Current Allogeneic Hematopoietic Stem Cell Transplantation for Pediatric Acute Lymphocytic Leukemia: Success,Failure and Future Perspectives—A Single-Center Experience, 2008 to 2016

Hematopoietic stem cell transplantation (HSCT) is the only curative option for a subset of patients with high-risk or relapsed acute lymphoblastic leukemia (ALL). Given evolving practices, it is important to continually evaluate outcomes for pediatric ALL following HSCT. Outcomes after HSCT are influenced by the type of donor used as this determines the degree and method of T cell depletion used and, consequently, specific transplant-related morbidities. We retrospectively analyzed HSCT data from our center for transplants performed between January 2008 and May 2016, comparing outcomes among different donor types. One hundred and twenty-four pediatric patients underwent HSCT from a matched sibling donor (MSD; n?=?48), an unrelated matched donor (UMD; n?=?56), or a haploidentical donor (n?=?20). We observed a similar 3-year event-free survival (EFS) for MSD recipients (of .64) and for UMD recipients (.62), but a significantly lower EFS for recipients of haploidentical transplants (.35; P?=?.01). Relapse was the main cause of HSCT failure and was significantly higher in the haploidentical donor group (.47 versus .19 for MSD and .24 for UMD; P?=?.02). Treatment-related mortality was evenly distributed among the donor groups (.17, .16, and .15 for the MSD, UMD, and haploidentical groups, respectively). Rates of infection-related mortality were lower than previously reported. Relapse is the main obstacle for successful HSCT in the contemporary era, and this effect is most evident in recipients of haploidentical donor grafts. Newer methods to improve graft-versus-leukemia effect are being evaluated and will need to be incorporated into the management of high-risk patients.     

Potassium release from the rat submaxillary gland in vitro. II. Induction by parasympathomimetic secretagogues.

The kinetics of K+ release from an in vitro system of rat submaxillary gland slices were studied after stimulation with parasympathomimetic secretagogues. The slices were incubated at 37degreesC in an oxygenated, enriched Krebs-Ringer bicarbonate medium in the presence and in the absence of Ca++ and of ouabain and, in some experiments, in the presence of the specific antagonists atropine (5 x 10(-6) and 2 x 10(-5) M), phentolamine (2 x 10(-5) M) or propranolol (2 x 10(-5) M. K+ release was elicited by the addition of acetylcholine (2 x 10(-5) M), pilocarpine (2 x 10(-5) M) and carbamylcholine (10(-9) to 2 x 10(-5) M). The results demonstrate that: 1) The selective stimulation of cholinergic receptors induces a rapid net release of K+ from the slices. After 10 minutes of incubation, the percent K+ released after a 2 x 10(-5) M dose of each of the three secretagogues was, respectively, 20.8%, 15.5%, and 19%. 2) The response to carbamylcholine does not occur when Ca++ is absent from the medium and is blocked by atropine but not by phentolamine or by propranolol. Atropine (5 x 10(-6) M) causes a 17-fold shift to the right on the dose-response curve to carbamylcholine. 3) The magnitude of K+ release is the ratio of two opposing mechanisms, a passive efflux and an active reuptake. The latter depends on the activity of the ouabain-sensitive Na+-K+-adenosine triphosphatase. 4) The sensitivity of the slice system to carbamylcholine seems to be greater than that to norepinephrine in terms of net K+ release after equimolar doses of 2 x 10(-5) M and also in terms of the dose required to induce a half maximal passive K+ efflux. However, the maximal passive K+ efflux is similar after both types of secretagogue and amounts of approximately 45% of the K+ present in the slices.     

Hypertrophic pyloric stenosis in the adult

In view of the low incidence of hypertrophic pyloric stenosis, we present a case of this pathology in a male aged 74. Stenosis was of the diffuse type, associated with gastric ulcer and chronic atrophic gastritis. The patient was admitted to our Service with upper digestive tract hemorrhage after deterioration of the ulcer.