• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.90-96
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• 1999

Background : Osteoporosis has been reported in patients with chronic obstructive pulmonary disease, but this association is not well established. This study was undertaken to determine whether the prevalence of osteoporosis was increased in patients with chronic obstructive pulmonary disease and we examined the relationship of corticosteroid administration with osteoporosis. Method: Subjects were 23 patients with chronic obstructive pulmonary disease and 20 control patients. We reviewed hospital records and measured bone mineral density using dual-energy x-ray absorptiometry(Lunar. USA). Results: Mean bone mineral density(BMD) of spine in COPD group was $0.683{\pm}0.154 g/cm^2$ and $0.971{\pm}0.212g/cm^2$ in controls(p<0.01). But there was no significant difference in femoral neck BMD. There were seventeen cases of osteoporosis and six cases of osteopenia in COPD group and three patients of osteoporosis and one case of osteopenia in controls. But, there was no significant correlation between disease duration of COPD and spinal T score(r=-0.395, p>0.05). Ten patients were received corticosteroid in COPD group. Spinal T score in steroid receiving patients were $-3.82{\pm}0.94(SD)$ and $-2.82{\pm}0.97(SD)$ in not having steroid patients(p<0.01). Cumulative dose of corticosteroid was associated with spinal T score(r=-0.424, p<0.05) and duration of corticosteroid administration also associated with spinal T score(r=-0.457. p<0.05). Spinal BMD of patients not having corticosteroid in COPD group(n=13) were significantly lower than that of controls($0.71{\pm}0.13 g/cm^2$ and $0.97{\pm}0.21 g/cm^2$, p<0.01). Conclusion : Prevalence of osteoporosis is increased in patients with chronic obstructive pulmonary disease. Especially patients who are receiving corticosteroid have high risk of osteoporosis or osteopenia and need for preventive management.

• Radiation Oncology Journal
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• v.4 no.1
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• pp.15-20
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• 1986

From 1979 to 1984, 39 local allograft irradiations were given to 29 patients: 10 irradiations were administered for prevention and 29 for reversal of acute rejection of transplanted kidney. Three doses of 150 cGy every other day were combined with high-dose of methylprednisolone pulse (1 gm/day) for 3 days. For prevention of acute rejection, local irradiation was delivered on the days 1, 3, and 5 after the transplantation, and for reversal, irradiation started after the diagnosis of acute rejection. Eight out of 10 patients irradiated for prevention had acute allograft rejection, and, what is more, there was no surviving graft at 15 months after transplantation. Reversal of acute rejection was achieved in $71\%$. When the pre-irradiation level of serum creatinine was below $5.5mg\%$, the reversal rate was $93\%$, but above $5.5mg\%$ the reversal rate was only $17\%$ (p<0.01). Reirradiation after failure was not successful. Among 15 reversed patients, $7(47\%)$ had subsequent rejection (s). The functional graft survivals at 6 month, 1, 2, and 3 year were $70\%,\;65\%,\; 54\%,\;and\;54\%$, respectively. Therapeutic irradiation resulted in better graft survival when serum creatinine was below $5.5mg\%$ (p<0.001) or when irradiation started within 15 days after the diagnosis of acute rejection (p<0.001).

• Development and Reproduction
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• v.13 no.4
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• pp.329-339
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• 2009

Cortisol is present in high concentration in the ovary and its receptor is expressed in the ovarian cells. Moreover, cortisol is known to have a role in steroid synthesis and cell metabolism in human granulosa and lutein cells. However, little is known of the role of cortisol presenting in high concentration in the follicles after LH surge on the granulosa-lutein cells. Therefore, the this study we evaluated the apoptosis and the production of progesterone $(P_4)$ and estradiol $(E_2)$ in the granulosa-lutein cells that are obtained during oocyte-retrieval after treatment with 5, 50, and $500{\mu}g/m\ell$ cortisol and 1 IU/$m\ell$ FSH. Results of DNA fragment analysis and TUNEL assay demonstrated that DNA fragmentation and the rate of apoptotic cells were increased in a dose-dependent manner showing a significant increase in 50 and $500{\mu}g/m\ell$ cortisol treated cells. We found, however, that FSH did not suppress the apoptosis of the cells induced by cortisol. In the results of chemiluminescence assay for $P_4$ and $E_2$, $P_4$ production was decreased by cortisol treatment, whereas $E_2$ was not changed. We also demonstrated that FSH did not inhibit the suppressive effect of GnRH on $P_4$ production as the result of apoptosis. The present study suggests that cortisol of high concentration could cause the apoptosis of human granulosa-lutein cells by suppressing the production of $P_4$. However, we need more studies to elucidate the mechanism by which cortisol induces apoptosis in human granulosa-lutein cells in view of the fact that our results are inconsistent with previous reported data.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.20 no.2
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• pp.55-62
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• 2020

A 22-month-old girl who had taken iron supplements due to iron deficiency anemia, presented bloody mucoid stool for one month. She had a bruise at the right periorbital area due to minor trauma and hepatosplenomegaly. Laboratory studies showed anemia, thrombocytopenia, elevated alkaline phosphatase (ALP), hypophosphatemia, decreased haptoglobin, hypocomplementemia, negative direct/indirect Coomb's test, normal vitamin D3 level and high PTHi. Wrist x-ray showed no signs of rickets. The abdominal ultrasound showed only accessory spleen. Tandem mass spectrometry was normal. During follow up, bloody stool regressed after seven days of withdrawal of iron supplement and cow milk, and the total CO2 level had been within 15-20 mEq/L with normal anion gap. NGS (next generation sequencing) panel test for evaluation of renal tubular acidosis showed negative results. After low dose steroid and vitamin D supplements under the impression of hypocomplementemic vasculitis, thrombocytopenia, C3/C4, decreased haptoglobin, and elevated ALP level became normal. At 57 months of age, laboratory findings showed elevated liver enzyme, ALP and gamma-glutamyl transferase again. And liver cirrhosis with splenomegaly and diffuse renal disease were reported with abdomen CT scan. Liver biopsy reported macro- and micronodular cirrhosis. Urine organic acid profile showed elevated succinylacetone level. Whole exome sequencing revealed novel compound heterozygous mutations (NM_00137.2:c.107T>C, NM_00137, 2:c.614T>C) in FAH gene and confirmed by Sanger sequencing. Consequently, the patient was diagnosed as chronic hereditary tyrosinemia type I. She started low phenylalanine/tyrosine diet and nitisinone treatment. Our case had presented symptoms very slowly, which is the first case of chronic tyrosinemia type I in South Korea.