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Complications and Comorbidities> Infectious Diseases>
Diabetes Guide Home PageEmail this module to a friend

HIV-Associated Diabetes

Todd T. Brown, M.D, Ph.D.
04-02-2010

DEFINITION

  •  Human immunodeficiency virus (HIV) is a retrovirus that causes AIDS by infecting helper T cells of the immune system, leading to immunosuppression and opportunistic infections. Modern antiretroviral therapy can effective control HIV replication and has greatly improved the prognosis for HIV-infected patients.
  • HIV-associated diabetes refers to diabetes occuring among individuals with HIV who may not otherwise have traditional risk factors for diabetes.

EPIDEMIOLOGY

  • Insulin resistance (IR) and diabetes mellitus (DM) are common among HIV+ individuals.
  • Incidence of DM is four times greater in HIV+ men on highly active anti-retroviral therapy (HAART) compared to HIV- men (Brown).
  • Complications such as kidney disease and cardiovascular disease may occur more frequently in HIV+ versus HIV- individuals (Neuhaus).
  • Risk factors for IR/DM in HIV: abdominal fat accumulation (i.e. lipodystrophy), peripheral lipoatrophy, family history of DM, obesity, age, hepatitis C positivity, low CD4 nadir, black/Hispanic race.
  • Certain protease inhibitors (PIs) may have a direct effect on insulin resistance. Lopinavir/ritonavir is the PI in current use most associated with IR.
  • Stavudine and zidovudine are also associated with insulin resistance.
  • Consider glycemic effects of other medications commonly used for HIV-related comorbidities: corticosteroids, growth hormone, megestrol acetate, immunosuppressants, atypical antipsychotics
  • In general population (and presumably in HIV+ pts), IR/DM increases risk for coronary artery disease.

DIAGNOSIS

  • DM is diagnosed using the same criteria with or without HIV.
  • HbA1c underestimates glycemia in HIV+ pts on HAART by ~ 0.8% (Kim)
  • No accepted role for clinical use of insulin levels to assess IR

CLINICAL TREATMENT

  • Balanced diet and regular exercise crucial. Recommend ADA diet.
  • Lifestyle modification shown to improve metabolic parameters in HIV-infected patients.
  • Aggressive risk factor modification for coronary disease: lipid control, HTN control (generally with ACE-I or ARB), smoking cessation, cocaine avoidance, aspirin therapy.
  • First line treatment: metformin. Some consider pioglitazone first line for HIV-infected patients with lipoatrophy, as this is associated with modest increases in subcutaneous fat.
  • Metformin: reduces hepatic IR. Associated with reduced visceral fat, BP, triglycerides (TG) (decreased 10-20%) in HIV+ pts. Some studies have shown decreased limb fat with metformin; use with caution in patients with lipoatrophy. Enhanced theoretical risk of lactic acidosis with nucleoside reverse transcriptase inhibitors (NRTIs), liver disease, and CHF.
  • TZDs (pioglitazone and rosiglitazone): reduce peripheral IR as peroxisome proliferator-activated receptor (PPAR) gamma agonists. Effect on lipoatrophy controversial. Pioglitzaone may be better than rosiglitazone for lipoatrophy, but no head-to-head trials. Effect present only on those not on stavudine or zidovudine. Some increase in TG with rosiglitazone but not pioglitazone. Rosiglitazone may increase CVD risk. Lipid profile with rosiglitazone less favorable than pioglitazone. Maximum effect after several weeks.
  • Use sulfonylureas, meglitinides, exenatide, sitagliptin or acarbose as second line therapies.
  • No accepted role for pharmacologic interventions for those with IR or pre-diabetes. Metformin can be considered in overweight, young patients with pre-diabetes per ADA guidelines.
  • Consider switching from PI to non-nucleoside reverse transcriptase inhibitor (NNRTI)-based regimen provided viral control not jeopardized. Consider low dose (10-15 units) bedtime glargine, detimer, or NPH insulin in combination with oral anti-diabetic agents if failing oral agents. Insulin effective for glucose control with individualized regimen.
  • Note: newer PIs (atazanavir, darunavir) are not associated with insulin resistance.

FOLLOW UP

  • In routine management of HIV, check fasting glucose at baseline, prior to, 3 and 6 months after HAART initiation, then yearly if normal.
  • In people with DM, self-monitor blood glucose 1-2 times per day on oral agents, 2-4+ times/day if on insulin. Monitoring may be more or less intensive depending on the stability of glycemia
  • Monitor HbA1c every 3-6 months, depending on control. Goal <7%, with caveat regarding accuracy of A1c in HIV-infected persons.
  • Patients with pre-DM should be screened at 3-6 month intervals.
  • Monitoring for complications: dilated fundoscopic exam by ophthalmology, spot urine for microalbumin and foot exam with inspection, monofilament, and vibration testing at baseline and every 6-12 months.

EXPERT COMMENTS

  • With effective  HAART, HIV+ pts are living longer and age-related co-morbidities, such as DM, are gaining importance.
  • Due to effects of antiretroviral medications and/or chronic infection, kidney disease and cardiovacular disease occur at higher than expected frequencies.
  • Multiple risk factor modification is essential.

REFERENCES


 
 
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