Alzheimer's disease(AD) is one of the most common causes of mental deterioration in elderly individuals, accounting for around 45~60% of the overall cases of dementia over 65 years of age. Although there is presently no "cure" for AD, a large number of potential therapeutic interventions have emerged to correct cholinergic dysfunctions. Currently, cholinergic therapy, particularly cholinesterase inhibition, represents the most realistic approach to the symptomatic treatment of AD. Modest efficacy for mild to moderate AD has been shown in well-designed clinical trials for tacrine, donepezil, rivastigmine, and galantimine. Among other treatment options, estrogen replacement therapy in postmenopausal women is under active investigation, but recent studies showed somewhat disappointing results. Epidemiological and clinical data suggest that nonsteroidal anti-inflammatory drugs are beneficial in the treatment and prevention of AD. But prednisone and COX-2 inhibitor, celecoxib showed no clinical benefit in recent studies. Alpha-tocopherol and gingko biloba showed some beneficial effect in delaying the progression of AD and enhancing cognitive functions. Immunization with beta amyloid peptide was considered to be the only method to prevent and halt disease progression in patients with AD. Recently, phase II clinical trial using synthetic beta amyloid peptide (AN-1792) was discontinued because some patients showed neuro-inflammation which may be caused by autoimmune responses.
Aged ; alpha-Tocopherol ; Alzheimer Disease* ; Amyloid ; Autoimmunity ; Celecoxib ; Cholinesterases ; Cognition ; Dementia ; Disease Progression ; Estrogen Replacement Therapy ; Female ; Ginkgo biloba ; Humans ; Immunization ; Methods ; Prednisone ; Rivastigmine ; Tacrine

No abstract available.
Hypertension, Renovascular*

No abstract available.
Child* ; Humans ; Male*

No abstract available.
Diabetes Mellitus* ; Insulin*

No abstract available.
Child* ; Humans

No abstract available.
Diagnosis*

No abstract available.
Animals ; Growth Hormone* ; Hypothyroidism* ; Rats*

No abstract available.

The final adult height in the children with true precocious puberty are destined to be short due to excessive bone maturation, compared to the growth velocity, regardless of its etiologies. To improve this final shortness, long-acting GnRH analog have been tried to the children with true precocious puberty. We evaluated the parameters of the growth. including the growth velocity, height SDS, predicted final adult height obtained by Bayley-Pinneau method in the 12 children with true precocious puberty after treatment of long-acting GnRH analog, Decapeptyl, The results were as belows; 1) The mean age of pubertal onset was 5.0 +/-2.9 year of age (1~8.6 years of age). The bone age (10.2+/-3.5 years of age) at diagnosis were significantly higher than the chronological age (7.2 +/-3.0)(Fig. 1,p<0.001). 2) During treatment with Decapeptyl, the progression of bone maturation seemed to be reduced, compared to the progression of chronological age, but there was no statistically significant difference (p>0.05). 3) The responses of LH and FSH to GnRH administration at 6 months of treatment with Decapeptyl were significantly reduced to prepubertal level, compared to those before the initiation of Decapeptyl treatment. 4) The height SDS before and at the first year of treatment with Decapeptyl were 1.5+/-0.3 and 1.4 +/-0.2, which had no significant change during treatment (Fig, 3, p>0.05). But the height velocity during the first year of treatment (4.9+/-1.7 cm/year) was significantly reduced, compared to the height velocity during the one year before treatment (10.1+/-1.5 cm/year)(Fig, 4, p=0.01). 5) The predicted final adult height, obtained by Bayley-Pinneau method, at second year of treatment (174.4 +/-1.8 cm) were significantly improved, compared to those at initial treatment (151.7 +/-2.3 cm) and 6 months of treatment (156.9+/-2.5 cm)(Fig, 5, p<0.05). 6) The predicted final adult height, obtained at the first year of treatment had significant inverse correlation with the bone age at the initiation of treatment with Decapeptyl (Fig. 6, p<0.05,r=-0.84), but had no corrleation with the chronological age at the initiation of treatment. 7) During this study, we could not find any adverse reaction, which could come with the therapy of Decapeptyl, such as facial flushing and hypotension. With these result, we can conclude that the final adult height can be improved if true precocious puberty could be diagnosed early and treatment with long-acting GnRH analog be given early.
Adult* ; Child* ; Diagnosis ; Flushing ; Gonadotropin-Releasing Hormone ; Humans ; Hypotension ; Puberty, Precocious* ; Triptorelin Pamoate

We studied the correlation between the bone age and the predicted adult height, final adult height in the 69 children (30 salt losing form and 39 non-salt losing form) diagnosed as 21-hydroxylase deficiency, retrospectively. The results were as belows; 1) The bone age was similar to the chronological age in the children with salt-losing form (5.3+/-2.3 and 6.3+/-3.5 years, respectively), but the bone age was much more advanced, compared to the chronological age in the children with non-salt losing from (7.8+/- 2.9 and 12.0 +/-3.5 years, respectively)(Table 1.p<0.001) 2) In the children with salt-losing form, the height SDS for the chronological age and bone age, were -0.3 +/-1.3 and -1.1+/-2.6, respectively, which has no difference. In the children with non-salt losing form, the height SDS for the bone age, were much lower than the height SDS for the chronological age (-2.1+/-1.3 and 1.5+/-1.5, respectively)(Table 2.p<0.001). 3) The incidence of true precocious puberty is significantly higher in the children with non-salt losing from (26 children) than in the children with salt losing from (6 children)(p<0.05). 4) All children with salt losing form received hydrocortisone and mineralocorticoid within the first month of life, but the average age at the first hydrocortisone therapy in the children with non-salt losing form was 5.0 3.3(0.1~13.1) years of age. The dosages of hydrocortisone were similar in two forms (24.3 +/-7.6 mg/m2 in non-salt losing form). 5) The predicted adult height, obtained by BP method, was shortest among three methods predicting adult height (RWT; 181.5 +/-14.6 cm, TW 169.2 13.2 cm, BP; 151.6 +/-9.3 cm)(Fig.1.p<0.001). 6) Seventeen children with 21-hydroxylase deficiency attained 152.1+/-8.8 cm of final adult height (152.2+/-1.5 cm in 12 salt losing form and 152+/-1.4 cm in 5 non-salt losing form). These final adult heights were closest to the predicted adult height, obtained by BP method, compared to other two methods (Fig. 2.p<0.05). 7) Among 7 children, whose mid-parental height could be obtained, one child could reach within the target height and other 6 children reached far below the target height (Fig. 3.p<0.005). In conclusion, to attain normal growth and normal final adult height, in is suggested that meticulous control should be needed for adequate suppression of adrenal androgen and mineralocorticoid should be given to all children who have high level of plasma renin activity in the children with 21-hydroxylase deficiency, with regular follow-up of laboratory tests and growth parameter. Additionally, even if patient has non-salt losing form, the diagnosis should be made and adequate hormonal therapy should be given as soon as after birth.
Adrenal Hyperplasia, Congenital* ; Adult* ; Child* ; Diagnosis ; Follow-Up Studies ; Humans ; Hydrocortisone ; Incidence ; Parturition ; Plasma ; Puberty, Precocious ; Renin ; Retrospective Studies ; Steroid 21-Hydroxylase*