Robert |.
Sjoberg, MD
Pancreatic Diabetes Mellitus
Diabetes mellitus caused by pancreatic exocrine disease
is a unique clinical and metabolic form of diabetes. The
diagnosis of pancreatic diabetes caused by chronic
pancreatitis may be elusive because it is occasionally
painless and often not accompanied by clinical
malabsorption until after hyperglycemia occurs. Diabetic
patients with pancreatic calcification or clinically
demonstrable pancreatic exocrine dysfunction will
manifest the unique aspects of pancreatic diabetes
described herein. Like other forms of diabetes, the
primary hormonal abnormality in pancreatic diabetes is
decreased insulin secretion. Patients with this disorder
are unique in that they have low glucagon levels that
respond abnormally to several physiological stimuli,
blunted epinephrine responses to insulin-induced
hypoglycemia, and malabsorption. In addition, they
often have concomitant alcohol abuse with hepatic
disease and poor nutrition. These characteristics result
in increased levels of circulating gluconeogenic amino
acids, decreased insulin requirements, a resistance to
ketosis, low cholesterol levels, an increased risk of
hypoglycemia while on insulin therapy, and the clinical
impression of brittle diabetes. Retinopathy occurs at a
rate equal to that of insulin-dependent diabetes but
may be less severe in degree. Other complications of
pancreatic diabetes have been less well studied but may
be expected to be seen more frequently as these
patients survive longer. The characteristics of pancreatic
diabetes suggest that a conservative approach be taken
in regard to intensive insulin therapy and tight blood
glucose control. Diabetes Care 12:715-24, 1989
From the Endocrine Service, Department of Medicine, Fitzsimons Army Medical
Center, Aurora, Colorado.
Address correspondence and reprint requests to Gerald S. Kidd, MD, Endo-
crine Service, Department of Medicine, Fitzsimons Army Medical Center, Au-
rora, CO 80045-5001.
The opinions and assertions contained herein are the private views of the
authors and are not to be construed as official or reflecting the views of the
Department of the Army or the Department of Defense.
DIABETES CARE, VOL. 12, NO. 10, NOVEMBER/DECEMBER 1989
Gerald S. Kidd, MD
lthough the exocrine and endocrine cells of the
A
pancreas are generally thought to function in-
dependently of each other, they are anatomi-
cally closely related. This anatomic relationship
allows pancreatic islet cell dysfunction to be associated
with and/or caused by pancreatic exocrine disease. The
pancreatic exocrine syndromes known to be associated
with so-called pancreatic diabetes include acute and
chronic pancreatitis, postpancreatectomy syndrome,
cystic fibrosis, tropical pancreatic diabetes, and pan-
creatic carcinoma. This association is historically im-
portant because the role of the pancreas in causing di-
abetes mellitus was initially postulated 200 yr ago in a
report of a patient with diabetes who had pancreatic
calcification (1). Pancreatic diabetes continues to be im-
portant because it is unique clinically, hormonally, and
metabolically, prompting the National Diabetes Data
Group to classify it as a distinct form of diabetes (2).
This review summarizes the clinical manifestations of
pancreatic diabetes, with particular emphasis on pan-
creatitis and postpancreatectomy syndrome. Diabetes
associated with cystic fibrosis and tropical pancreatic
diabetes is discussed briefly in comparison with other
forms of pancreatic diabetes, but it has recently been
reviewed in greater detail (3-5).
FREQUENCY AND DIAGNOSIS
Mild hyperglycemia may occur transiently in association
with acute pancreatitis up to 50% of the time and has
been used as a marker for the severity of pancreatitis
(6,7). Long-term follow-up of patients after a single ep-
isode of acute pancreatitis indicated that they had an
increased frequency of abnormal glucose tolerance
compared with an age-matched population (8). Such
715
PANCREATIC DIABETES MELLITUS
patients may have chronic painless pancreatic inflam-
mation in addition to their acute painful episode (6). A
distant history of acute pancreatitis may, however, be
etiologically important in any patient with diabetes.
The prevalence of abnormal glucose tolerance in pa-
tients with chronic pancreatitis was 60-70% and of overt
diabetes was 30-40% (6,9,10). Serial testing of individ-
ual patients with chronic pancreatitis demonstrated a
progressive deterioration of glucose tolerance over
time (6).
The presence of pancreatic calcification increased the
occurrence of endocrine dysfunction, resulting in a 70%
prevalence of diabetes (6). Thirty-three percent of pa-
tients with chronic pancreatitis and diabetes had pan-
creatic calcification (6). Pancreatic calcification was
present in 20% of patients with chronic pancreatitis
but was more common in alcohol-induced (30%) and
tropical (75%) pancreatitis (4-6).
Chronic pancreatitis is painless 5-10% of the time,
and steatorrhea is a late manifestation of chronic pan-
creatitis, often occurring after the onset of diabetes
(6,9-11). This implies that the diagnosis of diabetes as
a result of chronic painless pancreatitis can be elusive.
Approximately 30% of patients with diabetes and cal-
cific pancreatitis in one large series were diagnosed by
abdominal roentgenography of patients previously thought
to have genetic diabetes (6). The data reported below
regarding the clinical and hormonal status of patients
with chronic pancreatitis were derived from patients with
either pancreatic calcification on plain roentgenography
or well-documented recurrent episodes of pancreatitis
associated with pancreatic exocrine insufficiency and
usually a known etiology for chronic pancreatitis. With
these points in mind, proposals regarding who in the
diabetic population should be screened for and practical
clinical criteria for the diagnosis of pancreatic diabetes
are given in Table 1. Although these criteria may not be
inclusive, we feel that patients meeting these criteria will
manifest the unique aspects of pancreatic diabetes out-
lined below.
Little is known regarding the cause of chronic pan-
creatitis and any effect this may have on the diabetic
syndrome. Most patients studied have had alcohol abuse
as the cause for their pancreatic disease. This may sim-
ply reflect the most common etiology of chronic pan-
TABLE 1
Clues and criteria for diagnosis of pancreatic diabetes
Clues
Suspect pancreatic diabetes in any diabetic patient with:
One or more documented episodes of acute pancreatitis
A known historical cause for chronic pancreatitis
Previous pancreatic surgery
Criteria
Patients have pancreatic diabetes if:
Pancreatic calcification is present on plain roentgenography
Steatorrhea partially reversible with pancreatic enzyme therapy
is demonstrable
716
creatitis, but it has also been suggested that alcohol-
induced pancreatitis results in a higher prevalence of
diabetes than other etiologies of pancreatitis (6,9,11).
Cystic fibrosis results in diabetes less frequently than
chronic pancreatitis, its prevalence being 7-15% of cys-
tic fibrosis patients >18 yr of age (3). Tropical pan-
creatic diabetes differs from other causes of pancreatic
diabetes in its higher insulin requirements (4,5). Total
pancreatectomy generally results in a more severe de-
gree of endocrine dysfunction than chronic pancreatitis,
but resection of <90% of the pancreas rarely results in
diabetes unless the remaining pancreas is also damaged.
INSULIN AND GLUCAGON SECRETION
The histological appearance of the pancreas in chronic
pancreatitis and cystic fibrosis has been described as a
sea of fibrosis with islet cell neoformation, crowding,
and preservation (3,11). Despite this apparent lack of
islet cell damage, abnormal insulin secretion has con-
sistently been demonstrated in these patients (3). A
blunted insulin response to intravenous and oral glucose
occurred in 70 and 18%, respectively, of patients stud-
ied 7-48 mo after a single episode of acute pancreatitis
(8,12). Chronic pancreatitis frequently results in a blunted
insulin or C-peptide response to glucose given orally
and intravenously and to intravenous alanine, arginine,
glucagon, and tolbutamide (13-20; Fig. 1). Blunted in-
sulin or C-peptide secretion has also been positively cor-
related with exocrine pancreatic dysfunction and ab-
normal pancreatic structure, as determined by endoscopic
retrograde pancreatography (15-1 7,21). Because fat ab-
sorption and glucose homeostasis both become abnor-
mal after loss of at least 90% of pancreatic exocrine and
endocrine function, respectively, this correlation ex-
plains the observation that clinical steatorrhea often oc-
curs coincident with or subsequent to the onset of hy-
perglycemia.
Abnormal glucagon secretion also occurs in patients
with pancreatitis and cystic fibrosis (3). Hyperglucago-
nemia without hypoinsulinemia was the most consistent
hormonal pattern seen in acute pancreatitis, suggesting
that elevated glucagon release is the major pathogenetic
factor in causing the transient hyperglycemia of acute
pancreatitis (19). The mild degree of hyperglycemia in
acute pancreatitis is consistent with this theory. Chronic
pancreatitis resulted in normal basal glucagon levels,
but blunted glucagon responses to arginine, alanine, and
insulin-induced hypoglycemia were often demonstrable
(19,20,22-24).
In view of the histological lack of islet cell damage in
chronic pancreatitis, the causes for abnormalities of in-
sulin and glucagon secretion are unclear. Immunocy-
tochemical and ultrastructural studies of islets from a
small number of patients with chronic pancreatitis or
cystic fibrosis and diabetes revealed a mild decrease in
the percentage of P-cells and a mild increase in the
percentage of a-cells within each islet, but it is unclear
DIABETES CARE, VOL. 12, NO. 10, NOVEMBER/DECEMBER 1989
 R.J. SJOBERG AND G.S. KIDD

1050 subject of interest in terms of determining whether there

is an extrapancreatic source of physiologically active
(3500 Mr) glucagon in humans. Barnes and Bloom (27)
900
showed that immunoreactive glucagon was not detect-
able either basally or after arginine infusion postpan-
^ 750 createctomy (Fig. 2). Other studies, however, demon-
strated that pancreatectomy resulted in normal basal
glucagon levels that often increased after oral glucose,
<O ^ 600
were not changed by somatostatin or insulin-induced
^5 hypoglycemia, and occasionally increased after arginine
l l 450 infusion (28-30). At least 80% of the immunoreactive
glucagon detected in pancreatectomized patients has an
5* 300
M r >40,000, but low levels of 3500-Mr glucagon were
occasionally detectable in such patients (31-33). The
paradoxical increase in immunoreactive glucagon after
150 oral glucose ingestion was also caused by an increase

tl-
+ 80
250r
+ 60
200
+ 40
150
+ 20
100

30 31 35 40 60
-\ -1
MINUTES -20
FIG. 1. Serum insulin and plasma glucose responses of 16 140rB
patients with calcific pancreatitis (solid lines; 6 of whom
had frank diabetes) and 10 healthy control subjects (dashed
lines) to oral glucose (75 g) given at time 0 followed 30 120
min later by 500 mg tolbutamide i.v. and 1 mg glucagon
i.v. Values are means SE. (Reprinted from Joffe et al.
100
[14] with permission from Lancet. Copyright 1968.)

whether there was an absolute change in the total num-

ber of P- or a-cells (3,25). Given the dramatic decrease
I 8 0

in the number of (3-cells necessary to induce insulin- 60

dependent diabetes mellitus (IDDM), the abnormal glu-
cagon secretion typical of patients with chronic pan-
creatitis, and the correlation between exocrine and en-
docrine dysfunction in patients with chronic pancreatitis,
the hormonal abnormalities appear to be caused by pan- 3 20
creatic exocrine disease rather than by direct islet cell
damage. Impaired islet vascularity as a result of exocrine 0 L 5- -S--<SSS- 5--*--5- 5 5
tissue fibrosis may best explain this phenomenon, but
altered secretion of gut-derived insulin-releasing pep- 15 10 20 30 40 60
tides (incretins) due to malabsorption may also contrib- MINUTES
ute to abnormal insulin secretion. In this regard, treat-
ment of chronic pancreatitis patients with pancreatic FIG. 2. Plasma glucose and glucagon in 5 pancreatecto-
enzyme therapy augmented their blunted insulin and mized patients (O) and 5 patients with insulin-dependent
diabetes () in response to intravenous arginine (500
gastric inhibitory polypeptide (CIP) responses to a mixed
mg/kg over 30 min). Values are means SE. (Reprinted
meal (26). from Barnes and Bloom [27] with permission from Lancet.
Glucagon secretion postpancreatectomy has been a Copyright 1976.)

DIABETES CARE, VOL. 12, NO. 10, NOVEMBER/DECEMBER 1989 717

PANCREATIC DIABETES MELLITUS
in a 9000- to 15,000-Mr fraction of immunoreactive glu-
cagon (34).
The source of the low levels of 3500-Mr glucagon in
pancreatectomized humans is unclear. All pancreatec-
tomized patients studied have also had a partial duo-
denectomy and often an antrectomy, ruling out these
tissues as potential glucagon sources. The possibility of
peripheral conversion of gut-derived high-molecular-
weight glucagon to 35OO-Mr glucagon must also be con-
sidered (35).
AMINO ACID METABOLISM
Plasma amino acids, especially those that serve as
substrates for gluconeogenesis, were elevated postpan-
createctomy compared with normal or IDDM levels
(31,32,36-39). Maintenance of normoglycemia for 24 h
with a glucose-controlled insulin infusion system did not
decrease these gluconeogenic precursors to normal as
it did in IDDM (38). A physiological glucagon infusion
did, however, normalize amino acid levels, suggesting
0-
i i
-1 0 4 8 12
TIME (hours)
FIG. 3. Changes in blood concentrations of 3-hydroxybutyrate and glucose in 6 patients with insulin-dependent dia-
betes () and 4 pancreatectomized patients (O) after withdrawal of insulin. Values are means SE. *P < .05; **P <
.02. (Reprinted from Barnes et al. [40] with permission from N Engl / Med. Copyright 1977.)
718
that hypoglucagonemia mediates hyperaminoacidemia
(32,37,39).
FATTY ACID AND KETONE BODY METABOLISM
Studies concerning fatty acid metabolism postpancrea-
tectomy helped clarify the role of glucagon in the de-
velopment of ketoacidosis. Withdrawal of insulin from
fasting pancreatectomized patients resulted in ketoaci-
dosis, but blood ketones and glucose rise less markedly
over time than in IDDM patients (40,41; Fig. 3). No
difference was found between these two types of dia-
betes in free fatty acid increments (40). IDDM patients,
unlike pancreatectomized patients, had a marked in-
crease in glucagon concentration during development
of ketoacidosis (40; Fig. 4). These data suggest that
hyperglucagonemia promotes hepatic conversion of free
fatty acids to ketone bodies, but in view of the detect-
able plasma levels of 3500-Mr glucagon found in some
pancreatectomized patients, the absolute need for glu-
cagon in the development of ketoacidosis remains un-
15-i STOP
INSULIN
"2 10
o
o
5-
o
J
0
-10 4 8 12
TIME (hours)
DIABETES CARE, VOL. 12, NO. 10, NOVEMBER/DECEMBER 1989
 R.J. SJOBERG AND G.S. KIDD

sulin binding, glucose transport, and glucose oxidation,

but increased maximal erythrocyte and monocyte in-
sulin binding without a change in affinity has also been
reported (43,45,46).
30 1
GLUCOSE COUNTERREGULATION
STOP

INSULIN
It was shown 20 yr ago that chronic calcific pancreatitis
caused prolonged hypoglycemia in response to intra-
venous insulin (48), and the blunted glucagon response
20- to insulin-induced hypoglycemia in chronic pancrea-
titis was previously commented on. Pancreatectomized
patients also have a diminished or delayed epine-
o
o
<
o
ZD RECENT
CONTROL TYPE I TYPED Pi ONSET
o 10- p<0.003 p<0.003 p<0.0l
140-
1
120-
100- I
80-
3* 60-
40-
0- 20-
0

rr i B
l o 12 1400
p<0 003
4 X
Uj '200
2 ^ IOOO
X i
TIME (hours)
FIG. 4. Plasma glucagon concentrations in 6 patients
X E 800
W g 600 1
n
400
with insulin-dependent diabetes () and 4 pancreatecto- 8) 200
mized patients (O) after withdrawal of insulin. Values are
0
means SE. (Reprinted from Barnes et al. [40] with per-
mission from N Engl I Med. Copyright 1977.)
80
70
clear. Diabetes caused by either cystic fibrosis or trop-
ical pancreatitis also has a resistance to ketosis (3-5).
60
50
40
X
X I I I
30
INSULIN SENSITIVITY 20
10
Diabetes caused by either chronic pancreatitis or pan- 0
createctomy results in either decreased, normal, or in-
creased insulin sensitivity compared with normal sen- D 20- X
sitivity and either similar or increased insulin sensitivity l6 X
compared with IDDM (42-46). These discrepant results

may be due to the heterogeneity of the patients studied:
some had chronic pancreatitis, whereas others had var-
ious degrees of pancreatic resection. Hypoglucagone-
mia that occurs postpancreatectomy may increase
insulin sensitivity because a physiological glucagon in-
fusion decreases the insulin sensitivity of pancreatec-
tomized patients (47).
Results of in vitro studies of insulin binding and ac-
tion in pancreatic diabetes have also varied. Adipocytes
taken from pancreatic diabetic patients had normal in-
n
12
-
:
o
p volua v. control
FIG. 5. Increases in counterregulatory hormones (A, glu-
cagon; B, epinephrine; C, growth hormone; D, cortisol)
above basal levels in response to insulin-induced hypo-
glycemia in patients with various types of diabetes. Values
are means SE. (Reprinted from Polonsky et al. [49] with
permission from the American Diabetes Association.)

DIABETES CARE, VOL. 12, NO. 10, NOVEMBER/DECEMBER 1989 719

PANCREATIC DIABETES MELLITUS
phrine response to insulin-induced hypoglycemia (Fig.
5) (49,50). Subtle autonomic nervous system dysfunc-
tion due to alcohol-induced autonomic neuropathy may
be etiologic, although abnormal recovery from hypo-
glycemia also occurs with cystic fibrosis (3).
LIPIDS
Serum lipids in pancreatic diabetic patients are of inter-
est in determining their risk of developing macrovas-
cular disease. The most consistent finding regarding this
has been low total cholesterol in patients with diabetes
caused by either chronic pancreatitis or pancreatectomy
(37,51,52). This decrease is due primarily to decreased
low-density lipoprotein (LDL) cholesterol accompanied
by normal high-density lipoprotein cholesterol (37,52).
Triglycerides generally are normal in pancreatic diabe-
tes, but pancreatectomy results in triglyceride-rich very-
low-density lipoprotein, LDL, and high-density lipopro-
tein particles (37,51,52). These lipoprotein changes most
likely reflect dietary effects, malabsorption, and alcohol
abuse rather than the impact of diabetes itself.
OTHER GUT HORMONE SECRETION
Impaired secretion of other gut- and pancreatic-derived
hormones has been demonstrated with chronic pan-
creatitis and after pancreatectomy. Chronic pancreatitis
results in impaired pancreatic polypeptide and GIP se-
cretion, elevated motilin levels, and normal gastrin lev-
els (53,54). Pancreatectomy causes impaired pancreatic
polypeptide and GIP secretion, low gastrin levels (when
associated with antrectomy), and normal motilin and
somatostatin levels (55-57). Although altered GIP se-
cretion has been postulated to contribute to abnormal
insulin secretion in chronic pancreatitis (26), little is
known regarding the clinical sequelae of these abnor-
malities.
IS PANCREATIC DIABETES BRITTLE?
It has been thought that patients with pancreatic dia-
betes have an increased sensitivity to insulin resulting
in erratic swings of glucose concentration. Comparison
of 24-h insulin requirements of patients on a controlled
diet with a glucose-controlled insulin infusion system
showed that pancreatectomized patients required less
insulin to maintain normoglycemia than IDDM patients
(38). Malabsorption may be responsible for this effect
because these patients' insulin sensitivities are not con-
sistently increased. The only other hormonal character-
istic of pancreatic diabetes that may contribute to ap-
parent brittleness is the glucose counterregulatory
hormone secretory defect.
720
Many socioeconomic and nutritional factors aside from
diabetes probably account for the clinical impression of
brittle diabetes in these patients. The most common
etiology of chronic pancreatic exocrine disease is al-
cohol abuse, and poor nutritional intake and concom-
itant hepatic disease may contribute to poor glucose
control. In addition, malabsorption, altered gut motility,
and recurrent abdominal pain affect the consistency and
quality of nutrient intake and absorption. The therapy
and expected morbidity of pancreatic diabetes, there-
fore, must be individualized based on the presence of
these other factors.
LONG-TERM COMPLICATIONS OF DIABETES
The relative importance of genetics and metabolic dis-
turbances in the pathogenesis of diabetic microvascular
disease is still a point of much controversy (58). The
prevalence of microvascular disease in pancreatic dia-
betes has been used to help determine the impact of
metabolic disturbances on the development of diabetic
complications. This presumes, however, that those ge-
netic influences that may affect the development of mi-
crovascular disease in IDDM and non-insulin-depen-
dent diabetes mellitus (NIDDM) are not present in
pancreatic diabetes. This presumption may, in fact, not
be valid because little is known regarding the nature of
the genetic influence on this process (58). The preva-
lence of diabetic microvascular disease in pancreatic
diabetes may, however, influence the clinical manage-
ment of such patients.
CAPILLARY BASEMENT MEMBRANE
Thickening of the capillary basement membrane in the
retina, glomerulus, and skeletal muscle frequently oc-
curs early in the course of, and appears to be specific
for, diabetic microvascular disease (59). Siperstein et al.
(60) showed that only 1 of 8 patients with diabetes due
to chronic pancreatitis, as opposed to >90% of patients
with genetic diabetes, had thickened skeletal muscle
capillary basement membranes. Although Raskin (61)
also demonstrated that only 3 of 19 patients (16%) with
pancreatic diabetes had thickened skeletal muscle cap-
illary basement membranes, repeat biopsies conducted
1.5-9 yr later revealed a progressive increase in capil-
lary basement membrane thickness in 7 of 8 patients, 4
of whom had levels above the normal range. An earlier
study also revealed that 5 of 8 patients with diabetes
associated with chronic pancreatitis had thickened glo-
merular capillary basement membranes (62). These
studies indicate that, although capillary basement mem-
brane thickening may be less common in pancreatic
diabetes than in IDDM, it does occur and may be pro-
gressive over time.
DIABETES CARE, VOL. 12, NO. 10, NOVEMBER/DECEMBER 1989

RETINOPATHY
Studies concerning the occurrence of retinopathy in
pancreatic diabetes have also yielded variable results.
Earlier studies documented the occurrence of retinopa-
thy in 7-23% of diabetic patients with chronic pan-
creatitis (63,64). These patients had diabetes for <5 yr,
and the retinopathy seen was of a mild severity. More
recently, a close correlation was found between the du-
ration of pancreatic diabetes and prevalence of retinop-
athy, with mild retinopathy being present in 62% of
patients who had diabetes for >10 yr (65).
In a well-controlled study, it has been shown that the
overall prevalence of retinopathy was similar in pan-
creatic diabetes (41 %) and IDDM (45%) (Fig. 6), but no
specific comment was made regarding the severity of
retinopathy seen (66). Retinopathy has rarely been re-
ported with cystic fibrosis (3) but may occur in up to
33% of patients with tropical pancreatic diabetes (67).
Chronic pancreatitis also results in a high prevalence of
nondiabetic retinal abnormalities, possibly related to vi-
tamin A or zinc deficiency (68).
OTHER COMPLICATIONS
No studies have specifically addressed the occurrence
of nephropathy in pancreatic diabetes. The reasons for
this are twofold: 7) the clinical detection of nephropathy
before its late stages has previously been difficult, and
2) until recently, the 10-yr survival rate of patients with
chronic pancreatic insufficiency has been low (11). Uri-
nary microalbumin excretion, recently shown to be an
early predictor of nephropathy (69-72), has not been
studied in patients with pancreatic diabetes. In a retro-
100
75-
25
0
1-5 6-10 11-15 > 15
DURATION OF DIABETES ( Years)
FIG. 6. Prevalence of retinopathy according to duration
of diabetes in patients with chronic pancreatitis (dotted
box) and idiopathic diabetes {stripedbox). Number on top
of each column is total number of patients in that subgroup
and number in column is number of patients with reti-
nopathy. (Reprinted from Couet et al. [66] with permission
from the American Diabetes Association.)
DIABETES CARE, VOL. 12, N O . 10, NOVEMBER/DECEMBER 1989
R.J. SJOBERG AND G.S. KIDD
spective review of 146 patients with pancreatic diabe-
tes, only 2 patients with nephropathy were identified
(73), and the occurrence of biopsy-proved nephropathy
in pancreatic diabetes is in only a few case reports (74-
77). The distinguishing feature of these patients was their
long duration of diabetes before the onset of renal dis-
ease, the shortest being 14 yr.
The prevalence of other less-specific complications of
diabetes (neuropathy and macrovascular disease) in
pancreatic diabetes has also not been specifically ad-
dressed. Studies of macrovascular disease in these pa-
tients would be of interest in light of their low serum
LDL cholesterol concentrations and increasing survival
rate.
CONCLUSION
iabetes occurring as a result of pancreatic ex-
D
ocrine disease is an uncommon but unique
clinical, metabolic, and hormonal form of di-
abetes. Table 2 shows the hormonal and met-
abolic differences between this form of diabetes and
both IDDM and NIDDM. Patients with chronic pan-
creatic diabetes also often have coexisting features that
complicate their diabetes management. Chronic alco-
holism, poor nutritional status, malabsorption, and ab-
dominal pain all serve to thwart attempts to strictly attain
normoglycemia. The long-term complications of dia-
betes have not been well studied in pancreatic diabetes,
but retinopathy appears to occur at a rate equal to that
of IDDM. The hormonal, metabolic, gastrointestinal, and
socioeconomic factors that frequently accompany pan-
creatic diabetes require that the goals of metabolic con-
trol for such patients be individualized based on the
presence or absence of these factors.
ACKNOWLEDGMENTS
We thank Mitzi Myers for secretarial assistance and Dr.
Michael T. McDermott for reviewing the manuscript.
TABLE 2
Comparison of hormonal and metabolic aspects of
pancreatic diabetes, IDDM, and NIDDM
Pancreatic diabetes IDDM NIDDM
Insulin secretion 11 * 4* 4* 4
Insulin sensitivity 0 I 41
Glucagon secretion || tn VI
Plasma amino acids TT f/0 f/o
Ketosis prone TT TT! T
Glucose counterregulation | o/| o/j
Lipids 0 T TT
f , Increased; 0, normal; | , decreased; IDDM, insulin-dependent
diabetes mellitus; NIDDM, non-insulin-dependent diabetes mellitus.
721
PANCREATIC DIABETES MELUTUS
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