1
56
onset of steroid-sensitive nephrotic syndrome and type 1
diabetes has been reported, it is rare and the estimated
frequency is one case in every 3,300,000 inhabitants at
with ketoacidosis. The occurrence DKA might be
related to steroid-induced insulin resistance, activation
of lipolysis in the periphery and ketogenesis.
8
risk. In their report, polyuria, polydipsia, hyperglycae-
mia, ketonuria and glycosuria occurred three weeks after
commencement of prednisolone. Two months later, their
patient while on insulin relapsed with diabetic ketoaci-
dosis following an upper respiratory tract infection. In
contrast, our patient have not relapsed despite stoppage
of insulin administration for 12 months, suggesting that
the ketoacidosis was steroid-therapy induced as against
the simultaneous co-existence of steroid-sensitive
nephrotic syndrome and type 1 diabetes.
A review of the literature revealed that controversies
still exist mainly with regard to treatment of steroid-
induced new-onset diabetes mellitus (SINODM). Insulin
administration is the mainstay of therapy of SINODM.
In general, two approaches have been suggested with the
first, focusing on prandial insulin therapy and the sec-
ond, on basal insulin therapy. The prandial insulin ther-
apy approach is based on the observation that with once
daily dose of steroid, fasting blood glucose are typically
normal but rise steadily after breakfast and then lunch,
declining towards normal overnight. This rise in glucose
level throughout the day is believed to be an evidence
of a specific defect in postprandial insulin secretion,
which should be amenable to prandial insulin therapy.
Concerning the basal insulin therapy approach, Clore
The results of the fasting and postprandial blood glucose
values in our patient need consideration. Eight days after
the commencement of prednisolone, urinalysis revealed
glycosuria with random blood glucose of 14.2 mmol/L.
The fasting blood glucose was 6.5 mmol/L the next
morning. This discrepancy between the random and fast-
ing blood glucose values is not surprising as it is consis-
tent with the observation in other studies. For instance,
in a prospective study of patients without diabetes but
with primary renal disease who were treated with ster-
oid, 42% were found to have 2-hour postprandial blood
glucose greater than 11.1 mmol/L (200 mg/dl) but nor-
2
et al recommended the use of NPH for patients on pred-
nisolone based on the pharmacokinetics of this steroid.
The recommended dose in basal insulin therapy ap-
proach is 0.4 U/kg. However, it should be noted that this
recommendation is not based on randomized trial, and
so, there is no clear cut recommendation on insulin man-
agement of SINODM. Therapy should, therefore, be
individualized. The index case was managed with the
standard protocol for the treatment of diabetic ketoaci-
dosis and then switched to twice daily premixed (short
acting plus intermediate acting)insulin after resolution
6
mal fasting blood glucose values13. A similar observation
was reported by Iwamoto et al among patients with
neurological diseases treated with steroid. The clinical
implication for the diagnosis of steroid-induced diabetes
mellitus is that if fasting blood glucose values of 7.0
mmol/L (126 mg/dl) or greater is used as the only crite-
1
4
of DKA . The insulin therapy has been discontinued
about 12 months ago and blood glucose values have
remained with normal limits, representing a further evi-
dence that steroid-induced diabetes mellitus resolves
with discontinuation of steroid administration (steroid
therapy was discontinued 18 months ago). There is no
recurrence of DKA.
7
ria for its diagnosis, many cases will be missed . In pa-
tients with primary renal disease on high-dose steroid
therapy, both the random and fasting blood glucose val-
ues should be monitored to avoid missing the diagnosis
of steroid-induced diabetes mellitus. In this regard, in
one of the studies in Japan, it was specifically recom-
mended that the monitoring of blood glucose values two
hours after lunch should be performed in all patients on
high-dose steroid therapy because of the six sampling
points, the highest value was obtained two hours after
Conclusion
1
3
lunch . They further stated that fasting blood glucose
values did not contribute to detecting steroid-induced
diabetes mellitus.
In conclusion, in adolescents with steroid-sensitive
nephrotic syndrome, the risk of steroid-induced diabetic
ketoacidosis should be considered in the course of ster-
oid therapy. Both fasting and postprandial blood glucose
values should be monitored to prevent missing of cases
of steroid-induced diabetes mellitus and ultimately,
DKA.
This patient presented in our Children’s Emergency
Unit with diabetic ketoacidosis. As reported in other
studies, it is uncommon for patients with steroid-induced
9
diabetes mellitus to present with ketoacidosis . For in-
stance, none of the 25 patients o3n high-dose steroid ther-
Conflict of Interest: None
Funding: None
1
apy reported by Iwamoto et al in their study presented
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