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Letters to the Editor |
University of Keele Stoke-on-Trent, United Kingdom
Jill Belch
Ninewells Hospital & Medical School Dundee, United Kingdom
Serri et al. (1) reported recently an
interesting finding of altered monocyte behavior and increased
production of both plasma and monocyte-derived cytokines, tumor
necrosis factor alpha (TNF-
), and interleukin-6 (IL-6) as surrogates
of monocyte activation in patients with growth hormone deficiency. Also
they demonstrated increased adhesiveness of monocytes to cultured
bovine aortic endothelial cells. We were intrigued by the findings of
Serri et al., as our group has recently reported preliminary
results of increased plasma levels of soluble adhesion molecules,
intercellular cell adhesion molecule-1 (ICAM-1), and E-selectin in a
group of patients with growth hormone deficiency (n = 36) who were
free from any clinical evidence of vascular disease (2). Both
E-selectin and ICAM-1 are emerging as new markers of activated
endothelium (3), and ICAM-1 is a marker of interaction of activated
endothelium with monocytes and subsequent transendothelial migration of
white cells into the subendothelial space (4), an early step in the
formation of atherosclerotic vascular disease. We feel, however, that
the report by Serri and colleagues deserves some comments.
We don’t have enough clinical details of their group of patients, as
there is no mention in their report whether their patients were free
from any evidence of clinical vascular disease. Established and
advanced arteriopathy, especially with symptoms, undoubtedly was a
confounding factor that may have affected their findings. Furthermore,
one of their patients was described as having glucose intolerance, but
whether this patient had frank diabetes or impaired glucose intolerance
is another limiting factor in their results. Hyperglycemia is a known
trigger of altered white cell behavior (5, 6) and is associated with
excess production of cytokines like TNF- (7). Also, the smoking
habits of their patients was not stated, and cigarette smoking is known
to influence the cytokines TNF- and IL-6 production (8). Another
confounding factor in their study was the sex hormone
deficiency/replacement. If we exclude the patient with isolated growth
hormone deficiency, two other patients were not on sex steroid
replacement. The study did not indicate if they indeed had intact
pituitary-gonadal axis, or if they were deficient but, for one reason
or another, were not on sex steroid replacement. Sex steroid deficiency
is a factor, which should have been accounted for (9).
One further comment is related to the fact they could not find an increased plasma lipid peroxide level in their group, in contrast to the recent report by Anderson et al. (10), who reported increased levels of malondialdehyde in a slightly larger group of patients with growth hormone deficiency (n = 17). It is possible that the two groups may be different, so further research in this area is warranted.
Finally, it seems that the findings of Serri et al. are consistent with ours, and it might have been more exciting if they had examined the level of the soluble adhesion molecules in their group of patients. It seems to be an area they have explored before (11), and the scientific audience might have gained further insight in this area. It remains that Serri and colleagues have presented a novel finding that will undoubtedly shed more light on this interesting area of clinical endocrinology.
Footnotes
Address correspondence to: Tarik A. Elhadd, Department of Medicine, Keele University, North Staffordshire Hospital, Thornburrow Drive, Staffordshire, Stoke-on-Trent, United Kingdom.
Received May 13, 1999.
References
production in NIDDM patients after gliclazide treatment. Diabetes Care. 21:487–493.[Abstract]
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