in a natural environment (sapronosis).Infection occurs orally by contaminated food or water, f pseudotuberculosis and Y enterocolitica are gram-negative, rod-shaped bacterias of the genus Yersinia, belonging to the family' of Enterobacteriaceae.They are enteric pathogens, responsible for triggering a large number of different symptoms ranging from diarrhea and abdominal pain, to more systemic ones such as fever or scarlatinform skinrash.Others may include myocarditis, Crohn's disease.Reiter's syndrome, chronic pancreatitis, ankylosing spondylitis, acute interstitial nephritis, Kawasaki syndrome, conjunctivitis, erythema nodosum, lymphadenopathy (1) and arthritis (2, 3).Reactive arthritis develops 1-4 weeks after gastrointestinal or urogenital infections caused by Yersinia.The finding of LPS structures of Yersinia in the synovial fluid of human joints is widely regarded to be of pafarnouht importance in the pathogenesis of arthritis (4-6).Studies suggest that a superantigen YPM, which is produced in vivo by Yersinia, is responsible for the induction of IgG synthesis in infected patients.Significantly higher antibody level in the patients with systemic symptoms and the presence of YPM-responsive cells in their lymph nodes suggest that this superantigen may have a key role in the disease process ( I ).Owing to the wide diversify of symptoms, Kers/nfo-associated arthritis can pose a complicated diagnostic problem and suggest a rheumatic origin of the disease.In that case, due to the impossibility of isolating the microorganisms at this stage of infection, the basis for the confirmation of diagnosis is the measurement of specific antibody levels against antigen О of Y. enterocolitica and T pseudotuberculosis (t, 8).The aim of the study was to determine the relationship between symptoms of arthritis and infections caused by Y. enterocolitica and Y. pseudotuberculosis in children. MATERIAL AND METHODSBlood samples of 68 randomly chosen patients from the Pulmunology and Reumatology Ward, Children Hospital of Lublin.Poland, were examined for the presence of antibodies against Yersiniae.A group of 17 children patients with the highest levels of immunoglobulins IgA.IgM and IgG against Yersinia was consequently chosen and carefully studied.A broad array of different clinical
Health resort rehabilitation of the cardiological patientsHealth resort rehabilitation consists in the health improvement of the patients after sudden cardiological incidents.The volume of health resort rehabilitation has radically changed over the years.The reason is the development, which improves the general condition of patients, gives them an opportunity to return to activity, but at the same time keeps them from the correction of the existing factors of risk.Cardiological rehabilitation releases the physical strength of the organism, modifies risk factors, and is an introduction to the secondary prevention and physical rehabilitation (1-3).The treatment of the patients after myocardial infarction consists of three stages.They are: hospital rehabilitation, posthospital early rehabilitation (sanatorium), posthospital late rehabilitation (dispensary).Stage I. Hospital rehabilitation.The aim of the first stage of rehabilitation is the quickest achievement by the patient of the initiative in everyday activities.After the treatment in the hospital the patient is most often directed to a sanatorium for the continuation of treatment (4).Stage II.Posthospital rehabilitation.This stage consists in the complex influence on the patient and the introduction of the secondary prevention.It can be held in a sanatorium or in an outpatients' department.The second stage is held mostly in a sanatorium.The aim of the action in sanatorium is the continuation of treatment, physical rehabilitation, psychical rehabilitation and risk factors' modification.During this stage complex physical rehabilitation takes place.The authors of the articles referred to below say that the optimal physical programme gives physiological, biochemical, and haemodynamical effects for the patient after the myocardial infarction (5,6).A systematic physical activity releases heart spasms frequency, also in the state of rest, alleviates an increase in the blood pressure during the effort, which makes possible broadening of the physical activity of the patients after the myocardial infarction (7-9).Sanatorium rehabilitation is also a counteraction with risk factors.Implementation of the secondary preventive rules is necessary to prevent the next myocardial infarction and release the risk of complications.Psychical rehabilitation is an indisputable component of the full programme of cardiological rehabilitation affecting stress symptoms, reducing fear and anxiety and also teaching proper techniques of coping with stress (2,10,11).Stage III.Dispensary rehabilitation.Its aim is the improvement of the tolerance of effort, the support of temporary effects of treatment, and releasing the risk of disease relapse.It is realized in cardiological clinics and by family doctors, through conducting periodical control examinations and verification of pharmacological treatment.The aim of the research was the recognition of the rehabilitation benefit and rehabilitation influence on the tolerance of effort, lifestyle and the psychical condition of the cardiological patients.
Premalignant and malignant skin diseases Assessment of proliferation indexesMalignant diseases, such as proliferative skin lesions are characterized by inappropriate cell increase.Activation of proto-oncogenes and inactivation of tumour suppressor genes are the harmful genetic events that are responsible for malignant transformation (1).Carcinogenesis in the skin is a complicated process characterized by the appearance of cells which have escaped from the normal growth control mechanisms, following in an increase of proliferative activity in the cells (2).The prevalent risk factors for skin cancer are exposure to ultraviolet (UV) radiation and fair skin that is receptive to sunburn.Increasing frequency of exposure, immune status, age, male gender and DNA repair disorders such as xeroderma pigmentosum also assist to increased risk (3).The association between UV exposure and cancer is powerful for SCC but less well-defined for BCC, as nearly one third of all BCC originates in anatomical sites receiving minimal UV exposure.Skin temperature may also be a risk factor.Cultured immortalized human kératinocytes have been shown to spontaneously transform to a tumorigenic phenotype when incubated at elevated temperature (4).Some investigations indicate that human papilloma virus infection may be a risk factor for skin cancer, though the relationship is not clear (5).Solid-organ transplant recipients are at extremely high risk for SCC (6).The long-term immunosuppressive therapy is probably the cause of the increased frequency of SCC in these patients, particularly in persons with chronic actinic damage (7).The mechanism of UV-induced photo carcinogenesis appears to implicate the inactivation of the p53 tumour suppressor gene (8).Several studies have reported that p53 distortions play a critical role in the development and progression of various human malignancies.The p53 gene is involved in the regulation of cell cycle control and apoptosis'.Mutations in this gene could presumably cancel p53 function, allowing accumulation of mutant cells due to loss of the UV-induced apoptosis of DNA-damaged cells (9).This leads to clonal expansion of p53-mutated kératinocytes, which could eventually acquire the second mutation that leads to the progression to multiple mutations.They can be accumulated.Therefore, this clonal expansion is regarded as a key initiating step in epidermal carcinogenesis (10).Precancerous dermatoses occur prior to development of epidermal malignancies (6).Because skin lesions are visible and easily accessible, skin cancer provides us with an excellent model for studying the development and growth of cancer in humans.Furthermore, the carcinogenic agents to the skin are well known.This is of special interest so far as UV radiation is the most important carcinogen and puts a specific signature on the DNA (10).Actinic keratosis (AK), also known as senile or solar keratosis is the most common precancerous dermatosis and is attributable to UV radiation (11).This UV-induced lesion is usually seen as multiple lesions in sun-exposed skin in elderly persons.This sunrelated disease may develop into carcinoma in situ or invasive SCC.However, it is a controversial subject, based on the absence of a clear-cut distinction between AK and SCC (12).AK occur from proliferation of transformed
Cardiac involvement in systemic lupus erythematosusCardiac diseases are common in patients with systemic lupus erythematosus (SLE) and constitute the third cause of death in this disease after infections and kidney disorders (1).Cardiac abnormalities (pericardial, myocardial, valvular and/or coronary artery diseases) are noted in over 50 percent of SLE individuals (2).Valvular diseasemost often mitral regurgitation, usually hemodynamically insignificant is met in approximately 75 percent (2), pericardial disease, usually a clinically silent effusionin up to 55 percent (2), myocardial dysfunctionin up to 78 percent (2) and coronary artery diseasein up to 16 percent of patients (3).The frequency of cardiac involvement estimated by transthoracic echocardiography amounts 34% (4), by transoesophageal echocardiography -46-61% (4) and in autopsy 65-100% (2).Heart problems in SLE include: 1) pericarditis, 2) valvular disease, 3) coronary artery disease, 4) myocarditis, 5) pulmonary hypertension.Pericarditis is the most common manifestation.It is subclinical in 2/3 of patients and is present in 1/3 of SLE subjects with active disease (5).30% of SLE patients develop pericardial effusion, causing retrosternal or precardial pain, dry cough, dyspnoea, subfebrile state or fever, myalgias and artralgias.At presentation pericardial rub, the rise in ESR and CRP values as well as an increase in troponins' concentrations are detected.In ECG generalised ST segment elevation and T wave reversion are present (in contrast to local changes typical of myocardial infarction).Echocardiography is essential in quick assessment of pericardial morphology and its haemodynamic sequels.Pericardial effusion in SLE is usualy about 10 mm thick, serous, acidic, with low or normal glucose and high protein content, slightly elevated leucocytosis (< 5000 WBC/ml), lymphocytes, few macrophages, low complement and detectable antinuclear antibodies (ANA).It may contain LE cells.The pericardium may reveal foci of inflammatory lesions with immune complexes and predominant of mononuclear cells, but scaring may be the primary finding in healed disease.Heart tamponade is a condition of haemodynamic disturbances due to increased pericardial fluid pressure.It presents with dyspnoea in vertical body position, decreased effort tolerance, cough, syncope and the classic Beck's triad of symptoms: hypotension, silent heart sounds and overfilling of jugular veins.Chest X-ray reveals heart enlargement without pulmonary haemostasis, echocardiographypericardial fluid (the "dancing heart" sign), diastolic right atrium retraction and inferior caval vein enlargement.Pericardiocenthesis is a life-saving treatment.Large effusions, suggestive of tamponade or constrictive pericarditis are rare in SLE, however (5).Purulent pericarditis may occur in an immunosuppressed debilitated patient (6).Pericardiocentesis may be indicated to exclude potentially life-threatening causes of pericarditis, such as infections (e.g.tuberculosis), or neoplastic pericarditis or to drain the fluid in case of tamponade.In the absence of fever or a documented infection that could predispose to purulent pericarditis, we do not routinely perform diagnostic pericardiocentesis in patients with SLE pericarditis unless the symptoms persist despite treatment.
The problem of ionizing radiation exposure of the radiologists in the opinion of students of Medical Faculties of the Medical University of Lublin Ionizing radiation exposure is common in different diagnostic procedures in radiology.Knowledge and conventional wisdom of X-ray exposure consequences is necessary to avoid and protect from post exposure short-and long-term side-effects.General opinion about X-ray exposure in society is difficult to establish because of different relations with radiologists during diagnostic procedures and not well estimated knowledge level about the X-ray-related health risk.The aim of our study was to find out medicine students' opinion on ionizing radiation exposure in a radiologist speciality.
KRUPSKI2 Iodine influence on thyroid gland functionIodine is an essential microelement necessary for the synthesis of the thyroid hormones, thyroxin and triiodothyronine.The thyroid gland has ability to act against iodine excess by the Wolff-Chaikoff mechanism, which inhibits iodine organification and prevents large amounts of thyroid hormone synthesis.Thyroid peroxidase mRNA, protein synthesis and thyroglobulin iodination are temporary inhibited for 48-72 hours.Recent data shows that the Wolff-Chaikoff mechanism is caused by a decrease in the number of sodium-iodide symporter (NIS) proteins, resulting in a reduce of thyroidal iodine transport.The sodium iodide symporter protein was first cloned by Dai et al. in 1996 (1).After that, the escape phenomenon occurs and prolonged hypothyroidism does not happen.However in fetus, newborns, patients after episodes of subacute or postpartum thyroiditis, persons with severe diseases like chronic obstructive pulmonary disease, mucoviscidosis and autoimmune thyroid diseases, escape from inhibition of excess iodine does not occur and hypothyroidism can be observed.Patients with underlying autoimmune thyroid disease such as Hashimoto's thyroiditis are particularly susceptible to develop iodine induced hypothyroidism.The mechanism of it is an inability to escape from the Wolff-Chaikoff inhibitory effect.This leads to inhibition of organic iodine and iodothyronines synthesis (2).Thyroid gland diseases depend on the level of iodine intake, because it is an important environmental factor of several disorders.At the iodine deficiency areas most commonly first simple goiter occurs, and then morphologic reconstruction starts and nodules appear.Development of nodular goiter arises from iodine deficit.The consequence of decreased thyroid hormone concentration is the stimulation TSH formation and other growth factors.High iodine intake seen in Japan, USA or Iceland inclines to hypothyroidism and Graves' disease (3,4).The most frequent neoplasm of the endocrine system are thyroid gland carcinomas, which comprise up to 1.5% of all human malignances.Most common of the thyroid gland carcinomas are the differentiated forms such as follicular and papillary.Medullary and anaplastic thyroid carcinomas are more occasional.Iodine intake is considered to have particular influence on thyroid morphology.Less aggressive papillary thyroid carcinomas are observed in populations with iodine prophylaxis.The ratio of papillary to follicular carcinoma rose after introduction of potassium iodide to table salt.This similar effect is observed among the population touched by the Chernobyl accident.Iodine is also mentioned as an environmental factor of other cancers.It has suspected influence on the development of breast, ovarian, endometrial and even stomach cancer, which is indicated by large epidemiological studies (5,6).Hashimoto thyroiditis is the most common thyroid gland inflammation.It can develop in 19% of elderly women.Hypothyroidism can be detected in 1% of the population, especially in areas of high iodine intake.Among children with Hashimoto thyroiditis, hypothyroidism can be found in 1.2%, especially in areas of excesive iodine intake.Most of the children over 10 years old with
The C-reactive protein (CRP) is a constant component of the organism, it is present in blood serum in trace amounts of both healthy people and animals in physiological conditions (1, 2). Macrophage stimulation caused by tissue damage is a necessary condition for CRP synthesis (3, 4, 5). These cells produce pro-inflammatory cytokines which induce the expression of the APR gene. Interleukin 6 (IL-6) is the most important factor that stimulates CRP synthesis as well as all other acute phase proteins (5, 6). Interleukin 1 (IL-1) and tumor necrosis factor (TNF-a) stimulate macrophages, monocytes, fibroblasts, endothelium cells and others to produce IL-6 (6, 7, 8). CRP in the organism performs a defensive and reparative role (2, 3, 9, 10). This protein acts like an opsonin by joining with antigens and pathogen structure ligands and hastening their phagocytosis. CRP attaches to Fey receptors of human monocytes, neutrophils and other leucocytic system cells activating them. Cell stimulation results in a varied effector response, e.g. in the cytotoxic effect, phagocytosis, oxygen explosion or in the release of inflammatory mediators. C-reactive protein complexes with corresponding ligands activate the complement cascade mainly on the classical pathway (similarly to the antigen-antibody complexes). As a result of the
