Primary amyloidosis (AL) is a rare variety of plasma cell dyscrasia, the diagnosis of which is often difficult to establish. Pathogenesis of amyloidosis involves extracellular deposition of insoluble protein fibrils in tissues, leading to insufficiency of affected organs. According to various sources, mean survival rate of patients with primary amyloidosis ranges from 12 to 24 months, making primary amyloidosis a disease with a very poor prognosis. Survival rate is significantly lowered in case of cardiac manifestation of amyloidosis (about 6 months survival in untreated patients). In recent years a considerable progress in AL treatment has been observed. Nowadays we are able not only to delay progression of amyloidosis, but also to improve the function of the affected organs. Unfortunately as first signs and symptoms of AL are usually nonspecific, the diagnosis of AL is often delayed, resulting in late introduction of optimal therapy. There are many diagnostic tests which can be used in diagnostic process of amyloidosis, i.e. electrophoresis, serum and urine immunofixation or affected organs and bone marrow biopsy. On establishing the diagnosis in a patient with suspected amyloidosis it should be remembered that particular diagnostic methods vary considerably in sensitivity.The aim of this paper is to present a case report of a 27-year-old patient with primary amyloidosis focusing on diagnostic aspect of this condition. On the basis of this case, the authors would like to emphasize the value of precise diagnostic process, with immunological techniques playing undoubtedly a crucial role.

Background: The efficacy of interventions in ST-segment elevation myocardial infarction (STEMI) assessed by a decrease in inpatient mortality in Poland is very high. However, a rise in mortality rate is recorded within 3 years of the discharge from the intervention centre. In order to reduce out-of-hospital mortality, the treatment should be continued with cardiac rehabilitation after hospitalization. The aim of this retrospective study was to evaluate the effect of cardiac rehabilitation on exercise capacity increase patients with STEMI with regard to their age, gender, Body Mass Index (BMI), ejection fraction (EF), concomitant diabetes and nicotine dependence. The effectiveness of cardiac rehabilitation was assessed by exercise ECG (electrocardiogram) stress test or the 6-min walk test, prior to and after cardiac rehabilitation completion. Methods: The study group included 100 randomly selected patients undergoing cardiac rehabilitation after STEMI, aged 40–75 years, with BMI ≤ 40 kg/m2, with controlled arterial hypertension, without anemia and any pulmonary comorbidities. Results: The study patients’ exercise capacity was observed to have increased significantly (+1 metabolic equivalent (MET) in exercise ECG stress test and +75.4 m in the 6-min walk test) regardless of their gender, age, BMI and nicotine dependence. Conclusions: This study proved that every patient with STEMI could benefit from cardiac rehabilitation. Nicotine-dependents, males, patients aged ≤55 and those with reduced EF (<50%) were found to have benefitted most substantially.

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Concentrations of adiponectin were not correlated with levels of glycosylated hemoglobin in the diabetic and non-diabetic subjects examined.

Reduced serum levels of adiponectin in obesity and insulin resistance seem paradoxical, since adipose tissue is the only source of adiponectin, and reports on that subject are contradictory. The aim of this study was to investigate the concentrations of adiponectin in non-obese and obese normoglycemic humans, and to determine the correlation between adiponectin and HOMA index of insulin sensitivity. Based on the WHO definition of obesity, 145 obese subjects and 49 non-obese controls (aged 20-55 years) were studied. The serum adiponectin concentrations did not differ between subjects and controls (p=0.6398) and were not correlated with HOMA index (r=-0.0211; p=0.8048, and r=-0.0523; p=0.4757, for subjects and controls, respectively). Adiponectin was not correlated with HOMA index in females (r=-0.0521; p=0.6546, and r=-0.0825; p=0.3981, for female subjects and controls, respectively) as well as in males (r=0.0033; p=0.9791, and r=0.0123; p=0.9131, for male subjects and controls, respectively). These results lead to the conclusion that neither the concentrations of adiponectin differ between obese and non-obese humans, nor does any relationship between adiponectin concentration and insulin sensitivity exist.