Severe Impaired Deambulation

Anton Tedja Christensen, Torben Østergård, Vibeke Andersen
Medical Department, Viborg Regional Hospital. Viborg, Denmark
ABSTRACT
Context Skeletal muscle weakness and impaired gait function are common risk factors for disease and even death. Therefore,
identification of the modifiable causes of skeletal muscle weakness should have high priority. Knowledge regarding optimal vitamin
D treatment in cases of pancreatic insufficiency is scarce. Case report We report a case of a slow decrease in ability to walk
distances more than 100 m during the previous 6 months. Low exocrine pancreatic function resulting in phosphorus, magnesium and
vitamin D deficiency was found. Medical treatment with peroral pancreatic enzymes, phosphorus, magnesium and i.m. injections of
ergocalciferol (vitamin D2) was initiated. Gait function gradually increased to a walking distance of 1,500-3,000 m along with the
normalization of the vitamin D and mineral blood levels. Conclusions Vitamin D deficiency due to exocrine pancreatic insufficiency
should be kept in mind as one of the reasons for impaired gait and skeletal muscle weakness.
INTRODUCTION
Skeletal muscle weakness is a major health problem [1]
and as many as 40% of individuals over 60 years of age
may be affected [1]. The people affected are at high
risk of falling and immobilization, which may lead to
bone fractures, infection and death. Indeed, low gait
speed and poor balance have been found to be
associated with high mortality [2]. Thus, skeletal
muscle weakness has a high impact on the quality of
life of the affected individual and on health
expenditures in the community.
Skeletal muscle weakness is a major feature of several
conditions. These include primary muscle diseases,
such as muscular dystrophy, or endocrine diseases,
such as hypothyroidism, but also sarcopenia, the age-
related decline of muscle. Several neurological
disorders (e.g. Guillain Barre) or amyotrophic lateral
sclerosis give rise to muscle weakness. Peripheral
artery disease is a common manifestation of systemic
arteriosclerosis, which can present itself as skeletal
muscle weakness and reduced walking distance in the
form of intermittent claudication. Exocrine pancreatic
insufficiency is also associated with low vitamin D
levels, which is known to cause muscle weakness [3].
Identification of the modifiable causes of skeletal
muscle weakness should have a high priority as this
will lead to better treatment of patients. We present the
case of a patient showing a slow decrease in ability to
walk associated with low vitamin D and mineral levels
due to pancreatic insufficiency which improved as the
deficiencies were corrected.
CASE REPORT
A 62-year-old Caucasian male who was living by
himself contacted the outpatient clinic due to severely
reduced capacity of walking distances over the past 6
months. Quality of life was severely hampered and he
had recently put his house up for sale, as he was no
longer able to ascend the stairs to the first floor. Over
approximately the same time period, there had been a
10 kg weight loss.
Peripheral arterial disease was suspected. Therefore, a
walking test combined with measurement of the blood
pressure in the toes, ankle and brachia, including the
ankle-brachial index, was carried out and all blood
parameters were found to be normal. However, the
walking test confirmed that the patient had a severely
impaired capacity of walking distances, which was less
than 100 m. For the previous year, the patient had been
taking calcium with vitamin D 400 mg/400 IU bid.
Despite this, the laboratory findings showed severe
vitamin D and calcium deficiency as well as low levels
of vitamin A, phosphorus, magnesium and potassium
(Table 1). Stool elastase was found to be less than 50
µg/g of stool (reference: greater than 200 µg/g of
Received May 24th, 2011 - Accepted July 24th, 2011
Key words Mobility Limitation; Muscle Weakness; Pancreas;
Phosphorus; Vitamin D Deficiency
Correspondence Anton Tedja Christensen
Medical Department; Viborg Regional Hospital; 8800 Viborg;
Denmark
 

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483
stool), suggesting exocrine pancreatic insufficiency as
the cause of the hypovitaminosis and weight loss.
Peroral therapy with pancreatic enzymes (Creon®,
Solvay Pharma, Herlev, Denmark) 40,000 IU for
regular meals, vitamin A 50,000 IU od for 5 days
followed by 50,000 IU weekly, magnesium 360 mg tid,
zinc 100 mg tid and monthly i.m. injections of 300,000
IU ergocalciferol were initiated. However, after one
month, the patient was admitted to the gastro-
enterological ward as a result of electrolyte deficiency
and was treated with intravenous infusions of
phosphorous and magnesium. On several occasions, he
was asked to indicate his diet and medication in detail.
The diet was considered to be a “normal diet” in
regards to energy and nutrition content, his knowledge
on how and when to take his medication (especially the
pancreatic enzymes) was good and he said that there
were no compliance issues. The intramuscular
injections of ergocalciferol continued and the treatment
with pancreatic enzymes was increased to 80,000 IU
for regular meals and 40,000 IU for snacks.
Two months later, the vitamin D, phosphorous and
magnesium values were normalized whereas vitamin A
deficiency persisted, and calcium and parathyroid
hormone values remained suboptimal. (Figure 1, Table
1). Body weight and walking distance gradually
increased to near normal with a walking distance of
1,500-3,000 m.
DISCUSSION
We report the case of a patient with severe impaired
waling function due to low vitamin D and mineral
levels where walking distance improved upon
treatment of the deficiencies. Although several
treatments were initiated simultaneously, correction of
the vitamin D deficiency was credited with the
improvement in walking distance. In muscle cells, the
action of vitamin D on its receptor promotes protein
synthesis, uptake of inorganic phosphate and helps to
regulate intracellular calcium concentrations. This
affects a broad spectrum of chemical processes (e.g.
the production of energy rich compounds, such as
ATP), and the process of muscle contraction [4].
Vitamin D deficiency primarily causes atrophy of the
type-2 muscle fibers [4], which are fast contracting and
produce high power, and, as a result of this, can result
in muscle weakness and impaired deambulation.
The main reason for the deficiencies in our case was
found to be pancreatic insufficiency. Thus, fecal
elastase was found to be less than 50 µg/g of stool
(reference: greater than 200 µg/g of stool) which is
considered diagnostic for exocrine pancreatic
insufficiency. Low levels of vitamin D have previously
been found in subjects with chronic pancreatitis and
low fecal elastase [5]. An unbalanced diet could
contribute to the hypovitaminosis; however, the diet
reported by the patient was found to be sufficient.
Despite taking peroral calcium and vitamin D for the
previous year, the patient had developed a severe
vitamin D deficiency. Once i.m. injections of
ergocalciferol were initiated, there was a steady
increase in vitamin D. This is in accordance with a
recent Cochrane review on vitamin D supplementation
in children with exocrine pancreatic insufficiency due
to cystic fibrosis, which concluded that there was no
significant effect of peroral vitamin D treatment [6].
This may be in contrast to treatment of other patient
Table 1. Plasma values for a patient with severe impaired walking function.
Parameter
Initial value
3 months later
Reference ranges
25-hydroxy vitamin D2+D3
<10
63
50-160 nmol/L
Vitamin A
0.61
0.09
1.05-3.90 µmol/L
Beta-carotene
<0.04
<0.04
0.28-2.23 µmol/L
Calcium
1.12
1.16
1.18-1.32 mmol/L
Phosphorus
0.44
0.97
0.71-1.23 mmol/L
Magnesium
0.59
0.76
0.70-1.10 mmol/L
Sodium
136
137
136-147 mmol/L
Potassium
2.7
4.6
3.5-5.0 mmol/L
Parathyrin (intact parathyroid hormone)
9.8
14.1
1.6-6.9 pmol/L
Alkaline phosphate
160
109
35-105 U/L
Figure 1. Plasma values of 25-hydroxy vitamin D2+Dfor a patient
with severe impaired walking function due to pancreatic
insufficiency. The initial plasma 25-hydroxy vitamin D2+Dvalue
was found to be less than 10 nmol/L. Treatment with monthly i.m.
injections of 300,000 IU of ergocalciferol was initiated at day 15.
Levels steadily rose and were found to be within the reference levels
at day 79.

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JOP. J Pancreas (Online) 2011 Sep 9; 12(5):482-484.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 12 No. 5 - September 2011. [ISSN 1590-8577]
484
groups. For example, vitamin D supplementation in the
elderly has been well studied [7, 8, 9], and peroral
treatment was found to be effective concerning the
reduction in the number of falls as compared to the
placebo group [10].
To our knowledge, no comparative studies exist on the
use of parenteral or peroral vitamin D in patients with
pancreatic insufficiency. Thus, clinicians have to rely
on empirical knowledge when deciding for a peroral or
parenteral regime, depending on the case at hand.
In our case, peroral treatment with pancreatic enzymes
and minerals did not initially normalize the
phosphorous and magnesium insufficiencies. Non-
compliance was not suspected as the patient could
account for his medication in detail. Only after the
patient had received parenteral therapy with
phosphorous and magnesium, and an increase in
pancreatic enzyme therapy did the levels become
acceptable. A study by Schubert et al. suggests that it is
not the vitamin D deficiency per se but the
simultaneous phosphorus deficiency, which causes the
observed muscle weakness [11]. In our case, the
patient’s walking distance seemed to improve upon
normalization of the vitamin D and phosphorous
deficiency; however, we were not able to differentiate
between the two.
In conclusion, exocrine pancreas insufficiency and
vitamin D deficiency should be kept in mind as a
possible reason for impaired gait and skeletal muscle
weakness; knowledge regarding optimal vitamin D
treatment in cases of pancreatic insufficiency remains
scarce.
Acknowledgements We thank staff at the Information
Department and Library of Viborg Regional Hospital,
for their valuable assistance.
Conflicts of interests We report no conflicts of
interests
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