Background/Objectives: Postprandial hypotension (PPH) is an important clinical condition in patients presenting with postprandial symptoms. The aims of this study were to determine the prevalence of PPH in patients with postprandial symptoms and to investigate the relationship between PPH and insulin, particularly in healthy adults. Methods: This study was conducted with 111 adult patients who were admitted to the clinic due to postprandial symptoms. Patients underwent the mixed meal test (MMT). Blood glucose, insulin, and C-peptide levels were measured at 0, 30, 60, 90, 120, 180, 240, and 300 min. along with systolic blood pressure (sBP), diastolic blood pressure (dBP), and heart rate measurements during the MMT. Results: Serum adrenocorticotropic hormone (ACTH) levels were similar (p > 0.05), and cortisol levels were found to be higher in individuals without PPH compared to those with PPH before the MMT (p = 0.014). During the MMT, 23 patients (23.2%) had PPH. At the beginning of the test, serum glucose, insulin, C-peptide, and heart rate values were similar in patients with and without PPH; however sBP and dBP were significantly higher in the PPH group (p = 0.002 and p = 0.010, respectively). No correlation was found between sBP and insulin, glucose, and C-peptide at any time during the MMT except for a moderately significant positive correlation between glucose and sBP at 90 min. in patients with PPH (r = 0.490, p = 0.018). A moderately negative correlation was found between the magnitude of sBP fall between 30 and 60 min. and insulin and C-peptide levels in people with PPH (r = −0.420, p = 0.046; r = −0.564, p = 0.005; respectively). However, no significant relationships were observed between the magnitude of sBP fall at other time points and blood parameters (p > 0.05). Conclusions: A significant portion of adults with postprandial symptoms might have PPH, contributing to these symptoms. The lack of a relationship between insulin and glucose suggests that other physiological mechanisms beyond insulin and glucose may play a role in the pathogenesis of PPH in healthy individuals. Therefore, further research is needed to better understand the underlying causes of PPH.
Studies have demonstrated worse graft and patient survival among hepatitis C virus-positive patients following kidney transplant. Eradication of hepatitis C virus infection before renal transplant with interferon should be considered in hepatitis C virus-infected patients undergoing dialysis who are on the waiting list for transplant. We investigated whether pretransplant hepatitis C virus infection treatment affected graft and patient survival, and we evaluated other contributing factors to these outcomes.We enrolled 83 antihepatitis C virus-positive patients who were diagnosed with chronic hepatitis C virus infection by serology or histopathology and had renal transplant at Baskent University Ankara Hospital from 1982 to 2013. Data were obtained from patient medical files retrospectively. Patients were divided into 2 groups that had or did not have interferon treatment.In 83 renal transplant patients with chronic hepatitis C virus infection (57 male [69%] and 26 female [31%]), median age was 46 years (range, 26 - 69 y), and most patients were genotype 1-dominant (92%). Interferon monotherapy was received by 30 patients before renal transplant and 28 of 30 patients had long-term follow-up data. There were 14 of 28 patients (50%) who achieved sustained virologic response, and only 1 patient had relapse. Graft survival was significantly lower in patients who had treatment (6 y vs 9 y; P ≤ .003). However, patient survival rates were similar between groups. Patients who had interferon were younger and had longer hemodialysis duration before renal transplant than patients without treatment. Higher viral load was associated with higher mortality which was caused by sepsis.Patients with posttransplant lymphoproliferative disorder have high incidence of bone marrow involvement and high mortality rates. Therefore, bone marrow examination may be important in the diagnosis and staging evaluation of posttransplant lymphoproliferative disorder.
