531:
after 12 months of use (p<0.001). Patients also had decreased use of anti-diabetic medications, lipid-lowering medications, and insulin (p<0.001). In other clinical reports studying 3 patients diagnosed with AGL accompanied by hypoleptinemia, uncontrolled diabetes, and hypertriglyceridemia who were treated with metreleptin for 12–168 weeks, patients had great reduction in HbA1c, from 10.9% to 5.8%, and had normalized serum triglycerides with a mean decline of 90%. Patients reported improved quality of life and reduced need for other medications without significant adverse effects.
99:. After its onset, the disease progresses over a few days, weeks, months, or even in years. Clinical presentations of AGL are similar to other lipodystrophies, including metabolic complications and hypoleptinemia. Treatments are also similar and mainly supportive for symptomatic alleviation. Although HIV- or drug-induced lipodystrophy are types of acquired lipodystrophy, their origins are very specific and distinct and hence are usually not discussed with AGL (see
134:. Subcutaneous fat loss in AGL patients are visible in all parts of the body. AGL mostly affects face and the extremities and may look sunken or swollen in the eyes. However, the degree and location of severity may vary by person. Especially, intra-abdominal fat loss is variable. As subcutaneous fat is lost, affected areas show prominent structures of veins and muscle. Those with panniculitis-associated AGL may present erythematous nodules.
530:
According to a prospective, open-label clinical study at the NIH, metreleptin decreased the fasting glucose level from 180 mg/dL to 121 mg/dL, HbA1c from 8.4% to 6.4%, total cholesterol from 214 mg/dL to 146 mg/dL, and triglycerides from 467 (200-847)mg/dL to 180 (106-312)mg/dL
86:
is termed generalized lipodystrophy while the selective loss of adipose tissues is denoted as partial lipodystrophy. Thus, as the name suggests, AGL is a near-total deficiency of adipose tissues in the body that is developed later in life. It is an extremely rare disease with only about 100 cases
325:
Caliper measurements of skinfold thickness is recommended to quantify fat loss as a supportive information. In this measurement, skinfold thickness of less than 10 millimetres (0.39 in) for men and 22 millimetres (0.87 in) for women at the anterior thigh is suggestive cutoff for the
340:
The use of leptin levels should be carefully approached. While low leptin levels are helpful for making the diagnosis, they are not specific for the lipodystrophy. High leptin levels can help excluding the possible lipodystrophy, but there is no well-established standardized leptin ranges.
337:. Resistance to conventional therapy for hyperglycemia and hypertriglyceridemia serves as an indication for lipodystrophy. Specifically, the diagnosis is strongly considered for those requiring ≥200 units/day of insulin and persistent elevation of ≥250 mg/dl of triglyceride levels.
1134:
Hübler, A.; Abendroth, K.; Keiner, T.; Stöcker, W.; Kauf, E.; Hein, G.; Stein, G. (1998). "Dysregulation of insulin-like growth factors in a case of generalized acquired lipoatrophic diabetes mellitus (Lawrence
Syndrome) connected with autoantibodies against adipocyte membranes".
196:
About 25% of previously reported AGL is associated with panniculitis. Panniculitis is characterized by inflammatory nodules of the subcutaneous fat, and in this type of AGL, adipose destruction originates locally at the infection or inflammation site and develops into generalized
534:
One research published in 2017 reported a middle-aged patient developed AGL after treatment and recovery for autoimmune thrombocytopenia that included immunoglobulin therapy and prednisone, which suggests the autoimmune trigger may contribute to the development of AGL.
538:
Other researches focus on genetics of lipodystrophy; however its relevance to acquired generalized lipodystrophy has not been confirmed so far. One clinical report published in July 2017 stated two brothers with juvenile-onset generalized lipodystrophy was due to
184:. Overlap between panniculitis and autoimmune types also exists. Another theory suggest that AGL is an autoimmune disease itself, as panniculitis can be described as an autoimmune disease, however its triggering factors remains to be unknown. Underlying
115:: the only difference is that AGL patients are born with normal fat distribution and symptoms develop in childhood and adolescence years and rarely begins after 30 years of age. Females are more often affected than males, with ratio being 3:1.
1405:
445:. It is available as 11.3 mg powder in a vial for subcutaneous injection upon reconstitution and needs to be protected from the light. For treatment, patients and their doctors need to be enrolled and certified in the
546:
There have been many published case reports. Meta-analysis of published case reports published within the decade will be very helpful in establishing patient demographic, etiologies, and prognosis of the diagnosis.
996:
Billings, J. K.; Milgraum, S. S.; Gupta, A. K.; Headington, J. T.; Rasmussen, J. E. (December 1987). "Lipoatrophic panniculitis: a possible autoimmune inflammatory disease of fat. Report of three cases".
1469:
248:
The exact pathophysiologic mechanism is mostly unknown; however, each of three main origins, autoimmune, panniculitis, or idiopathic, may have different mechanisms of pathogenesis.
642:
Brown, Rebecca J.; Chan, Jean L.; Jaffe, Elaine S.; Cochran, Elaine; DePaoli, Alex M.; Gautier, Jean-Francois; Goujard, Cecile; Vigouroux, Corinne; Gorden, Phillip (2016-01-02).
137:
Metabolic complications include insulin resistance, high metabolic rate, and uncontrolled lipid levels such as hypertriglyceridemia, low HDL, and high LDL. Patients may develop
1731:
322:
Diagnosis is made comprehensively, together with visual observation, body fat assessment, a review of lab panels consisting of A1c, glucose, lipid, and patient history.
1093:
Oral, Elif
Arioglu; Simha, Vinaya; Ruiz, Elaine; Andewelt, Alexa; Premkumar, Ahalya; Snell, Peter; Wagner, Anthony J.; DePaoli, Alex M.; Reitman, Marc L. (2002-02-21).
209:
AGL with autoimmune origin is responsible for about 25% of all AGL reports. Those with autoimmune origin stems from other autoimmune diseases, most commonly with
527:
Much research for the treatment of lipodystrophy focuses on the safety and efficacy of leptin replacement therapy and the outlook is positive in many studies.
1761:
1611:
1462:
1544:
449:
853:
Handelsman, Yehuda; Oral, Elif A.; Bloomgarden, Zachary T.; Brown, Rebecca J.; Chan, Jean L.; Einhorn, Daniel; Garber, Alan J.; Garg, Abhimanyu;
1455:
271:
of energy and sensitize insulin. In AGL patients, adipose tissues are insufficient and leads to fat deposition in non-adipose tissues, such as
1766:
623:
598:
407:
deficiency. It is the only drug option approved for generalized lipodystrophy-related symptoms and is not intended to use for patients with
1721:
1510:
920:
1571:
403:
analog and was approved by FDA in 2014 for generalized lipodystrophy as an adjunct therapy to diet to treat the complication of
1726:
1680:
415:. Although it is a recombinant human leptin analog, it is not completely the same as natural leptin as it is produced in
1690:
1638:
566:
561:
408:
237:
Although idiopathic AGL accounts for about 50% of all AGL, it can vary in its origin and it is unclear how it develops.
222:
100:
1566:
502:
442:
327:
1205:"Intensive, long-term plasma exchange therapy for severe hypertriglyceridemia in acquired generalized lipoatrophy"
1685:
1554:
1626:
1576:
1339:"Juvenile-onset generalized lipodystrophy due to a novel heterozygous missense LMNA mutation affecting lamin C"
543:
C-specific mutation but it is unknown at this point if this will fall into acquired or familial lipodystrophy.
362:
210:
112:
1705:
1525:
434:
295:
in the body is proportional to the amount of adipose tissue present, AGL patients also have a deficiency of
1249:"Partial and Generalized Lipodystrophy: Comparison of Baseline Characteristics and Response to Metreleptin"
1695:
1621:
1530:
1515:
1435:
334:
742:
498:
412:
72:
1203:
Bolan, Charles; Oral, Elif
Arioglu; Gorden, Phillip; Taylor, Simeon; Leitman, Susan F. (January 2002).
1561:
280:
218:
214:
911:
Gardner, David G.; Shoback, Dolores M. (2017-10-10). Gardner, David G.; Shoback, Dolores M. (eds.).
1600:
1549:
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226:
119:
80:
68:
59:
affecting large areas of the body, particularly the face, arms, and legs. There are four types of
1590:
1586:
1520:
512:
Lifestyle modifications are also recommended, including changes into less fat diet and exercise.
300:
288:
160:
There is no known cause for this disease; however, three origins of AGL are generally suspected:
142:
131:
127:
349:
Initial and general approach for AGL patients are to treat the metabolic complications such as
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960:
878:
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800:
700:
663:
655:
417:
188:
factors may be implicated; however their existence has neither been confirmed nor rejected.
1045:"Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies"
1736:
430:
426:
1363:
1338:
1273:
1248:
973:
948:
883:
874:
859:"THE CLINICAL APPROACH TO THE DETECTION OF LIPODYSTROPHY – AN AACE CONSENSUS STATEMENT"
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813:
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643:
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479:
386:
252:
83:
76:
52:
1247:
Diker-Cohen, Talia; Cochran, Elaine; Gorden, Phillip; Brown, Rebecca J. (2015-05-01).
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60:
56:
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483:
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Program because people on this treatment has a risk of developing anti-metreleptin
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92:
88:
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1010:
1447:
461:
446:
396:
390:
268:
947:
Musso, Carla; Major, Maria Laura; Andres, Eugenia; Simha, Vinaya (2017-01-05).
804:
422:
1337:
Patni, Nivedita; Xing, Chao; Agarwal, Anil K.; Garg, Abhimanyu (2017-09-01).
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516:
370:
311:
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173:
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96:
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1323:
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1204:
1148:
1120:
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892:
822:
712:
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152:
is present in some patients but its prevalence is not known at this time.
1430:
1354:
1264:
1111:
1094:
1061:
1044:
964:
704:
491:
472:
and fasting glucose level, and reduced caloric intake as well as fasting
457:
453:
438:
326:
diagnosis of lipodystrophy. Less commonly, biphotonic absorptiometry and
307:
185:
149:
1397:
949:"Metreleptin Treatment in Three Patients with Generalized Lipodystrophy"
691:
Garg, Abhimanyu (2004-03-18). "Acquired and
Inherited Lipodystrophies".
589:
Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L., eds. (2007).
465:
382:
366:
358:
260:
1298:"Acquired Generalized Lipodystrophy Following Immune Thrombocytopenia"
456:
that decrease the effectiveness of metreleptin, and increased risk of
87:
reported worldwide. There are three main etiologies of AGL suspected:
1409:
614:
James, William D.; Berger, Timothy G.; Elston, Dirk M., eds. (2006).
404:
400:
378:
350:
296:
292:
272:
264:
123:
494:, but its use has been decreased after the approval of metreleptin.
79:, in the absence of nutritional deprivation. The near-total loss of
540:
354:
276:
425:
residues at is amino terminus. It works by binding to the human
1451:
55:
that appears during childhood or adolescence, characterized by
353:-replacement therapy and/or to control the abnormal levels of
75:. Both acquired or inherited lipodystrophy present as loss of
377:
are used for insulin-resistance or high glucose levels, or
287:
levels further contributes to metabolic problems including
1296:
Cunningham, Julia; Nadal, Rosa; Broome, Catherine (2017).
1179:
915:(Tenth ed.). New York: McGraw-Hill Education Lange.
1253:
The
Journal of Clinical Endocrinology & Metabolism
1137:
Experimental and
Clinical Endocrinology & Diabetes
333:
Other forms of insulin resistance may be assessed for
299:
which contributes to excessive eating and worsens the
793:
Endocrinology and
Metabolism Clinics of North America
482:
was previously an option for lowering extremely high
1387:
1209:
The
Journal of Clinical Endocrinology and Metabolism
118:
The hallmark characteristics are widespread loss of
111:
The clinical presentation is similar to people with
1714:
1660:
1651:
1599:
1495:
1486:
1421:
1391:
741:Vantyghem, Pr Marie-Christine, ed. (January 2009).
616:
330:(MRI) can be done for the measurement of body fat.
240:No known preventive measurement has been reported.
63:based on its onset and areas affected: acquired or
26:
21:
644:"Lymphoma in acquired generalized lipodystrophy"
519:of the disease is unknown as of December 2017.
1095:"Leptin-Replacement Therapy for Lipodystrophy"
913:Greenspan's Basic & Clinical Endocrinology
743:"Orphanet: Acquired generalized lipodystrophy"
450:Risk Evaluation and Mitigation Strategy (REMS)
1463:
8:
306:In a few patients with AGL, the presence of
1612:Alpha-1 antitrypsin deficiency panniculitis
1343:American Journal of Medical Genetics Part A
460:. Clinical study with GL patients who took
1732:Marfanoid–progeroid–lipodystrophy syndrome
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812:
667:
1545:Subcutaneous fat necrosis of the newborn
953:Clinical Medicine Insights: Case Reports
787:Hussain, Iram; Garg, Abhimanyu (2016).
578:
468:sensitivity, as indicated by decreased
180:, or any disease state that can induce
1242:
1240:
437:. The receptor belongs to the Class I
1174:
1172:
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1086:
1084:
1082:
1080:
1038:
1036:
1034:
1032:
1030:
1028:
782:
618:(Ninth ed.). Saunders Elsevier.
7:
1722:Congenital generalized lipodystrophy
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1762:Conditions of the subcutaneous fat
1671:Acquired generalized lipodystrophy
875:10.4158/endp.19.1.v767575m65p5mr06
37:Acquired generalized lipodystrophy
22:Acquired generalized lipodystrophy
14:
399:(MYALEPT) is a recombinant human
71:or familial), and generalized or
1572:Lupus erythematosus panniculitis
1302:The American Journal of Medicine
1099:New England Journal of Medicine
693:New England Journal of Medicine
259:to store fat for energy during
1727:Familial partial lipodystrophy
1681:Acquired partial lipodystrophy
1:
660:10.3109/10428194.2015.1040015
497:Cosmetic treatments, such as
1767:Syndromes affecting the skin
1691:HIV-associated lipodystrophy
1639:Superficial thrombophlebitis
1315:10.1016/j.amjmed.2017.04.035
1011:10.1001/archderm.123.12.1662
567:HIV-associated lipodystrophy
562:List of cutaneous conditions
223:systemic lupus erythematosus
101:HIV-associated lipodystrophy
192:Panniculitis-associated AGL
172:AGLs. Triggers may include
148:Case reports revealed that
1783:
328:magnetic resonance imaging
283:. Continuous elevation in
122:, ectopic fat deposition,
1686:Centrifugal lipodystrophy
1555:Post-steroid panniculitis
1049:Journal of Human Genetics
805:10.1016/j.ecl.2016.06.012
789:"Lipodystrophy Syndromes"
591:Dermatology: 2-Volume Set
505:, can be done to replace
409:HIV-related lipodystrophy
363:Anti-diabetic medications
205:Autoimmune-associated AGL
1577:Sclerosing lipogranuloma
211:juvenile dermatomyositis
113:congenital lipodystrophy
1706:Localized lipodystrophy
1567:Weber–Christian disease
999:Archives of Dermatology
648:Leukemia & Lymphoma
389:. If symptoms persist,
217:, but also occurs with
128:metabolic abnormalities
126:deficiency, and severe
1696:Lipoatrophia annularis
1511:Cytophagic histiocytic
1222:10.1210/jcem.87.1.8176
1149:10.1055/s-0029-1211955
486:levels for preventing
335:differential diagnosis
49:Lawrence–Seip syndrome
30:Lawrence-Seip syndrome
499:facial reconstruction
413:partial lipodystrophy
314:has been identified.
1562:Lipodermatosclerosis
1540:needle-shaped clefts
1355:10.1002/ajmg.a.38341
1265:10.1210/jc.2014-4491
1180:"Homepage | Myalept"
1112:10.1056/nejmoa012437
1062:10.1038/jhg.2013.107
965:10.4137/ccrep.s40196
705:10.1056/nejmra025261
593:. St. Louis: Mosby.
433:, and activates the
411:or complications of
281:hypertriglyceridemia
219:rheumatoid arthritis
215:autoimmune hepatitis
1609:without vasculitis:
1550:Sclerema neonatorum
1502:without vasculitis
1043:Nolis, Tom (2013).
393:can be prescribed.
263:period and release
176:that aggravate the
1591:Erythema induratum
1587:Nodular vasculitis
1422:External resources
863:Endocrine Practice
855:Garvey, W. Timothy
375:thiazolidinediones
301:metabolic syndrome
291:. As the level of
289:insulin resistance
143:insulin resistance
132:insulin resistance
1749:
1748:
1745:
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1308:(10): e445–e446.
1005:(12): 1662–1666.
699:(12): 1220–1234.
625:978-0-7216-2921-6
600:978-1-4160-2999-1
168:-associated, and
139:diabetes mellitus
45:Lawrence syndrome
43:), also known as
34:
33:
16:Medical condition
1774:
1658:
1636:with vasculitis:
1617:Erythema nodosum
1584:with vasculitis:
1493:
1480:subcutaneous fat
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1366:
1349:(9): 2517–2521.
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1259:(5): 1802–1810.
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443:JAK/STAT pathway
441:and signals the
227:Sjogren syndrome
120:subcutaneous fat
95:-associated, or
19:
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507:adipose tissues
439:cytokine family
427:leptin receptor
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253:adipose tissues
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1392:Classification
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1384:External links
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1379:
1378:
1329:
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1236:
1215:(1): 380–384.
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1105:(8): 570–578.
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480:Plasmapheresis
464:had increased
421:and has added
387:hyperlipidemia
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233:Idiopathic AGL
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84:adipose tissue
53:skin condition
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1653:Lipodystrophy
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484:triglyceride
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267:to regulate
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178:panniculitis
162:panniculitis
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81:subcutaneous
51:, is a rare
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397:Metreleptin
391:metreleptin
269:homeostasis
27:Other names
1756:Categories
1715:Congenital
1703:localized:
1526:Pancreatic
1189:2017-11-07
752:2017-11-07
573:References
454:antibodies
423:methionine
308:antibodies
257:adipocytes
251:Normally,
174:infections
170:idiopathic
166:autoimmune
97:idiopathic
89:autoimmune
69:congenital
1531:Traumatic
1516:Factitial
931:995848612
517:prognosis
371:metformin
345:Treatment
318:Diagnosis
312:adipocyte
244:Mechanism
65:inherited
1678:partial:
1661:Acquired
1431:Orphanet
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551:See also
523:Research
503:implants
492:xanthoma
476:levels.
458:lymphoma
435:receptor
383:fibrates
365:such as
361:levels.
310:against
255:contain
150:lymphoma
130:such as
107:Symptoms
57:fat loss
1627:Chronic
1496:Lobular
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466:insulin
447:Myalept
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379:statins
367:insulin
359:glucose
261:fasting
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124:leptin
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1521:Gouty
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541:lamin
470:HbA1c
373:, or
277:liver
156:Cause
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