Cardiovascular Journal of Africa: Vol 26 No 2 (March/April 2015)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 2, March/April 2015

AFRICA

Epidemiological data from the literature support a significant

association of

Hpylori

seropositivity with CVD, insulin resistance

and elevated parameters of the metabolic syndrome.

12,13

The risk of the MetS is greater in HIV-infected individuals

compared with the general population because of a greater

prevalence of lipid and glucose abnormalities.

14,15

HIV infection

itself is associated with disturbances in lipid metabolism such

as hyperglyceridaemia, and a decrease in total cholesterol and

high-density lipoprotein (HDL) cholesterol levels.

Treatment

of HIV infection with highly active antiretroviral therapy

(HAART) can also induce severe metabolic complications

including lipodystrophy, dyslipidaemia, and insulin resistance.

Patients with HIV infection and the MetS had increased intima–

media thickness (IMT), similar to that found in diabetes.

While inflammation is recognised as a major contributor

in the pathogenesis of both diabetes and atherosclerosis, little

is known about the key inflammatory molecules involved in

atheroma and diabetes in HIV-positive HAART recipients.

However, epidemiological studies have shown that

H pylori

infection has become a common cause of chronic gastritis in

HIV/AIDS patients.

It is possible that prevalent infection by

H pylori

enhances the inflammatory process observed in the

atheroma of HAART-recipient HIV-positive individuals, leading

to CVD and the MetS.

In many central African countries, the first-line anti-retroviral

therapy (ART) protocol in the public health sector recommends

the combination of three drugs (stavudine, lamivudine and

efavirenz), commonly referred to as ‘regimen 1A’. In ‘regimen

1B’, efavirenz is substituted with nevirapine, particularly in

females of reproductive age.

There is a paucity of data on

H pylori

seropositivity, socio-

economic status and the use of HAART in patients with the

MetS and HIV co-infection among black Africans. Hence, the

aim of this study was to determine the relationship between

H pylori

infection and the MetS among HIV-infected black

Africans.

Methods

This was a cross-sectional study design. The study population

consisted of HIV-infected patients, aged 20 years and above;

all black Africans attending LOMO specialised heart clinic in

Kinshasa, Democratic Republic of the Congo between January

2004 and December 2008.

The study protocol was designed according to the Helsinki

Declaration II,

and approved by the local ethics committee.

Patients were consecutively enrolled in the study if they were

HIV infected, and diagnosed with or without the MetS.

Exclusion criteria included pregnancy, dysfunctional thyroid

gland, nephrotic syndrome, hepatic cirrhosis, and use of any of

beta-blocker, digoxine, lipid-lowering drugs or insulin. All study

participants were enrolled by informed consent. Associations

between

H pylori

infection and the MetS were assessed among

HIV-infected patients with and without the MetS.

Data were collected using structured and standardised

questionnaires. Demographic data (gender, age), lifestyle (socio-

economic status) and behavioural risk factors (intravenous

drug use, current cigarette smoking and excessive alcohol

intake) were recorded. Low and high socio-economic status

(SES) were defined according to our previous work.

Patients’

anthropometric parameters (body weight and height, waist

and hip circumferences) were measured following a physical

examination.

For patients diagnosed as having HIV infection, we used

World Health Organisation (WHO)

and Centres for Diseases

Control and Prevention (CDC)

staging systems to classify

their disease stages. Information on the use of highly active

anti-retroviral therapy (HAART) was obtained from all study

participants.

Blood pressure (BP) was measured after the participant

had rested for 10 minutes, seated in a quiet waiting room. BP

was measured on the left arm with elbow flexed at heart level,

by the same physician using an Omron HEM 705 electronic

BP manometer (Omron Life Science Co, Ltd, Tokyo, Japan).

Three readings were obtained, and the average was used for the

analysis.

Definitions and criteria for the MetS

Criteria defined by the 2005 International Diabetes Federations

(IDF) report were used to ascertain cases of the MetS.

Participants with three of the following criteria were defined

as having the metabolic syndrome: prerequisite was waist

circumference

≥

94 cm in men and

≥

80 cm in women;

triglycerides

≥

150 mg/dl (1.7 mmol/l); HDL cholesterol

40mg/

dl (1.03 mmol/l) in men and

50 mg/dl (1.29 mmol/l) in women;

systolic blood pressure

≥

130 mmHg, diastolic blood pressure

≥

85 mmHg; and fasting glucose

≥

100 mg/dl (5.6 mmol/l) or

previously diagnosed type 2 diabetes. Other participants met the

criteria for high blood pressure or high fasting glucose levels if

they were currently on antihypertensive or oral hypoglycaemic

therapies, respectively.

The cardiometabolic co-morbidities included arterial

hypertension, type 2 diabetes, myocardial infarction, stroke, long

QTc

≥

0.420 ms, gout/hyperuricaemia (uric acid

≥

7 mg/dl), and

subclinical atherosclerosis (pulse pressure

≥

60 mmHg + IMT

≥

1 mm or carotid plaque).

4,22,23

Laboratory investigations

The initial HIV test was performed using HIV rapid test

(SmartCheck test, World Diagnostics Inc, USA) while a

confirmatory test following an initial positive HIV result was

performed using Uni-Gold

Recombigen

HIV (Trinity Biotech

PLC, USA) from the blood samples. CD4

lymphocyte cell

count was measured using CyFlowR Counter (Partec GmbH;

Munstar, Germany) and HIV RNA viral load was quantified by

means of Nuclisens Easy Q HIV-1 system (Biomérieux, Box tel,

the Netherlands).

Haemoglobin and haematocrit levels were measured in blood

using standard haematological techniques. Fasting glucose

levels were measured from plasma samples using the glucose-

oxydase method and spectrophotometer (Hospitex Diagnostics,

Florence, Italy). Total cholesterol, HDL cholesterol, uric

acid and triglyceride levels were measured using enzymatic

colorimetric methods (Biomérieux, Marcy l’Etoile, France).

Oxidised low-density lipoprotein (LDL) cholesterol, a biomarker

of oxidative stress, was measured using solid-phase two-side

enzyme immunoassay (Mercodia AB, Sylveniusgatan 8A, SE754

50, Uppsala, Sweden).