Facial-acquired Partial Lipo Dystrophy Associated with Diabetes : Journal of Diabetology

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Facial-acquired Partial Lipo Dystrophy Associated with Diabetes

Agrawal, Prabhat1; Pursnani, Nikhil1,; Gautam, Ashish2; Gupta, Prashant3

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Journal of Diabetology 14(1):p 62-63, Jan–Mar 2023. | DOI: 10.4103/jod.jod_118_22
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Lipodystrophy can be characterized by the type of fat loss (partial vs. generalized) and by inheritance (congenital vs. acquired).[1] Partial lipodystrophy of limbs is a relatively common form of lipodystrophy in diabetes and is characterized by insulin-resistant diabetes and symmetrical distal lipoatrophy of limbs.[2] Patients usually present with loss of subcutaneous fat in forearm, thigh, and calves. Very rarely, limbs’ sparing lipodystrophy is also reported.

Here, we present a case of middle-aged female diabetic patient presented with partial lipodystrophy of face. The patient agreed to participate in the study and provided written and informed consent.


A 49-year-old woman presented to outdoor department with wasting of facial muscle on both sides of her face for the last 8–10 months [Figure 1A and B]. She is a known case of type 2 diabetes for the last 17 years and hypertension for the last 6 years.

Figure 1:
(A and B) Lipodystrophy evident on the left and right side of face marked with red arrow. A 49-year-old woman presented to outdoor department with complaint of fat loss in the form of dimples on both sides of face for the last 8–10 months initially progressively over 3–4 months but are now nonprogressive for the last 4–5 months

Currently, she is on glimepiride, metformin, vildagliptin, and amlopidine + telmisartan combination. Her random blood sugar was 290 mg/dL and hemoglobin A1c (HbA1c) was 9.6%. Her lipids were high (serum cholesterol 280; serum triglyceride 313, and high-density lipoprotein 36). Her body mass index was 32.3. Her renal function, thyroid function, and pulmonary function were normal. Her serum glutamic pyruvic transaminase was 76 mg/dL (0–40 mg/dL). Rheumatoid factor, antinuclear antibodies, human immunodeficiency virus (HIV), hepatitis B surface antigen, and hepatitis C antibody were normal. Her insulin levels were high 32.30 µU/mL (2.60–24.90 µU/mL). On ultrasonography of abdomen, she was having fatty liver. We advised magnetic resonance imaging of face to see the loss of buccal fat pad but she refused. Her blood pressure, pulse, temperature, and oxygen saturation were within normal limit. Over the patient’s neck, acanthosis nigricans was present. She noticed this fat loss in the form of dimples on face for the last 8–10 months; these dimples of face (fat atrophy) increased initially progressively over 3–4 months but are now nonprogressive for the last 4–5 months. These lesions were painless and symmetric but patient was cosmetically uncomfortable. Patient did not have generalized weight loss. There was no history neither on physical examination and evidence of dystrophy/hypertrophy on trunk, abdomen, and both upper and lower limbs. There was no family history of similar disease, and patient noticed loss of fat on face in the late 40s. On taking her menstrual history, she told that she had irregular menstrual cycle during her early days. We started biphasic insulin before meals and dapagliflozin along with previous oral hypoglycemic agents. Her blood sugar started improving; for the management of dyslipidemia, atorvastatin was added. After 2 months, her HbA1c was 6.8% and blood sugar fasting and post prandial were 110 and 168, respectively. Her lipids also became normal but there was no change in her facial atrophy even after metabolic improvement.


Lipodystrophy syndrome refers to rare heterogenous disorders characterized by defining adipose tissue and out evidence of nutrition deprivation or a catabolic state. Because of rarity and heterogenicity, lipodystrophy disorders are usually unrecognized or misdiagnosed.

Acquired partial lipo-dystrophy includes HIV-associated lipodystrophy, Barraquer–Simens syndrome, and others.[3] Barraquer–Simens syndrome is a very rare disorder possibly autoimmune in origin and fat loss usually occurs in late childhood. Fat loss is usually cephalocaudal.

Treatment of lipodystrophy includes aggressive treatment of comorbidities such as diabetes, dyslipidemia, and leptin treatment (in selected cases).[4] We report this case because very rarely facial atrophy can be associated with diabetes or insulin resistance.


This is a case of acquired partial atrophy of face associated with insulin-resistant diabetes (supported by hyperinsulinemia, hepatic steatosis, acanthosis nigricans, and history of polycystic ovary syndrome). To the best of our knowledge, this is the first case reported from Asia of facial partial lipodystrophy associated with diabetes.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1. Brown RJ, Araujo-Vilar D, Cheung PT, Dunger D, Garg A, Jack M, et al The diagnosis and management of lipodystrophy syndromes: A multi-society practice guideline J Clin Endocrinol Metab. 2016;101:4500–11
2. Shah M, Saboo B. Partial lipodystrophy of limbs in type 2 diabetes: A case report J Diabetol. 2021;12:371–5
3. Araújo-Vilar D, Santini F. Diagnosis and treatment of lipodystrophy: A step-by-step approach J Endocrinol Invest. 2019;42:61–73
4. Oral EA, Simha V, Ruiz E, Andewelt A, Premkumar A, Snell P, et al Leptin-replacement therapy for lipodystrophy N Engl J Med. 2002;346:570–8

Acquired partial lipodystrophy; diabetes; lipoatrophy

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