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The morbidity of a bout of AP persists in some patients after recovery. Long‐term assessment is addressed in Table 1.8. An episode of AP increases a patient’s risk of developing diabetes mellitus, progressing to chronic pancreatitis with EPI, and is associated with an increased risk of harboring or developing pancreatic cancer. Ventre et al. [96] reported that patients who had severe AP that required critical care were found to have a high risk for developing new‐onset diabetes mellitus. In addition, as expected, greater pre‐hospitalization comorbidity, as determined by the Charlson score, negatively influenced survival. Das et al. [97] conducted a systematic review of diabetes mellitus prevalence after AP and found pre‐diabetes mellitus in 16%; this is important, as 40% of patients with pre‐diabetes progress to diabetes over 5–10 years. Diabetes mellitus was found in 23% and requirement for insulin treatment in 15%. Newly diagnosed diabetes (so‐called type 3c diabetes) developed in 15% within 12 months after the first episode of AP. Interestingly, they found that there was no effect of disease severity on the risk of developing diabetes mellitus. Conversely, in a study of patients who had severe pancreatitis, of whom almost three‐quarters underwent open necrosectomy, new‐onset diabetes mellitus was found in 45%, and pancreatic insufficiency requiring pancreatic enzyme replacement was found in 25% [98].

Shen et al. [99] reported a cohort study that included almost 3000 patients with their first attack of AP and approximately 12 000 individually matched controls. The incidence of developing diabetes within the first three months after AP was 60.8 per 1000 person‐years in the AP group compared with 8.0 per 1000 person‐years in the control group (hazard ratio, HR, 5.9). The adjusted HR was 2.54 for developing diabetes mellitus beyond three months. Similar to other studies, the results for patients with mild AP were similar to those for all AP groups. We should therefore be aware that after AP of all severities, the risk of developing diabetes mellitus is increased, so‐called “diabetes of the exocrine pancreas” [100].

Table 1.8 Long‐term sequelae after resolution of acute pancreatitis.

Chronic pancreatitis Exocrine pancreatic insufficiency Diabetes mellitus Pancreatic ductal adenocarcinoma Decreased quality of life

Hollemans et al. [101] reported on the follow‐up of almost 1500 patients with AP at 36 months. They found a pooled prevalence of EPI of 27%. Using fecal elastase levels, EPI occurred significantly more often in patients with alcoholic pancreatitis than in those with other etiologies. EPI was significantly more common in patients with severe than mild AP [101]. The presence of pre‐diabetes and/or diabetes mellitus in patients after AP should necessitate a search for coexistent EPI. In patients after AP, Das et al. [102] found a prevalence of concomitant EPI of 40% in patients with newly diagnosed pre‐diabetes or diabetes.

Machicado et al. [103] reported the long‐term deleterious effect on physical health‐related quality of life using a physical‐ and mental health‐related quality of life telephone survey. Individuals who had experienced AP had a significantly lower physical component survey (PCS) score than did controls and this was associated with the presence of multisystem organ failure during hospitalization, which is similar to other ICU survivors. In addition, at time of follow‐up lower PCS scores were associated with abdominal pain, analgesic use, disability, and cigarette use. Thus, support to discontinue smoking and alcohol use and to control pain on discharge should be a focus of ongoing care.

The long‐term (median of 10.5 years) follow‐up of pancreatic function after the first episode of acute alcoholic pancreatitis was reported by Nikkola et al. [104]. As expected, 35% had one or more recurrent episodes of AP during a maximum follow‐up of 13 years. New pancreatogenic diabetes developed in 19%, all of which had recurrent AP. Exocrine pancreatic dysfunction occurred in 77 (24%) patients, which was associated with abnormal endocrine function [104]. In alcoholic patients with RAP, progression to chronic pancreatitis occurred in 19% [104] and in 38% mainly in alcoholics as reported by Lankisch et al. [105].

The risk of pancreatic cancer after a primary episode of AP was reported by Rijkers et al. [106] in 731 patients who were followed for a median of 55 months. Pancreatic cancer incidence rate (per 1000 patient‐years) in the group who progressed to chronic pancreatitis was 9.0 compared with 1.1 in those did not progress to chronic pancreatitis. The median time to developing pancreatic cancer was 47 months in those with chronic pancreatitis and 12 months in those who did not have chronic pancreatitis. One wonders if the AP was secondary to the underlying pancreatic cancer in this group without chronic pancreatitis. No comparative group was utilized in this study [106].

Sadr‐Azodi et al. [107] performed a population‐based cohort study including all Swedish residents diagnosed with AP in order to determine the relationship between AP and pancreatic cancer. Approximately 70% of patients with pancreatic cancer had a history of AP. The risk of pancreatic cancer was increased during the first few years after the episode of AP and then gradually declined. The risk of pancreatic cancer between two months and two years after hospitalization for AP was highest in individuals aged 60 and above without gallstone‐related pancreatitis but with diabetes mellitus. Those cancers diagnosed within six months of AP were more likely to be localized [107].

A follow‐up, nationwide, matched cohort study from Denmark by Kirkegard et al. [108] found that patients with AP had increased risk of pancreatic cancer. Their risk for developing pancreatic cancer decreased with time but was still elevated at two and five years post episode and this included a three‐year washout period to reduce the likelihood of including prevalent cases of pancreatic cancer. Thus, we must continue to follow up and search for an underlying neoplasm in patients with AP who are older than 40 years of age, irrespective of the presumed cause of their AP. The reason(s) for this association may be similar etiologies, including alcohol, smoking, diet, diabetes, and obesity [109].

Thus, patients with a history of AP regardless of cause should likely undergo screening for pancreatic cancer in the five years after their initial episode.