Anaphylaxis following psyllium ingestion

Psyllium is a hydrophilic agent found in many bulk laxative preparations. We report the occurrence of an anaphylactic reaction in a patient after ingestion of a psyllium-containing laxative. IgE mediation of the reaction was suggested by a positive immediate skin test to psyllium, positive passive transfer skin test, lack of skin response during passive transfer with heat treated serum, and an elevated IgE (RAST) to psyllium seed.     

A longitudinal evaluation of thyroid function in critically ill surgical patients.

Thyroid hormone alterations (known as the "sick-euthyroid syndrome") are common following major surgery, but the time course for appearance and recovery from these alterations has not previously been longitudinally studied in a large group of surgical patients. The authors prospectively studied 59 patients undergoing major surgery (coronary artery bypass grafting, pneumonectomy, or subtotal colectomy). Compared with preoperative values, the mean serum T4, T3, free T3, and TSH concentrations decreased significantly (p less than 0.05) following surgery. Serum reverse T3 and T3 resin uptake index increased, while free T4 levels remained unchanged. These changes were seen within 6 hours of surgery and normalized by 1 week after surgery. Although the serum TSH response to TRH was normal before and after surgery in 56 of the 59 patients, the maximal TRH-induced increase in serum TSH and the integrated serum TSH response to TRH were suppressed in the early perioperative period. This postoperative TSH suppression correlated with elevated postoperative plasma dopamine concentrations (r = 0.57, p less than 0.05). Three patients with compensated primary hypothyroidism were detected in the study and represent the first documentation of serial thyroid hormone and TSH levels in hypothyroid patients undergoing major surgery. These patients had similar changes in thyroid hormone values compared with euthyroid patients. The serum TSH response to TRH was suppressed into the normal range in two of these patients on the day following surgery. The authors conclude that the sick-euthyroid syndrome occurs within a few hours of major surgery and remits with convalescence. Postoperative decreases in serum TSH may mask the diagnosis of hypothyroidism. Surgical consultants should be aware of these rapid postoperative changes so that thyroid function tests are properly interpreted in patients who have undergone major surgery.     

Postprandial hypoglycemia after Nissen fundoplication for reflux esophagitis

The motility of the stomach is modulated by the complex interplay of muscular, humoral, and neuronal factors. Rapid gastric emptying has been described after gastrectomy, gastrojejunostomy, vagotomy with pyloroplasty, and with active peptic ulcer disease. Rapid emptying may result in "dumping" syndrome and in postprandial hypoglycemia. We report a patient who developed postprandial hypoglycemia after a Nissen fundoplication for reflux esophagitis. This is the first report of this complication after this surgical procedure. The hypoglycemia was secondary to a combination of rapid gastric emptying, rapid absorption of glucose causing hyperglycemia, and excessive insulin secretion. This syndrome should be considered in patients who develop hypoglycemic symptoms after fundoplication. Treatment with a low carbohydrate diet and anticholinergic agents may offer symptomatic relief.     

Effect of rate of enteral nutrient supply on gut mass.

Early enteral feeding after injury is important for maintenance of gut integrity. However, enteral nutrients are frequently administered at low rates because of decreased gastrointestinal motility. These low rates are said to "maintain the gut." This study was performed to evaluate the effect of rate of enteral nutrient delivery on gut mass. Six male Sprague-Dawley rats had no surgery and served as controls (ad libitum rat chow diet). Twenty-four male Sprague-Dawley rats underwent abdominal surgery for placement of gastroduodenal feeding tubes (tip located 2 cm into intestine from pylorus) and were randomized (n = 6 per group) to ad libitum rat chow, 1/2 strength peptide diet (Reabilan HN, RHN) at 1 mL/h (1/2RHN-1 mL), full-strength peptide diet at 2 mL/h (RHN-2 mL), or full-strength peptide diet at 4 mL/h (RHN-4 mL). These diets supplied approximately 30%, 13%, 50%, and 100% of rat recommended daily allowances. The control animals gained weight (38 +/- 3 g over 5 days) whereas all postsurgery animals lost weight. Weight loss was greatest in the 1/2 RHN-1 mL (-55 +/- 3 g over 5 days) and RHN-2 mL (-52 +/- 6 g over 5 days) groups compared with the RHN-4 mL animals (-41 +/- 5 g over 5 days). All animals fed liquid enteral diets had reduced gut weights compared with chow-fed animals. Gut weights did not differ between control and postsurgery ad libitum chow animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arginine: mediator or modulator of sepsis?

Arginine is a conditionally essential amino acid that plays pivotal roles in maintaining body homeostasis. Arginine is a substrate for protein synthesis but can also be metabolized to various bioactive compounds that include nitric oxide, ornithine, polyamines, creatine phosphate, agmatine, and dimethylarginines. Arginine produces physiologic effects via nitric oxide dependent and independent pathways. Nitric oxide is important for the modulation of vascular tone, inflammation, immune function, endothelial function, platelet and leukocyte adherence, and neurotransmission. Nitric oxide modulates many biochemical processes important for the response to sepsis. Arginine, independent of nitric oxide, is important for growth, wound healing, cardiovascular function, immune function, inflammatory responses, energy metabolism, urea cycle function, and other metabolic processes. Arginine supplementation improves outcomes in animals with sepsis, wounds, ischemia-reperfusion injury, and following thermal injury. Enteral administration of arginine improves endothelial function but has little effect upon hemodynamics during human sepsis. An analysis of clinical studies using enteral formulas with supplemental arginine suggests benefits upon outcome, with no evidence of significant detrimental effects.     

Innate immunity of surfactant protein A and D in urinary tract infection with uropathogenic Escherichia coli

Objective To investigate the role of surfactant protein (SP) - A and SP - D in urinary tract infection mouse model, and evaluate the effects of SP-A and SP-D absence on urinary tract infection. Methods SP-A and SP-D double knockout (SP-A/D KO) mice were made. SP-A/D KO and wild-type (WT) C57BL/6 female mice were used for this study. The expression of SP-A and SP-D in kidney was detected by immunohistochemistry (IHC). The levels of p - p38 and p38 protein in kidneys were measured by Western blotting. Uropathogenic Escherichia coli or buffer was delivered into the bladder of female mice. At 24 and 48 h after inoculation, CFU of Escherichia coli in the kidney and urine of the treated and control mice were measured. Histological, cellular and molecular analysis were performed by several methods of H/E staining, IHC and Western blotting. The effects of SP-A and SP-D on bacterial growth were studied in vitro. Results SP-A and SP-D in kidney were located in the proximal tubules and collecting tubules. Compared with WT mice, infected SP - A/D KO mice with UPEC had higher CFU in kidneys and urine at 24 h and 48 h, increased inflammatory cells infiltration in kidneys（P＜0.05）. Compared with WT mice, SP - A/D KO mice had higher p38 MAPK phosphorylation levels in kidneys（P＜0.05）. Growth of Escherichia coli was greatly inhibited by both SP-A and SP-D（P＜0.05）. Conclusions Both SP-A and SP-D are expressed in kidney. SP-A and SP-D can attenuate UTI induced by UPEC which may be through inhibiting bacterial growth and modulating renal inflammation.     

Hypercalcemia and disseminated cytomegalovirus infection in the acquired immunodeficiency syndrome

Two patients with the acquired immunodeficiency syndrome and disseminated cytomegalovirus infection developed hypercalcemia associated with suppressed parathyroid gland activity. Neither patient had evidence of a malignant, endocrinologic, granulomatous, or drug-related cause for hypercalcemia. Increased osteoblastic bone resorption induced by cytomegalovirus infection may have been the cause for the hypercalcemia. Physicians should be alert for the occurrence of endocrinologic and metabolic problems in immunosuppressed patients.     

Trace Element Homeostasis During Continuous Sedation With Propofol Containing EDTA Versus Other Sedatives in Critically Ill Patients

Objective: To evaluate changes in serum and urinary zinc, cobalt, copper, iron, and calcium concentrations in critically ill patients receiving propofol containing disodium edetate (disodium ethylenediaminetetraacetic acid [EDTA]) versus sedative agents without EDTA. Design: This was a randomised, open-label, parallel-group study with randomisation stratified by baseline Acute Physiology and Chronic Health Evaluation (APACHE II) scores. Setting: Intensive care units (ICU) in 23 medical centres. Patients: Medical, surgical, or trauma ICU patients 17 years of age or older who required mechanical ventilator support and sedation. Interventions: A total of 106 patients received propofol containing 0.005 % EDTA (propofol EDTA), and 104 received other sedative agents without EDTA (non-EDTA). Only the first 108 patients were assessed for urinary trace metal excretion. Twenty-four–hour urine samples were collected on days 2, 3, and 7 and every 7 days thereafter for determination of zinc, cobalt, copper, iron, and calcium excretion; EDTA levels; urine osmolality; albumin levels; and glucose levels. The first 143 patients were assessed for serum concentration of zinc, cobalt, copper, iron, and calcium; creatinine; blood urea nitrogen; and albumin at baseline and once during each 24-hour urine collection. Measurements and Results: For the assessment of trace metals, patients receiving propofol EDTA demonstrated increased mean urinary excretion of zinc, copper, and iron compared with the normal range. All patients receiving sedatives demonstrated increased urinary excretion of zinc and copper above normal reference values. Compared with the non-EDTA sedative group, the propofol EDTA group demonstrated increased urinary excretion of zinc and iron. Mean serum concentrations of zinc and total calcium were decreased in both patient groups. Serum zinc concentrations increased from baseline to day 3 in the non-EDTA sedative group but not in the propofol EDTA group. Renal function, measured by blood urea nitrogen, serum creatinine, and creatinine clearance, did not deteriorate during ICU sedation with either regimen. Conclusion: This study showed that critical illness is associated with increased urinary losses of zinc, copper, and iron. Propofol EDTA– treated patients had greater urinary losses of zinc and iron and lower serum zinc concentrations compared with the non-EDTA sedative group. No adverse events indicative of trace metal deficiency were observed in either group. The clinical significance of trace metal losses during critical illness is unclear and requires further study.