Changing trends in penetrating keratoplasty indications at a tertiary eye care center in Budapest, Hungary between 2006 and 2017

AIM: To analyse the changing trends in penetrating keratoplasty (PKP) indications. METHODS: This retrospective study included all patients with PKP between 2006 and 2017. Patients were classified using histological diagnoses. Our groups were more than 10 various keratopathies. Additionally, two different time-periods (2006-2012 and 2013-2017) were analysed. Results: Totally 1721 histological analyses of 1214 patients were available for review. The diagnoses were pseudophakic or aphakic bullous keratopathy in 487 (28.3%), regraft in 443 (25.7%), acute necrotizing and ulcerative keratitis in 313 (18.2%), corneal scar in 153 (8.9%), keratoconus in 140 (8.1%). Fuchs’ dystrophy in 61 (3.5%), corneal dystrophy other than Fuchs’ in 46 (2.7%), other diagnoses in 44 (2.6%) and failed endothelial keratoplasty graft in 34 (2.0%) cases. From the first to the second analysed time-period, incidence of acute necrotizing and ulcerative keratitis, corneal scar, Fuchs’ dystrophy increased (P≤0.032 for all) and incidence of keratoconus significantly decreased (P=0.015). Conclusion: Pseudophakic or aphakic bullous keratopathy is the leading indication for PKP, followed by regraft and acute necrotizing and ulcerative keratitis.     

Sphincter of oddi manometry in patients with acute biliary pancreatitis: evidence for sphincter of oddi dysfunction in acute biliary pancreatitis

We calculated morphometrically the amount of antral gastrin-producing (G) cells and body parietal and chief cells in gastric biopsy specimens from 30 undialysed patients with chronic renal failure (CRF) and from sex- and age-matched controls. The CRF patients had raised fasting serum gastrin levels, whereas these were normal in the controls (mean, 290 ± 283 (±SD) ng/1 (n = 27) versus 33 ± 36 (n = 30)). Serum gastrin values of the patients and controls correlated positively with G-cell density (r = 0.501, n = 36, p = 0.002), as did the maximal acid output of the CRF patients with parietal cell density (r = 0.617, n = 14, p = 0.019). In CRF patients the densities of G, parietal, and chief cells were higher than those in the controls (G cells, 351 ± 151 (±SD) cells/mm², n = 21 versus 211 ± 90, n = 16, p = 0.002; parietal cells, 299 ± 94, n = 15 versus 224 ±72, n = 14, p = 0.025; chief cells, 886 ± 346, n = 15 versus 743 ± 182, n = 14, p = 0.181). The results agree with previous findings indicating that hyposecretion of gastric acid in CRF does not derive from decreased capacity for acid secretion but rather from the inhibition of acid output. Increased parietal cell density in CRF patients gives cause to suspect that the maximum acid output might even be raised, possibly depending on the permanent hypergastrinaemic state with its trophic influence on the gastric body mucosa.