Early-stage chronic pancreatitis may be undetected as a clinical entity. However, it may carry a definite risk for subsequent secondary damage, depending on the etiology of the disease. Therefore, the most important question is whether indeed the patient in question does have early-stage chronic pancreatitis rather than oligosymptomatic advanced-stage chronic pancreatitis. This can be easily determined by appropriate imaging such as abdominal computed tomography. For early changes, endoscopic ultrasound is superior to any other technique. Endosonography may also tell about anatomical obstacles (e.g., papillary stenosis, pancreas divisum) that may be treated to prevent progression of the disease. Treatment options at this stage are endoscopic for the most part. Depending on the etiology and familiar/hereditary background of the given patient, one must look further into molecular markers. Such markers may give an estimate on the progression or dynamics of the disease in the future and include mutations in the cationic (PRSS1) and anionic (PRSS2) trypsinogen genes as well as mutations in the serine protease (SPINK1) or cystic fibrosis (CFTR) genes. Admitted ly, these are not markers of early-stage chronic pancreatitis but must be investigated if and when such pathogenesis is suspected. Further, rare forms of chronic pancreatitis, such as autoimmune pancreatitis, which can be cured by appropriate medical treatment with steroids, must be excluded. Markers for autoimmune pancreatitis are elevated serum IgG, especially IgG4, and autoantibodies to carbonic anhydrase (type II) and lactoferrin. It is noteworthy that these markers, present in almost every Asian patient with autoimmune pancreatitis, are mostly lacking in Caucasian populations of patients with autoimmune pancreatitis.