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Biomedical subjects

J R Tucci

Publications and source records attributed to J R Tucci.

At least 19 recordsLinked to original sources
PubMed1991

Hyperphosphatemia in multiple myeloma due to a phosphate-binding immunoglobulin.

Hyperphosphatemia (HP) is usually seen in patients with hypoparathyroidism, renal failure, and tumor lysis. The authors described a patient with HP due to a phosphate-binding immunoglobulin (Ig). An 86-year-old woman had serum phosphate levels as high as 4.75 mmol/l, (normal, 0.77 to 1.45 mmol/l). Serum ionized calcium, blood urea nitrogen (BUN), creatinine, and N-terminal parathyroid hormone (PTH) levels were normal, but serum 1,25-dihydroxyvitamin D level was subnormal at less than 12 pmol/l (normal, 36 to 146 pmol/l). Serum total protein was elevated at 105 g/l (normal, 60 to 80 g/l), and additional studies confirmed a diagnosis of immunoglobulin G (IgG) multiple myeloma. Results of in vitro studies using anti-human IgG antibodies showed that the IgG of the patient bound inorganic phosphate. Several isolated case reports have documented spurious HP due to interference of the paraprotein in the routine serum phosphate assay. In only one patient, however, has actual binding of phosphate to a myeloma protein been documented. The studies of the authors document phosphate binding by an IgG paraprotein and suggest that in this setting HP may be of physiologic significance as evidenced by depressed serum levels of 1,25-dihydroxyvitamin D.

Aged↗
PubMed1989

Cyproheptadine may act at the pituitary in Cushing's disease: evidence from CRF stimulation.

Cyproheptadine has been reported to effect remissions in up to 50% of patients with Cushing's disease presumably at a hypothalamic level. Endocrine studies including CRF testing were performed in a 37-year-old woman with Cushing's disease. Cyproheptadine therapy resulted in a clinical and chemical remission. During therapy, basal plasma and urinary steroid levels were normal as were responses to dexamethasone, metyrapone, and insulin induced hypoglycemia. CRF administration in the untreated patient resulted in a markedly exaggerated increase in plasma ACTH and cortisol levels, while with cyproheptadine therapy responses were considerably blunted but still greater than normal. These observations are the first to provide evidence supporting a pituitary effect of cyproheptadine in Cushing's disease in vivo and raise questions regarding the assumption of hypothalamic dysfunction in those patients with Cushing's disease responding to cyproheptadine.

17-Hydroxycorticosteroids↗
PubMed1989

Idiopathic isolated ACTH deficiency and the response to CRF.

A 26-year-old woman, intermittently symptomatic over 8 yr, was evaluated for weakness, lightheadedness, and gastrointestinal complaints. She was found to have negligible plasma cortisol and low to low-normal plasma ACTH levels. Although serum cortisol was responsive to ACTH stimulation, metyrapone and insulin-induced hypoglycemia were unable to stimulate pituitary driven adrenal activity. Hypothalamic and pituitary functions were otherwise intact. CRF administration failed to stimulate any increase in plasma ACTH or cortisol levels and CT scanning failed to reveal any anatomic abnormality of the sella or suprasellar areas consistent with an acquired isolated defect in pituitary ACTH secretion. These studies support the impression that the primary defect in isolated idiopathic ACTH deficiency is failure of pituitary ACTH-secreting cells.

Adrenocorticotropic Hormone↗
PubMed1989

Virilizing granulosa cell tumor responsive to human chorionic gonadotropin and oral contraceptive with 8-year followup.

Urinary and serum steroid measurements were obtained in a 48-year-old female before and after the removal of a virilizing granulosa cell tumor (GCT). Preoperatively, serum testosterone was markedly elevated while 17-ketosteroid (17-KS) and estrogen excretion were normal. Chorionic gonadotropin administration effected a marked rise in urinary 17-KS excretion and serum testosterone while oral contraceptive therapy for 21 days decreased serum testosterone to normal. With tumor resection, serum testosterone fell to normal and subsequent administration of HCG had no stimulatory effect on serum testosterone or urinary 17-KS excretion. The patient's clinical response and 8-year followup attest to the tumor's unusual virilizing role.

17-Ketosteroids↗
PubMed1989

C-cell hyperplasia of the thyroid in a patient with goitrous hypothyroidism and Hashimoto's thyroiditis.

A 63-year-old man with a goiter and primary hypothyroidism due to Hashimoto's thyroiditis was found to have hypercalcitonemia and, though hypothyroid, markedly elevated serum total and free T3 levels. The latter findings were attributable to circulating T3 autoantibodies and interference with radioimmunoassay. An infusion of calcium and pentagastrin resulted in abnormal increases in serum calcitonin levels. Because there was no evidence of a nonthyroidal cause for the hypercalcitonemia, the patient had a total thyroidectomy. Pathological examination of the thyroidectomy specimen revealed typical Hashimoto's thyroiditis and extensive C-cell hyperplasia symmetrically distributed throughout the upper and middle thirds of each lobe. The C cells stained strongly with immunoperoxidase stains for calcitonin, chromogranin, and CEA using absorbed polyclonal anti-CEA antibody. Less extensive staining for CEA was obtained using the monoclonal antibodies for CEA, 374/14, 250/183, and 431/31; only a few reactive cells were noted using 431/31. Postoperatively, serum calcitonin levels fell to normal and did not rise with a repeat calcium-pentagastrin infusion test. This patient appears to be the first instance of C-cell hyperplasia associated with Hashimoto's thyroiditis, while elsewhere an association with medullary thyroid carcinoma has been reported. These observations raise questions regarding a possible pathogenetic relationship between Hashimoto's thyroiditis and C-cell neoplasia.

Calcitonin↗
PubMed1987

Idiopathic hypoparathyroidism with extensive brain calcification and persistent neurologic dysfunction.

Idiopathic hypoparathyroidism is an uncommon cause of movement disorders. The following case illustrates the persistence of a parkinsonian gait 2 years after the restoration of normal serum calcium levels. The extensive calcifications in the brain presumably account for this as well as for the persistent mild dementia. The importance of identifying hypoparathyroidism early in the course is graphically illustrated.

Brain Diseases↗
PubMed1987

A case of thyroxine thyrotoxicosis.

A 57-year-old woman presented with palpitations, muscle weakness, bilateral proptosis, goiter, and tremor. The thyroxine (T4) level and the free T4 index were increased while the total triiodothyronine (T3) level was normal. Iodine 123 uptake was increased, and a scan revealed an enlarged gland with homogeneous uptake. Repeated studies again revealed an increased T4 level and free T4 index and normal total and free T3 levels. A protirelin test showed a blunted thyrotropin response. Treatment with propylthiouracil was associated with disappearance of symptoms and normal T4 levels, but after 20 months of therapy, hyperthyroidism recurred and the patient was treated with iodine 131. This was an unusual case of T4 toxicosis because the patient was not elderly and was not exposed to iodine-containing compounds or drugs that impair T4-to-T3 conversion. There was no evidence of abnormal thyroid hormone transport or antibodies.

Autoantibodies↗
PubMed1977

Urinary excretion of cyclic 3',5'-adenosine monophosphate and cyclic 3',5'-guanosine monophosphate during and after pregnancy.

Urinary cyclic AMP and cyclic GMP excretions were measured in 24-h urine specimens obtained from 89 women at various times during their normal uncomplicated intrauterine pregnancies and from 49 women at various times after the births of their normal healthy infants. Cyclic AMP excretion increased steadily from the beginning of the second trimester or earlier until late in the third trimester, reaching a peak excretion approximately 40% greater than that of normal nonpregnant women. The cyclic AMP excretion dropped abruptly by the first day after parturition to levels which were not significant different from those of normal non-pregnant women. In contrast, cyclic GMP excretion increased rapidly during the first trimester and remained relatively constant during the remainder of the pregnancy, reaching a peak excretion of about 140% greater than that of normal nonpregnant women. Furthermore, it decreased slowly toward normal levels, but was still significantly elevated six weeks after parturition. The factors responsible for the increased excretion of cyclic AMP during pregnancy and for the increased cyclic GMP during and after pregnancy are not known.

Cyclic AMP↗
PubMed1977

Circadian rhythms in the urinary excretion of cyclic 3',5'-adenosine monophosphate (cyclic AMP) and cyclic 3',5'-guanosine monophosphate (cyclic GMP) in human subjects.

Significant circadian rhythns in urinary excretion of cyclic AMP, cyclic GMP, creatinine, 17-hydroxycorticosteroids and inorganic phosphorus were demonstrated in three normal subjects (two males and one post-menopausal female) who collected serial 4-h specimens for periods of 33, 22, and 14 days, respectively. Peak excretion of the above substances occurred, respectively, at approximately 1500-1700, 2300-0200, 1700-1800, 1100-1300, and 1800-2200 h. The estimated amplitudes of the rhythms expressed as a percentage of the mean 4-h excretion rate were 12-13%, 9-13%, 9-15%, 30-78% and 22-26%, respectively. With the possible exception of cyclic GMP, all of the observed rhythms appeared to be sinusoidal, with normal periods of 24 h. The rhythms in both cyclic AMP and creatinine excretion, but not in the remaining substances may be explained largely in terms of the known rhythm in glomerular filtration rate. The factors responsible for the rhythm in cyclic GMP excretion are unknown.

17-Hydroxycorticosteroids↗
PubMed1977

The effect of pituitary-adrenal manipulations upon urinary cyclic AMP excretion in man.

The present studies demonstrate that the administration of pharmacologic amounts of ACTH is associated with small but significant increases in urinary cyclic AMP excretion and in urinary cyclic AMP/creatinine ratios which are most likely related to a release of cyclic AMP from adrenocortical tissue. Acute suppression of the pituitary-adrenal axis with dexamethasone and stimulation with metyrapone, however, is not associated with changes in urinary cyclic AMP excretion. These results suggest that physiological levels of ACTH and cortisol contribute little, if any, to the urinary excretion of cyclic AMP in man.

17-Hydroxycorticosteroids↗
PubMed1976

Urinary cyclic nucleotide levels in patients with hyper- and hypothyroidism.

Urinary cyclic AMP, cyclic GMP and creatinine excretion were measured in 38 patients with hyperthyroidism, 32 patients with hypothyroidism and in 57 normal subjects. The excretion of both cyclic nucleotides was significantly increased in hyperthyroid females, but not in hyperthyroid males. The cyclic nucleotides/creatinine ratios, however, were uniformly elevated in both male and female hyperthyroid subjects and this was due, in part, to decreased creatinine excretion. Cyclic AMP excretion was significantly decreased in the hypothyroid subjects, but the cyclic AMP/creatinine ratios were not significantly different from normal. There were no significant alterations in cyclic GMP and cyclic GMP/creatinine ratios in the male hypothyroid patients, but ratios in the female patients were slightly greater than in the normals. These results demonstrate that hyper- and hypothyroidism may be associated with appreciable alterations in urinary cyclic nucleotide levels and that there may be sex-related differences in the patterns of urinary excretion of these nucleotides. The cyclic nucleotide levels herein described in patients with hyper- and hypothyroidism are qualitatively and, in some instances, quantitatively similar to those found in patients with hyper- and hypoparathyroidism, respectively.

Creatinine↗
PubMed1975

Metyrapone test in Cushing's disease.

The urinary 17-hydroxycorticosteroid response to 2 g of metyrapone given orally at 10 PM was compared with that following the standard test in which 750 mg of metyrapone was given at 4 hourly intervals for 6 doses. Both tests were performed on four occasions in 3 patients with Cushing's disease. Increments in urinary 17-hydroxycorticosteroid excretion during the modified test were 7.0, 7.5, 8.4 and 23.3 mg/day, whereas with the standard test, increments ranged from 29.5 to 56.8 mg/day. The urinary 17-hydroxycorticosteroid response to the 2 g dose of metyrapone at 10 PM was marginal in 3 of the 4 studies. Urinary 17-hydroxycorticosteroid excretion with the modified metyrapone test varied from 10.7 to 44% of that found with the standard test. Since urinary steroid excretion may vary considerably in patients with Cushing's syndrome as was evident in 2 of the 3 patients studied, the data suggest that the modified metyrapone test should not be used in preference to the standard test in evaluating Cushing's syndrome. It appears that the modified test could lead to erroneous conclusions.

17-Hydroxycorticosteroids↗
PubMed1975

Mixed gonadal dysgenesis.

Mixed gonadal dysgenesis (MCG) is a rare intersexual disorder, characterized in most cases by the presence of a testis and a contralateral streak gonad; in some cases the contralateral gonad may be rudimentary not having differentiated into an ovary or into a testis and in other cases it may be absent. A personal case was recently studied by the authors in some detail: A 51-year-old individual reared as a female with primary amenorrhea, short stature, subnormal intelligence, male type habitus, hirsutism, moderate breast development, ambiguous external genitalia with a 5 x 2 cm phallus, labia majora with scrotal type skin, and a urogenital sinus. Internal genitalia consisted of a hypoplastic vagina and uterus, a streak gonad on the right and intraabdominal testis, fallopian tube, and epididymis on the left side. The dysgenetic testis contained a gonadoblastoma and the streak a gonadoblastoma and dysgerminoma. A buccal smear was chromatin negative and karyotype analysis revealed XO/XY mosaicism. Thyroid and adrenocortical function was normal. A plasma testosterone level of 0.15 mu-g% rose to 0.45 mu-g% with 3 days of HCG administration. With bilateral gonadectomy the plasma testosterone level fell to 0.06 mu-g% and there was no response following HCG administration. 109 cases of MGD and 2 cases of unilateral gonadal dysgenesis reported in the world literature between 1937 and 1973 were reviewed. On the basis of their clinical and pathological features, the latter two patients were excluded from the category of MGD. In 15 of the 109 cases of MGD, a gonadoblastoma obscuring the gonad of origin was opposed by a dysgenetic gonad with or without a gonadoblastoma or no gonad. In these cases the presence of a testis was not proven histologically and their clinical-pathological features were similar to those found in pure gonadal dysgenesis. Of the remaining 94 cases of MGD, 72 had testicular tissue on one side and a streak or embryonic gonad on the other while 22 had a testis and no contralateral gonad...

Amenorrhea↗