Pancreas Transplant Clinical Trial
Official title:
Assessing Arginine-Stimulated Native Pancreas Insulin Production Via Selective Venous Sampling in Patients With Long-Functioning Pancreas Allografts
This study will examine whether insulin-producing cells in the pancreas (beta cells) can
recover in patients with type 1 diabetes who have had a pancreas transplant. In type 1
diabetes, the body's immune system destroys the beta cells. Patients are treated with insulin
shots or a pancreas transplant to control their blood sugar. Some experiments suggest that
the pancreas may have the capacity to recover some of its insulin-producing capacity, but
that ability is negated by factors such as the continuing immune attack and erratic blood
sugar levels in patients.
Patients who have had a pancreas transplant may be in a unique situation to allow their own
pancreas to regrow beta cells for two reasons: 1) the medicines they take to prevent
rejection of the transplanted pancreas weaken their immune system; and 2) they have
near-normal blood sugar levels because of their functioning transplanted pancreas. This study
will test this hypothesis by sampling blood from patients' hepatic vein, which drains the
liver and native pancreas and from their iliac vein, which drains the transplanted pancreas.
This will determine whether insulin is coming from the transplanted pancreas (iliac vein) or
the liver and native pancreas (hepatic vein).
Patients 18 years of age and older who have had stable pancreatic transplant function for
more than 5 years may be eligible for this study. Candidates are screened with a medical
history and physical examination.
Participants are admitted to the hospital for 2 days for a full medical examination, blood
tests and procedures to determine insulin production. The procedures will include the
placement of catheters in the neck and groin for blood sampling. Participants will be closely
monitored after the procedures and discharged home if there are no complications.
Type 1 diabetes mellitus (T1DM) is thought to result from an autoimmune destruction of insulin producing beta-cells found within the pancreatic islets of Langerhans. In addition to the autoimmune process however, many studies have shown that hyperglycemia is also toxic to islets. Interventional studies have shown, for instance, that either tight glycemia control or immunosuppression can preserve C-peptide production. We hypothesize that patients who are immunosuppressed and euglycemic will display evidence that their native pancreas has recovered beta-cell function. We have asked whether pancreas transplant recipients, due to the immunosuppression required to prevent allograft loss, and the improved glycemia control resulting from the transplanted pancreas, might display some recovery of their native pancreatic islet function. Our preliminary data suggest that patients without C-peptide production prior to receiving an islet transplant appear to recover some endogenous pancreatic insulin secretion after islet transplantation. We will study whole pancreas transplant recipients, specifically those with grafts functioning for at least 5 years. We will test for native pancreas insulin production by infusing arginine into a peripheral vein, then selectively/simultaneously sampling blood for C-peptide levels from the hepatic veins and the vein draining the pancreatic allograft . Unlike our previous study of islet transplant recipients, a study that required portal vein cannulation, this study will require only hepatic and iliac vein cannulations, both much easier to accomplish, and associated with much less risk to the patient. Samples obtained from these sites will be tested for C-peptide levels. In addition, if we find evidence of native pancreas insulin production, we will look at a variety of clinical variables to see if any correlate with recovery of function. ;
| Status | Clinical Trial | Phase | |
|---|---|---|---|
| Not yet recruiting |
NCT06407232 -
Letermovir (Prevymis) for CMV in Kidney and Pancreas Transplant Recipients
|
Phase 3 |