Lipoatrophy

Published on 05/05/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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168 Lipoatrophy

Instruction

Look at this patient.

Look here (examiner pointing at the patient’s thighs).

Salient features

History

• Ask whether the patient is taking insulin for diabetes.

• Is there a past history of renal disease (mesangiocapillary glomerulonephritis)?

• History of HIV and whether patient is receiving antiretroviral agents

• Family history.

Examination

• Atrophy of the subcutaneous fat leading to disfiguring excavations and depressed areas (Figs 168.1 and 168.2).

image

Fig. 168.1 Lipoatrophy.

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Fig. 168.2 Lipoatrophy.

Diagnosis

This patient has atrophy of subcutaneous fat or lipoatrophy (lesion) caused by local injection of subcutaneous insulin (aetiology).

Advanced-level questions

With which conditions is lipoatrophy associated?

• Mesangiocapillary glomerulonephritis

• Localized scleroderma

• Morphea

• Chronic relapsing panniculitis

• HIV.

What advice would you give this patient on insulin?

The insulin should be changed to a more purified form. The purified form should be injected directly into the atrophic area, which often results in the restoration of the local contours.

What is the mechanism of lipoatrophy?

It results from an immune reaction.

Can lipohypertrophy occur with insulin injections?

Yes, as a consequence of insulin being deposited in the same location repeatedly; it has an estimated prevalence of 3.6%. The condition can be unsightly clinically and theoretically could lead to erratic insulin absorption. The precise pathogenesis remains unclear, but possible mechanisms include immune reaction to insulin or excipients of the injection solution, injury from cold insulin, or trauma from repeated local injections. Rotation of injection sites can prevent this complication. It can occur with purified insulins and responds best to liposuction.

What is relationship between lipoatrophy and human immunodeficiency virus?

HIV-1-infected patients receiving antiretroviral therapy have been reported to have abnormal fat distribution including (a) lipoatrophy or loss of subcutaneous fat and (b) central or visceral fat accumulation. Typically these patients have wasting of face and limbs along with adipose tissue accumulations in the abdomen and back of the neck, the latter giving a ‘buffalo hump’ appearance. It was initially considered to be only caused by HIV-1 protease inhibitors but subsequently this has not been substantiated. It has also been associated with nucleoside reverse transcriptase inhibitors (NRTI), via mitochondrial toxicity and interference with lipid metabolism (Lancet 2001;357:592–8). Stavudine-based regimens have a higher cumulative prevalence of lipoatrophy than regimens based on zidovudine, abacavir or tenofovir. Regimens based on nelfinavir are associated with more rapid fat loss than efavirenz. In general, thymidine-based nucleoside analogues have been most associated with lipoatrophy and protease inhibitor drugs most associated with the metabolic syndrome. Leptin deficiency contributes to the insulin resistance and other metabolic abnormalities associated with severe lipodystrophy. Leptin-replacement therapy improves glycaemic control and decreased triglyceride levels in patients with lipodystrophy and leptin deficiency.

What are genes implicated in familial lipoatrophy?

• Familial partial lipodystrophy of the Dunnigan variety. Genes encoding lamins A and C

• Congenital generalized lipodystrophy (Berardinelli–Seip syndrome). Two molecularly distinct forms have been defined:

• Type 1: mutations in AGPAT2, the gene for 1-acylglycerol-3-phosphate O-acyltransferase
• Type 2: mutation in Bscl2, the gene encoding seipin gene.

• Some patients have neither type, so that additional genes are most likely involved, possibly mutation affecting the gene for the peroxisome-proliferator–activated receptor-γ.

The 1923 Nobel Prize in Medicine was awarded for the discovery of insulin to a Canadian surgeon, Sir Fredrick G Banting (1891–1941), and a Scottish physiologist, John JR Macleod (1876–1935) working in Toronto. Banting shared his monetary prize with Charles Best whereas Macleod shared his prize with JJ Collip (the latter purified insulin to the point that it could be used in humans). Macleod corrected Banting’s deficiencies on carbohydrate metabolism and provided him with laboratory support including the services of a graduate student in physiology viz., Charles Best. Macleod was from Aberdeen.

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