Abdominal pain is one of the most prominent symptoms in patients with chronic pancreatitis (CP) and can manifest intermittently or persistently. The mechanism of pain is not yet clear, and no effective treatment is currently available. This study aimed to explore the risk factors for pain in patients with CP, which may provide new insights for developing effective pain control modalities.

This clinical study was based on a single-centre research database that included 570 patients with CP. We compared the differences in baseline data, clinical characteristics, and psychophysiology traits between patients with and without pain. Subsequently, patients will be followed up to assess changes in their risk factors and explore their relationship with pain.

In the final risk factor model, young age (P = .031; odds ratio [OR] = 0.986 [0.973, 0.999]), prolonged disease duration (P < .001; OR = 1.307 [1.127, 1.516]), heavy smoking (P = .014; OR = 1.331 [1.060, 1.617]), alcohol consumption (P = .003; OR = 1.419 [1.127, 1.788]), low body mass index (P < .001; OR = 0.786 [0.703, 0.879]), pancreatic exocrine insufficiency (P = .040; OR = 1.683 [1.024, 2.767]), acute pancreatitis attacks (P = .027; OR = 1.759 [1.067, 2.902]), anxiety, and depression (P = .016; OR = 1.047 [1.009, 1.088]; P = .014; OR = 1.068 [1.013, 1.126]) were associated with CP pain. Reducing tobacco and alcohol intake (P = .001; OR = 2.367 [1.525, 4.637]; P = .024; OR = 2.011 [1.085, 3.199]), increasing the body mass index (P = .005; OR = 1.968 [1.265, 3.805]), and improving anxiety (P = .001; OR = 1.164 [1.081, 1.340]) were identified to be beneficial for pain relief. Compared to the effects on persistent pain, pancreatic enzyme supplementation (P = .004; OR = 1.794 [1.186, 2.502]) had a clear effect on intermittent pain in patients with CP.

We identified a multifactorial model of pain risk factors for CP and confirmed that modifying these risk factors could influence patient pain symptoms.

Effective chronic pancreatitis (CP) treatment requires accurate severity evaluation, but no histopathology grading system exists. This study aimed to develop and validate a novel CP pathological grade (Histopathology-derived CPpG) using quantified pathological and radiological characteristics through deep learning.

Patients with pathologically/clinically confirmed CP or recurrent acute pancreatitis were retrospectively enrolled (2011-2023). Whole-slide CP images were automatically segmented and quantified via DeeplabV3+, followed by latent class analysis to develop Histopathology-derived CPpG. A deep learning radiomics score (DLRS) was created to predict Histopathology-derived CPpG using preoperative CT scans of patients with pathologically confirmed CP. CT-predicted CPpG was then validated in an independent group of patients with clinically confirmed CP and recurrent acute pancreatitis.

The study included 2054 patients with CP and recurrent acute pancreatitis, with 181 cases of pathologically confirmed CP. Histopathology-derived CPpG I had a higher proportion of acini, acinus-to-stroma ratio, acinus-to-islet ratio, islet-to-stroma ratio, and (acinus + islet)-to-stroma ratio, and a lower proportion of stroma and lymphocytes compared to CPpG II. The DLRS demonstrated high performance in the validation (AUC, 0.84; 95 % CI: 0.75-0.92) and test (AUC, 0.76; 95 % CI: 0.65-0.87) sets. In a large-scale clinical validation, CT-predicted grades were significantly associated with endocrine and exocrine function, as well as prognosis (P < .05).

This study developed a novel pathological classification, Histopathology-derived CPpG, which accurately reflects disease severity. Additionally, the non-invasive DLRS shows great potential for dynamically monitoring CP severity and evaluating pancreatic endocrine and exocrine function, as well as prognosis.

Chronic pancreatitis is defined as a disease of the pancreas in which recurrent inflammatory episodes result in replacement of the pancreatic parenchyma by fibrous connective tissue in individuals with genetic, environmental, and other risk factors. Pain is one of the most important symptoms of chronic pancreatitis and, in many cases, has chronic visceral nociceptive, nociplastic, and even neuropathic components, with evidence of both central and peripheral sensitization, neuroplasticity, and neurogenic inflammation.

The literature on the diagnosis and treatment of pain in chronic pancreatitis was reviewed and summarized.

Treatment of abdominal pain in chronic pancreatitis is guided by pancreatic morphology on imaging, although the correlation between pain symptoms and pathoanatomical changes is not always straightforward. Patients with pancreatic duct obstruction are initially offered endoscopic or surgical therapies, while non-obstructive disease is mostly managed medically. Lifestyle changes and psychological support are of particular importance for all chronic pancreatitis patients. Analgesic options range from non-opioid medications to opioids and adjuvant agents. Interventional pain management may consist of radiofrequency treatment of the splanchnic nerves and spinal cord stimulation. To date, there are no randomized trials supporting their efficacy in the treatment of chronic pancreatitis pain, and the recommendation to consider these treatment options is justified by evidence from observational studies. Possible opioid-sparing effects of interventional pain treatments are important to consider because opioid use and dependency are common in chronic pancreatitis patients and associated with worse outcomes. Celiac plexus block is not generally recommended for chronic pancreatitis due to the limited quality of evidence, overall short duration of effect, and invasiveness of the procedure. Central sensitization can impact the effectiveness of invasive treatments.

Managing pain in chronic pancreatitis is a complex task that requires a multidimensional and individualized approach. Due to the lack of randomized trials, treatment decisions are often guided by expert opinion. Integrating pharmacological and non-pharmacological interventions and collaborating with a multidisciplinary team are key components of effective chronic pancreatitis pain management.

Chronic pancreatic pain is one of the most severe causes of visceral pain, and treatment response is often limited. Neurostimulation techniques have been investigated for chronic pain syndromes once there are pathophysiological reasons to believe that these methods activate descending pain inhibitory systems. Considering this, we designed this systematic literature review to investigate the evidence on neuromodulation techniques as a treatment for chronic pancreatic pain.

We performed a literature search using the databases MEDLINE, Cochrane Central Register of Controlled Trials (CENTRAL), and Embase until April 2024. The included studies used neurostimulation techniques in participants with chronic pancreatic pain and reported pain-related outcomes, with a focus on pain scales and opioid intake. Two reviewers screened and extracted data, and a third reviewer resolved discrepancies. We assessed the risk of bias using the Jadad scale. The authors then grouped the findings by the target of the neurostimulation, cortex, spinal cord, or peripheral nerves; described the findings qualitatively in the results section, including qualitative data reported by the articles; and calculated effect sizes of pain-related outcomes.

A total of 22 studies were included (7 randomized clinical trials [RCTs], 14 case series, and 1 survey), including a total of 257 clinical trial participants. The two outcomes most commonly reported were pain, measured by the visual analogue scale (VAS), numeric rating scale (NRS), and pressure pain threshold scores, and opioid intake. Two RCTs investigated repetitive transcranial magnetic stimulation (rTMS), showing a reduction of 36% (±16) (d = 2.25; 95% CI, 0.66-3.83) and 27.2% (±24.5%) (d = 2.594; 95% CI, 1.303-3.885) in VAS pain scale. In another clinical trial, transcranial direct-current stimulation (tDCS) and transcranial pulsed current stimulation were not observed to effect a significant reduction in VAS pain (χ2 = 5.87; p = 0.12). However, a complete remission was reported in one tDCS case. Spinal cord stimulation (SCS) and dorsal root ganglion stimulation were performed in a survey and 11 case series, showing major pain decrease and diminished opioid use in 90% of participants after successful implantation; most studies had follow-up periods of months to years. Two noninvasive vagal nerve stimulation (VNS) RCTs showed no significant pain reduction in pain thresholds or VAS (d = 0.916; 95% CI, -0.005 to 1.838; and d = 0.17; -0.86 to 1.20; p = 0.72; respectively). Splanchnic nerve stimulation in one case report showed complete pain reduction accompanied by discontinuation of oral morphine and fentanyl lozenges and a 95% decrease in fentanyl patch use. Two RCTs investigated transcutaneous electrical nerve stimulation (TENS). One found a significant pain reduction effect with the NRS (d = 1.481; 95% CI, 1.82-1.143), and decreased opioid use, while the other RCT did not show significant benefit. Additionally, one case report with TENS showed pain improvement that was not quantitatively measured.

The neuromodulation techniques of rTMS and SCS showed the most consistent potential as a treatment method for chronic pancreatic pain. However, the studies have notable limitations, and SCS has had no clinical trials. For VNS, we have two RCTs that showed a non-statistically significant improvement; we believe that both studies had a lack of power issue and suggest a gap in the literature for new RCTs exploring this modality. Additionally, tDCS and TENS showed mixed results. Another important insight was that opioid intake decrease is a common trend among most studies included and that adverse effects were rarely reported. To further elucidate the potential of these neurostimulation techniques, we suggest the development of new clinical trials with larger samples and adequate sham controls.

Spinal cord stimulation (SCS) has emerged as a treatment option for patients with chronic pancreatitis (CP) who experience pain that does not respond to standard interventions. However, there is a lack of sham-controlled trials to support its efficacy.

This randomized, double-blinded, sham-controlled, cross-over trial enrolled 16 CP patients with insufficient pain relief from standard therapies. Patients underwent high-frequency (1000 Hz) paraesthesia-free SCS or sham for two 10-day stimulation periods, separated by a 3-day washout period. The primary outcome was daily pain intensity registered in a pain diary based on a numeric rating scale (NRS). Secondary outcomes included various questionnaires. Quantitative sensory testing was used to probe the pain system before and after interventions.

The average daily pain score on the NRS at baseline was 5.2 ± 1.9. After SCS, the pain score was 4.2 ± 2.1 compared to 4.3 ± 2.1 in the sham group (mean difference -0.1, 95% CI [-1.4 to 1.1]; P = 0.81). Similarly, no differences were observed between groups for the maximal daily pain score, secondary outcomes or quantitative sensory testing parameters. During an open-label, non-sham-controlled and non-blinded extension of the study, the average daily NRS was 5.2 ± 1.7 at baseline, 3.2 ± 1.8 at 3 months, 2.9 ± 1.9 at 6 months and 3.4 ± 2.2 at 12 months of follow-up (P = 0.001).

In this first sham-controlled trial of SCS in painful CP, we did not find evidence of short-term pain relief with paraesthesia-free high-frequency (1000 Hz) stimulation. However, evaluation of the long-term effect by larger sham-controlled trials with long-term follow-up is warranted.

In this first sham-controlled trial to apply high-frequency (1000 Hz) spinal cord stimulation in patients with visceral pain due to chronic pancreatitis, we did not find evidence for clinically relevant pain relief. Taken together with potential procedure-related complications, adverse effects and costs associated with spinal cord stimulation, our findings question its use for management of visceral pain.

Chronic pancreatitis (CP) is a fibroinflammatory disease characterized by irreversible destruction of pancreatic tissue. With the development of the disease, it may lead to exocrine and/or endocrine insufficiency. CP is one of the common diseases that cause abdominal pain, which will not get permanent spontaneous relief as the disease evolves. The American College of Gastroenterology clinical guidelines recommend computed tomography or magnetic resonance imaging as the first-line examination for the diagnosis of CP. CP common imaging findings include pancreatic atrophy, irregular dilatation of the pancreatic duct, calcification of pancreatic parenchyma, pancreatic duct stones, etc. In clinical practice, whether any correlations between CP-induced abdominal pain patterns (no pain/constant/intermittent pain) and corresponding imaging findings present are not well known. Therefore, this review aims to comprehensively sort out and analyze the relevant information by collecting lots of literature on this field, so as to construct a cross-bridge between the clinical manifestations and imaging manifestations of CP patients. Also, it provides an imaging basis and foundation for the classification and diagnosis of abdominal pain types in clinical CP patients.

Pain, the hallmark symptom of chronic pancreatitis (CP), remains difficult to assess. To capture the variability of pain that patients can experience day to day, this study used pain diaries to describe daily pain experiences and identify pain phenotypes.

This study is a secondary data analysis from a pilot trial examining cognitive behavioral therapy for pain treatment in CP. Before treatment, patients completed an online daily pain diary using the Brief Pain Inventory for 7 days. Using indicators of pain magnitude, pain variability, pain synchrony along with least, worst, and average pain intensity levels, we identified pain patterns using K-means clustering.

Of 30 patients in the pilot trial, a total of 27 patients (mean age of 49.8 years, 80% women) had complete data to include in this report. Four clusters were identified: cluster 1, lowest pain magnitude (n = 3); cluster 2, moderate pain magnitude and high pain variability (n = 4); cluster 3, moderate pain magnitude and low pain variability (n = 9); and cluster 4, highest pain magnitude and lowest pain variability (n = 11).

Daily pain diaries offer a novel way of evaluating the dynamic pain experiences in CP. Although 4 distinct pain patterns were identified, further studies are needed to validate these findings.

The quality of life (QoL) of patients with chronic conditions is a function of factors associated with the illness, its natural course, and treatment as well as those related to the patient. Chronic pancreatitis (CP) is a critical public health problem. Chronic pancreatitis patients can experience chronic pain with different mechanisms, malabsorption, diabetes, and cachexia.

Chronic pancreatitis (CP) is a critical public health problem. CP patients can experience chronic pain with different mechanisms, malabsorption, diabetes, and cachexia. The aim of the study was to assess the Quality of Life (QoL) of patients with CP and identify factors affecting QoL.

104 patients diagnosed with CP from the hospital in Wrocław, Poland, were included. The study was conducted using our own questionnaire, the World Health Organization Quality of Life-BREF (WHOQOL-BREF) scale, the 36-Item Short Form Health Survey (SF-36), and the Visual Analog Scale (VAS).

The mean total SF-36 score was 47.7, with the highest mean rating for the physical functioning domain. The mean VAS pain score was 5.13. Pain intensity was significantly correlated with impairments in activities of daily living (P = 0.001), the need to reduce their duration (P = 0.001), and the performance of physical activity (P = 0.003). Comorbidities, education, and age have a significant relationship with only some domains of SF-36.

One aspect that has an impact on QoL impairment is pain which perception is governed by the same brain regions in which abnormalities result in depression and anxiety. QoL in CP patients also depends on the patient's age, comorbidities, and level of education.

Although abdominal pain is the most prevalent and disabling symptom in patients with chronic pancreatitis (CP), there are also patients who have painless CP.

We performed a retrospective analysis of patients with a diagnosis of CP. A total of 279 patients with definite CP with completed demographic and clinical data were included in the final analysis.

There were 75 (26.9%) patients with painless CP. These patients had a significantly higher mean age at diagnosis, 61.7 years, than the 52.5 years of patients with pain (p < 0.001). Painless and painful CP had similar rates of diabetes mellitus (DM) (28.4% vs. 31.6%) and pancreatic exocrine insufficiency (PEI) (50.0% vs. 52.3%). Painless CP had lower rates of alcoholic etiology, 36.0%, than the 52.5% in painful CP (p < 0.05). Patients older than 55 at the time of CP diagnosis were associated with painless CP with an adjusted odds ratio (aOR) of 3.27 [95% confidence interval (CI): 1.62-6.60]. Alcoholic etiologies were not associated with painless CP, aOR of 0.51 (95% CI: 0.25-0.91).

Patients with painless CP had a significantly higher mean age than patients with painful CP and increased aOR for those older than 55 at CP diagnosis. Painless and painful CP patients had similar rates of DM and PEI, confirming the necessity of routine follow up in all patients with CP.