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Indian Pediatr 2012;49: 920-921
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Diabetic Ketoacidosis Following Mumps
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Manish Agrawal, SP Goel and Ashish Prakash
From the Department of Pediatrics, Subharti Medical
College, Meerut, India.
Corresponding Address: Dr Manish Agrawal, L-863,
Shastri Nagar, Meerut 250 004, India.
Received: February 9, 2012;
Initial review: March 01, 2012;
Accepted: June 23, 2012.
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A-13-year-old girl presented with diabetic ketoacidosis with convincing
clinical signs of parotitis (fever, drooling of saliva, inability to
swallow with development of bilateral parotid swelling) and pancreatitis
(fever, abdominal pain and vomiting), along with high serum amylase and
positive mumps IgM titer. This suggests that mumps virus may have been
the causative factor, probably as a result of concomitant involvement of
the pancreas.
Key words: Diabetic ketoacidosis, Mumps.
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The common complications of mumps are
meningitis with or without encephalitis, gonadal involvement and
myocarditis while pancreatitis is an uncommon complication of mumps.
Epidemiological studies have suggested that mumps pancreatitis may
be associated with subsequent development of diabetes mellitus, but
a causal link has not been established. The following is a report of
a case of diabetic ketoacidosis (DKA), apparently due to mumps
pancreatitis, with involvement of parotid glands.
Case Report
A-13-year-old girl, developed low-grade fever,
drooling of saliva and vague abdominal pain. Next day, it progressed
to inability to swallow and speak, and vomiting. Two days later, she
had twitching of face and generalized convulsions and became
unconscious. She was then admitted to our institution.
She was drowsy but oriented and following verbal
commands. Moderate dehydration was present. Her temperature was
101ºF, pupils were bilateral normal size and reacting and Glasgow
coma score was 15. Her cardiac examination was normal. The abdomen
was soft and non-tender. Liver was 2 cm below costal margin, soft,
smooth and non-tender. Spleen was not palpable. On central nervous
system examination, there was no focal neurological deficit or signs
of meningeal irritation.
Investigations revealed high random blood sugar
values (462 mg/100mL), urine was postive for sugar and ketone, and
blood gas analysis revealed metabolic acidosis. She was diagnosed as
a case of diabetic ketoacidosis and treated with intravenous fluids,
regular insulin and other supportive treatment. Hyperglycemia was
controlled within 24 hours. On the third day of admission, she
developed swelling of right parotid gland followed by involvement of
the left parotid gland following day. Serum amylase was 918 U/L. USG
abdomen showed. hepatomegaly and bilateral enlarged kidneys (right
kidney- 11.5 × 4.5 cm, left kidney- 11.2 × 4.6 cm) with increased
cortical echotexture. Cortico-medullary distinction was maintained.
Mumps IgM by ELISA was positive.
On 5 th
day of admission, drooling became less and she was able to swallow
liquids. Her parotid swellings subsided on the 8th
day of the admission and she was discharged on subcutaneous human
mixtard insulin.
Discussion
Type I diabetes mellitus (T1DM) results from the
interaction of genes, the environment, and the immune system. The
presence of disparate geographic prevalence, rising worldwide
incidence, and 50% discordance rate in identical twins provides
evidence that environmental agents are operative. As there is a
latent period between the appearance of T1DM-associated
autoantibodies and onset of disease, additional environmental
factors –probably interacting with genetic factors – also seem to
modulate the rate of development of the disease [1].
Early nutrition and infection have been the most
frequently implicated early environmental influences. There is,
however, no direct evidence to date that either nutrition or
infection plays a major role in causation, albeit one example of
prenatal rubella infection which is associated with beta-cell
autoimmunity in up to 70%, and diabetes in up to 40% of infected
children [2,3]. A relationship between beta-cell autoimmunity and
intrauterine exposure to enteroviral (mainly Coxsackie B 4)
infection has been proposed [3-5]. Studies from Finland and Sweden
suggested that maternal enterovirus infection may increase the
likelihood of subsequent T1DM development in offspring [5]. Higher
levels of antibodies to procapsid enterovirus antigens were found in
the pregnant sera of mothers of children who developed diabetes.
However, the presence of antibodies against enteroviruses in people
with autoimmunity does not prove a causal relationship. Persons with
autoimmunity also may be more prone to enteroviral infection, may
have a stronger humoral response to infection because of their
particular HLA genotype, or may be in a nonspecific hyperimmune
state marked by elevation of antibody levels to various exogenous
antigens. Islet related autoantibodies also have been detected after
mumps, measles, chickenpox and rotavirus infections [7,8]. But of
all the viral infections, mumps seems to be most frequently
associated with diabetes [8-9]. In most of these instances, symptoms
of diabetes developed within one-to-eight weeks after infection
[8,9].
In the case presented in this report, presence of
clinical features of mumps and the postive IgM indicates a recent
mumps infection. This report further strengthens the reported
association of mumps infection and diabetes.
Contributors: All authors contributed to
diagnosis of case and drafting the paper.
Competing interests: None stated; Funding:
None.
References
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