VOLUME 8 NUMBER 3 • SEPTEMBER 2011
135
SA JOURNAL OF DIABETES & VASCULAR DISEASE
CDE WATCH
Metformin’s discovery predated an
understanding of how it works. Its primary
mechanism of action is now known to be
related to its actions at a mitochondrial
level through activation of protein kinases.
An important practical aspect to remember
is metformin’s slow onset of action, with
maximum effects taking two weeks. ‘Also,
if you care about your patient’s well-being,
use only the extended-release formulation
of metformin’.
Metformin is not a first-line therapy in
polycystic ovarian syndrome (PCOS), Dr
Hough believes. ‘In the 113 randomised
clinical trials of metformin used in this con-
dition, very little evidence emerged to sup-
port its use in endometrial protection. In my
view, it is a useful second-line therapy when
other treatments to achieve pregnancy are
not tolerated or are not wanted by the
patient. Its use in patients with POS who
are dysglycaemic and diabetic is warranted
in the interests of improving glycaemic con-
trol’, Dr Hough said.
There is a significant lower risk of
cancer mortality in patients receiving
metformin
Dr Gregory Hough
Haemochromatosis and diabetes
Prof Peter Jacobs and Lucille Wood, Cape
Town
Familial haemochromatosis associated
with diabetes, cirrhosis, joint pathology
and porphyria represent diverse genetically
determined syndromes requiring special-
ist haemotologist evaluation and manage-
ment. Once thought of as a single entity
and treated by venesection until plasma fer-
ritin levels are at the lower limit of normal,
current understanding of the molecular
pathophysiology has elucidated aspects of
this approach.
In suspected cases of iron accumula-
tion, once secondary causes such as acute
inflammation have been excluded, genetic
testing is needed, with interventions based
on the precise mutations present. Liver-
function and ferritin tests, radiological
imaging with liver biopsy, and response to
therapeutic phlebotomy underpin clinical
decision-making.
While venesection is central to avoid-
ing the late complications that range from
diabetes to cardiovascular disease, the
process cannot be arbitrary, as evidence is
emerging that as stores are depleted, there
is activation of the regulatory pathways
and enhanced iron absorption, resulting in
increasing need for phlebotomy. In this situ-
ation, hepcidin levels provide a better meas-
ure of when to stop red cell removal than
plasma ferritin levels.
‘Aside from a specialist endocrinolo-
gist, the cardiologist and rheumatologist
should also be involved in the care of these
patients’, Dr Jacobs concluded.
Fear and diabetes
Dr Rayan S Pillay, Dot Shuttleworth Centre,
Durban
Dr Pillay was a representative of the Cardiff
graduates who dedicated this lecture to the
late Dr Majopela Mhlakaza, a fellow stu-
dent.
‘Fear is the static that prevents me from
hearing myself’ – Samuel Butler
Fear is a factor that may well interfere
with patients’ retention of information
about their diabetes. Using research that
focuses on assessing increased blood flow,
and evaluated by sophisticated imaging
techniques, the role of the amygdala nuclei
has emerged as the guard dog for fear in
the human brain.
‘Unconscious fear exists in our patients
and we need to re-regulate their anxiety
levels’, Dr Pillay noted. We can do this by
a simple process of interaction with our
patients, aimed at increasing their feeling
of being SAFER.
Use the technique of RE-SOLVE: focus
1.
on what we can control about the dis-
ease, not on what we cannot control.
RE-ASSESS: continually emphasise the
2.
positive, as the patient’s inattentiveness
is frequently due to anxiety/fear.
RE-FOCUS: our brains are wired to over-
3.
attend to disaster. Refocus on what has
been achieved.
RE-ENGAGE: engage with patients
4.
about their upside, their achievements,
and desires of their life.
RE-FRAME: emphasise the solutions to
5.
problems by cognitive reflection not emo-
tional introspection on the problem itself.
Obesity is a systemic inflammatory
disorder
Dr David Segal, CDE Johannesburg and
Witwatersrand
The changing gut microbiome:
is it killing us?
Dr David Segal, Johannesburg
In a journey to examine childhood obes-
ity differently and in the context of the
increase in both type 1 and type 2 diabetes,
Dr David Segal, paediatric endocrinologist
with academic commitments at Wits Univer-
sity Medical Faculty and also in private prac-
tice at CDE, Parktown, explored the available
medical literature and interpreted new data
to provide concepts for clinical intervention.
He targeted two main features of modern
obesity. The first is neuro-economics or the
cost–benefit of obtaining food. Secondly, he
noted the consequences of increased fat and
carbohydrate intake, which are challenging
the
β
-cell and altering the gut microbiota so
that food transition and absorption is modi-
fied.
‘While genetic studies have added to our
knowledge of the gene control of appetite,
satiety and feedback mechanisms, they
have failed to give us a practical option
to control obesity’, he said. The field of
neuro-economics applied to food calculates
the price-cost in energy expended, and the
risk and effort to procure the food that we
eat, and relates it to demand, which is ever
present as appetite, and supply, which in
urban areas is plentiful at the nearest super-
market.
