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VOLUME 8 NUMBER 2 • JUNE 2011
99
SA JOURNAL OF DIABETES & VASCULAR DISEASE
REPORTS
a delay before diagnosis (up to eight weeks).
This results in infection extending to the cra-
nium and even the meninges with resultant
cranial osteomyelitis and meningitis. Manage-
ment is at the specialist ear, nose and throat
level, and it requires culturing and the involve-
ment of a histopathologist to exclude cancer.
MRI and gallium SPECT are used to determine
the extent of the invasive infection.
Rhinocerebral mycormycosis
Fifty per cent of cases occur in diabetics, and
keto-acidosis is an important co-factor. The
causative organism is most frequently
Rhizopus
species. Symptomatology is that of a bad cold
and invasion of the sinuses then occurs. Diag-
nosis is made by biopsy and culture and even
by microscopy of the nasal discharge. If inva-
sion of the sinuses has occurred, these must
be drained and the affected tissue debrided.
Amphotericin B is the most often-required
antifungal agent but the response is not
always favourable. There is anecdotal evidence
that combination therapy of Amphotericin B
and one of the newer azoles, Voriconazole or
Posaconazole may be more efficacious.
DIABETES AND HIV INFECTION
Dr Cloete van Vuuren, 3 Military Hospital
The most important principle is to treat both
conditions on their own merit and manage the
disease processes as completely as possible. ‘In
South Africa, we have 5.7 million people who
are infected with HIV. In addition, 440 000 new
infections occur annually and we are recruiting
about 200 000 patients into the HAART pro-
gramme annually.’
It is important to note that as HIV-positive
patients prolong their lives on anti-retroviral
therapy (HAART), they will develop diabetes,
cardiovascular disease and non-AIDS defining
malignancies, and this could happen much
earlier than in non-infected persons.
‘Ten per cent of American women on HIV
therapy develop diabetes, but this rises to
almost 20% in Hispanics and African-Ameri-
cans, while traditional risk factors for diabetes
are still valid in HIV infection. Protease inhibi-
tors increase diabetes risk. HIV-treated women
are also likely to be obese’, said Dr van Vuuren.
‘While HAART is rewarding, as you see
patients get better, we need to understand
that weight loss pre-HAART is due to muscle
loss, and weight gain is due to deposition of
fat viscerally and peripherally in the limbs. Pro-
tease inhibitors (PI) interfere with PPAR-gamma
receptors and cause hyperlipidaemia, insulin
resistance (IR) and adipose maldistribution. Not
all PIs are the same, and atazanavir, daruna-
vir and saquinavir are lipid neutral and do not
affect insulin sensitivity. Unfortunately, these
agents are not yet available in the state sector’,
Dr van Vuuren noted.
Diabetes mellitus is the commonest
co-morbidity in HIV
Anti-retroviral therapy improves health over-
all and also results in the deposition of fat in
the limbs and visceral areas, leading to insu-
lin resistance. Protease inhibitors inhibit glut-
4, causing hyperlipidaemia, insulin resistance
and maldistribution of adipose tissue. Indinavir
and lopinavir are the worst culprits, while the
newer protease inhibitors such as atazana-
vir are lipid neutral with no effect on insulin
resistance. Other drugs such as zidovudine and
stavudine cause lipo-atrophy, and within six
weeks of treatment, cause insulin resistance
because of mitochondrial toxicity. This differ-
ent phenotype from non-HIV diabetics leads to
increased cardiovascular risk over non-infected
diabetics.
It is important to note that antiretrovirals
interfere with the HbA
1c
levels and if you use
the normal cut-off point of 7%, you will only
diagnose 40% of HIV-positive patients with
diabetes. The cut off for diabetes diagnosis in
HIV-treated patients should be 5.8%.
In conclusion, HIV-infected patients must
be treated with antiretrovirals to suppress their
viral load and the metabolic consequences
must be managed with medication and the
usual lifestyle factors. There is still great benefit
in smoking cessation.
THE DIABETIC FOOT
Dr RG Botha, vascular surgeon, Universitas and
Netcare Hospitals
‘The most important aspect to remember is
that injuries to the diabetic foot are caused by
repetitive trauma from everyday activity. The
consequences of foot wounds plus infection
can lead to amputation, the most feared con-
sequence of diabetes’, said Dr Botha.
Three pathological processes, neuropathy,
vascular disease and an impaired response to
infection are the basis of damage to the feet.
‘We can change the vascular disease, not the
neuropathy, so we need to offer these solu-
tions to our patients. The principle is to identify
injuries early, and treat the trauma zone imme-
diately’, commented Dr Botha.
The characteristics of the neuropathic dia-
betic foot of being dry and warm may falsely
reduce the suspicion of ischaemia. One must
test for foot pulses at every visit.
Treating the vascular deficiencies with
bypass surgery is important in re-establishing
blood flow to the foot and is very beneficial.
Today primary patency rates of 60% over three
years are readily achieved by competent vas-
cular surgery.
‘Palpate the pulses and be vigilant for
ischaemia so as to prevent the stairway to
amputation. Please sit down with your patient
and explain the necessity of daily foot care.
Also advise them to quit smoking’, noted Dr
Botha.
Doppler detects flow, not ischaemia. A
useful technique is to raise the foot. If there is
pallor on elevation then there is ischaemia and
the patient should be referred to a vascular
surgeon for assessment and treatment.
DIABETES AND THE GUT
Dr OC Buchel
Autonomic neuropathy can manifest in many
ways: dysmotility (oesophagus, stomach, large
bowel), diarrhoea and faecal incontinence.
Insulin resistance is associated with non-
alcoholic fatty liver disease and an increased
risk of cancers such as liver, pancreas and colon
cancer. Associated conditions may be coeliac
disease, hepatitis C and haemochromatosis.
Infections include small bowel bacterial
overgrowth and
Candida
infections.
Gastroparesis is important to diagnose as
it can lead to malnutrition and dehydration. It
can be difficult to diagnose and treat. Manage-
ment includes advising small, frequent meals,
avoiding fibre and limiting fat intake. Prokinet-
ics like metoclopramide or drugs such as tricy-
clics can be tried.
Take-home message
• The holy grail of HIV therapy
is to achieve undetectable viral
load AND manage the metabolic
consequences.
Management of diabetes in HIV-positive
patients on treatment
• manage diabetes in its own right
• metformin has proven efficacy in this situation
• glitazones can also be used but not with
metformin
• choose antiretrovirals (atazanavir) less likely to
cause lipodystrophy
• pravastatin and fluvastatin are the best statins
to use
• it may be difficult to reach target triglyceride
and HDL cholesterol targets.
