УДК: 616.33–089:616.71–007.234]–06–055.1–008.9
Introduction. The problem of osteoporosis (OP) has become an epidemic unprecedented in its scale. Numerous studies of various aspects of OP leave out men with a history of gastric resection (GR) as a result of complicated peptic ulcer disease (PUD). Therefore, a detailed characteristics of clinical parameters and hormonal and metabolic homeostasis in men with postgastric resection disease (PGRD) and comorbid OP will allow the improvement of the treatment and prevention of osteodeficiency conditions in this category of patients.
The aim of the study. To characterize clinical parameters and hormonal and metabolic homeostasis in men with postgastric resection disease and comorbid osteoporosis.
Materials and methods. 164 men with PGRD and comorbid OP were examined with preliminary random stratification by the presence of a history of five or more years of GR surgery as a result of complicated PUD. In addition to routine examinations, hormonal homeostasis was studied by the effect of hormones on protein metabolism: anabolic (growth hormone, parathyroid hormone, gastrin, and testosterone) and catabolic (triiodothyronine, thyroxine, glucagon, and cortisol) hormones and cyclic nucleotides. Plasma electrolytes and protein profile were also analyzed.
Results. It was established that the vast majority of patients who underwent the surgery with PGRD and comorbid OP have clinical signs of calcium metabolism disorders. They had significant abnormalities in hormonal and metabolic homeostasis manifested by dyshormonemia, dyselectrolytemia and dysproteinemia. We believe that these scientific facts will help to improve the treatment and prevention of secondary osteoporosis complications in this category of patients.
Conclusions. Among the clinical parameters in men with PGRD and comorbid OP, bone pain and muscle cramps prevailed. Hormonal homeostasis was characterized by dyshormonemia with a significant decrease in almost all studied anabolic hormones and an increase in almost all studied catabolic hormones. Deviations in metabolic homeostasis were manifested by dyselectrolytemia (hypophosphatemia, hypomagnesemia, decreased ionized calcium) and dysproteinemia (hypoalbuminemia, hyper-a1-globulinemia, hyper-β-globulinemia, sharply reduced glycoproteins).