Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report an 18-year-old male patient who developed chronic hepatitis C after blood transfusion and had testicular dysfunction after irradiation for a testicular relapse of childhood acute lymphocytic leukemia after cessation of maintenance therapy, and the initiation of testosterone replacement therapy at puberty. Concomitant administration of estradiol resulted in a reduction in serum alanine aminotransferase and ferritin levels and hepatic iron concentration and staining after 2 years of estrogen therapy, although interferon therapy was withdrawn because of adverse effects. This observation suggests that endogenous estradiol may play a beneficial role in male patients with chronic hepatitis C.
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PMID:Estrogen therapy in a male patient with chronic hepatitis C and irradiation-induced testicular dysfunction. 1130 Jan 39

We studied 12 adolescent boys with beta-thalassemia major and delayed puberty (age, 15.8 +/- 1 years) with Tanner I sexual development treated with a long-term low-transfusion regimen. Ten nonthalassemic adolescents (> 14 years) with constitutional delay of growth and puberty (CDGP) served as controls. Auxologic parameters and testicular size were measured, and bone age was determined. Measurement of basal gonadotropin (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) and testosterone (T) levels taken at 8 am revealed prepubertal levels in both groups of patients. Human chorionic gonadotropin (hCG, 2500 U/m(2)) was injected intramuscularly twice weekly for 6 months, and anthropometric data, testicular diameter, and serum T concentrations were remeasured after 1 and 6 months. The testicular diameter after 6 month of hCG therapy was significantly correlated with the testicular diameter and T level after 1 month of therapy (r = 0.93 and 0.39, respectively, P < .01). After 6 months of hCG therapy, the mean growth velocity (GV) increased from 4.1 to 8.6 cm/y in thalassemic patients and from 4.6 to 10.3 cm/y in those with CDGP during hCG therapy. In thalassemic boys, the mean T concentration increased from 0.93 to 2.7 nmol/L (mean increase = 1.8 nmol/L) vs an increase from 0.47 to 4.81 nmol/L (mean increase = 4.32 nmol/L) in those with CDGP. All adolescents with CDGP, but only 7 the 12 thalassemic adolescents, had T secretion above 2 nmol/L after 6 months of hCG therapy and maintained their growth and pubertal development for a year after stopping hCG. The 5 thalassemic patients with defective T secretion after hCG therapy had significantly higher ferritin level (1985 +/- 658 ng/mL) vs the other 7 patients (1100 +/- 425 ng/mL). These findings denoted significant testicular dysfunction in those patients with higher iron overload (testicular siderosis). Statural GV was significantly correlated with insulin-like growth factor 1 (IGF-1) concentrations and testicular diameter after hCG therapy (r = 0.5 and 0.43 respectively, P < .001). In summary, hCG therapy was effective in treating 7 of 12 (58%) of thalassemic adolescents with delayed puberty. In the rest of patients (5/12, 46%) with significantly higher iron overload, hCG therapy failed to stimulate testicular growth and adequate T. Proper iron chelation appears to protect against testicular dysfunction. In the first group of patients, hCG therapy can be used for the treatment of their hypogonadism, whereas T replacement remains the therapy of choice for the second group.
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PMID:Human chorionic gonadotropin therapy in adolescent boys with constitutional delayed puberty vs those with beta-thalassemia major. 1556 75