Dermoscopy of apocrine hidrocystomas: a morphological study.

BACKGROUND: The dermoscopic morphology of apocrine hidrocystomas remains to be elucidated. OBJECTIVE: To evaluate the morphological findings of apocrine hidrocystomas under dermoscopic observation. METHODS: Dermoscopic examination of 22 cases of apocrine hidrocystomas was performed to evaluate specific dermoscopic criteria and patterns. RESULTS: The most frequently occurring dermoscopic features were found to be: (i) A translucent to opaque, homogeneous area which occupies the whole lesion in all apocrine hidrocystomas (100%). The colour of this homogeneous area was skin-colored in 31.8% of our cases; yellow, in 31.8% and blue, in 22.7% of apocrine hidrocystomas. (ii) Vascular structures were identified in 81.8% of our cases; arborizing vessels, in 68.2% and linear-irregular vessels in 9.1% of our cases; and (iii) Whitish structures were identified in 22.7% of the lesions. The results of our study reveal that the presence of a homogeneous area that occupies the whole lesion and arborizing vessels is the most common dermoscopic pattern in apocrine hidrocystomas (68.2%). CONCLUSION: Apocrine hidrocystomas, above all in its pigmented variant, may represent a dermoscopic pitfall, being difficult to differentiate clinically and dermoscopically from basal cell carcinomas.

Calbindin D-28k immunoreactivity in the temporal neocortex in patients with Alzheimer's disease.

Calbindin D-28k immunoreactivity in the temporal isocortex was examined in seven patients with Alzheimer's disease (AD) and in six controls. In normal brains, calbindin D-28k-immunoreactive cells were bitufted neurons, multipolar cells with ascending dendrites and large double-bouquet cells mainly located in layers II and III. Immunoreactive fibres were seen in the molecular layer and in vertical bundles in layers III and V/VI. Calbindin D-28k immunoreactivity was reduced in patients with AD, although with differences from one patient to another. Immunoreactivity was decreased in the plexus of the molecular layer and in the vertical bundles in the cellular layers in every case. Most patients had, also, decreased immunoreactivity in the dendritic arbors. The number of calbindin D-28k-immunoreactive cells was significantly decreased in three of five patients with moderate or severe dementia, and was normal in two cases with mild dementia.

Calbindin immunoreactivity in normal human temporal neocortex.

Calbindin immunoreactivity in the temporal neocortex was examined in 4 subjects with no neurological, metabolic or malignant disease. The brains were obtained between 1 and 4 h after death and rapidly fixed by perfusion with 4% paraformaldehyde through the carotid arteries, cut into slabs, cryoprotected and stored at -80 degrees C. Sections of the whole left temporal lobe obtained with a freezing microtome were processed free-floating with a well known monoclonal antibody against calbindin according to the peroxidase-antiperoxidase (PAP) method. Calbindin-immunoreactive (CaBP-ir) neurons were found to be local-circuit neurons (interneurons) mainly distributed in the upper cortical layers (layers I, II and III), and were categorized as small multipolar neurons with ascending dendrites ramifying in the molecular layer, small bitufted cells, pyramid-like cells in layer II, horizontal neurons in the molecular layer, multipolar neurons with long descending dendrites, and large double-bouquet cells, some of them exhibiting a very long dendrite with claw-shaped terminals in layer V. Less than 10% of all CaBP-ir neurons were localized in the remaining cortical layers. Pyramidal cells were only very weakly or not stained at all. In addition, CaBP-ir fibres formed a dense plexus in the molecular layer, and vertical bundles 8-10 microns thick and 500-600 microns long, separated by blank spaces 20-40 microns wide were distributed in layers III and V/VI.(ABSTRACT TRUNCATED AT 250 WORDS)

Parvalbumin immunoreactive neurons in normal human temporal neocortex and in patients with Alzheimer's disease.

Parvalbumin-immunoreactive (PARV-ir) neurons were studied in the temporal neocortex of 4 normal subjects and in 7 patients with Alzheimer's disease (AD) whose brains were removed from the skull between 1 and 4 h after death and immediately fixed by perfusion through the carotid arteries to minimize pitfalls related to delayed tissue processing. Freezing microtome sections were immunostained free-floating for PARV using a well characterized monoclonal antibody diluted at 1:5000 and the peroxidase-antiperoxidase method. PARV-ir cells predominated in layers III, IV and V and were classified as bitufted cells and small, medium and large multipolar neurons according to their dendritic arbors. Immunoreactive cell processes surrounding the soma of neighbouring cells and immunoreactive vertical strings of buttons were consistent, respectively, with terminal axons of basket cells and chandelier neurons. The number of PARV-ir cells in the superior (T1), middle (T2) and inferior (T3) temporal gyri was variable from one case to another in both normal and pathological cases. Only 1 of 7 patients with AD had significantly reduced numbers of PARV-ir neurons, thus suggesting that PARV-ir cells in the neocortex are relatively resistant to degeneration in Alzheimer's disease.

[A study of senile plaques with a combined method in brains of patients suffering from Alzheimer's disease]. / Estudio de las placas seniles con un método combinado en el cerebro de pacientes con enfermedad de Alzheimer.

Combined immunocytochemistry to phosphorylated neurofilament epitopes and periodic-acid methenamine silver (PAM) were used in the study of senile plaques (SP) in 6 patients with Alzheimer disease. SP are categorized as diffuse, primitive, mature and burned-out. Amyloid deposits are found in all of them, which is loose in diffuse and primitive plaques, and condensed in mature and burned-out types. Dystrophic neurites are only found in primitive and mature plaques. Combined methods have also shown that apparently isolated dystrophic neurites in the neuropil are always associated to amyloid deposits. These features suggest that amyloid deposition is a primary event in SP formation.

Arteriolosclerotic leucoencephalopathy in the elderly and its relation to white matter lesions in Binswanger's disease, multi-infarct encephalopathy and Alzheimer's disease.

Arteriolosclerotic leucoencephalopathy in the elderly (ALE) is characterized by white matter lesions associated with atherosclerosis and arteriolosclerosis. Mild lesions are focal and probably represent early status cribosus or incomplete lacunar infarcts. Moderate and severe lesions are diffuse areas of demyelination in the centrum semiovale in which lacunar infarcts are seldom observed. The incidence of ALE in a consecutive necropsy series of 50 cases (mean age 62.6 +/- 13.1 years) was 52%, it was rare in the fourth and fifth decades but increased thereafter to reach a prevalence of 100% at the age of 80 years. Mild lesions occurred in 19 patients and lesions were moderate or severe in 7 (14%). The mean age was higher in this group (74.7 +/- 7.6 years) than in patients with white matter changes as a whole. Dementia occurred only in 3 patients with moderate or severe ALE. These data suggest that (a) ALE is common in old age and is probably the cause of leuko-araiosis in most CT scans in the elderly; (b) ALE may be asymptomatic; (c) the severity of white matter changes may be not related to the severity of neurological deficits; and (d) multiple lacunar infarcts or associated degenerative diseases (i.e., Alzheimer's disease) may be the main cause of dementia in patients with ALE. White matter lesions in ALE, Binswanger's disease, transition areas in multi-infarct encephalopathy (MIE) and Alzheimer's disease (AD) are similar in morphology and are probably the result of a subacute hypoperfusion/hypoxic process. Increased arterial blood pressure is a frequent risk factor in ALE, Binswanger's disease and MIE, whereas congophilic angiopathy of the meningeal and cortical vessels, in addition to mild or moderate arteriolar hyalinosis in the white matter, may play a role in the pathogenesis of incomplete infarctation of the white matter in patients with AD.

Gallium-67 scan for distinguishing follicular hyperplasia from other AIDS-associated diseases in lymph nodes.

We have studied gallium-67 citrate scan (Ga-67) in the diagnosis of lymphadenopathy in patients with HIV-associated symptoms. Thirty HIV-infected patients with lymphadenopathy, fever and/or weight loss were evaluated with Ga-67. Lymph-node biopsy and/or needle aspirations were done in all patients. Twelve of 17 patients with grade 2 or 3 Ga-67 (uptake equal to or greater than that in the liver) had mycobacteriosis, three had lymphoma, one had Kaposi's sarcoma plus Castleman's disease and one had follicular hyperplasia. The three patients with grade 1 Ga-67 (uptake greater than that in soft tissue but less than that in the liver) had follicular hyperplasia. Of the 10 patients with grade 0 Ga-67 (less than or equal to that in soft tissue), nine had follicular hyperplasia and one had Kaposi's sarcoma. Sixteen of 17 patients with grade 2 or 3 Ga-67 versus one of 13 with Ga-67 grade 1 or 0 had diseases other than follicular hyperplasia (P less than 0.0001). Ga-67 may be a practical diagnostic tool in HIV-infected patients with lymphadenopathy and constitutional symptoms. A grade 1 or 0 Ga-67 suggests the presence of follicular hyperplasia, and lymph-node biopsy may be avoided unless Kaposi's sarcoma is suspected.

Studies with the Golgi method in central gangliogliomas and dysplastic gangliocytoma of the cerebellum (Lhermitte-Duclos disease).

The rapid Golgi method, combined with current optical and electronmicroscopical techniques, was used in three central gangliogliomas and in one dysplastic gangliocytoma of the cerebellum to study the morphology of ganglionic cells. Gangliogliomas were composed of bipolar, fusiform and radiate cells with dense core and clear vesicles in the perikaryon and cellular processes, the number of each cellular type varying from one case to another. These features, together with the fact that isodendritic neurons are considered to be phylogenetically old neurons, suggest that these tumours are composed of "primitive" neurons that are not homogeneous with regard to their morphology. In contrast, ganglionic cells in dysplastic gangliocytoma are huge cells with long, stereotyped neurites that establish unique asymmetric contacts with neighbouring perikarya and neurites by means of claw-shaped processes covered with synaptic buttons. These morphological characteristics are different from those of any other neuron of the CNS.

Neuronal alterations in patients with dementia: a Golgi study on biopsy samples.

Golgi-impregnated neurons in biopsy samples of the cerebral cortex (area 8) of patients with Alzheimer's disease (AD), Pick's disease (PD) and Creutzfeldt-Jakob disease (CJD), but not in control samples, have swellings in the proximal and mid regions of dendrites of pyramidal and non-pyramidal cells that differ from normal dendritic varicosities. Dendritic outgrowths, isolated or in clusters, and covered with spines occur only in neurons with reduced dendritic arbors mainly located in the vicinity of senile plaques. Degenerating pyramidal and non-pyramidal neurons, although distributed throughout the cerebral cortex in CJD and PD, predominate in layers II, III and VIb in patients with AD.