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                    <p class="art-type" id="articleinfo">Case Report</p>
		    <p class="art-title">Post-Delivery Hypoglycemia in Type 1 Diabetic Patient is associated with Lactation: A Case Presentation</p>
		    <p class="art-author"><?php $authors="Jos&eacute; G Jim&eacute;nez-Montero<sup>*</sup>"; echo (stristr($authors,$coauthor))?str_replace($coauthor,"<a href='".$extpath."authors/".$courl."' target='_blank'>".$coauthor."</a>",$authors):$authors; ?></p>
<p class="art-affl">Department of Endocrinology Hospital CIMA, San Jos&eacute;, Costa Rica and Postgraduate Studies, Universidad de Ciencias M&eacute;dicas, PO
Box 638 -1007, Centro Colon, San Jos&eacute;, Costa Rica</p>
		    <p class="art-aff"><b>*Corresponding author: <?php $corresponding_author="Jos&eacute; G Jim&eacute;nez-Montero"; echo ($coauthor!="" && $coauthor==$corresponding_author)?"<a href='".$extpath."authors/".$courl."' target='_blank'>".$coauthor."</a>":$corresponding_author;?></b>,
Department of Endocrinology Hospital CIMA
San Jos&eacute;, Costa Rica and Postgraduate
Studies,
Universidad de Ciencias M&eacute;dicas,
PO Box 638 -1007, Centro Colon,
San Jos&eacute;, Costa Rica,
Tel: 506 2549 0128,
E-mail: <a href="mailto:jimenezmj@ucimed.com">jimenezmj@ucimed.com</a>;<a href="mailto:jjimenez@hospitalcima.com">jjimenez@hospitalcima.com</a></p>
<p class="art-aff"><b>Received:</b>  September 28, 2015
<b>Accepted:</b>   October 20, 2015
<b>Published:</b>  October 28, 2015</p>
<p class="art-aff"><b>Citation:</b>  Jim&eacute;nez-Montero JG. Post-Delivery
Hypoglycemia in Type 1 Diabetic Patient is
associated with Lactation: A Case Presentation.
<i>Madridge J Diabetes</i>. 2015; 1(1): 5-10.
doi: <a href="https://doi.org/10.18689/mjd-1000102">10.18689/mjd-1000102</a></p>

<p class="art-aff"><b>Copyright:</b> &copy;  2015 The Author(s). This work is licensed under a Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p>
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<div class="articlecontent">
<p class="art-subhead" id="abstract">Abstract</p>
<p class="art-para"><b>Objective:</b>  To describe diabetes management during pregnancy and after delivery of a
pregnant type-I diabetic patient with hyperemesis gravidarum.</p>
<p class="art-para"><b>Methods:</b> The patient's history, laboratory results, and glycemic control were obtained.
Diabetes control was done using an insulin pump and a glucose monitoring system
during pregnancy, post-partum and at six month after delivery.</p>
<p class="art-para"><b>Results:</b>  A 27-year-old pregnant patient with history of hypothyroidism, type 1 diabetes,
and hyperemesis gravidarum, receiving multiple daily insulin injections, presented
marked glycemic fluctuations starting on week 6 of gestation. Before conception
laboratory results showed glycosylated hemoglobin A1c (HbA<sub>1c</sub>) at 6.7% and Thyroid-Stimulating Hormone (TSH) at 4.40 uUI/ml. An insulin pump and a continuous glucose
monitoring system improved glycemic control as mean glucose changed from 139&plusmn;77
mg/dL in the first trimester to 113.0&plusmn;44 mg/dL and 106.0&plusmn;39 mg/dL, in the second and
third trimester (p<0.01) respectively. HbA<sub>1c</sub> declined from 6.7% to 5.6%. Adjustment in
levothyroxine doses optimized thyroid hormone levels. The patient gave birth on week
39 of pregnancy by Caesarean section to a child of 2,700 g and 48 cm, and an Apgar
score of 9/10. Recurrently poglycemic episodes occurred 10-15 minutes after initiating
lactation followed by rebound hyperglycemic events; once the patient ceased lactation
six months later glycemic controls improved.</p>
<p class="art-para"><b>Conclusions:</b> Optimal glycemic control was achieved during pregnancy, but the lactation
period induced sudden glucose fluctuations. Recurring hypoglycemic events lead to a
decline in post-partum glycemic control. Thus, lactation-induced hypoglycemia may
explain the frequent deterioration in glycemic control in type-I diabetic patients.</p>
<p class="art-para"><b>Keywords:</b>  Type 1 diabetes; Lactation-induced hypoglycemia; Continuous insulin infusion;
Continuous glucose monitoring system.</p>
<p class="art-para"><b>Abbreviation:</b>TSH: Thyroid-Stimulating Hormone; CSII: Continuous Insulin Infusion;
CGMS: Glucose Monitoring System</p>

<p class="art-subhead" id="intro">Introduction</p>
<p class="art-para">In diabetic pregnant patients, a strict glycemic control is critical to avoid fetal
malformations, neonatal morbidity and obstetrical complications <a href="#1" id="ref1">[1</a>-<a href="#5" id="ref5">5]</a>. However, in
type 1 diabetics an aggressive insulin treatment increases the risk of severe hypoglycemia
and has potential adverse maternal effects <a href="#6" id="ref6">[6</a>,<a href="#7" id="ref7">7]</a>. Recurrent hypoglycemic events induce
rebound hyperglycemia due to counter regulatory mechanisms and food intake <a href="#8" id="ref8">[8]</a>.
Postprandial hyperglycemia during pregnancy has been identified as the best prognosis
of neonatal macrosomia, despite excellent HbA<sub>1c</sub> levels throughout pregnancy <a href="#9" id="ref9">[9]</a>.
Moreover, glycemic fluctuations may adversely affects diabetic complications <a href="#10" id="ref10">[10]</a>.</p>

<p class="art-para">This case study first describes the clinical course of a type
1 diabetic pregnant patient suffering from hyperemesis
gravidarum since the first trimester up until six months postpartum. Secondly, it documents the occurrence of sudden
glycemic reductions and recurrent hypoglycemic events soon
after beginning the lactation period.</p>

<p class="art-subhead" id="case">Case Presentation</p>
<p class="art-para">A 27-year-old, Venezuelan, type 1 diabetic patient,
receiving treatment with multiple daily insulin injections (16 U
glargine insulin plus 10 U prandial lispro insulin) came to the
clinic for a regular check-up. She followed an adequate diet,
was engaged in regular physical activity, and performed selfmonitoring blood glucose tests three times a day. During the
first visit to the clinic her HbA<sub>1c</sub> was at 6.2 %, there was no
evidence of diabetic-related complications. She had rare
symptomatic or unawareness hypoglycemic episodes. At age
24 she was diagnosed with hyperthyroidism. She was treated
with radioactive iodine, developing hypothyroidism. She was
treated with 125 uglevothyroxine daily, and was tested for
TSH receptor antibodies resulting in negative findings. Her
thyroid-stimulating hormone (TSH) level was 3.96 uUI/ml. The
patient's blood pressure was 90/60 mmHg, her height was
159 cm, weight 50.7 kg and Body Mass Index (BMI) 20.6 kg/
mts <a href="#2" id="ref2">[2]</a>. There were no outstanding findings in the physical
examination. Minor adjustments in insulin and levothyroxine
doses were done.</p>
<p class="art-para">The second visit occurred three months later when the
patient reported nausea, daily vomiting, and nocturnal and
post-exercise hypoglycemia. The patient's finger stick test
glucose levels fluctuated from 40-290 mg/dL at any time of
the day. She was found to be six weeks pregnant with
hyperemesis gravidarum. Her HbA1c was at 6.7% and the TSH
was at 4.4 uUI/ml. Her weight was 52 kg and blood pressure
90/70 mmHg. Glargine insulin was discontinued, prandial
insulin was reduced to 6 U, and levemir 16 U was initiated.
Domperidone 10 mg and folic acid 5 mg were prescribed.</p>
<p class="art-para">One week later, the patient continued vomiting and
experiencing severe and recurrent hypoglycemic events and
rebound postprandial hyperglycemia. She was hospitalized,
and a Continuous Insulin Infusion (CSII) (Paradigm Medtronic,
Minneapolis, MN) and Glucose Monitoring System (CGMS,
Medtronic, Northridge, CA) were placed <a href="#10" id="ref10">[10</a>,<a href="#11" id="ref11">11]</a> in order to
improve glucose control <a href="#11" id="ref11">[11</a>-<a href="#15" id="ref15">15]</a>. During a short inpatient
period, we conducted carbohydrate counting and insulin
pump management sessions. The insulin infusion rate was
determined based on the total MDI regimen previously used
and adjusted according to daily glucose profiles.</p>
<p class="art-para">The patient's weight rose to 57.5 kg and 61 kg during the
second and third trimester, respectively. She maintained
normal blood pressures, did not have albuminuria, and
sequential ultrasounds did not reveal fetal abnormalities. On
week 39 the patient gave birth to a child of 2,700 g, 48 cm,
and an Apgar score of 9/10, by cesarean section with no
complications and no evidence of thyrotoxicosis. The patient
received a 5% glucose IV infusion while the CSII was still in
place. Immediately after delivery, the insulin infusion was
stopped transitorily, and then re-started at a reduced infusion
rate. Glucose levels ranged between 120-140 mg/dl during
the following hours. The patient was counseled to adjust her
food intake, and began breastfeeding eight hours after
delivery. In the next three months, she noticed abrupt glycemic
declines 10-15 minutes after she began breast feeding,
followed by rebound hyperglycemia.</p>
<p class="art-para">The patient was under observation to monitor the
fluctuation glucose levels. She did not perform physical
activity during this time. The patient ceased lactation and had
gradual improvements in glucose control with few
hypoglycemic levels compared to the previous months. After
the patient stopped breastfeeding, she occasionally extracted
breast milk manually to feed her baby and to avoid mastitis.
Interestingly, doing so caused glycemic declines minutes after
milk extraction. This observation was not documented with
the CGMS.</p>
<p class="art-para">The changes in HbA1c, blood glucose, the area under the
curve above and below target levels, the standard deviation
of glucose, and the glucose variation coefficient were analyzed
during pregnancy, in the early post-partum period and three
and six months later. Compared to the first trimester, the
glucose variation coefficient declined from 55% to 13.5% and
the area under the curve above target was reduced by 77% at
the end of pregnancy, as illustrated in Table 1 and Figure 1.
The average daily carbohydrate intake, average daily insulin,
and the carbohydrate/insulin ratio during pregnancy and
post-partum periods were obtained from the CGMS, as shown
in Table 2. Total insulin requirements increased from 0.55 U/
kg in the first trimester to 0.80 U/kg at the end of pregnancy;
the changes in insulin demand were mainly driven from
increments in insulin bolus, which changed from 0.23 to 0.45 U/kg in the same time period. Three days, one month and six
months post-partum, insulin requirements dropped, as total
daily insulin requirement was 0.44, 0.53 and 0.6 U/kg,
respectively. Table 2 shows average daily insulin dose during
different trimesters and in the post-partum period.</p>
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<p class="art-para">Due to hyperemesis, the absorption of levothyroxine was
affected as TSH increased to 5.0 uU/ml on week 16 of
pregnancy (Figure 2). Thus, levothyroxine was increased to
175 ug daily and, as a result of that, total T4 concentrations
ranged from 11.5 to 12.5 ug/dl and the TSH levels were
maintained below 3.0 uUI/ml during the rest of the pregnancy.</p>




<p class="art-subhead" id="discussion">Discussion</p>
<p class="art-para">The present report describes a type 1 diabetic hypothyroid
female patient with hyperemesis gravidarum who presented
large glycemic fluctuations and hypoglycemia during the first
weeks of pregnancy. Physical activity was not associated with
the glucose fluctuations, as the patient was sedentary during
the observation period. This patient did not report unnoted
hypoglycemia prior to the pregnancy and, although she was
diagnosed with diabetes twenty years ago, no other risk
indicators for hypoglycemia were documented <a href="#16" id="ref16">[16]</a>. In
addition to the glucose variability seen in type 1 pregnant
diabetic patients <a href="#8" id="ref8">[8</a>,<a href="#17" id="ref17">17]</a>, hyperemesis gravidarum predisposed
severe hypoglycemic episodes. This condition precluded an
optimal diabetes management and added high risks to the
patient and fetus. The prenatal insulin treatment provided a
good glycemic control as HbA1c was at 6.7%, but glucose
levels fluctuated along the hyperglycemic and hypoglycemic
range, predisposing obstetrical complications and congenital
abnormalities, as aforementioned <a href="#2" id="ref2">[2</a>,<a href="#3" id="ref3">3]</a>.</p>
<p class="art-para">The intensive insulin treatment with CSII has not proven
to be superior to MDI in pregnancy complicated by diabetes
<a href="#13" id="ref13">[13</a>,<a href="#18" id="ref18">18]</a>, and macrosomia has been documented in wellcontrolled type 1 diabetics with CSII <a href="#8" id="ref8">[8</a>,<a href="#9" id="ref9">9]</a>. In this patient, the
glucose fluctuations were high and she suffered from frequent
and severe hypoglycemic events, therefore, the use of both
the CSII with the CGMS was clearly indicated <a href="#14" id="ref14">[14</a>,<a href="#15" id="ref15">15]</a>.</p>
<p class="art-para">As pregnancy progressed, glycemic control improved and
glucose recordings significantly declined, similarly to previous
studies <a href="#13" id="ref13">[13</a>,<a href="#18" id="ref18">18]</a>. The patient's average carbohydrate intake
increased throughout pregnancy and as expected, insulin
needs increased. While basal insulin requirements remained
relatively constant, the overall insulin demand was provided by the prandial insulin boluses, as reported previously <a href="#11" id="ref11">[11</a>-<a href="#13" id="ref13">13]</a>.</p>

<p class="art-para">In the post-partum period, the patient experienced
unexpected glucose declines and hypoglycemic episodes 10-
15 min after she initiated lactation as observed previously
<a href="#19" id="ref19">[19]</a>. In non-diabetic women, no significant glucose changes
occur during the period before or after lactation, nor do they
develop hypoglycemia in response to lactation <a href="#20" id="ref20">[20</a>,<a href="#21" id="ref21">21]</a>. Fasting
glucose demand was associated with an increased glucose
production derived from glycogenolysis; while during
breastfeeding, normal glucose levels were maintained by
increasing insulin sensitivity <a href="#21" id="ref21">[21]</a>. Lactation has beneficial
effects on glucose and lipid metabolism <a href="#22" id="ref22">[22]</a>, and it was shown
that the intensity of lactation improved fasting glucose and
lower insulin levels as compared to non-lactating women <a href="#23" id="ref23">[23]</a>.
The basal insulin dose was reduced to minimize the risk of
hypoglycemia in breastfeeding in type 1 diabetic patients
using CSII <a href="#24" id="ref24">[24</a>,<a href="#25" id="ref25">25]</a>, as done to our patient during the lactation
period. Thus, hyperinsulinization does not seem to have
played a role in the hypoglycemic episodes seen in our
patient. The recurrent falls in the glucose levels and the
hypoglycemic episodes documented soon after she initiated
breastfeeding could be explained by the increased glucose
demand associated with lactation and to the post-partum
changes in insulin sensitivity <a href="#21" id="ref21">[21</a>,<a href="#22" id="ref22">22]</a>. In addition to the changes
in insulin sensitivity and glucose demand to produce lactose
for milk production, other mechanisms, such as the neurohormonal stimulus of suckling, could have elicited this
phenomenon. Nevertheless, this is only speculative.</p>
<p class="art-para">In conclusion, in this type 1 diabetic, hypothyroid,
pregnant patient complicated with hyperemesis, who gave
birth to a normal child on week 39, the CGMS and CSII had a
favorable effect to optimized glucose control. Thus, lactationinduced hypoglycemia could have played a role in the post
delivery deterioration of glucose control in our patient.</p>
<p class="art-para"><b>Acknowledgments:</b> Lic. Kathya Arrieta-Morera for assistance
in literature search,to Lic. Grettel Rodr&igrave;guez-Rodr&iacute;guez for
technical assistance and to Miss Constanza Gonzalez for their
for technical assistance in preparing the manuscript.</p>
<p class="art-para"><b>Financial Disclosure:</b> Dr. JG. Jim&eacute;nez-Montero has been on
the insulin advisory board, received a research grant from
Sanofi-Aventis and has been speaker for Merck Sharp &
Dohme, and Novartis.</p>
<p class="art-para"><b>Consent:</b> Patient has provided written consent for publication
of this study.</p>

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