Calcitonin levels in autoimmune atrophic gastritis-related hypergastrinemia.

PURPOSE: Calcitonin (Ct) is currently the most sensitive biochemical marker of C-cell disease (medullary thyroid cancer [MTC] and C-cell hyperplasia), but its specificity is relatively low. Our aim was to examine whether autoimmune atrophic gastritis (AAG) and chronic hypergastrinemia, with or without chronic autoimmune thyroiditis (AT), are conditions associated with increased Ct levels. METHODS: Three groups of patients were consecutively enrolled in this  multicentric study: group A consisted of patients with histologically-proven AAG (n = 13; 2 males, 11 females); group B fulfilled the criteria for group A but also had AT (n = 92; 15 males, 77 females); and group C included patients with AT and without AAG (n = 37; 6 males, 31 females). RESULTS: Median Ct levels did not differ between the three groups. Ct levels were undetectable in: 8/13 cases (61.5%) in group A, 70/92 (76.1%) in group B, and 27/37 (73.0%) in group C. They were detectable but ≤ 10 ng/L in 4/13 (30.8%), 20/92 (21.7%) and 7/37 (18.9%) cases, respectively; and they were > 10 ng/L in 1/13 (7.7%), 2/92 (2.2%) and 3/37 (8.1%) cases, respectively (P = 0.5). Only three patients had high Ct levels (> 10 ng/L) and high gastrin levels and had an MTC. There was no correlation between Ct and gastrin levels (P = 0.353, r = 0.0785). CONCLUSIONS: High gastrin levels in patients with AAG do not explain any hypercalcitoninemia, regardless of whether patients have AT or not. This makes it mandatory to complete the diagnostic process to rule out MTC in patients with high Ct levels and AAG.

The role of erythrocytapheresis in secondary erythrocytosis therapy.

In chronic respiratory insufficiency secondary erythrocytosis (SPC), causing pulmonary hypertension and dx ventricular insufficiency, is often noticed. An alternative therapy to phlebotomy for SPC is isovolemic large volume erythrocytapheresis performed with cell separator (CSE) in order to quickly remove a large volume of red blood cells (RBC) while saving plasma proteins and clotting factors. In order to evaluate the efficiency and safety of CSE in SPC we reported a retrospective analysis of our experience with 61 SPC patients: from April 1996 to May 1998 we performed 208 CSE using Haemonetics MCS3P (TAE protocol). Before every apheresis procedure we verified Hb (in median 18.8 g/dl), Ht (in median 58.4%), viscometry, coagulation test, EGA, PFR and ECG. 11 patients were treated with 1 CSE, 12 with 3, 29 with 4 and 9 with 5. The mean volume of RBC removed was 576 ml (range 426-800); Hb post CSE averaged 14.4 g/dl and Ht post CSE averaged 42.7%; hematic viscosity post CSE was significantly reduced while tissue oxygen tension increased: the improvement of symptomatology and hematochemical parameters was maintained on the average for 6.5 months. All the procedures were well tolerated and light side effects (paresthesias citrate-depending in 27 apheresis) were easily controlled. CSE, compared to phlebotomy, has the advantage of selectively removing RBC without loss of clotting factors, platelets and plasma proteins. Although CSE has relatively high costs we noticed a decrease of hospital recurrence (about 50-65%) in SPC patients treated with apheresis.