Nihon Naibunpi Gakkai zasshi最新文献

A 57-year-old woman came to our hospital with complaints of neck swelling and headache in 1991. She was diagnosed as having chronic thyroiditis in euthyroidism because she had a diffuse goiter with both antithyroglobulin antibody (TGHA) and antimicrosomal antibody (MCHA). In 1992, she complained of the rapid growth of her thyroid gland and a swallowing disturbance. Atypical lymphocytes were observed in 16.5% of leukocytes in peripheral blood and similar atypical cells were found in bone marrow. Although an ultrasound scan of the thyroid gland revealed a symmetrical enlargement without a pseudocystic appearance, cytological study with fine needle aspiration biopsy of the thyroid gland demonstrated an abundance of atypical lymphoid cells. A whole body scintigram with 67gallium citrate showed no significant accumulation except in the thyroid gland. With a diagnosis of suspected primary thyroid lymphoma, total thyroidectomy was performed. However the diagnosis of malignant lymphoma was not confirmed histologically. A study of lymphocytes subset with two-color flow cytometry, which was performed for both lymphocytes in peripheral blood and infiltrating lymphocytes in the resected thyroid gland, revealed abnormal increased CD4 positive T cells and decreased HLA-DR expression. Additionally, southern blot DNA analysis for abnormal lymphocytes using restriction enzymes, EcoRI and BamHI, demonstrated rearrangement of the T-cell antigen receptor, which indicates a monoclonal proliferation of lymphocytes. After total thyroidectomy, atypical lymphocytes in peripheral blood decreased, and circulating autoantibodies including TGHA and MCHA disappeared. From these data, this patient was finally diagnosed as having a primary T-cell lymphoma of the thyroid gland, which is a very rare type of thyroid lymphoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Recently we developed a sandwich enzyme immunoassay (EIA) specific for intact molecular osteocalcin (I-OC), produced only by osteoblast cell and partially released into blood circulation, to establish a specific biochemical marker of bone formation. In order to confirm whether serum I-OC levels constitute a specific marker for bone formation and to assess the relationship between serum I-OC levels and growth response to growth hormone (GH) therapy, we measured the serum I-OC in serial serum samples using this EIA from 61 children with GH deficiency who showed significant bone growth during GH therapy. The serum I-OC levels in children with GH deficiency before GH therapy were slightly lower than those in normal children (Kanzaki S. et al., J. Clin Endocrinol Metab. 1992;75:1104-9), and had a wide distribution overlapped with the normal range. These levels were apparently increased during GH treatment; that is, in contrast to the levels of 22.9 +/- 1.5 ng/ml (mean +/- SE) before GH treatment, the levels after 1 and 2 months of GH treatment were 29.1 +/- 1.6 ng/ml and 32.5 +/- 1.8 ng/ml, respectively. However, they decreased slightly at 3 months and then they gradually rose to 37.5 +/- 2.8 ng/ml after 12 months, I-OC ratios, represented by the I-OC level at each month of GH therapy in relation to pretreatment level, correlated well with the growth response (growth velocity, growth velocity SD score and delta growth velocity SD score) after 12 months of GH treatment. Correlation coefficients of the growth velocity versus I-OC ratio at 1 and 6 months of GH treatment were 0.677 (p < 0.001, N = 58) and 0.752 (p < 0.001, N = 55), respectively. However, both IGF-I and ALP ratios represented in the same way as the I-OC ratio, correlated poorly as compared with the I-OC ratio. These results demonstrate that the change of serum I-OC levels indicates a direct and sensitive reflection of bone formation, because serum I-OC levels significantly increased with the growth response to GH therapy. The measurement of serum I-OC levels after 1 month of GH treatment may be a useful tool in predicting improved growth velocity during long-term GH therapy.

It is well accepted that testicular function is controlled by gonadotropins. Androgen secretion is regulated by LH, whereas spermatogenesis is controlled by FSH and locally produced androgens. However, evidence has accumulated to indicate that this extratesticular control system is modulated by equally important intratesticular cell-cell interactions. The study of this local control system has received major impetus from the development techniques which have allowed isolation and culture of purified testicular cells and has revealed that testicular cells respond to previously unexpected variable humoral factors which are produced by testicular cells themselves, namely testicular paracrinology. Numerous reviews with regard to cell-cell interactions have been published. In this paper, we attempted to summarize recent topics of para and autocrinology of testicular androgen biosynthesis and spermatogenesis.

A 26-year-old female was admitted to our hospital on December 4, 1992, because of recurrent fever. She had experienced recurrent fever of over 38 degrees C, occurring at irregular intervals 4-6 times a year with chest or abdominal pain, since the age of 19. After delivery of a baby at the age of 25, her symptoms had increased to once a week. In the febrile phase, leukocytosis, an increased erythrocyte sedimentation rate and positive CRP were recognized. These symptoms and laboratory findings spontaneously disappeared within a few days. Despite systemic and careful examinations, no evidence of infectious diseases, collagen diseases or malignant diseases were found. There were no significant differences of serum and urine catecholamines, and urine etiocholanolone between the febrile phase and the afebrile phase. An intravenous infusion of metaraminol induced symptoms similar to a spontaneous attack, and the metaraminol rechallenge test became negative after she was treated with oral colchicine. Based on these findings, she was diagnosed as having familial Mediterranean fever. Since she was treated with colchicine, the febrile attacks have decreased. Significantly, her elder brother has had similar recurrent fever with abdominal pain. He was diagnosed as having familial Mediterranean fever due to a positive metaraminol provocative test, and his febrile attacks have also been suppressed by colchicine. This is the first case of familial Mediterranean fever with obvious family history in Japan.

In order to differentiate silent thyroiditis (SLT) from Graves' disease, the usefulness of the measurement of the urinary concentration of iodine was evaluated in this study. The subjects employed were 39 patients with SLT and 40 patients with Graves' disease. Patients were advised to avoid any iodine-containing food or medication for a week before the examination. The urinary concentration of iodine (UI) and the serum concentration of thyroid hormones were determined. UI was calculated from the amount of iodine in the spot urine by multiplying it by the ratio of iodine to creatinine. Since the UI value thus obtained was significantly well correlated with the UI value for 24 hour urine, the former value was used instead of the latter value thereafter. Mean UI value in the patients with SLT was 482.4 +/- 296.4 mu g/day and that in the patients with Graves' disease was 169.8 +/- 75.2 mu g/day, the former value being significantly higher than the latter (p < 0.0001). A strong and significant correlation between UI and the serum concentration of FT4 or T3 (TT3) was found in the patients with SLT (r = 0.76, p < 0.0001 and r = 0.54, p < 0.02), but not in those with Graves' disease (r = 0.34, p = 0.07 and r = 0.24, p = 0.14) Mean UI/FT4 ratio and mean UI/TT3 ratio was significantly higher in patients with SLT than those with Graves' disease and the overlaps in the ratios between these two groups were very slight. These results indicate that both the ratios of UI/FT4 and UI/TT3 were useful parameters to differentiate SLT from Graves' disease. The higher UI value observed in the patients with SLT was thought to be due to the increase in the amount of inorganic iodine which was liberated from the iodinated material leaked from the damaged thyroid tissue by the deiodinating mechanism in the peripheral tissues.

The present study was conducted to investigate the effects of the transient increase of serum prolactin levels on the gonadotropin secretion system in patients with occult hyperprolactinemia (OHP). 216 cases of normoprolactinemic hypothalamic anovulatious were selected by LH-RH and TRH loading tests, and 5mg/day of bromocriptine was administered for more than 8 weeks. The effectiveness of the bromocriptine administration was estimated by the ultrasonic examination of the follicular development. The endocrinological backgrounds were compared between bromocriptine effective (154 cases, group A) and non-effective (62 cases, group B) patients. Serum prolactin levels 30min. after LH-RH and TRH loading (PRL30 in group A were significantly higher than those of group B (74.1 +/- 36.5 vs. 38.0 +/- 18.2ng/ml, p < 0.01). From this result, it was thought that many of the OHP patients were selected in group A. Serum LH levels 30min. after loading test (LH30) in group A also increased compared to those of group B (65.0 +/- 66.5 vs. 43.1 +/- 34.3mIU/ml, p < 0.02). The LH/FSH ratio before loading was also higher in group A (1.3 +/- 0.6) than that of group B (1.0 +/- 0.5, p < 0.02). This fact showed that group A also contained patients with hyper-LH hypothalamic anovulation, which is known as the endocrinological PCOD. There were also significant inverse correlations between serum levels of prolactin and FSH in group A (before loading values: r = 0.272, 30min. after loading: r = 0.224, p < 0.01). By the administration of bromocriptine, serum prolactin levels decreased both in group A and B, and the elevated serum LH/FSH ratio (1.0 +/- 0.4, p < = 0.02), LH30 (46.1 +/- 37.0mIU/ml, p < 0.005) also decreased significantly. Serum levels of FSH in group A increased significantly with treatment (before loading: 5.4 +/- 2.6-->6.2 +/- 2.0, 30min. after loading: 10.6 +/- 6.0-->14.6 +/- 9.9mIU/ml, p < 0.005). From these facts, it was concluded that FSH secretion was suppressed even by a slight increase of serum prolactin levels which was usually seen in the OHP, and bromocriptine administration was effective not only for the suppression of serum prolactin and LH levels, but also for the improvement of FSH secretion in the OHP patients.

We employed two different methods of 131I treatment for Graves' disease in 285 patients and compared the results between the two. (We also analyzed the factors affecting the treatment outcome.) A single dose of 131I adjusted to the patients' thyroid weight was administered to 180 patients in group 1, while a relatively lower dose of 131I (approximately 30Gy) was given repeatedly to 105 patients in group 2. A 5-year follow-up showed that in group 1, 34% of the patients were euthyroid, 11% hypothyroid, 11% subclinical hypothyroid and 44% still remained hyperthyroid. In group 2, 43% of the patients were euthyroid, 5% hypothyroid, 35% subclinical hypothyroid and 17% hyperthyroid. The factors affecting the outcome of the treatment in group 1 patients were their thyroid weight, the duration of the disease and TRAb levels. No significant correlation was observed between the efficacy of 131I treatment and the patients' sex, age, 24hr 131I-uptake, effective half life of administered 131I or titers of antithyroid antibodies. We conclude that the repeated low dose administration of 131I provides the best outcome in a 5-year follow-up. However, we suggest that an adjusted dose of 131I in relation to the patients' thyroid weight should be employed to obtain a faster therapeutic response.

It is well known that the renal nerve plays an important role in the regulation of renal functions such as sodium and water reabsorption in the tubules as well as in the pathogenesis of essential hypertension. The renal sympathetic nerves innervate to the basement membranes of almost all nephron segments. Specific adrenergic receptors and intracellular signal transduction systems are located in these nephron segments. By the recent progress of molecular biological techniques, at least three alpha 1-, three alpha 2- and three beta-adrenergic and five dopaminergic receptors have been identified and characterized. Using micromethods such as microperfusion, micropuncture techniques and the reverse transcription and polymerase chain reaction (RT-PCR) methods applied to the microdissected tubules, more detailed localizations and functions of these adrenergic and dopaminergic receptors are being classified. Future studies in this field may provide further information concerning the physiological and pathophysiological roles of these receptors in the kidney.

A 58-year-old woman was admitted to our hospital for impaired consciousness, hyperglycemia and bitemporal hemianopsia. She was diagnosed as having NIDDM one year ago and was treated with diet and glibenclamide (1.25 mg/day) for 6 months. However, she stopped her medical treatment one month ago and then polydipsia and general fatigue were manifested. She was admitted to a hospital five days ago at which time hyperglycemia (405 mg/dl) and anemia (Hb8.0g/dl) were detected. She was transferred to our hospital for control of blood glucose and further examination of bitemporal hemianopsia. She showed typical acromegalic features including enlargement of the nose, lips and tongue, increased heel pad and acral growth. Conscious disturbance was cured by the infusion of saline and the administration of insulin. Endoscopy revealed an active gastric ulcer (A1). Endocrine data disclosed increased GH levels in plasma and urine, whereas plasma IGF-1 levels were low. Plasma GH paradoxically increased following the administration of TRH. A water deprivation test showed an impaired increase in urinary osmolarity, indicating partial central diabetes insipidus (DI). MRI with Gd-contrast revealed a macroadenoma which progressed toward suprasella. She was diagnosed as having acromegaly, partial DI and probable hyperosmolar hyperglycemic nonketotic diabetic pre-coma. Polyuria (5-101/day) due to partial DI was controlled by the administration of DDAVP (10 micrograms/day). The constant subcutaneous administration of octreotide (240 micrograms/day) resulted in normal plasma GH levels and a marked shrinkage of the pituitary tumor. The pituitary tumor was finally removed by the transsphenoidal approach following treatment with octreotide for 4 months. HE staining of the pituitary tumor showed atrophic and acidophilic cells surrounded by hyaloid connective tissue. After the surgery, plasma GH levels were normalized and complications were cured. In conclusion, this is a very rare case of acromegaly associated with diabetic pre-coma and partial DI, and effectively treated with constant subcutaneous infusion of octreotide.