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Biomedical subjects

E Elkhammas

Publications and source records attributed to E Elkhammas.

6 recordsLinked to original sources
PubMed1995

Obesity as a risk factor after combined pancreas/kidney transplantation.

The impact of pretransplant overweight/obesity was analyzed in a group of 268 consecutive primary pancreas renal transplant recipients. Obesity was defined as body mass index (BMI) greater than 27 kg/m2. BMI was available for 240 of the 268 patients. A total of 88% (212/240) of the patients had a BMI < or = 27 and 28/240 (12%) had BMI > 27. There were no significant differences in age, sex, or race between obese and nonobese patients. The incidence and degree of posttransplant hypertension, weight gain, increase in BMI, and hyperlipidemia did not differ on the basis of pretransplant BMI. Serum creatinine at one year posttransplant was slightly increased in obese patients, but the increase was not statistically significant. Cumulative prednisone dose (mg/kg) as well as cyclosporine (CsA) dose (mg/kg) at one year was not significantly different between obese and nonobese patients. However, there was a marginally significant negative correlation between BMI and one-year cumulative (mg/kg) prednisone dose (P = .06). Types and frequency of posttransplant complications were similar between obese and nonobese patients, although there was a slightly higher incidence of wound related complications in obese patients (11% vs. 6.8%) (P = NS). There was no difference in the frequency of acute rejection episodes in obese and nonobese patients. Actuarial patient survival was comparable between patients with BMI < or = 27 versus those with BMI > 27 (P = .10). However, actuarial graft survival, both pancreas and renal, were significantly decreased in patients with BMI > 27 (P = .029). The decrease in pancreas and kidney graft survival in obese patients could not be attributed to decreased "early" patient survival, increased incidence of perioperative or postoperative complications, differences in hypertension, acute rejection episodes, serum lipids, or immunosuppression dosage. The most common causes of graft loss were rejection and patient death in both obese and nonobese patients. After three years posttransplant, the decreased pancreas and renal graft survival in obese patients corresponded to decreased patient survival. The most common cause of patient death was cardiovascular complications in both obese and nonobese PKT recipients.

Adult↗
PubMed1988

Clinical observations and lessons learned in the treatment of patients with thoracoabdominal aortic aneurysms.

Thoracoabdominal aortic aneurysms can be repaired successfully with acceptable rates of morbidity and mortality. Twenty-three men and seven women (an average age of 67 years) underwent 23 elective and seven emergency operations. Pulmonary complications were the most common, but renal insufficiency and paraplegia were the most serious postoperative problems. The average time of suprarenal aortic occlusion was 47 minutes, but neither renal insufficiency nor paraplegia was directly related to suprarenal clamp time. Four deaths occurred after elective procedures, two from postoperative bleeding (one death from a technical error) and two deaths from multisystem organ failure. Four late deaths were caused by myocardial infarction. The remaining patients are alive at two to 79 months after infarction. DeBakey's technique (multiple sidearm grafts from the main aortic graft) was used in the first three procedures, and the graft inclusion technique of Crawford, in the remainder. The graft inclusion technique reduced operating time and loss of blood by 50 per cent and intraoperative fluid requirements by 33 per cent. Hypothermia was minimized by extraperitoneal, rather than intraperitoneal, abdominal aortic exposure, heated ventilation and warmed intravenous fluids. Selective renal cooling was performed by catheter perfusion of the renal arteries. Extreme care must be taken in making openings and attaching grafts to visceral arteries to avoid troublesome hemorrhage. In contrast with patients with infrarenal aneurysms, those with thoracoabdominal aneurysms require prolonged ventilatory support and have considerably higher fluid requirements. Precise surgical technique is mandatory.

Aged↗
PubMed1986

Characterization of the in vivo and in vitro inhibition of gastrin secretion from gastrinoma by a somatostatin analogue (SMS 201-995).

Earlier experiments characterized the effect of SMS 201-995 on gastrin secretion from gastrinoma in vivo. The results showed that the somatostatin analogue inhibits basal as well as secretin- and calcium-stimulated gastrin secretion. The current study examined the effect of SMS 201-995 on gastrin secretion from gastrinoma in vitro. Gastrinoma cells were prepared in cell culture or acute cell dispersion to study basal gastrin release. In cell culture, SMS 201-995 at 10(-9) M, 10(-8) M, and 10(-7) M significantly stimulated gastrin secretion (basal medium gastrin, 157 +/- 7.9 pg/ml; with SMS 201-995 10(-9) M, 786 +/- 62 pg/ml; with SMS 201-995 10(-8) M, 569 +/- 72 pg/ml; and with SMS 201-995 10(-7) M, 258 +/- 26 pg/ml). In contrast, in acute cell dispersion, the somatostatin analogue inhibited gastrin secretion (basal medium gastrin, 12.8 +/- 1.3 ng/ml; with SMS 201-995 10(-9) M, 9.0 +/- 0.1 ng/ml; with SMS 201-995 10(-8) M, 8.4 +/- 1.5 ng/ml; and with SMS 201-995 10(-7) M, 7.9 +/- 0.2 ng/ml). Gastrinoma cells were prepared in cell culture to study the effect of SMS 201-995 on gastrin secretion stimulated by secretin and by post-receptor increases in adenosine cyclic nucleotide. The somatostatin analogue inhibited gastrin secretion stimulated by secretin (10(-6) M) (797 +/- 48 pg/ml for secretin alone, compared with 396 +/- 9.4 pg/ml for secretin plus SMS 201-995). SMS 201-995 did not inhibit gastrin secretion stimulated by dibutyryl cyclic AMP (10(-7) M) (617 +/- 62 pg/ml for dibutyryl cyclic AMP alone, compared with 778 +/- 55 pg/ml for the two together). In vitro, SMS 201-995 inhibits basal gastrin secretion from gastrinoma prepared in acute cell dispersion, but not gastrinoma in cell culture, probably due to differences in basal secretory rates. The effect in vitro is less than that in vivo. SMS 201-995 does not inhibit postreceptor increases in adenosine nucleotide. This indirectly supports the hypothesis that SMS 201-995 acts in gastrinoma cells to inhibit gastrin secretion by inhibition of adenylate cyclase activity.

Adult↗