Frey’s procedure - does it improve quality of life? A single centre experience of long term outcome following Frey’s procedure

Background: The objective of the study was to find out long term outcome of patients who underwent Frey’s procedure for chronic calcific pancreatitis.Methods: This is a prospective observational study from retrospectively collected data of all patients who underwent Frey’s procedure for chronic calcific pancreatitis in Institute of Surgical Gastroenterology, Rajiv Gandhi Government General Hospital, Chennai from January 2012 to December 2014. All patients who have completed at least 48 months after surgery were followed up and their long-term postoperative quality of life were analyzed.Results: Totally 48 patients underwent Frey’s procedure during this period. Eight patients lost follow up. Preoperatively all patients had pain score above six in numerical rating scale but after surgery only two patients in the long term required stronger opioids for pain relief. Exocrine deficiency was present in 24 (60%) patients preoperatively, out of which seven patients showed improvement, eight patients had worsened exocrine deficiency and weight loss. Post operatively there were six patients who developed exocrine deficiency. Endocrine deficiency was seen in 23 (57.5%) patients preoperatively and during follow up none showed improvement, with two (5%) patients developed endocrine deficiency. Seven patients showed worsened endocrine deficiency as documented by increasing insulin requirement. Quality of life analysis using SF 36 showed poor quality of life in patients with worsened exocrine deficiency.Conclusions: Frey’s procedure although in long term showed improved outcome in terms of pain free survival and overall quality of life, exocrine and endocrine deficiency persisted in most and worsened in some patients.

Non-alcoholic chronic calcific pancreatitis in a patient of celiac disease: a rare presentation

Celiac disease is a common malabsorptive disorder in the Indian subcontinent and autoimmune dysfunction of thyroid and pancreas is frequently encountered along with. Chronic Calcific pancreatitis is a unique entity commonly seen in alcoholics but very rare in a patient of celiac disease. This case report includes the interesting constellation of calcific pancreatitis with celiac disease in a young adult male patient known case of insulin dependent diabetes and hypothyroidism. We believe it to be the only case report from north India. A 32 year old Indian male patient known case of Diabetes and hypothyroidism presented with features of malabsorption and was diagnosed with Celiac disease and calcific pancreatitis on imaging. The symptoms and insulin requirement also improved with the treatment of Celiac disease. Although a common involvement of pancreas in celiac disease, calcific pancreatitis is a rare finding and improvement of both the insulin requirement and malabsorptive symptoms with the treatment of celiac disease and pancreatitis vice-a-versa.

Painless Tropical Chronic Pancreatitis with Extensive Calcification.

Chronic pancreatitis (CP) is caused by a wide variety of causes such as alcohol, biliary diseases, trauma, infections, autoimmune diseases, and hereditary disorders. Patients with CP present with disabling abdominal pain, weight loss, exocrine insufficiency, and diabetes and are at risk for malignant transformation. Pancreatic calcification narrows down the diagnosis of CP. Uncommon causes of calcific pancreatitis include autoimmune pancreatitis, hereditary pancreatitis, tropical pancreatitis, groove pancreatitis, and pancreatitis associated with cystic fibrosis, Ascaris, and ectopic pancreatic tissue. Calcific pancreatitis in young diabetics of tropical countries could be either due to alcohol or tropical pancreatitis. We report a young man with weight loss and steatorrhea, but without abdominal pain whose evaluation led to a diagnosis of tropical CP and diabetes.

Chronic Calcific Pancreatitis in a 9-Year-Old Boy.

Chronic pancreatitis is defined as continuing inflammatory disease of pancreas, characterised by irreversible morphological changes leading to pancreatic insufficiency. Chronic pancreatic insufficiency without pancreatitis is also seen in children suffering from cystic fibrosis which is a disease with congenital enzyme deficiency. Mean age of chronic pancreatitis is about 40 years. We present a case of a 9-year-old boy who was diagnosed as a case of chronic calcific pancreatitis. He was admitted with the complaints of paraumbilical pain and vomiting and was found diabetic. Diagnosis was established by X-ray, USG and CT scan of abdomen and ERCP. He was treated surgically in the form of lateral pancreaticojejunostomy (Puestow’s procedure).

Extracorporeal shock wave lithotripsy and endotherapy for pancreatic calculi—a large single center experience.

Aim Large pancreatic ductal calculi and pain are a feature of chronic calcific pancreatitis (CCP) in the tropics. This large single center study evaluates the role of extracorporeal shock wave lithotripsy (ESWL) in fragmentation of large pancreatic stones and relief of pain in patients with CCP. Methods Patients with CCP presenting with pain and large pancreatic duct (PD) calculi (>5 mm diameter) not amenable to extraction at routine endoscopic retrograde cholangio pancreatography (ERCP) were taken up for ESWL using a 3rd generation lithotripter. Stones in the head and body of pancreas were targeted at ESWL; 5,000 shocks were given per session. The calculi were fragmented to <3 mm size and then cleared by endotherapy. Pancreatic duct stents were deployed when indicated. A total of 1,006 patients underwent ESWL. Complete clearance was achieved in 762 (76%), partial clearance in 173 (17%) and unsuccessful in the rest. More than 962 (90%) of patients needed less than three sessions of ESWL. At 6 months, 711 (84%) of 846 patients who returned for follow up had significant relief of pain with a decrease in analgesic use. Complications were mild and minimal. Conclusion ESWL is an effective and safe modality for fragmentation of large PD calculi in patients with CCP.

Pancreatic diabetes.

Pancreatic endocrine insufficiency secondary to destruction of acinar cells is a well known complication of chronic pancreatitis (CP). Of all patients with diabetes mellitus, 0.5-1% is secondary to CP. The frequency of occurrence of diabetes in CP is about 40-60%. This figure varies according to the aetiology, extent of calcification, and duration of the disease. Pancreatic diabetes is more commonly associated with alcoholic and tropical calcific pancreatitis of long duration. The pathophysiology of pancreatic diabetes is related to beta cell failure and reduced insulin secretory capacity. The development of pancreatic diabetes calls for careful evaluation and management to prevent long term complications. Pancreatic cancer is a known complication of chronic pancreatitis and sometimes manifests with new onset diabetes. As destruction of pancreatic tissue in CP leads to depletion of both insulin and glucagonproducing cells of the islets of Langherhans, pancreatic diabetics are usually not prone to ketoacidosis. A trial of oral hypoglycemic agents followed by insulin therapy when the need arises has been the line of management thus far in these patients. This review focuses on the prevalence, unique pathophysiological aspects, clinical features and special issues in the management of diabetes secondary to chronic pancreatitis.

Genotype–phenotype correlation in 9 patients with tropical pancreatitis and identifi ed gene mutations.

The etiopathogenesis of tropical chronic pancreatitis (TCP) remains unclear. Malnutrition, dietary toxins like cyanogens in cassava and micronutrient deficiency are proposed factors. The description and characterization of genetic factors in TCP has added a new dimension to the understanding of pathogenesis of the disease. However, there is sparse data on the association of TCP with cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations. We report 8 patients of TCP with CFTR gene mutations, including one with a novel mutation, and describe the clinical profile of these patients. Further prospective genetic studies on the association of CFTR gene mutations are essential in order to unravel the genetic basis of TCP.