JURNAL: Fulminant Type 1 Diabetes Mellitus (a case report)

Rezky Ramadhani Syarif / 10542060615

Case Presentation
A male, 27 years old, came with fatigue and dyspnea as a chief complaint that has been for one day. The patient has complained
to have a fever that suddenly spiked about four days ago, and has been given antibiotics in a clinic. About two days before fever,
the patient was having an episode of fatigue, but no other complaints such as a cough, fever, and vomit. Aside from chief
complaint, the patient was having urination more than usual, about ten times a day. Random blood glucose examination with
blood glucose meter shows a level of 360 mg/dL, and 3 hours before admission, the patient had a series of vomit followed by
lightheadedness and extreme fatigue. From physical examination, the patient was awoken, and having a normal body mass index
with a weight of 67 kilograms and a height of 168 centimeters. Physical examination of eyes, neck, lungs, heart, abdomen are
within normal range, but thestudy of extremities shows a minimal edema in the left lower extremity. Peripheral blood
examination revealed elevated leukocyte count, metabolic acidosis with a pH level of 7,202 and declined C-peptide level. The
patient was admitted to diabetic ketoacidosis and suspected type 1 diabetes mellitus, fulminant type. The patient was given
glargine insulin at 21 units, and insulin aspart at 34 units. On follow-up at the hospital ward after ketoacidosis have been resolved
(February 1st, 2017), blood glucose was 131 mg/dL at night with 21 units of insulin glargine and 101 mg/dL at the following
morning with 16 units of insulin aspart. On the next day (February 2nd, 2017), blood glucose levels were 106 mg/dL at noon with
16 units of insulin aspart,an85 mg/dL at night with ten units of insulin glargine. At February 3rd, 2017 blood glucose levels were
92 mg/dL at the morning without insulin and having an incidence of hypoglycemia after an injection of 16 units insulin aspartat
noon (38 mg/dL).The midday and nighttime blood glucose were 62 and 207 with an injection of 16 units insulin aspart at noon
and 21 units insulin glargine at night, respectively. On the third day (February 4th, 2017), the patient was normoglycemic with a
stable dose of 3 times, 12 units injection of insulin aspart and 21 units once daily injection of insulin glargine until discharge three
days later.
Discussion
1. Definition
Type I diabetes An absolute deficiency in insulin secretion due to
Mellitus the destruction of B-cells in the pancreas
ADA & WHO Type I DM is autoimmune type (1A) and
idiopathic type (1B)
• Type IA diabetes : was a result of
thedestruction of β-cells by autoantibodies
• Type IB diabetes : exact cause of type 1B
diabetes is not fully known.
Nowadays, Fulminant type 1 diabetes because the disease
there is a new progress rapidly and leaving a unique
category of characteristic when blood examination is
type 1 performed
diabetes
Discussion
Fulminant type 1 is defined by a sudden onset of ketosis or ketoacidosis, no
or decreased C-peptide secretion, and high level of plasma glucose
accompanied with normal glycosylated hemoglobin level.
These extremely abrupt characteristics happen within only a few days and
rarely exceeds one week

Type IA diabetes VS Type IA diabetes : will take years to

Fulminant Type I DM develop autoantibodies to the clinical
onset of ketosis or ketoacidosis

Fulminant T1DM : within only a few days

and rarely exceeds one week.
Discussion
2. Pathophysiology
• Pathogenesis of fulminant type 1 diabetes is around class II HLA susceptibility; even the
exact mechanism is not known.
• There is a possibility that HLA molecule could interact with viruses and can cause
fulminant type 1 diabetes.
• Among thevast array of viruses, enteroviruses,and herpes viruses seem to be frequently
associated with fulminant diabetes, particularly human herpesvirus 6 (HHV-6), which can
cause hypersensitivity syndrome and reactivation of HHV-6.
• It is also worth noting that IgA antibodies were significantly higher in patients with
fulminant type 1A diabetes than in type 1A diabetes.
• Although viruses were said to be preceding this type of diabetes, immune reactions
might also play a role in thedevelopment of the disease, mainly by the T-lymphocytes
response to GAD.
Discussion
3. Signs and Symptoms
Consist of thirst (93.7%), flu-like symptoms (71.7%), and abdominal symptoms (72.5%).
• Flu-like symptoms can manifest as : fever (60%), sore throat (25.2%), and cough (12%)
• The most common abdominal symptoms are : nausea or vomiting (65.4%), upper
abdominal pain (39.2%) and lower abdominal pain (11%).
• In some cases : the patients can experience a loss of consciousness ranging from
drowsiness to coma, which is in about half of fulminant type 1 diabetes patients.
• Along with predictable symptoms, there has been a report of acardiopulmonary arrest
in one patient with fulminant type 1 diabetes with a complaint of fatigue, and the patient
was thought to have anunderlying cardiac disorder such as T-wave inversion or atrial
fibrillation
Discussion
4. Laboratory Findings
• High blood plasma glucose with normal glycosylated hemoglobin because of the abrupt nature of the disease that
caused by the quick destruction of β-cells, while glycosylated hemoglobin reflects an average in blood glucose over the
period of 1-2 months.
• Plasma ketone bodies are elevated (ketosis) and arterial blood gas had a pH below 7.35 in more than 90% patients
with fulminant type 1 diabetes and ketoacidosis is usually seen at the onset of fulminant type 1 diabetes
• Serum levels of exocrine pancreas enzymes such as amylase, elastase-1 and lipase are also elevated at the onset of
fulminant type 1 diabetes. This elevation does not warrant pancreatitis, but in some cases, there will be a swelling of
the pancreas that can be from CT-scan or abdominal echograms.
• Sodium and chloride levels are markedly lower,and potassium is higher. These electrolyte abnormalities are more
severe than type 1A diabetes.
• The increment in AST and ALT levels can also be after starting insulin for treating patients, but the exact
phenomenon is yet to be known
• These patients have negative islet cell antibodies (ICA), insulin autoantibody (IAA), anti-glutamic acid decarboxylase
antibody (GADAb), and anti-insulinoma-associated antigen twoantibodies (IA-2Ab).
• In fulminant type 1 diabetes, the β-cells is only about 14,5% after 1-9 months of overt diabetes. Along with β-cells
damage, there is damage in the α-cells portion about 33,1%, but this phenomenon was not with autoimmune type 1
diabetic patients
Discussion
5. Treatment
Treatment in fulminant type 1 diabetes does not differ from autoimmune type 1 diabetes, which
consists of intravenous infusion and regular insulin regiment. Once the acute phase of ketoacidosis
can be managed, the patients can revert to daily or twice-daily injections with either very long-acting
insulin together with twice or thrice daily doses at each meal with rapid-acting or regular insulin
Conclusion
• Fulminant type 1 diabetes mellitus is a disease that centered around β-cells destruction by an
autoimmunity process.
• It can be precipitated by viral infection, especially HHV-6 and enteroviruses.
• Clinical characteristics of fulminant type 1 diabetes consist of high blood glucose, normal
glycosylated hemoglobin level, thepresence of ketosis or ketoacidosis, abnormalities of potassium and
ALT/AST level, and negative autoantibody examination such as ICA, IAA, GADAb, IA-2Ab.
• Treatment in fulminant type 1 diabetes does not differ from another type 1 diabetes, which consists
of glycemic control via the use of insulin (intravenous for initial therapy for diabetic ketoacidosis),
intravenous infusion of isotonic saline, and corrections of acid-base and potassium abnormalities if
the levels fall within therapeutic initiation range
Thank you
#Fastabiqul Khaerat