A Case of Pseudo-Bartter's Syndrome Associated with Hypergastrinemia, Thrombocytosis and Increased Serum Thyroxine-Binding Globulin.

Abstract

A housewife, 40 years of age, was admitted with dysesthesia of the extremities, muscle weakness, and attacks of adynamia and thirst. She had been taking a laxative for more than 20 years. On physical examination, blood pressure was 94/56 mmHg. Laboratory tests revealed thrombocytosis, low serum K and marked increases in both plasma renin activity and serum aldosterone.Serum TBG was increased. Serum gastrin was also markedly increased and could not be enhanced by exogenous secretin. Both angiotensin 11 loading test and noradrenalin loading test failed to increase blood pressure. Ammonium chloride loading to examine the disturbance of urinary acidification was abnormal in the short term test and borderline in the long term test. Following a diagnosis of pseudo-Bartter's syndrome induced by long term intake of laxative and repeated diarrhea, the administration of laxative was interrupted and potassium, indomethacin and spironolactone were administered. However, serum K remained low. Hypergastrinemia, thrombocytosis and a high serum TBG level also persisted, the causes of which remain unknown. This is the first reported case of pseudo-Bartter's syndrome associated with hypergastrinemia, thrombocytosis and increased serum TBG.

Cardiac and intestinal tissue conduct developmental and reparative processes in response to lymphangiocrine signaling

“…By acting in an autocrine fashion, reelin expressed in LECs aids the development of collecting vessels and produces monocyte chemotactic protein 1 (MCP-1), a factor that recruits SMCs important for stimulating the secretion of reelin from LECs and for lymph propulsion ( Lutter et al, 2012 ) ( Figure 1 ). Although the source of SMCs remains unknown, MCP-1 is known for the recruitment of myeloid-monocytic cells ( Fujimoto et al, 2009 ) which can harbor precursors of SMCs ( Okano et al, 1990 ). While the study demonstrated the secretion of reelin from the conditioned media of cultured LECs by immunoprecipitation and western blotting ( Liu et al, 2020 ), its actual concentration produced by LECs remains to be elucidated.…”