ARTICLE
Auteur(s) : Caterina FOTI1, Nicoletta
CASSANO2, Vincenzo O. PALMIERI3, Piero
PORTINCASA3, Anna CONSERVA1, Michele
LAMURAGLIA3, Giuseppe PALASCIANO3, Gino A.
VENA1
1 Unit of Dermatology, Department of Internal
Medicine, Immunology and Infectious Diseases, University of Bari,
Piazza Giulio Cesare 11, 70124 Bari, Italy
2 Istituto Dermopatico dell'Immacolata, I.D.I.,
I.R.C.C.S., 00167, Rome, Italy
3 Section of Internal Medicine, Department of
Internal Medicine and Public Medicine, University of Bari, Piazza
Giulio Cesare 11, 70124 Bari, Italy
Article accepted on 2/10/2003
Case report
A 26-year-old man developed in summer 2002 acral tetany and
muscular cramps. In December 2002, laboratory examinations showed
low serum calcium levels (3.8 mg/dL; normal range
8-10.3 mg/dL), and low plasma levels of parathyroid hormone
(PTH) (8.2 pg/mL; normal range 10-73 pg/mL). For this
reason, he started a therapy with calcium lactogluconate, calcium
carbonate and calcitriol. In February 2003 he presented to our
clinic with transverse leukonychia on all the fingernails. The
patient reported that this had appeared in August 2002 in
association with muscle cramps; he complained of mild paresthesias
and carpal spasms. Chvostek's and Trousseau's signs were both
positive. Investigations revealed normal haemoglobin, leukocyte
count, blood glucose, urea, serum creatinine, electrolytes,
albumin, magnesium, liver and thyroid function tests. Laboratory
evaluation was significant for calcium (6.2 mg/dL),
phosphoremia (5.0 mg/dL; normal range 2.5-4.9 mg/dL), and
PTH (< 10pg/ml). Ionized calcium levels were 2.6 mg/dL
(normal range 4.6-5.3 mg/dL), and calciuria was 11 mg/24h
(normal range 42-352 mg/24 h). The erythrocyte
sedimentation rate was 21 mm/h (normal range 0-10 mm/h);
anti-nuclear, liver, kidney, microsomal, and smooth muscle
autoantibodies were negative. IgA anti- tissue transglutaminase
were 18.2 UA/mL (normal value < 7), IgG
anti-tissue transglutaminase were 27.9 UA/mL (normal
value < 30) and IgA anti-endomysium were positive.
Chest radiograph, electrocardiogram, echocardiogram and ultrasound
examination of thyroid and abdomen were unremarkable. Bone
radiographs were normal and revealed no fracture lines. Bone
mineral density, measured by dual-energy x-ray absorptiometry, was
normal. The diagnosis of hypoparathyroidism was made, whereas
malabsorption was suspected but not clearly confirmed.
On physical examination, multiple transverse white bands on the
fingernails were observed (Fig. 1). The white
lines extended across the entire width of the nail and presented a
rounded edge; they did not disappear on pressure. The nail plate
curvature, cuticles and lunulae were normal; there were neither
signs of onychodystrophy or periungual lesions. The toenails and
hairs were normal. Repeated nail scrapings did not demonstrate
fungal infection and capillaroscopic examination was normal.
Diagnosis of transverse leukonychia associated with
hypoparathyroidism was made and the continuation of treatment with
calcium supplementation and calcitriol was recommended.
After three months, calcium levels improved (7.6 mg/dl) but
were still below the normal range, whereas muscular cramps and
transverse leukonychia disappeared. The patient did not report any
gastrointestinal symptoms. The measurement of transglutaminase
antibodies was repeated, with the following results: IgA
20.8 UA/mL e IgG 53.1 UA/mL. Gastrointestinal endoscopy
and intestinalbiopsy confirmed celiac disease, so that a
gluten-free diet was added. After one month the calcium levels
raised (9.8 mg/dL) as well as PTH values (68 pg/mL).
Discussion
Transverse leukonychia is characterized by single or multiple
homogeneous, complete transverse white lines found on one or more
nail plates [1, 2], which can be traumatic, toxic, infectious or
due to pharmacological damage [3-6]. It can be also associated with
systemic diseases [5]. The term “Mees' lines” refers to transverse
leukonychia observed in arsenic intoxication, while transverse
leukonychia should be used in all other cases [1]. In Mees' lines
and in transverse leukonychia the damage results from abnormal
keratinization of the nail plate due to transient injury to the
nail matrix [4, 5, 7-9], but in Mees' lines it is also the result
of the deposition of arsenic in the nail plate [10].
Hypocalcemia may be associated with nail alterations [11].
Simpson, in 1954, described various types of nail changes in
association with low calcium levels [12]. It has been hypothesized
that hypocalcemia can cause nail abnormalities through spasm of the
arterioles of the fingertips [13]. Moreover, it has been shown that
calcium plays an important role in the synthesis of hard keratins
[14] and modulates the expression of α2β1-
and α3β1-integrins in the nail plate
[15].
To our knowledge, this is the first report of transverse
leukonychia associated with hypocalcemia. The causal role of low
calcium levels in our patient was clearly demonstrated by the
disappearance of nail changes after calcium supplementation, which
resulted in increased calcium levels, even if they remained lower
than normal range, probably due to the concomitant presence of
celiac disease.
In our opinion, the mechanisms responsible for
hypocalcemia-induced leukonychia are represented by angiospasm and
disorganization of keratin, with formation of empty spaces and
consequent transverse bands of reflectance [8].
This case report underlines also the possible association of
transverse leukonychia with severe systemic diseases. n
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