With treatment Achalasia patients exhibit some restoration in peristalsis as well as improved bolus clearance. After Heller Myotomy, the return of peristalsis correlates with esophageal clearance, which may partly explain its superior relief of dysphagia.
Patients treated with total parenteral nutrition (TPN) receive high concentrations of IV dextrose. TPN usually contains from 30% to 100% of nonprotein calories as dextrose. The final dextrose concentration in TPN fluids may be as high as 40%.Hyperglycemia is a common complication of continuous dextrose infusion with TPN. This occurs when the infused dextrose cannot be metabolized as a result of an inability of the pancreas to supply an adequate amount of insulin, an increased rate of insulin catabolism or the development of insulin resistance. Treatment requires reduction in the dextrose dose, adding exogenous insulin to the TPN solution, or correction of the underlying causes of insulin resistance. It is important to treat hyperglycemia because moderate to severe hyperglycemia can lead to fluid and electrolyte abnormalities and increased susceptibility to infection. 1 Occasionally, however, hypoglycemia can occur in some patients when TPN is stopped. Decreasing the rate of TPN infusion before discontinuation can be used to minimize the development of hypoglycemia. This maneuver is referred to as tapering. This is often done for patients receiving TPN at home where the solution is given overnight and discontinued in the morning. There are several other reasons why TPN might need to be discontinued, including marked fluid and electrolyte abnormalities, loss of vascular access, infusion device complications, and during medical emergencies. Under these circumstances, a 10% solution of dextrose can be infused for 1 hour and then replaced with standard IV fluid until the patient can resume receiving TPN. 2 This article will discuss the events surrounding dextrose infusion while maintaining euglycemia, the ways that TPN infusions can be modified to maintain euglycemia, and when it is appropriate to taper TPN infusions. Minimum Glucose RequirementsGlucose is required for normal brain, kidney, and erythrocyte function. The body maintains glucose levels via 2 processes: glucose production (ie, gluconeogenesis and glycogenolysis) and reduced glucose use (use of ketone bodies for energy). When normal adult volunteers are infused with 100 g of dextrose per day, gluconeogenesis can be significantly suppressed. This diminishes the reliance on protein breakdown for the provision of amino acids for gluconeogenesis. Proteolysis is maximally suppressed when approximately 250 g of dextrose are infused per day. Therefore, if IV dextrose is the only source of carbohydrate, at least 100 g should be infused each day to minimize nitrogen depletion. 3 Maximum Dextrose Infusion RatesIt has been clearly shown that hypermetabolic patients have difficulty using large quantities of IV dextrose from TPN. 4 In uncomplicated postoperative patients, glucose oxidative rates were not overwhelmed until dextrose infusions exceeded 7 mg/kg/ minute. 5 Although plasma glucose can remain in the normal range beyond this rate of infusion, the excess dextrose is used for lipogenesis. In critically ill patients, the upper infusion rate for glucose disposal w...
Purpose: Helicobacter pylori could theoretically induce ocular adnexal lymphoma (OAL) via 2 mechanisms: the first is that of infection within the ocular adnexa and the second is that of infection within the gastric mucosa, leading to the malignant transformation of lymphocytes that migrate to the ocular adnexa, forming a primary “ectopic” cancer. This study investigated if an association exists between gastric H. pylori or ocular adnexal H. pylori and OAL. Methods: Prospective case-control study including cases with OAL and controls with nonlymphomatous pathologies. Gastric H. pylori infection was assessed via serologic antibody testing. Ocular adnexal infection was assessed via polymerase chain reaction testing for H. pylori and Chlamydia psittaci within ocular adnexal samples. Results: Seventy-two patients were enrolled, of whom 18 had lymphoma and 54 nonlymphomatous pathologies. H. pylori antibodies were present in 5 cases (28%) and 18 controls (33%) (95% CI, 0.24%–2.50%, p = 0.78). All ocular adnexal specimens were negative for H. pylori and C. psittaci infection. The only relevant statistically significant difference between cases and controls was a history of gastric ulcer (95% CI, 1.23%–44.80%, p = 0.03). Conclusions: In the study’s population, infection of gastric mucosa with H. pylori does not appear to influence the development of OAL. Also, H. pylori or C. psittaci infection within the ocular adnexa does not appear to influence the development of OAL. In the study’s practice, authors do not recommend antibiotic administration or routine gastroscopy for patients with OAL. The authors do recommend referral of OAL patients with gastric symptoms to a gastroenterologist.
Background. Despite improvements in immunosuppression, acute and chronic allograft rejection remains a problem in renal transplantation. Monitoring serum creatinine is of poor prognostic value in predicting acute rejection. Renal allograft biopsy is invasive and predisposes the patient to serious complications. Immune monitoring may provide an early and non-invasive means for identifying patients at risk of acute (AR) and chronic rejection and help tailor immunosuppression. Methods. Thirty-six renal allograft recipients were serially monitored following transplantation for expression of T cell activation markers in the peripheral blood and for development of anti-HLA antibodies. Samples were collected weekly during the first 8 weeks and then at weeks 13, 18, 26, 39 and 52. Gene expression of perforin and granzyme B was quantitated by Real-Time PCR and results reported as normalized values to the endogenous control. Anti-HLA antibodies were characterized using soluble HLA class I and class II antigens in a solid-phase luminex assay. Assay results were correlated with histologic changes in the renal biopsy and clinical data. Results. Ten of 36 patients were evaluated by 14 renal allograft biopsies. In 4 patients with biopsy confirmed AR, mean expression of granzyme B during the first month post-transplantation (122) was significantly elevated compared to patients without evidence of rejection (51) (p<0.006). Similarly, expression of perforin was higher in patients with AR (115) compared to non-rejectors (50) (p<0.003). Expression of perforin (141) and granzyme B (127) was highest during the time of rejection, which was set as one week before and after a positive biopsy. In 2 patients with AR, elevations in perforin and granzyme B gene expression preceded increases in serum creatinine. No correlation was found between serum creatinine levels and episodes of AR or T cell activation markers. Serial monitoring of anti-HLA antibodies showed that 3 out of the 4 patients diagnosed with AR developed anti-HLA class II antibodies. Conclusion. The data indicate that a program of immune monitoring of renal allograft recipients may serve as a noninvasive aid in the diagnosis of acute rejection and help to tailor immunosuppression. Further studies are in progress to determine the predictive value of these assays.
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