Radioiodine-induced changes in lymphocyte subsets in patients with differentiated thyroid carcinoma.

This study evaluated changes in lymphocyte subsets in patients with thyroid carcinoma who received iodine-131 for diagnostic and therapeutic purposes. Twenty thyroid cancer patients were entered in the study after total thyroidectomy: ten patients (group A) underwent whole-body scintigraphy with 185 MBq of (131)I and the other ten (group B) received 3700 MBq of (131)I therapy. All patients were in a hypothyroid state at the time of administration of (131)I and started L-thyroxine 150 microg/day 3 days after (131)I administration. Free and bound triiodothyronine and thyroxine, thyroid-stimulating hormone, thyroglobulin, thyroglobulin antibodies, thyroid peroxidase/microsomal antibodies, white blood cell, lymphocyte counts and lymphocyte subsets were serially determined at baseline and at days 2, 7, 15, 30 and 60 after (131)I administration. Twenty healthy age- and sex-matched individuals were used as a reference population for lymphocyte subset values. In group A only a reduction in NK cells at days 7 (P=0.043) and 15 (P=0.037) was observed. In group B, patients showed a delayed reduction in the total lymphocyte count at days 15, 30 and 60 (P=0.008, 0.004 and 0. 018, respectively), and a decrease in B cells throughout the study (at days 7, 15, 30 and 60: P=0.006, 0.0017, 0.0017 and 0.0017 respectively). A transient decrease in NK cells was observed at days 15 (P=0.025) and 30 (P=0.008). Among T cells, the helper phenotype (CD4+) was mainly affected, resulting in a reduction in the CD4+/CD8+ ratio at day 60 (P=0.046). Comparing the two groups, the numbers of B lymphocytes at day 30 (P=0.023) and NK cells at days 2 (P=0.037) and 30 (P=0.023) were significantly lower in group B. Neither group showed any clinical sign of immunosuppression during the follow-up period. In patients with thyroid cancer the sensitivity of lymphocytes to the effects of (131)I administered for diagnostic or therapeutic purposes depends upon lymphocyte phenotype and (131)I activity. NK cells are the most radiosensitive cells, being reduced even by low (131)I activity. At higher activity all subtypes show a reduction, which is more marked and prolonged for B lymphocytes and, to a lesser extent, for T-helper lymphocytes. These changes do not result in clinically relevant immunosuppression.

S-100 and NSE as serum markers in melanoma.

S-100 protein and neuron-specific enolase (NSE) have recently been proposed as serum markers for melanoma. In this study NSE and S-100 serum levels were assayed by commercial IRMA methods in 53 patients with melanoma. The overall prevalence of abnormal marker levels was similar for NSE (26%) and S-100 (30%). The 24 patients in stages I and II had uniformly normal S-100 levels, but abnormal NSE levels were observed in 3 out of the 12 patients in stage II (33%) and in 1 out of 12 in stage I. NSE appears thus to be the marker of choice in the early stages, where its increase points to disease progression. In patients in stages III and IV the prevalence of abnormal values was 34% for NSE and 55% for S-100 (p = < 0.05). In the latter group diagnostic sensitivity increased to 62% if isolated elevation of each marker was considered. In patients with advanced stage disease, both NSE and S-100 should be assayed.

Multiple sclerosis associated with peripheral demyelinating neuropathy.

We report clinical, electrophysiological, magnetic resonance imaging, and nerve biopsy findings of 2 patients with definite multiple sclerosis and peripheral demyelinating disease. Although it is not easy to assess the real incidence of peripheral neuropathy in patients with multiple sclerosis, this association seems to be rare. The combination of central and peripheral demyelination may be a fortuitous coincidence, but it appears improbable. Alternatively, these patients may represent a specific subpopulation and common immunopathogenetic mechanisms (such as immunological factors, endothelial alterations, and abnormal expression of adhesion molecules) may underly both central and peripheral myelin involvement. The study of these cases might clarify specific mechanisms of pathogenetic significance in demyelinating diseases.

In-111 octreotide scintigraphy in the diagnostic evaluation of en plaque meningioma. A case report.

A 44-year-old woman had a 13-year history of a small bulge of the left frontal region which had increased in size during the last year. At admission, an orange-sized, hard, fixed left frontal mass was found. Magnetic resonance imaging showed hyperostosis in the left frontal region which was causing a skull deformity and marked focal meningeal enhancement. A hyperostotic plaque meningioma was hypothesized. In-111 octreotide scintigraphy confirmed the diagnosis before surgery. In-111 octreotide scintigraphy allows biologic characterization of neoplasms in vivo.

Indium-111 octreotide scintigraphy in neurofibromatosis.

Scintigraphy with the radiolabelled somatostatin analogue indium-111-DTPA-D-Phe-1-octreotide has recently been proposed for the imaging of CNS neoplasms expressing somatostatin receptors. While meningiomas are imaged with high sensitivity, neurinomas do not take up octreotide owing to the lack of somatostatin receptors. Neurofibromatosis is a relatively uncommon disorder in which meningiomas and neurinomas often occur in the same patient. Differential diagnosis between these two tumours by computed tomography and magnetic resonance imaging can be difficult. This study reports on 111In-octreotide scintigraphy in four patients with neurofibromatosis. 111In-octreotide scintigraphy was shown to be very helpful in the in vivo differential diagnosis: all four meningiomas showed intense tracer uptake, while all 15 neurinomas were negative (P < 0.001 by Fisher's exact test). It may be concluded that scintigraphy with 111In-octreotide is a useful diagnostic procedure in neurofibromatosis, complementing standard neuroradiological imaging procedures.

Magnetic resonance imaging in multiple sclerosis: an overview.

In less than a decade, Magnetic Resonance Imaging (MRI) has become the examination of choice in patients with suspected multiple sclerosis (MS). It is the best paraclinical test in assessing dissemination in space of lesions. With serial MRI scans, even dissemination in time can be detected. Using serial Gd-DTPA-enhanced MRI scans, the evolution of lesion can be easily followed. MRI studies in MS patients have contributed to shape current ideas about the pathogenesis of the disease showing that focal breakdown of the blood-brain barrier (BBB) is an early event, if not the first, in the evolution of MS lesions. A number of asymptomatic lesions can be detected by MRI in MS patients, suggesting an ongoing disease activity independent of the clinical appearance. Thus, besides its diagnostic usefulness, MRI will represent the best tool to evaluate effectiveness of treatments in therapeutical trials in MS.

An in vivo and post mortem MRI study in multiple sclerosis with pathological correlation.

A young woman affected by multiple sclerosis (MS) was examined by magnetic resonance (MRI) during a relapse. Three months later the patient died from acute pulmonary embolism. An imaging and quantitative MRI study was performed on the formalin-fixed brain. Finally, the left hemisphere was examined by light microscopy after histological and immunocytochemical staining. While fixation significantly reduced T1 and T2 relaxation times, MRI signal and image contrast of the fixed brain were satisfactory. Lesion distribution was very similar in corresponding MRI slices and histological sections. The post mortem MRI scan and pathological study detected several new lesions, as expected from the patient's clinical course. Thus, it was possible to evaluate the age of lesions by comparing the MRI scans. In this study, signal intensity of MS lesions varied according to their histological features, i.e. to their age.

Crossed cerebello-cerebral diaschisis: a SPECT study.

A scintigraphic single photon emission computed tomographic (SPECT) evaluation of frontal perfusion alteration was performed in five patients with known cerebellar lesions but with normal supratentorial computed tomographic (CT) or magnetic resonance (MR) scans. A clearly evident asymmetry was found in prefrontal areas in the four subjects with acquired cerebellar damage. The fifth subject, who had congenital left cerebellar hypoplasia, did not show any frontal flow asymmetry. The data support the growing clinical evidence that the cerebellum contributes to the cognitive processes of the frontal lobes and suggest a possible role for SPECT examination in the assessment of functional cognitive impairment in patients with acquired cerebellar lesions.

Four year double-blind controlled study of levamisole in multiple sclerosis.

41 patients with definite multiple sclerosis (MS) in the stationary phase entered this four year double-blind levamisole-placebo controlled study. 22 patients were treated with levamisole, 150 or 200 mg once a week for a 4 year period, and other 19 with placebo with the same schedule. Patients were put in one of the two groups at random. The treatment was then stopped for those patients who presented a clear exacerbation before the end of the 4 year trial period, and these cases have been considered as negative. Of the group treated with levamisole 8 patients presented an exacerbation during the observation period, and 14 did not. The group treated with placebo presented 14 subjects who had exacerbations and 5 patients who did not. The difference between the two groups was statistically significant. This study demonstrates that levamisole significantly reduced the number of MS patients with acute relapse during the 4 year period of treatment. Nevertheless, not all patients were free from relapse: that could probably suggest that different immunopathological backgrounds may underlie what we usually call MS.