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VOLUME 9 NUMBER 1 • MARCH 2012
35
SA JOURNAL OF DIABETES & VASCULAR DISEASE
REPORT
burning feet, especially at night, and lanci-
nating pain is also a useful descriptor.’
At the very outset, it is important to try
and assess the severity of pain, using the
variety of severity scales available. A pain
diary may also be useful, and a detailed
medical history and psychosocial assessment
is essential.
In treating pain, there are numerous
guidelines that the clinician can follow, for
example, the ADA, NICE or South African
SEMDSA guidelines. ‘There is no single drug
panacea that works in every patient all the
time. In fact there are significant unmet
needs for drugs directed at the underlying
nerve pathology’, Dr Kaplan noted.
Most commonly, we start with a tricyclic
antidepressant and progress to other avail-
able modalities. Ideal starting therapy would
be the use of duloxetine or pregablin. ‘Of
concern however is that these agents are not
inexpensive and are not covered by medical
aids. We need to initiate a process whereby
painful diabetic neuropathy is included in the
list of chronic conditions requiring full pay-
ment under the prescribed minimum benefits
(PBM) legislation’. Dr Kaplan advocated.
Tramadol may be a useful adjuvant but
should be used with caution with drugs from
the group of selective serotonin reuptake
inhibitors, as there may be an added sero-
tonergic action. Anti-epileptic drugs are also
useful. Dr Kaplan discussed these classes of
drugs and outlined the potential of some
newer agents.
In conclusion, Dr Kaplan noted that pre-
vention is better than cure and clinical trials
have shown that a reduction in HbA
1c
level
of 1% can reduce the prevalence of diabetic
neuropathy by up to 30%. Once neuropathy
is present, tight control of the blood sugar
level also helps to reduce the severity of the
symptoms, and more so in type 1 than type
2 diabetes.
The individualisation of therapy
for haemochromotosis
Hepcidin, the ‘ultimate’ iron regulatory hor-
mone, is the key determinant for assessing
the frequency with which venesection ther-
apy should be used to treat haemochroma-
tosis. ‘Assays for this protein will soon be
available’, noted Prof Peter Jacobs.
Prof Jacobs, emeritus professor, UCT, has
been involved in the early clinical assessment
of iron overload since the 1960s, in associa-
tion with Prof Tom Bothwell and others. He
presented a view of this fascinating jour-
ney from clinical assessment to the recent
determinations of the aberrant genes of iron
absorption. In addition to mutations in the
HFE gene, defects in four additional genes
have been found to cause hereditary haemo-
chromatosis: hepcidin, transferrin receptor 2
(TFR2), haemojuvelin (HJV) and ferroportin.
12
‘In the 1950s, Bothwell and others pub-
lished the first report of the juvenile occur-
rence of haemochromatosis. We now know
that this early clinical appearance which
leads to early cardiovascular abnormalities
is due to a defective haemojuvelin gene.
Similarly, other manifestations reflecting
a series of clinical syndromes can now be
related to the individual genetic abnormal-
ity, which ultimately affects hepcidin levels’,
Prof Jacobs explained.
For the clinician today, Prof Jacobs advised
the following:
• Imaging studies with MRI can be very
helpful in assessing iron stores in the liver,
pancreas and heart tissues.
• Early diagnosis and multidisciplinary sup-
port for the haemochromatosis patient
involving an endocrinologist, biochemist
and cardiologist is essential to prevent
organ damage. Sole-practice support of
a haemochromatosis patient is unwise.
• Advice to patients should be based
on the underlying genetic abnormality
so as to re-assure patients concern-
ing their and their children’s on-going
risk. The University of Stellenbosch is
involved in the local genetic studies and
Prof Jacobs urged that clinicians should
make use of these services to build up
a picture of our South African environ-
ment.
• Fifty per cent of patients will be symp-
tomatic of diabetes, as iron selectively
destroys the
β
-cells of the pancreas.
• The prevalence of haemochromatosis is
1.3% in affected families; six times the
prevalence in the general population.
• Therapeutic use of proton pump inhibi-
tors, dietary and lifestyle modifications,
and iron chelates are not helpful.
• Venesection should be managed, to bal-
ance the loss of iron (venesection activates
intrinsic mechanisms of iron absorption
in the diet). Hepcidin measurement will
in future be definitive in the balancing of
a venesection programme.
3
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‘He who understands pain, understands
medicine’ – William Osler