Pancreas Vol. 5 , No. 4, pp. 479483 8 1990 Raven Press, Ltd., New York
Chronic Pancreatitis in Mexico City Guillermo Robles-Diaz, "Florencia Vargas, Luis Uscanga, and Carlos Fernhdez-del Castillo Pancreas Clinic and the *Department of Gastroenterology, Instituto Nacional de la Nutricibn "Salvador Zubirbn," Mexico City,Mexico
Summary: The incidence, etiology, clinical characteristics, and long-term outcome of patients with chronic pancreatitis (CP) studied at the Instituto Nacional de la Nutricidn in a 1Zyear period were retrospectively analyzed. One hundred fifty cases were identified, with an overall incidence of 4.4 per 1,OOO hospital admissions and of 5.4 per 1,OOO in the last 6 years. In 68% of the cases, CP was secondary to alcoholism, in 29% it was idiopathic, and in the rest it was secondary to other causes. Overall, 74% of patients had pancreatic calcifications at time diagnosis was established, and 21% were asymptomatic regarding pain. Patients with idiopathic CP had an earlier age of onset than did patients with alcoholic CP, and in addition the former developed symptoms of diabetes or pancreatic exocrine insufficiency less frequently than alcoholic patients did (p < 0.05). The sex ratio was different in both groups, with a marked male predominance in alcoholic CP and an equal distribution in the idiopathic group. A 30% actuarial mortality was found in the first 10 years after the onset of the disease, which remained the same at 20 years with a tendency to better survival in nonalcoholic patients. Five patients developed pancreatic cancer throughout the study period. Key Words: Pancreatitis, chronic-Mexico City.
teristics and the long-term outcome of this group of patients.
The frequency, etiology, and clinical picture of chronic pancreatitis (CP) has wide geographical variations (1). Its incidence has increased significantly in the last years throughout the world (2). In Mexico, we have described the etiological and nutritional features of patients with CP (3), most of whom are alcoholic individuals with similar characteristics to those reported by other authors in temperate areas of the world. However, there are no epidemiological studies in our country. The aim of this study was to determine the incidence of CP in a tertiary care hospital in Mexico City during the last 12 years and to review some of the clinical charac~~~
PATIENTS AND METHODS The study was conducted at the Instituto Nacional de la Nutrici6n Salvador Zubiriin in Mexico City, which is a referral center for gastrointestinal disorders. We reviewed the discharge diagnosis lists of all patients admitted to our hospital between 1975 and 1987 (except 1981, when lists were incomplete) and recorded the number of admissions and the number of patients with acute and CP. Further analysis was made of the charts of all cases with CP. Criteria for diagnosis of CP included at least one of the following: (a) radiological evidence of pancreatic calcification, (b) abnormalities in the pancreatic duct by endoscopic retrograde cholangiopancreatography
~
Manuscript received August 8, 1989; revised manuscript accepted January 16, 1990. Address correspondence and reprint requests to Dr. G . Robles-Diaz at Department of Gastroenterology,Instituto Nacional de la Nutrici6n, Vasco de Quiroga 15, Tlalpan 14Oo0, Mexico D.F.. Mexico.
479
G.ROBLES-DIAZ ET AL.
480
(ERCP) and (c) histological findings of CP. Patients with CP, secondary to duct obstruction from cancer were excluded. All patients were seen by one or more of the authors. Specific data regarding age at onset, sex, etiology of CP, length of alcohol intake, and clinical characteristics such as pain, diarrhea, diabetes, and calcifications were recorded. The onset of the disease was determined by the age at which pain or chronic diarrhea related to pancreatic insufficiency was first experienced. Patients who were discharged alive were followed up in the outpatient clinic. Follow-up was defined as the period between diagnosis and date of death or last visit to the clinic. Development of pancreatic insufficiency, compliance with follow-up, and survival rates were determined by means of the actuarial method (4). Data from alcoholic and nonalcoholic patients were analyzed separately. Patients with nonalcoholic CP in whom no etiology was found were considered to have idiopathic CP. RESULTS
During the 12-year study period, the overall incidence of pancreatitis was 9 per 1,000 hospital admissions. However, this figure varied with time, and a significant increase in the incidence rate was found in recent years, as shown in Table 1 and Fig. 1. In the first study period (1975-1980), diagnosis of CP was mainly established with the demonstration of pancreatic calcifications in abdominal plain films (55 of 59). In the 91 patients of the second study period, diagnosis of CP was made as follows: by plain abdominal films in 56 patients, by ERCP in 17, by computed tomography scan in 12 and histologically in the remaining 6. The etiology, sex ratio, and mean age at onset are shown in Table 2. CP secondary to alcoholism was predominant. The percentage of alcoholic CP was similar in both the first (1975-1980) and the second (1982-1987) 6-year periods of study, 68 and 66%, respectively. The age at onset differed with etiology
20
I I975 , 7b h 7b
I
79
8b
I
1
1
,
81 d2 d3 84 85 d6 87
YEARS FIG. 1. Incidence of pancreatitis in a tertiary care hospital in Mexico City. The shaded areas represent 95% confidence limits.
(Fig. 2); in alcoholic persons a peak was found between 21 and 40 years, whereas the onset of idiopathic CP occurred at a younger age, showing a peak between 11 and 20 years. In the alcoholic group, the mean duration of alcoholism before the clinical onset of CP was 18.1 k 9.2 years. Nine patients had not complained of abdominal pain or diarrhea when the diagnosis of CP was established. They had been admitted to the hospital because of complications of diabetes mellitus (eight patients) or because of hyperparathyroidism (one patient). The etiology was alcoholism in five, hyperparathyroidism in one, and in three patients no etiologic factor was found. The clinical features at the onset of the disease (pain, diarrhea, or diabetes) did not differ between etiologic groups. At the time diagnosis was established, 111 patients (74%) had pancreatic calcifications (72 alcoholic and 39 nonalcoholic patients). In patients with abdominal pain at the onset of the disease, this symptom decreased significantly with TABLE 2. Etiology, sex ratio and mean age of onset of patients with chronic pancreatitis
TABLE 1. Incidence" of pancreatitis in a Mexican hospital population Acute pancreatitis
Chronic pancreatitis
Period (yr)
Incidence
95% CI*
Incidence
95% CI*
1975-1980 1982-1987
2.86 5.62
2.07-3.65 4.49-6.75
3.38 5.38
2.52-4.24 4.28-6.47
* Confidence interval. a
Per 1.OOO admissions.
Pancreas, Val. 5 , No. 4, 1990
Alcoholic Etiology Sex (M:F) Mean age (*I SD)(yr) Male Female
(n
=
loo)
24: 1
*
38.7 12.3 54.6 C 4.2
Idiopathic (n = 44)
Othersu (n = 6)
1.3:1
1:l
29.0 2 19.8 20.7 -t 9.9
35.0 & 23.6 23.0 k 12.1
a Hyperparathyroidism (n = 3 ) , hereditary (n = 2), obstructive (n = 1).
CHRONIC PANCREATITIS IN MEXICO CITY ALCOHOLIC h. 95
i
IDIOPATHIC n * 4 I
0-10
11-20
21-30
31-40
AGE
4144
51-60
61-10
I
481
‘“9
p--*
TI-00
(YEARS1
FIG. 2. Age of clinical onset of alcoholic and idiopathic chronic pancreatitis.
time, whereas symptoms related to pancreatic insufficiency such as diabetes mellitus and diarrhea increased (p < 0.01; x2 test) (Fig. 3). Thirty-one patients never had abdominal pain; 18 were alcoholic and 13 were nonalcoholic. Alcoholic patients without diabetes or diarrhea at the onset of the disease developed these complications earlier and more frequently than did nonalcoholic patients with idiopathic CP (p < 0.05, Wilcoxon test) (4) (Fig. 4). Forty-four patients were followed up for more than 4 years. Mean duration of follow-up was 4.2 years. By actuarial analysis, almost one-half of all cases had dropped out by the 4th year of the followup. There were no differences in the drop-out rate between alcoholic and nonalcoholic patients. We observed a 30% actuarial mortality in the first 10 years after the onset of the disease, which remained the same at 20 years with a tendency to better survival in nonalcoholic patients. Five patients (three with alcoholic and two with idiopathic CP) devel-
v q l , , 2 DIABETES@ DIIRRHEAB
4
6
8
,‘I
, 10
12
14
16
l8
20
Y E A R S
@ Number of patients at risk immediately prior to end of interval. FIG. 4. Development of diabetes mellitus and diarrhea in patients with alcoholic and idiopathic chronic pancreatitisthroughout their illness.
oped pancreatic cancer. Twenty-five patients died. Death was related to sepsis in 17 cases (predominantly pneumonia), pancreatic cancer in four, complications of diabetes mellitus in three, and in one case the cause of death was not dearly established. DISCUSSION
The frequency of pancreatitis in our hospital has increased significantly in the past few years. An increasing incidence of CP has been common throughout the world. We believe that the higher frequency in our second study period is probably due to an increased awareness of the disease, changes in practices of patient referral, and a better availability of diagnostic methods. The last possibility is supported by the fact that in the second study period more patients were diagnosed by methods other than the demonstration of calculi in plain abdominal films. Another interesting finding is that although alcohol consumption has increased in Mexico (9,the proportion of alcoholic CP has remained constant. The overall incidence of CP in our study was of 4.4 per 1,000 hospital admissions, an incidence that is similar to that found in other studies (6,7).
NABOOMINAL PAIN
%
DIARRHEA
‘ 80 O01
ONSET
ADMISSION
LAST CONSULT
FIG. 3. Clinical manifestations of chronic pancreatitis at onset, hospital admission, and last consult.
Pancreas, Vol. 5 , No.4, 1990
482
G . ROBLES-DfAZ ET AL.
Alcohol was the predominant etiologic factor (67%), followed by the group of patients with CP in whom etiology could not be determined (idiopathic CP). These relative percentages of different forms of pancreatitis are similar to those reported by Worning in 1984 in his review of the literature (2). Differences in sex and age distribution according to the etiology of pancreatitis were consistent with our previous findings (3) and with data from Brazil (8), i.e., patients with alcoholic CP were predominantly male, whereas in young patients with nonalcoholic CP the ma1e:female ratio was approximately equal. We did not find any cases of CP associated with malnutrition even though 20% of our cases with idiopathic CP were under 10 years of age at the time of diagnosis. In alcoholic CP the length of alcohol consumption before the development of CP was similar to that reported by others (8-10); however, it was longer than in our previous study (3). This difference may be due to changes in the quantity of alcohol consumed and in the quality of the diet, which are factors that may modify the time necessary to develop a pancreatic lesion (10); however, these factors were not evaluated in the present study. Of our total of 150 patients with CP, 31 (21%) can be considered asymptomatic because pain was not present at any time during their illness. Although pancreatic pain has been described more often in alcoholic CP and less frequently in the nonalcoholic CP of tropical countries (9,11,12), we did not find this difference, and asymptomatic cases were distributed equally between alcoholic and nonalcoholic CP. The diagnosis of CP was incidental in nine patients (6%) because neither abdominal pain nor diarrhea were present. We therefore consider that CP should be investigated in any chronic alcoholic patient with diabetes or in patients with hyperparathyroidism because, in our experience, 10% of the latter have an associated CP (13). In our study, approximately three-fourths of the patients had radiologically evident pancreatic calcification. The incidence of pancreatic calcifications reported in the literature varies from 25 to 85%, which probably reflects the different diagnostic criteria used by different authors in the evaluation of CP at the time of diagnosis (8,9,12,14,15). We did not find differences in the frequency of calcifications according to the etiology of CP, as has been suggested previously (9,12). The disappearance of pancreatic pain and the dePancreas, Vol. 5 , No. 4, 1990
velopment of pancreatic insufficiency as observed in this study are part of the natural history of CP (9,11,12,14,15). Five of our patients developed pancreatic carcinoma, which is considered by some groups as a complication of CP that occurs with variable frequency (8,9,12). Although no differences in clinical presentation, pancreatic calcifications, and length of follow-up could be found between alcoholic and idiopathic CP, we did find a difference in the age at onset (earlier ‘in nonalcoholic patients), as well as in the sex ratio (marked male predominance in the alcoholic group and equal distribution in the nonalcoholic patients). Also, in agreement with the study of Amman et al. (15), we found that patients with nonalcoholic CP have a delayed progression to exocrine and endocrine insufficiency as compared with those with alcoholic CP. In conclusion, CP in Mexico City seems to have clinical characteristics that are similar to CP described in other temperate regions of the world. We have not yet found cases of tropical pancreatitis, but further studies in the rural parts of our country will disclose whether this variety of the disease exists in Mexico, and whether the incidence and clinical features of CP are the same as in the urban areas. Acknowledgment: We thank
Dr. Guadalupe Garcia-
Tsao for reviewing the manuscript.
REFERENCES 1 . Sarles H. Etiopathogenesis and definition of chronic pancreatitis. Dig Dis Sci 1986;31:91-1078.
2. Worning H. Chronic pancreatitis. Epidemiology, etiology and clinical picture 1946-1984. In: Gyr KE, Singer MV, Sarles H, eds. Pancreatitis. Concepts and classification. Amsterdam; Excerpta Medica, 1984:347-50. (Excerpta Medica international congress series 642). 3. Uscanga L, Robles-Diaz G, Sarles H. Nutritional data and etiology of chronic pancreatitisin Mexico. Dig Dis Sci 1985; 3O:llO-3. 4. Coldman AJ, Elwood JM. Examining survival data. Can Med Assoc J 1979;121:1065-71. 5. Molina Pifieiro V, Berruecos VLA, Shnchez Medal L. El alcoholismo en Mkxico. 11: Aspectos sociales, culturales y econbmicos. Fundacibn de investigaciones sociales. Mtxico, D.F.: A.C. Impresiones Modernas S.A., 1985. 6. Marks IN, Girwood AH, Bornam PC, Feretis C. The prevalence and etiology of pancreatitis in Cape Town. In: Gyr KE, Singer MV, Sarles H, eds. Pancreatitis. Concepts and classification. Amsterdam: Excerpta Medica, 1984:3454. (Excerpta Medica international congress series 642). 7. Durbec JP, Sarles H. Epidemiology of chronic pancreatitis. Alcohol and dietary habits. In: Cyr KE, Singer MV, Sarles H, eds. Pancreatitis. Concepts and classification. Amster-
CHRONIC PANCREATITIS IN MEXICO CITY
8. 9.
10.
11.
dam: Excerpta Medica, 1984:351-3. (Excerpta Medica international congress series 642). Dani R, Penna FJ, Nogueira CED. Etiology of chronic calcifying pancreatitis in Brazil: a report of 329 consecutive cases. Int J Pancreatol 1986;1:399406. Sarles H, Sahel J, Staub JL, Bourry J, Laugier R. Pancreatites chroniques. In: Sarles H, Howat HT, eds. Le pancreas exocrine. Paris: Flammarion Medecine-Sciences, 1980:385-420. Durbec JP, Sarles H. Multicentric survey of etiology of pancreatic disease. Relationship between the relative risk of developing chronic pancreatitis and alcohol, protein and lipid consumption. Digestion 1978;18:337-50. Kondo T, Hayakawa T, Noda A, et al. Follow-up study of chronic pancreatitis. Gastroenterol Jpn. 1981;16:4&53.
483
12. Bank S. Chronic pancreatitis: clinical features and medical management. Am J Gastroenterol 1986;81:153-67. 13. Fernhdez del Castillo C, CanM-Gonzhlez G, Robles-Diaz G, Campuzano M. Hiperparatiroidismo primario y pancreatitis. Evidencia de una verdadera asociaci6n. Rev Gastroenterol Mex 1988;53:61-6. 14. Bernardes P, Belghiti J, Athouel M, Mallard0 N, Breil P, Fekete F. Histoire naturelle de la pancratite chronique: etude de 120 cases. Gastroenterol Clin Biol 1983;7:&13. 15. Amman RW, Buchier H, Muench R, Freiburghavs AW, Siegenthaler W. Differences in the natural history of idiopathic (nonalcoholic) and alcoholic chronic pancreatitis. A comparative long-term study of 287 patients. Pancreas 1987;2:368-77.
Pancreas, Vol. 5, No. 4, 1990
Chronic Pancreatitis in Mexico City Guillermo Robles-Diaz, "Florencia Vargas, Luis Uscanga, and Carlos Fernhdez-del Castillo Pancreas Clinic and the *Department of Gastroenterology, Instituto Nacional de la Nutricibn "Salvador Zubirbn," Mexico City,Mexico
Summary: The incidence, etiology, clinical characteristics, and long-term outcome of patients with chronic pancreatitis (CP) studied at the Instituto Nacional de la Nutricidn in a 1Zyear period were retrospectively analyzed. One hundred fifty cases were identified, with an overall incidence of 4.4 per 1,OOO hospital admissions and of 5.4 per 1,OOO in the last 6 years. In 68% of the cases, CP was secondary to alcoholism, in 29% it was idiopathic, and in the rest it was secondary to other causes. Overall, 74% of patients had pancreatic calcifications at time diagnosis was established, and 21% were asymptomatic regarding pain. Patients with idiopathic CP had an earlier age of onset than did patients with alcoholic CP, and in addition the former developed symptoms of diabetes or pancreatic exocrine insufficiency less frequently than alcoholic patients did (p < 0.05). The sex ratio was different in both groups, with a marked male predominance in alcoholic CP and an equal distribution in the idiopathic group. A 30% actuarial mortality was found in the first 10 years after the onset of the disease, which remained the same at 20 years with a tendency to better survival in nonalcoholic patients. Five patients developed pancreatic cancer throughout the study period. Key Words: Pancreatitis, chronic-Mexico City.
teristics and the long-term outcome of this group of patients.
The frequency, etiology, and clinical picture of chronic pancreatitis (CP) has wide geographical variations (1). Its incidence has increased significantly in the last years throughout the world (2). In Mexico, we have described the etiological and nutritional features of patients with CP (3), most of whom are alcoholic individuals with similar characteristics to those reported by other authors in temperate areas of the world. However, there are no epidemiological studies in our country. The aim of this study was to determine the incidence of CP in a tertiary care hospital in Mexico City during the last 12 years and to review some of the clinical charac~~~
PATIENTS AND METHODS The study was conducted at the Instituto Nacional de la Nutrici6n Salvador Zubiriin in Mexico City, which is a referral center for gastrointestinal disorders. We reviewed the discharge diagnosis lists of all patients admitted to our hospital between 1975 and 1987 (except 1981, when lists were incomplete) and recorded the number of admissions and the number of patients with acute and CP. Further analysis was made of the charts of all cases with CP. Criteria for diagnosis of CP included at least one of the following: (a) radiological evidence of pancreatic calcification, (b) abnormalities in the pancreatic duct by endoscopic retrograde cholangiopancreatography
~
Manuscript received August 8, 1989; revised manuscript accepted January 16, 1990. Address correspondence and reprint requests to Dr. G . Robles-Diaz at Department of Gastroenterology,Instituto Nacional de la Nutrici6n, Vasco de Quiroga 15, Tlalpan 14Oo0, Mexico D.F.. Mexico.
479
G.ROBLES-DIAZ ET AL.
480
(ERCP) and (c) histological findings of CP. Patients with CP, secondary to duct obstruction from cancer were excluded. All patients were seen by one or more of the authors. Specific data regarding age at onset, sex, etiology of CP, length of alcohol intake, and clinical characteristics such as pain, diarrhea, diabetes, and calcifications were recorded. The onset of the disease was determined by the age at which pain or chronic diarrhea related to pancreatic insufficiency was first experienced. Patients who were discharged alive were followed up in the outpatient clinic. Follow-up was defined as the period between diagnosis and date of death or last visit to the clinic. Development of pancreatic insufficiency, compliance with follow-up, and survival rates were determined by means of the actuarial method (4). Data from alcoholic and nonalcoholic patients were analyzed separately. Patients with nonalcoholic CP in whom no etiology was found were considered to have idiopathic CP. RESULTS
During the 12-year study period, the overall incidence of pancreatitis was 9 per 1,000 hospital admissions. However, this figure varied with time, and a significant increase in the incidence rate was found in recent years, as shown in Table 1 and Fig. 1. In the first study period (1975-1980), diagnosis of CP was mainly established with the demonstration of pancreatic calcifications in abdominal plain films (55 of 59). In the 91 patients of the second study period, diagnosis of CP was made as follows: by plain abdominal films in 56 patients, by ERCP in 17, by computed tomography scan in 12 and histologically in the remaining 6. The etiology, sex ratio, and mean age at onset are shown in Table 2. CP secondary to alcoholism was predominant. The percentage of alcoholic CP was similar in both the first (1975-1980) and the second (1982-1987) 6-year periods of study, 68 and 66%, respectively. The age at onset differed with etiology
20
I I975 , 7b h 7b
I
79
8b
I
1
1
,
81 d2 d3 84 85 d6 87
YEARS FIG. 1. Incidence of pancreatitis in a tertiary care hospital in Mexico City. The shaded areas represent 95% confidence limits.
(Fig. 2); in alcoholic persons a peak was found between 21 and 40 years, whereas the onset of idiopathic CP occurred at a younger age, showing a peak between 11 and 20 years. In the alcoholic group, the mean duration of alcoholism before the clinical onset of CP was 18.1 k 9.2 years. Nine patients had not complained of abdominal pain or diarrhea when the diagnosis of CP was established. They had been admitted to the hospital because of complications of diabetes mellitus (eight patients) or because of hyperparathyroidism (one patient). The etiology was alcoholism in five, hyperparathyroidism in one, and in three patients no etiologic factor was found. The clinical features at the onset of the disease (pain, diarrhea, or diabetes) did not differ between etiologic groups. At the time diagnosis was established, 111 patients (74%) had pancreatic calcifications (72 alcoholic and 39 nonalcoholic patients). In patients with abdominal pain at the onset of the disease, this symptom decreased significantly with TABLE 2. Etiology, sex ratio and mean age of onset of patients with chronic pancreatitis
TABLE 1. Incidence" of pancreatitis in a Mexican hospital population Acute pancreatitis
Chronic pancreatitis
Period (yr)
Incidence
95% CI*
Incidence
95% CI*
1975-1980 1982-1987
2.86 5.62
2.07-3.65 4.49-6.75
3.38 5.38
2.52-4.24 4.28-6.47
* Confidence interval. a
Per 1.OOO admissions.
Pancreas, Val. 5 , No. 4, 1990
Alcoholic Etiology Sex (M:F) Mean age (*I SD)(yr) Male Female
(n
=
loo)
24: 1
*
38.7 12.3 54.6 C 4.2
Idiopathic (n = 44)
Othersu (n = 6)
1.3:1
1:l
29.0 2 19.8 20.7 -t 9.9
35.0 & 23.6 23.0 k 12.1
a Hyperparathyroidism (n = 3 ) , hereditary (n = 2), obstructive (n = 1).
CHRONIC PANCREATITIS IN MEXICO CITY ALCOHOLIC h. 95
i
IDIOPATHIC n * 4 I
0-10
11-20
21-30
31-40
AGE
4144
51-60
61-10
I
481
‘“9
p--*
TI-00
(YEARS1
FIG. 2. Age of clinical onset of alcoholic and idiopathic chronic pancreatitis.
time, whereas symptoms related to pancreatic insufficiency such as diabetes mellitus and diarrhea increased (p < 0.01; x2 test) (Fig. 3). Thirty-one patients never had abdominal pain; 18 were alcoholic and 13 were nonalcoholic. Alcoholic patients without diabetes or diarrhea at the onset of the disease developed these complications earlier and more frequently than did nonalcoholic patients with idiopathic CP (p < 0.05, Wilcoxon test) (4) (Fig. 4). Forty-four patients were followed up for more than 4 years. Mean duration of follow-up was 4.2 years. By actuarial analysis, almost one-half of all cases had dropped out by the 4th year of the followup. There were no differences in the drop-out rate between alcoholic and nonalcoholic patients. We observed a 30% actuarial mortality in the first 10 years after the onset of the disease, which remained the same at 20 years with a tendency to better survival in nonalcoholic patients. Five patients (three with alcoholic and two with idiopathic CP) devel-
v q l , , 2 DIABETES@ DIIRRHEAB
4
6
8
,‘I
, 10
12
14
16
l8
20
Y E A R S
@ Number of patients at risk immediately prior to end of interval. FIG. 4. Development of diabetes mellitus and diarrhea in patients with alcoholic and idiopathic chronic pancreatitisthroughout their illness.
oped pancreatic cancer. Twenty-five patients died. Death was related to sepsis in 17 cases (predominantly pneumonia), pancreatic cancer in four, complications of diabetes mellitus in three, and in one case the cause of death was not dearly established. DISCUSSION
The frequency of pancreatitis in our hospital has increased significantly in the past few years. An increasing incidence of CP has been common throughout the world. We believe that the higher frequency in our second study period is probably due to an increased awareness of the disease, changes in practices of patient referral, and a better availability of diagnostic methods. The last possibility is supported by the fact that in the second study period more patients were diagnosed by methods other than the demonstration of calculi in plain abdominal films. Another interesting finding is that although alcohol consumption has increased in Mexico (9,the proportion of alcoholic CP has remained constant. The overall incidence of CP in our study was of 4.4 per 1,000 hospital admissions, an incidence that is similar to that found in other studies (6,7).
NABOOMINAL PAIN
%
DIARRHEA
‘ 80 O01
ONSET
ADMISSION
LAST CONSULT
FIG. 3. Clinical manifestations of chronic pancreatitis at onset, hospital admission, and last consult.
Pancreas, Vol. 5 , No.4, 1990
482
G . ROBLES-DfAZ ET AL.
Alcohol was the predominant etiologic factor (67%), followed by the group of patients with CP in whom etiology could not be determined (idiopathic CP). These relative percentages of different forms of pancreatitis are similar to those reported by Worning in 1984 in his review of the literature (2). Differences in sex and age distribution according to the etiology of pancreatitis were consistent with our previous findings (3) and with data from Brazil (8), i.e., patients with alcoholic CP were predominantly male, whereas in young patients with nonalcoholic CP the ma1e:female ratio was approximately equal. We did not find any cases of CP associated with malnutrition even though 20% of our cases with idiopathic CP were under 10 years of age at the time of diagnosis. In alcoholic CP the length of alcohol consumption before the development of CP was similar to that reported by others (8-10); however, it was longer than in our previous study (3). This difference may be due to changes in the quantity of alcohol consumed and in the quality of the diet, which are factors that may modify the time necessary to develop a pancreatic lesion (10); however, these factors were not evaluated in the present study. Of our total of 150 patients with CP, 31 (21%) can be considered asymptomatic because pain was not present at any time during their illness. Although pancreatic pain has been described more often in alcoholic CP and less frequently in the nonalcoholic CP of tropical countries (9,11,12), we did not find this difference, and asymptomatic cases were distributed equally between alcoholic and nonalcoholic CP. The diagnosis of CP was incidental in nine patients (6%) because neither abdominal pain nor diarrhea were present. We therefore consider that CP should be investigated in any chronic alcoholic patient with diabetes or in patients with hyperparathyroidism because, in our experience, 10% of the latter have an associated CP (13). In our study, approximately three-fourths of the patients had radiologically evident pancreatic calcification. The incidence of pancreatic calcifications reported in the literature varies from 25 to 85%, which probably reflects the different diagnostic criteria used by different authors in the evaluation of CP at the time of diagnosis (8,9,12,14,15). We did not find differences in the frequency of calcifications according to the etiology of CP, as has been suggested previously (9,12). The disappearance of pancreatic pain and the dePancreas, Vol. 5 , No. 4, 1990
velopment of pancreatic insufficiency as observed in this study are part of the natural history of CP (9,11,12,14,15). Five of our patients developed pancreatic carcinoma, which is considered by some groups as a complication of CP that occurs with variable frequency (8,9,12). Although no differences in clinical presentation, pancreatic calcifications, and length of follow-up could be found between alcoholic and idiopathic CP, we did find a difference in the age at onset (earlier ‘in nonalcoholic patients), as well as in the sex ratio (marked male predominance in the alcoholic group and equal distribution in the nonalcoholic patients). Also, in agreement with the study of Amman et al. (15), we found that patients with nonalcoholic CP have a delayed progression to exocrine and endocrine insufficiency as compared with those with alcoholic CP. In conclusion, CP in Mexico City seems to have clinical characteristics that are similar to CP described in other temperate regions of the world. We have not yet found cases of tropical pancreatitis, but further studies in the rural parts of our country will disclose whether this variety of the disease exists in Mexico, and whether the incidence and clinical features of CP are the same as in the urban areas. Acknowledgment: We thank
Dr. Guadalupe Garcia-
Tsao for reviewing the manuscript.
REFERENCES 1 . Sarles H. Etiopathogenesis and definition of chronic pancreatitis. Dig Dis Sci 1986;31:91-1078.
2. Worning H. Chronic pancreatitis. Epidemiology, etiology and clinical picture 1946-1984. In: Gyr KE, Singer MV, Sarles H, eds. Pancreatitis. Concepts and classification. Amsterdam; Excerpta Medica, 1984:347-50. (Excerpta Medica international congress series 642). 3. Uscanga L, Robles-Diaz G, Sarles H. Nutritional data and etiology of chronic pancreatitisin Mexico. Dig Dis Sci 1985; 3O:llO-3. 4. Coldman AJ, Elwood JM. Examining survival data. Can Med Assoc J 1979;121:1065-71. 5. Molina Pifieiro V, Berruecos VLA, Shnchez Medal L. El alcoholismo en Mkxico. 11: Aspectos sociales, culturales y econbmicos. Fundacibn de investigaciones sociales. Mtxico, D.F.: A.C. Impresiones Modernas S.A., 1985. 6. Marks IN, Girwood AH, Bornam PC, Feretis C. The prevalence and etiology of pancreatitis in Cape Town. In: Gyr KE, Singer MV, Sarles H, eds. Pancreatitis. Concepts and classification. Amsterdam: Excerpta Medica, 1984:3454. (Excerpta Medica international congress series 642). 7. Durbec JP, Sarles H. Epidemiology of chronic pancreatitis. Alcohol and dietary habits. In: Cyr KE, Singer MV, Sarles H, eds. Pancreatitis. Concepts and classification. Amster-
CHRONIC PANCREATITIS IN MEXICO CITY
8. 9.
10.
11.
dam: Excerpta Medica, 1984:351-3. (Excerpta Medica international congress series 642). Dani R, Penna FJ, Nogueira CED. Etiology of chronic calcifying pancreatitis in Brazil: a report of 329 consecutive cases. Int J Pancreatol 1986;1:399406. Sarles H, Sahel J, Staub JL, Bourry J, Laugier R. Pancreatites chroniques. In: Sarles H, Howat HT, eds. Le pancreas exocrine. Paris: Flammarion Medecine-Sciences, 1980:385-420. Durbec JP, Sarles H. Multicentric survey of etiology of pancreatic disease. Relationship between the relative risk of developing chronic pancreatitis and alcohol, protein and lipid consumption. Digestion 1978;18:337-50. Kondo T, Hayakawa T, Noda A, et al. Follow-up study of chronic pancreatitis. Gastroenterol Jpn. 1981;16:4&53.
483
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