ABSTRACT
This 20 year old man suffered increasingly from multifocal bone- and back pain over the last 6 months. Painful weakness of the left leg with dysesthesia of the 4th and 5th toe, a weight loss of 15 kg and polydipsia and pollakiuria had developed. The clinical workup disclosed hard tumors in the right mandible and tibia, a waddling gait with bilateral sign of Trendelenburg, reduced muscular force in the left leg with missing achilles tendon reflex and a loss of sensibility in the distal S1 segment, epigastric tenderness on pressure and hypertension with a value of 160/100 mmHg. X-rays revealed multiple cystic bone lesions at all sites. Hypercalcemia and massively elevated parathyroid hormone were measured. Since the parathyroids were enlarged on sonography, primary hyperthyroidism with fibrosing osteitis v. Recklinghausen was diagnosed.
Subject(s)
Bone Diseases/etiology , Hyperparathyroidism/complications , Osteitis Fibrosa Cystica/complications , Polyuria/etiology , Adenoma/complications , Adenoma/diagnosis , Adult , Bone Diseases/physiopathology , Drinking Behavior , Humans , Hyperparathyroidism/diagnosis , Male , Osteitis Fibrosa Cystica/diagnostic imaging , Pain , Parathyroid Neoplasms/complications , Parathyroid Neoplasms/diagnosis , RadiographyABSTRACT
The effect of angiotensin II (AII), transforming growth factor-beta (TGF-beta), and insulin-like growth factor-I (IGF-I) on platelet-derived growth factor (PDGF)-BB-, basic fibroblastic growth factor (bFGF)-, and epidermal growth factor (EGF)-induced DNA synthesis in vascular smooth muscle cells (VSMCs) was investigated. TGF-beta, AII, IGF-I increased concentration-dependent cell protein. No increase in [3H]thymidine incorporation could be detected. TGF-beta, AII, and IGF-I enhanced PDGF-BB-, bFGF-, and EGF-induced DNA synthesis. Our results suggest that growth factors that possess a weak mitogenic effect on vascular smooth muscle cells such as TGF-beta, AII, and IGF-I may enhance the mitogenicity of PDGF-BB, bFGF, and EGF.
Subject(s)
Angiotensin II/pharmacology , DNA/biosynthesis , Epidermal Growth Factor/pharmacology , Fibroblast Growth Factor 2/pharmacology , Insulin-Like Growth Factor I/pharmacology , Insulin/pharmacology , Muscle, Smooth, Vascular/cytology , Muscle, Smooth, Vascular/metabolism , Platelet-Derived Growth Factor/pharmacology , Transforming Growth Factor beta/pharmacology , Animals , Aorta/metabolism , Cells, Cultured , Dose-Response Relationship, Drug , Drug Synergism , Female , Rats , Rats, Inbred WKY , Thymidine/metabolism , TritiumABSTRACT
High concentrations of high-density lipoprotein (HDL) are known to decrease the risk of coronary artery disease. In order to study the underlying cellular mechanisms, the influence of HDL on the epidermal growth factor (EGF)-induced vascular smooth muscle cell (VSMC) proliferation was investigated. Approximately 40% of the EGF-induced increase of the cell DNA synthesis was abolished in the presence of 30 micrograms/ml HDL. The EGF-induced dose-dependent (10 pg/ml to 100 ng/ml) increase in DNA synthesis was blunted by 30 micrograms/ml HDL. In addition HDL (3-300 micrograms/ml) caused a dose-dependent inhibition of EGF (20 ng/ml)-induced DNA synthesis, yielding a half maximal effective dose (ED50) of 30 micrograms/ml. Similar experiments with the HDL-protein and HDL-lipid fraction indicated that the HDL-protein fraction is most probably responsible for the observed inhibiting effects of HDL. This was confirmed by using purified apolipoprotein (apo) A-I and apo A-II. Both induced an approximately 80% inhibition of the EGF-induced DNA synthesis. These results may help to explain the observed beneficial effects of HDL on cardiovascular diseases that are described in many epidemiological studies.
Subject(s)
DNA/biosynthesis , Epidermal Growth Factor/pharmacology , Lipoproteins, HDL/pharmacology , Muscle, Smooth, Vascular/metabolism , Animals , Aorta/cytology , Aorta/metabolism , Cell Division , Cells, Cultured , Female , Lipoproteins/pharmacology , Muscle, Smooth, Vascular/cytology , Rats , Rats, Inbred WKY , Thymidine/metabolismABSTRACT
The hypophyses of 13 patients with Nelson syndrome following bilateral adrenalectomy were examined by MRI and CT. Diffuse enlargement of the hypophysis was demonstrated in 8 patients by CT and in 9 by MRI. Compared with CT, MRI provides better demonstration of tumour development, such as abnormal convexity of the cranial margin of the hypophysis (MRI 4/13, CT 1/13), displacement of the infundibulum (MRI 4/13, CT 0/13) or optic chiasm (MRI 2/13, CT 0/13). MRI also provides diagnostically important differentiation between scar tissue and recurrence of tumour following hypophysectomy (MRI 1/3, CT 0/3) and more accurate demonstration of infiltration of the cavernous sinus (MRI 4/13, CT 2/13). CT is superior only in showing the floor of the sella. MRI is the method of choice for imaging in cases of Nelson syndrome.
