Purtscher's retinopathy: a rare complication of acute non-alcoholic pancreatitis

Purtscher's retinopathy is a rare complication of acute alcoholic pancreatitis that is characterized by the development of cotton-wool exudates and retinal hemorrhages located around the optic disk. Its development is due to ischemic phenomena in the posterior pole of the retina due to microemboli in the retinal arterioles and capillaries. This complication is not related to a poorer prognosis of acute pancreatitis and the retinopathy usually has a favorable outcome with disappearance of the ophthalmic lesions and restoration of visual acuity after 4-6 weeks in most cases. However, some patients may show residual lesions, especially if optical atrophy occurs. We present a 40-year-old woman with loss of visual acuity due to Purtscher's retinopathy during the course of mild acute idiopathic pancreatitis.     

Hospital contacts with alcohol problems prior to liver cirrhosis or pancreatitis diagnosis

AIM To evaluate prior hospital contacts with alcohol problems in patients with alcoholic liver cirrhosis and pancreatitis. METHODS This was a register-based study of all patients diagnosed with alcoholic liver cirrhosis or pancreatitis during 2008-2012 in Denmark. Hospital contacts with alcohol problems(intoxication, harmful use, or dependence) in the 10-year period preceding the diagnosis of alcoholic liver cirrhosis and pancreatitis were identified.RESULTS In the 10 years prior to diagnosis, 40% of the 7719 alcoholic liver cirrhosis patients and 40% of the 1811 alcoholic pancreatitis patients had at least one prior hospital contact with alcohol problems. Every sixth patient(15%-16%) had more than five contacts. A similar pattern of prior hospital contacts was observed for alcoholic liver cirrhosis and pancreatitis. Around 30% were diagnosed with alcohol dependence and 10% with less severe alcohol diagnoses. For the majority, admission to somatic wards was the most common type of hospital care with alcohol problems. Most had their first contact with alcohol problems more than five years prior to diagnosis.CONCLUSION There may be opportunities to reach some of the patients who later develop alcoholic liver cirrhosis or pancreatitis with preventive interventions in the hospital setting.     

Prevalence of normal serum amylase levels in patients with acute alcoholic pancreatitis

Acute alcoholic pancreatitis is uncommonly diagnosed when the serum amylase level is normal. We defined acute alcoholic pancreatitis as a clinical syndrome in which hyperamylasemia was not a necessary component and sought support for the diagnosis by ultrasonography and computed tomography of the pancreas. In 68 episodes of acute alcoholic pancreatitis identified in a one-year period, the serum amylase level was normal at the time of hospital admission in 32%. In 40 episodes, we performed ultrasonography and computed tomography within 48 hr of admission. The diagnosis was supported by ultrasonography in 43%, by computed tomography in 68%. Ultrasonography and computed tomography supported the diagnosis as frequently in patients with normal serum amylase levels as in patients with hyperamylasemia. We conclude that patients with acute alcoholic pancreatitis frequently have normal serum amylase levels. The widespread clinical practice of relying solely on hyperamylasemia to establish the diagnosis of acute alcoholic pancreatitis is unjustified and should be abandoned.     

Acute Septic Pancreatitis Presenting as Colonic Necrosis

A 43-year-old alcoholic male homosexual developed acute ischemic necrosis of the descending colon secondary to acute necrotizing pancreatitis. CT scan was diagnostic of pancreatitis. Necrosis of the left colon required colectomy with colostomy. Postoperatively recovery was slow but ultimately complete. The patient is in excellent health 18 months postoperatively.     

Alcoholic chronic pancreatitis

Opinion statement The most important intervention in the treatment of alcoholic chronic pancreatitis is alcohol cessation, and therefore, it should be a primary treatment goal. This measure alters the natural course of the disease and may improve long-term survival. Smoking cessation should also be encouraged, since the risk of pancreatic cancer increases with prolonged chronic pancreatitis, and is again doubled by smoking. Maldigestion is treated in a way similar to other types of chronic pancreatitis. Treatment of pain should begin with an effort to identify reversible causes, including pseudocysts and duct obstruction. Chronic pain management should follow a multi-step treatment regimen that reserves narcotics for only the most severe cases. Since pain tends to diminish during the natural history of pancreatitis, treatment of pain needs to be continually reevaluated. Endoscopic or surgical interventions are indicated only for the management of complications, but have no significant effect on the natural history of alcoholic chronic pancreatitis. In the future, diagnosis of patients within the earliest stages of alcoholic chronic pancreatitis, and intervention with effective strategies to prevent progression of fibrosis and other complications, may offer the best solution for eliminating this disease. Thus, the focus of management should be early identification of patients at risk, and institution of effective new therapies.     

Alcohol intake, cigarette smoking, and body mass index in patients with alcohol-associated pancreatitis

The differential diagnosis between acute and chronic alcohol-associated pancreatitis is often difficult or impossible at onset of the disease. A study was conducted to determine possible relationships between patients suffering from a first episode of acute alcoholic pancreatitis and patients with unequivocal chronic alcoholic pancreatitis, comparing age, drinking and smoking habits, and body mass index (BMI). Two groups of men were considered. The first group consisted of 67 patients with a diagnosis of acute alcohol-associated pancreatitis in the absence of other potential pathogenic factors; in this group, 48 of the 56 patients surviving the acute attack were submitted to imaging studies for a median period of 9 years. The second group consisted of 396 patients with chronic alcoholic pancreatitis with a median follow-up period of 12 years. The variables that differed significantly in the two groups were BMI (p < 0.009) and number of smokers (p < 0.001). Logistic regression analysis selected only BMI with an odds ratio of 1.19 (95% CI, 1.07-1.33; p < 0.00015) in favor of acute alcoholic pancreatitis. In male patients, from an epidemiologic standpoint, only smoking habits and BMI are significant differences at clinical onset between the two types of pancreatitis.     

Malignant hypertension presenting as acute pancreatitis

We report a patient who was admitted to hospital with acute pancreatitis but who also had malignant phase hypertension. Whilst his alcohol intake was high, there was no objective evidence of alcoholic liver disease and no other underlying cause for pancreatitis was found. The pancreatitis may therefore have been due to pancreatic infarctions associated with fibrinoid necrosis. In all patients with acute pancreatitis, the diagnosis of malignant hypertension should be considered.     

Modern diagnostics of chronic pancreatitis

Chronic pancreatitis is a well-defined disease on histopathological grounds, but for clinical purposes diagnosis is generally not based on histological specimens. Imaging procedures, non-invasive or with different degrees of invasiveness, and pancreatic function tests are therefore the diagnostic mainstay in patients with suggestive clinical history. The correct diagnosis of chronic pancreatitis is easy in late stages but difficult in an early stage of the disease. A particular challenge is the differentiation between acute or recurrent acute and early chronic pancreatitis. Earlier classifications (Cambridge and Marseille) did not consider the complex interrelationship between (especially alcoholic) acute and chronic pancreatitis. A possible solution is to separate the entities into probable and definite alcoholic chronic pancreatitis, with the assignment into the latter category achieved by follow-up investigations. Up to now the best diagnostic accuracy at an early stage is achieved by the detection of abnormalities of the ductal system in endoscopic retrograde pancreatography or by assessing exocrine function with the secretin-ceruletide test. The endoscopic ultrasound may substitute the endoscopic retrograde pancreatography as superior imaging modality that detects both parenchymal and ductal changes of chronic pancreatitis at an early stage. Magnetic resonance pancreatography is a further promising diagnostic tool without the risk of pancreatitis after endoscopic retrograde pancreatography, but imaging of the side branches, which is crucial for detection of early chronic pancreatitis, is not yet sufficient. Faecal elastase is a progress in non-invasive testing of exocrine pancreatic function, but its value for the diagnosis of chronic pancreatitis under conditions of clinical practice is limited. Several (13)C breath tests have been developed, but their availability and their diagnostic accuracy in chronic pancreatitis is still limited. Light to moderate exocrine pancreatic insufficiency is not detectable with adequate accuracy by tubeless function tests. A specific serum marker of pancreatic fibrosis which would reliably indicate the presence of chronic pancreatitis or its progression to is not available.     

Prognosis and prognostic factors in chronic pancreatitis

To evaluate the prognosis and prognostic factors of chronic pancreatitis, 84 patients with alcoholic chronic pancreatitis and 51 with nonalcoholic chronic pancreatitis have been followed for 1-21 years (average of 7.1 years). The follow-up period was defined as the period from diagnosis to death in those who died and to the present in those still alive. The following conclusions were obtained. (1) Patients with alcoholic chronic pancreatitis showed a significantly higher mortality rate (26.2%) and cancer death rate (8.3%) than the age- and sex-matched population. In patients with nonalcoholic chronic pancreatitis, however, the difference did not reach the level of statistical significance, although both rates tended to be higher. (2) Patients with alcoholic chronic pancreatitis showed a significantly poorer prognosis than those with nonalcoholic chronic pancreatitis. (3) Frequent causes of death in chronic pancreatitis were cancer (11 cases) and diabetes-associated conditions (renal failure in three cases, intractable pneumonia in one, hypoglycemic shock in two, and myocardial infarction in two). Death directly from pancreatitis was observed in four. (4) Unfavorable prognostic factors in alcoholic chronic pancreatitis included heavy drinking, continuance of drinking after diagnosis, smoking, insulin-dependent diabetes, and an advanced age. In nonalcoholic chronic pancreatitis, however, patients' age was the only significant prognostic factor; smoking did not reach the level of statistical significance, although it tended to lead to a poorer prognosis.     

Alcohol consumption in patients with acute or chronic pancreatitis.

Understanding of the relation between the alcoholic consumption and the development of pancreatitis should help in defining the alcoholic etiology of pancreatitis. Although the association between alcohol consumption and pancreatitis has been recognized for over 100 years, it remains still unclear why some alcoholics develop pancreatitis and some do not. Surprisingly little data are available about alcohol amounts, drinking patterns, type of alcohol consumed and other habits such as dietary habits or smoking in respect to pancreatitis preceding the attack of acute pancreatitis or the time of the diagnosis of chronic pancreatitis. This review summarizes the current knowledge. Epidemiological studies clearly show connection between the alcohol consumption in population and the development of acute and chronic pancreatitis. In the individual level the risk to develop either acute or chronic pancreatitis increases along with the alcohol consumption. Moreover, the risk for recurrent acute pancreatitis after the first acute pancreatitis episode seems also to be highly dependent on the level of alcohol consumption. Abstaining from alcohol may prohibit recurrent acute pancreatitis and reduce pain in chronic pancreatitis. Therefore, all the attempts to decrease alcohol consumption after acute pancreatitis and even after the diagnosis of chronic pancreatitis should be encouraged. Smoking seems to be a remarkable co-factor together with alcohol in the development of chronic pancreatitis, whereas no hard data are available for this association in acute pancreatitis. Setting the limits for accepting the alcohol as the etiology cannot currently be based on published data, but rather on the 'political' agreement.     

The Lipase to Amylase Ratio in Acute Pancreatitis

Objectives : The ratio of serum lipase to serum amylase has been proposed to distinguish acute episodes of alcoholic from nonalcoholic pancreatitis. We evaluated the efficacy of this test in a community hospital setting. Methods : Charts of all patients discharged with a diagnosis of acute pancreatitis over 19 months were retrospectively reviewed. Patients were excluded if their cre-atinine was greater than 3.0 mg/dl, if the amylase and lipase were not measured within 72 h of the onset of symptoms, or if the cause of pancreatitis was not known by the time of discharge. Results : Of the 56 patients, 31 had alcoholic pancreatitis. The lipase to amylase ratio did not differ significantly between patients with alcoholic and nonalcoholic pancreatitis. Median amylase and lipase were significantly higher in nonalcoholic pancreatitis; however, the wide ranges of both meant that neither amylase nor lipase accurately determined the cause of pancreatitis. Conclusion : The lipase to amylase ratio does not appear to be sufficiently sensitive or specific to distinguish alcoholic from nonalcoholic acute pancreatitis.     

Differences in the natural history of idiopathic (nonalcoholic) and alcoholic chronic pancreatitis. A comparative long-term study of 287 patients

Controversies in the literature regarding definition, diagnosis, and therapy of chronic pancreatitis may be related in part to differences in the natural history of alcoholic and idiopathic (nonalcoholic) chronic pancreatitis. In order to evaluate this problem the long-term course of 205 patients with alcoholic (85.4% with calcifications) (group A) and 82 patients with idiopathic (nonalcoholic) chronic pancreatitis (76.8% with calcifications) (group B) has been analyzed prospectively since 1963. The patients were studied at regular intervals with particular regard to pain, pancreatic exocrine, and endocrine function and calcifications. The observation time was 2 years or longer in 230 patients with a median observation time of 6.7 years from diagnosis in group A and 10.6 years in group B. In group B over 50% of the cases had primary painless chronic pancreatitis. Progressive deterioration of exocrine and endocrine function was observed in both groups. However, in group A the rate of progression of exocrine dysfunction after diagnosis was more rapid and the incidence of diabetes in relation to marked exocrine insufficiency was much higher than in group B. Steatorrhea preceded diabetes in 56% (group A) and 80% (group B), respectively. Onset of pancreatic calcifications was closely associated with pancreatic exocrine insufficiency in group A in contrast to group B. In addition lasting pain relief occurred spontaneously in about 30% of patients in group B despite a normal exocrine function for 6 years or longer which is in disaccord with the results in alcoholic chronic pancreatitis. In conclusion group A and B have many features in common, in particular the high incidence of pancreatic calcifications and the progressive pancreatic dysfunction. However, the long-term profile of both groups differs in some important aspects, particularly in the clinical pattern and in the rate of progression of pancreatic dysfunction and morphology. These differences should be appreciated in the discussion of problems regarding definition, diagnosis, and surgical therapy of chronic pancreatitis.     

CD14 promoter polymorphism in Chinese alcoholic patients with cirrhosis of liver and acute pancreatitis

AIM: To investigate the relationship between genetic polymorphism of the CD14 promoter and the occurrence of alcoholic cirrhosis and alcoholic pancreatitis, and to challenge the conclusion made earlier that the patients with acute alcoholic pancreatitis and patients with alcoholic cirrhosis of liver are two different subpopulations. METHODS: Using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, we determined the polymorphism of CD14 gene and aldehyde dehydrogenase gene 2 (ALDH 2) in 335 alcoholic patients with different organ complications i.e., cirrhosis of liver (n = 100), acute pancreatitis (n = 100), esophageal cancer (n = 82) and avascular necrosis of hip joint (AVN) (n = 53) and 194 non-alcoholic controls in a Chinese group. RESULTS: The results showed that the carriage of T allele was not different among alcoholic patients with cirrhosis of liver, alcoholic patients with other complication and non-alcoholic controls. On the other hand, the carriage of the C allele was significantly more prevalent for alcoholic pancreatitis than for esophageal cancer (0.79 vs 0.60, P<0.001), alcoholic AVN (0.79 vs 0.65, P<0.025) and nonalcoholic controls (0.79 vs 0.68,P<0.025). Furthermore, when only subjects with ALDH2 1-1 genotype were examined, the C allele frequency was significantly more prevalent for alcoholic pancreatitis than for alcoholic liver cirrhosis (0.82 vs 0.69,P<0.025), esophageal cancer (0.82 vs 0.61,P><0.01), alcoholic AVN (0.82 vs 0.64, P<0.01) and non-alcoholic controls (0.82 vs 0.69, P<0.05). CONCLUSION: The C allele may be associated with some mechanism, which is important in the pathogenesis of alcoholic pancreatitis, and that alcoholic patients with acute pancreatitis and cirrhosis of liver are probably two different subpopulations.     

Serum amylase isozymes in patients with chronic pancreatitis with hyperamylasemia

In order to clarify the relationship between hyperamylasemia and clinical states in chronic pancreatitis, serum amylase isozymes were studied in 39 cases of chronic pancreatitis including 13 cases of alcoholic pancreatitis. Hyperamylasemia in chronic pancreatitis is generally due to high pancreatic type isoamylase (P-amylase) activity in acute exacerbation, sometimes accompanied by a transient elevation in salivary type isoamylase (S-amylase). On remission, however, hyperamylasemia due to high S-amylase activity has been found. These were cases of advanced alcoholic pancreatitis, which exhibited a characteristic pattern of low serum P-amylase and high serum S-amylase activities while the clearance ratio (Cam/Ccr) was normal despite high S-amylase activity. It should be noted that hyperamylasemia in chronic pancreatitis may be caused by high S-amylase activity in addition to high P-amylase activity, especially in alcoholic pancreatitis.     

Cigarette smoking accelerates progression of alcoholic chronic pancreatitis

BACKGROUND: Smoking is a recognised risk factor for pancreatic cancer and has been associated with chronic pancreatitis and also with type II diabetes. AIMS: The aim of this study was to investigate the effect of tobacco on the age of diagnosis of pancreatitis and progression of disease, as measured by the appearance of calcification and diabetes. PATIENTS: We used data from a retrospective cohort of 934 patients with chronic alcoholic pancreatitis where information on smoking was available, who were diagnosed and followed in clinical centres in five countries. METHODS: We compared age at diagnosis of pancreatitis in smokers versus non-smokers, and used the Cox proportional hazards model to evaluate the effects of tobacco on the development of calcification and diabetes, after adjustment for age, sex, centre, and alcohol consumption. RESULTS: The diagnosis of pancreatitis was made, on average, 4.7 years earlier in smokers than in non-smokers (p = 0.001). Tobacco smoking increased significantly the risk of pancreatic calcifications (hazard ratio (HR) 4.9 (95% confidence interval (CI) 2.3-10.5) for smokers v non-smokers) and to a lesser extent the risk of diabetes (HR 2.3 (95% CI 1.2-4.2)) during the course of pancreatitis. CONCLUSIONS: In this study, tobacco smoking was associated with earlier diagnosis of chronic alcoholic pancreatitis and with the appearance of calcifications and diabetes, independent of alcohol consumption.     

Alcoholism and alcoholic organ damage and genetic polymorphisms of alcohol metabolizing enzymes in Chinese patients

It is still not clear why some alcoholic patients acquire certain organ-specific complications of alcoholism whereas other alcoholic patients acquire different ones. As we know the liver alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and cytochrome P4502E1 (P4502E1) are polymorphic at the ADH2, ADH3, and ALDH2 loci and the 5'-flanking region of the P4502E1. The aim of this study was to investigate the differences between Chinese alcoholic patients with cirrhosis and acute pancreatitis by studying the genetic polymorphisms of ADH2, ADH3, ALDH2, and P4502E1. Genotyping of ADH2, ADH3, ALDH2, and P4502E1 was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods on peripheral white blood cell DNA from 75 alcoholic cirrhotic patients, 48 acute alcoholic pancreatitis patients, 19 heavy drinkers without liver disease or pancreatitis, and 235 controls. The results showed that the frequencies of the alleles ADH2*1 and ALDH2*1 in the alcoholic cirrhotic patients were significantly higher than those in the nonalcoholic controls. In acute alcoholic pancreatitis patients, only the frequency of allele ALDH2*1, not ADH2*1 was significantly higher than in the nonalcoholic controls. The allele frequency of ADH2*1 in acute pancreatitis patients was significantly lower (P < .01) than in alcoholic cirrhotic patients. The daily amount of alcohol consumption was significantly lower in patients with acute pancreatitis than in patients with cirrhosis (P < .0005). The genotype distributions of P4502E1, detected by RsaI and PstI, were not different among alcoholic cirrhotic patients, alcoholic pancreatitis patients, heavy drinker, and nonalcoholic controls. In conclusion, ALDH2*1 is the most important alcohol metabolizing gene affecting predisposition to alcoholism whereas the ADH2*2 gene may influence susceptibility to acute alcoholic pancreatitis. The patients with alcohol-induced cirrhosis and with alcohol-induced acute pancreatitis are of two different subpopulations.(Hepatology 1997 Jan;25(1):112-7)     

Pancreatitis in a native American Indian population

We have studied pancreatitis in a population of Southwestern American Indians where gallstones are frequent, alcohol consumption is presumably high, but where smoking is an uncommon habit. Over a 5-year period, 131 cases of pancreatitis (65 males, 66 females) were observed: 66 (50%) were thought to be biliary pancreatitis, 54 cases (41%) alcoholic pancreatitis, and 5 cases (4%) were caused by injuries. In 6 cases (5%) no definite cause was found. Smoking appeared to be increased in male subjects with alcoholic pancreatitis when compared to subjects with alcoholic liver cirrhosis--a group with similar drinking habits. (Adjusted odds ratio = 12.5, p = 0.008). No such relationship was observed for females. Our findings suggest that in this population smoking may be an additional important risk factor for male subjects with alcoholic pancreatitis.     

Prevalence of Markers of Hepatotrophic Viruses in Alcoholics with Symptomatic Liver Cirrhosis or Pancreatitis

The reason why similar amounts of alcohol consumption cause different types of organ damage in alcoholics is obscure. Recent studies indicate that hepatitis B virus infection may influence the development of liver cirrhosis in alcoholics. We investigated the prevalence of markers of viruses known to cause hepatitis (HAV, HBV, EBV, CMV) in two groups of patients, one with alcoholic pancreatitis without known liver cirrhosis and one with alcoholic liver cirrhosis without known pancreatitis. We found signs of past infection with HAV and HBV more often in alcoholics with liver cirrhosis than in patients with alcoholic pancreatitis or in age-matched controls.