DYSREGULATION OF INSULIN-LIKE GROWTH-FACTORS IN A CASE OF GENERALIZEDACQUIRED LIPOATROPHIC DIABETES-MELLITUS (LAWRENCE-SYNDROME) CONNECTEDWITH AUTOANTIBODIES AGAINST ADIPOCYTE MEMBRANES
A. Hubler et al., DYSREGULATION OF INSULIN-LIKE GROWTH-FACTORS IN A CASE OF GENERALIZEDACQUIRED LIPOATROPHIC DIABETES-MELLITUS (LAWRENCE-SYNDROME) CONNECTEDWITH AUTOANTIBODIES AGAINST ADIPOCYTE MEMBRANES, EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 106(1), 1998, pp. 79-84
We report on a 33-year-old male patient with generalized acquired lipo
dystrophy, insulin resistant diabetes mellitus and acanthosis nigrican
s (Lawrence Syndrome). First probable symptoms of lipodystrophy (weigh
t loss, shrinkage of subcutaneous fatty tissue, and loss of muscular s
trength) became evident three years ago, with the onset of diabetes me
llitus occurring about six months later. The patient suffered from the
following clinical symptoms: IDDM with increasing insulin-requirement
, extreme reduction of fatty tissue, fatty liver hepatitis with elevat
ed liver enzymes, glomerulopathy, muscular and neuropathic pains, as w
ell as hypertriglyceridaemia. A basal C-peptide concentration is rathe
r high. Definitely, the endogenous insulin secretion is increased. In
other words, insulin resistance is documented. In an effort to identif
y the pathogenetic mechanisms of lipoatrophic diabetes mellitus in thi
s patient and to develop a therapeutic strategy, antibodies against di
fferent tissues and endocrinologic regulation were investigated. It wa
s possible to demonstrate the presence of serum autoantibodies against
lipocytes of the subcutis and other tissues, against hepatic stellate
cells, together with autoantibodies against different endocrine organ
s. By studying the basis of diabetic abnormalities relating to the gro
wth hormone (GH), the insulin-like growth factor (IGF) dynamics in thi
s patient, i.e. reductions of GH, IGF-I, IGF-II, IGF-Binding protein (
IGF-BP) 2 and IGF-BP 3, were detected. An immunosuppressive treatment
strategy was not beneficial.