Biomedical subjects

M Ozata

Publications and source records attributed to M Ozata.

64 records · Page 4Linked to original sources

PubMed1995

Can we use plasma fibronectin levels as a marker for early diabetic nephropathy.

Although increased plasma fibronectin (PF) levels have been found in diabetic patients with microalbuminuria, there is still controversy about its clinical implication for detecting early diabetic nephropathy. To evaluate the PF concentration as a possible marker for early diabetic nephropathy, three groups of sex-and age-matched patients were studied I) 22 insulin dependent diabetic (IDDM) patients with microalbuminuria (mean age +/- SEM: 23.3 +/- 3.6 years, mean urinary albumin excretion rate (AER) +/- SEM: 47.1 +/- 39.5 micrograms/min); II) 17 IDDM patients with normoalbuminuria (mean age: 23.4 +/- 4.4 years, mean AER: 7.8 +/- 2.1 micrograms/min) and III) 20 healthy control subjects (mean age: 22.6 +/- 4.1 years, mean AER: 6.7 +/- 2.1 micrograms/min). PF and urinary excretion of albumin were measured by an immunoturbidimetric method using commercially available kits (Boehringer Mannheim GMBH FRG, and Miles Lab., UK). The mean PF was significantly higher in the group with microalbuminuria (406.5 +/- 122.9 micrograms/ml) than in the group with normoalbuminuria (295.6 +/- 96.9 micrograms/ml, P < 0.01) or in the control group (299.54 +/- 105.5 micrograms/ml, P < 0.01). A weak positive correlation was found between PF and urinary albumin values (r = 0.35, P < 0.05). There were no significant correlations between PF and the other variables such as age, duration of diabetes, body mass index, arterial blood pressure, fasting blood glucose, fructosamine and HbA1 in the diabetic patients or in the control group. Our results suggest that the PF concentration could be a weak marker for early diabetic nephropathy. We cannot therefore use PF instead of microalbuminuria because there is only a weak correlation between PF and microalbuminuria.

Adult↗

PubMed1994

Serum thyroglobulin in the follow-up of patients with treated differentiated thyroid cancer.

To determine the significance of serum thyroglobulin (Tg) level in terms of presence or absence of thyroid cancer, we evaluated available serum Tg data on and off T4 therapy in 180 patients with differentiated thyroid cancer who have now been followed up to 18 yr. The presence of cancer was established by radioiodine scans, x-rays, and clinical examination. Thirty-two patients with detectable serum Tg autoantibodies were excluded from this analysis. Tg was measured by RIA with a sensitivity of 1 ng/mL. Patients who had all stages of cancer, but who had no evidence of active disease after treatment, were grouped according to operative and 131I ablative therapy. In patients with a partial thyroidectomy with or without ablation, the presence of Tg did not indicate the presence of cancer since levels were often above either a 5 ng/mL or a 10 ng/mL cutoff. The presence of residual normal thyroid tissue decreases the diagnostic value of serum Tg assay. In patients who underwent near total (NTT) or total thyroidectomy (TT) and 131I ablation, 3 of 55 (5.5%) patients had Tg greater than 5 ng/mL and 1 of 55 (1.8%) patients had Tg greater than 10 ng/mL during therapy, whereas off therapy 13 of 57 (22.8%) patients had Tg greater than 5 ng/mL and 6 of 57 (10.5%) patients had Tg levels greater than 10 ng/mL. In this group of patients, a Tg level less than 10 ng/mL during suppressive therapy indicated the absence of apparent tumor in 54 of 55 (98.2%) of patients. Whereas sensitivity of the assay was increased by withdrawal of hormone, "false positives" increased especially at lower (3-6 ng/mL) cut-off levels. No cut-off value properly categorized all patients. These data suggest, that even in patients who underwent 131I ablation and total thyroidectomy and were thought to be cured, small foci of thyroid tissue which are undetectable by standard 2 mCi 131I scans may exist and produce some Tg. However, these residual cells do not appear to cause an adverse prognosis in most patients. In patients with recurrent or continued disease, during T4 treatment, Tg levels ranged between 2-21,000 ng/mL and 5 of 11 patients had a Tg less than 5 ng/mL. Off treatment, Tg levels ranged between 6-10,700 ng/mL and 3 of 13 patients had a Tg less than 10 ng/mL. In 4 patients Tg levels were less than 10 ng/mL on treatment but greater than 10 ng/mL off therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMedDate not supplied

Event-related brain potentials in male hypogonadism.

Several studies based on psychometric tests have determined an impairment of cognitive functions in patients with androgen deficiency. However, little is known about event-related potentials (ERPs) alterations in male hypogonadism. We investigated alterations of ERP in male hypogonadism before and 3 months after gonadotropin treatment. ERPs were elicited in 20 untreated male patients with idiopathic hypogonadotropic hypogonadism (IHH) (mean age: 21.1+/-1.4 years) and in a group of 30 male controls with comparable mean age and educational level. ERP recordings were repeated 3 months after hCG/hMG treatment. Untreated hypogonadal patients had longer mean P300 latencies and increased P300 amplitudes when compared to those in controls (321.6+/-18.5 vs 299.3+/-20.1 msec, p=0.0002; 12.15+/-4.47 vs 9.38+/-3.02 microV, p=0.011, respectively). The mean P300 latencies did not change significantly 3 months after gonadotropin treatment, while P300 amplitudes were decreased significantly. P300 latencies did not correlate with serum testosterone and other hormone levels. We conclude that prolongation of P300 latencies and increased P300 amplitudes are associated with male hypogonadism, but P300 prolongation is not reversed 3 months after gonadotropin treatment. These findings confirm the occurrence of cognitive defects in hypogonadal patients and would support the hypothesis that perinatal androgen deficiency contributes to an insufficient cognitive development.

Adult↗

PubMedDate not supplied

Central and peripheral neural responses in males with idiopathic hypogonadotropic hypogonadism.

It has previously been shown that abnormal neurophysiologic responses are associated with Kallmann's syndrome. However, little is known about neurophysiologic responses in idiopathic hypogonadotropic hypogonadism (IHH). Fifty-six untreated male patients with IHH (mean age: 20 +/- 0.7 years) were compared with a control group of 20 age-matched male subjects to determine whether IHH can lead to alterations in somatosensory evoked potentials (SSEPs) and brainstem auditory evoked potentials (BAEPs). We have also investigated the effect of gonadotropin replacement (hCG/hMG) therapy on these tests in 20 randomly selected patients. Significant cervical 7 (N13), Erb (N9) and thoracic 12 (N22) latency prolongation was observed in median and tibial nerve SSEPs in patients with IHH as compared with a matched control group. Other components of SSEPs and interpeak latencies of BAEPs yielded no significant difference between untreated patients and control group. Abnormal components of SSEPs did not correlate with basal hormone levels and did not improve with gonadotropin therapy. We conclude that IHH results abnormalities in peripheral but not central nervous system components of SSEPs and that short term gonadotropin treatment cannot correct these abnormalities.

Adolescent↗

PubMedDate not supplied

Central and peripheral neural responses in acromegaly.

OBJECTIVE: To assess the function of the central and peripheral nervous systems in patients with untreated acromegaly. METHODS: We recorded the somatosensory evoked potentials (SSEPs) and brain stem auditory evoked potentials (BAEPs) in 10 patients with untreated acromegaly of brief duration and in 20 age- and sex-matched healthy control subjects to evaluate the function of the central nervous system and at least the median and tibial components of the peripheral nerves. Electrophysiologic studies were done at the time of diagnosis and before the initiation of any treatment for acromegaly. We also studied the distal motor latency, nerve conduction velocity, compound muscle action potentials, and F response in the peroneal nerve; the sensory nerve conduction velocity and sensory potential amplitude were measured in the sural nerve. RESULTS: The mean duration of acromegaly (expressed as time elapsed since patients first recognized signs or symptoms) was 2.4 years. The N(9) and N(13) latencies in median SSEPs and the N(22) latency in tibial SSEPs were significantly prolonged in patients with acromegaly in comparison with the control group; however, central nervous system components of SSEPs and all components of BAEPs were normal. We also noted abnormalities in peroneal motor and sural sensory nerves. No correlation was found between the neurophysiologic data and the basal growth hormone level, the fasting blood glucose level, or the duration of disease. CONCLUSION: Our results suggest that peripheral, but not central, nervous system involvement exists in patients with untreated acromegaly of short duration.

Journal Article↗

PubMedDate not supplied

Event-related brain potentials in patients with hypothyroidism.

OBJECTIVE: To evaluate the cognitive function of patients with hypothyroidism, based on long-latency auditory event-related potentials (ERPs). METHODS: We investigated alterations of P300 latency in patients with hypothyroidism before treatment and after restoration of euthyroidism. ERPs were elicited in 14 untreated patients with hypothyroidism (mean age, 26.71 +/- 2.39 years) and in a group of 30 control subjects with comparable mean age, sex distribution, and educational level. ERP recordings were repeated at 1 and 6 months after attainment of euthyroidism. RESULTS: Untreated patients with hypothyroidism had longer P300 and N1 wave latencies in comparison with those in the control subjects (P = 0.003 and P = 0.018, respectively). The mean P300 latencies did not change significantly 1 month after restoration of euthyroidism. At 6 months after attainment of euthyroidism, however, the mean P300 latencies returned to normal values, similar to those in the control subjects. CONCLUSION: We conclude that P300 latencies are impaired in patients with hypothyroidism, which is indicative of cognitive dysfunction. These alterations, however, may be reversed 6 months after attainment of euthyroidism.

Journal Article↗

PubMedDate not supplied

A case of Noonan's syndrome with numerous cardiac abnormalities.

OBJECTIVE: To report a case of Noonan's syndrome in a patient with numerous cardiac abnormalities. METHODS: We present a case report of a patient with Noonan's syndrome, including clinical, laboratory, and radiologic findings, and discuss the characteristic features of this condition. RESULTS: A 19-year-old male patient had most of the typical clinical findings of Noonan's syndrome-dysmorphic face, short stature, ear abnormalities, cryptorchidism, webbed neck, and high palate. In addition, mitral valve prolapse, secondary mitral insufficiency, left ventricular hypertrophy, and secondary tricuspid insufficiency were diagnosed. Although some cardiac abnormalities have been reported in patients with this syndrome, a case with numerous cardiac abnormalities has not been described previously. CONCLUSION: Noonan's syndrome is a rare disorder with characteristic clinical features and cardiac abnormalities. Although previously reported cases have described cardiovascular anomalies, on review of the literature we found no other case with numerous cardiac abnormalities.

Journal Article↗

PubMedDate not supplied

A case of Klinefelter's syndrome associated with unilateral renal aplasia.

We describe a 22-year-old patient with Klinefelter's syndrome associated with unilateral renal aplasia. Unilateral absence of kidney was detected in our ongoing screening for renal abnormalities by renal ultrasound in male hypogonadism. The present abnormality may be a co-existing entity or previously unrecognized abnormality associated with Klinefelter's syndrome since there is not reported systematic screening for urinary tract abnormalities in patients with Klinefelter's syndrome in the literature.

Adult↗

PubMedDate not supplied

Vitamin d-receptor gene polymorphisms and vertebral bone density in men with idiopathic hypogonadotrophic hypogonadism.

BACKGROUND: Optimal peak bone mass is closely related to sufficient and appropriately timed androgen release. However, attainment of peak bone mass in men, as in women, is under genetic control, as well as being subject to hormonal and mutational effects. With increasing recognition of osteoporosis and related fractures in men, it is of interest to consider whether there is relationship between bone density and vitamin D receptor (VDR) polymorphisms, as described in women. MATERIAL AND METHODS: To assess the influence of allelic variation in the VDR gene on vertebral bone density in men with idiopathic hypogonadrotrophic hypogonadism (IHH), 27 patients (mean age 21.4 +/- 0.4 yrs) and 25 age-and-BMI matched healthy males (mean age 21.2 +/- 0.3) were genotyped using three restriction enzymes (Apa I, Bsm I, and Taq I). Vertebral bone mineral density was measured using dual energy X-ray absorptiometry (DEXA). RESULTS: As expected, vertebral bone density was reduced significantly in patients with IHH (p < 0.001). Despite weak evidence for an association between Apa I polymorphism and vertebral bone density in the IHH group (r = 0.454, p = 0.017 and r2 = 0.20), VDR genotype was not associated with vertebral bone density in either group. When analyzing homozygous haplotypes, the probability of carrying the favorable BAt haplotype was greater in the control group (OR = 2.000 vs. 0.500). CONCLUSION: We conclude that VDR genotype has no influence on vertebral bone density in men with IHH. Thus, allelic variation in the VDR cannot help define those at increased risk for osteoporosis and related fractures among such patients.

Absorptiometry, Photon↗

PubMedDate not supplied

Plasma leptin concentrations in patients with Graves' disease with or without ophthalmopathy.

BACKGROUND: Recent studies have demonstrated that human preadipocyte fibroblasts in orbital connective tissues from patients with Graves' ophthalmopathy differentiate into cells resembling adipocytes and acquire expression of leptin and functional thyroid stimulating hormone receptors. These finding imply that leptin may play a role in the pathogenesis of Graves' ophthalmopathy. However, little is known about plasma leptin concentration in patients with Graves' disease with or without ophthalmopathy. MATERIAL AND METHODS: To investigate this relationship; 28 patients with active Graves' ophthalmopathy (19 female and 9 male, mean age: 32.7+/-10.5 years, mean BMI: 24.8+/-3.7 kg/m2) and 10 patients without ophthalmopathy (6 female and 4 male, mean age: 24.6+/-5.6, mean BMI: 23.02+/-2.4 kg/m2) all with untreated Graves' disease were included in the study at first diagnosis in our endocrinology out-patient clinic. Sex-, BMI- and age-matched twenty healthy subjects (13 female, 7 male, mean age: 31.9+/-10.0, mean BMI: 24.2+/-3.0 kg/m2) were selected as a control group. Plasma leptin levels were measured by a RIA method with a sensitivity of 0.5 ng/ml. RESULTS: Results showed any significant differences neither between patients and controls (7.97+/-5.2 ng/ml vs. 7.83+/-3.7 ng/ml) nor between patients with or without Graves' ophthalmopathy (8.29+/-5.0 ng/ml vs. 7.06+/-5.8 ng/ml) (both P>0.05). Moreover, no correlation was found between plasma leptin levels and ophthalmopathy index score, or proptosis. CONCLUSIONS: Although effects of local leptin production in the orbit cannot be excluded, our data suggest that circulating plasma leptin does not have a significant direct influence on ophthalmopathy index score or pathophysiology of Graves' ophthalmopathy.

Adult↗