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Biomedical subjects

F Azizi

Publications and source records attributed to F Azizi.

At least 73 records · Page 4Linked to original sources
PubMed1978

Effect of starvation on hypothalamic-pituitary-thyroid function in the rat.

Total starvation in the rat for 2 days did not alter the hypothalamic content of thyrotropin-releasing hormone (TRH), but did decrease both pituitary TSH content and serum TSH concentration. Five days starvation resulted in a significant decrease in serum TSH and a slightly enhanced serum TSH response to exogenous TRH, suggesting that the pituitary retains its sensitivity to TRH. Fasting for 5 days resulted in a decreased 1 and 4th, but an increased 24th thyroid 131I uptake. Other starvation-induced abnormalities of intrathyroid 131I metabolism were a consistent increase in the percent of organified 131I present as MIT and DIT and a decreased percent 131I labeled T4 AND T3. These alterations in the intrathyroid metabolism of 131I in the starved rat probably reflect both a decrease in serum TSH concentration and a decrease in urinary and fecal loss of administered 131I. The serum total and free T4 and total and free T3 concentrations were decreased following 2 and 5 days of starvation.

Animals↗
PubMed1978

The free triiodothyronine (T3) index.

In a large number of normal men (n = 111) and women (n = 110) the free triiodothyronine (T3), index, calculated from serum total T3 and T3-uptake, was highly correlated with free T3, measured by equilibrium dialysis. The correlation was almost as high as that of the free thyroxine (T4) index with free T4. The correlations of the total T3, free T3, and free T3 index with, respectively, the total T4, free T4, and free T4 index were much lower, though still statistically significant. The free T3 index is clinically useful because serum total T3 may sometimes be misleading. Hyperthyroid patients with apparent T4-toxicosis and normal total T3 may have an elevated free T3 index and thus physiologically elevated levels of both thyroid hormones. Calculation of the free T3 index might also make possible the diagnosis of T3-toxicosis in a patient with a normal free T4 index and normal total T3. Total T3 may be elevated without an elevated total T4 in women taking oral contraceptives; thus the free T3 index may prevent a misdiagnosis of T3-toxicosis. The free T3 index seems no better than total T3 in the diagnosis of primary hypothyroidism, but it can confirm the diagnosis of T3-hypothyroidism.

Adult↗
PubMed1977

Clinical, pathologic, and genetic findings in a case of 46,XY pure gonadal dysgenesis (Swyer's syndrome).

Cytogenetic, pathologic, and clinical studies were conducted on a phenotypically female patient with primary amenorrhea and infertility. Analysis of blood cultures with routine and Giemsa-banded preparations indicated that the chromosomal complement of the patient was 46,XY. Buccal and peripheral blood smears prepared for fluorescent analyses confirmed the presence of a single F-body (Y chromosome). Pathologic examination of tissues removed at total hysterectomy and bilateral salpingo-oophorectomy revealed a gonadoblastoma of the right gonad, dysgerminoma of the left gonad, and an infantile hypoplastic uterus. The data were consistent with a diagnosis of 46,XY pure gonadal dysgenesis (Swyer's syndrome).

Adolescent↗
PubMed1977

Uptake of bone imaging agents by diffuse pulmonary metastatic calcification.

Three cases of diffuse lung uptake of the bone scanning agent 99mTc diphosphonate, which appears to reflect metastatic pulmonary calcification, are described. Each patient had hypercalcemia and renal failure. Clinical features common to patients with this scan pattern were ascertained from a review of the literature. Renal failure was present in all, and the majority have had hypercalcemia. The bone scan may prove to be a valuable adjunct to the diagnosis of metastatic pulmonary calcification; this characteristic pattern should be more widely appreciated.

Adolescent↗
PubMed1977

Follow-up study of male and female offspring of DES-exposed mothers.

This follow-up study presents the effects of DES on the genital tract of male and female offspring of mothers who were part of a double-blind, placebo-controlled investigation during 1951 and 1952 aimed at determining the effect of DES on pregnancy. Epididymal cysts, hypotrophic testes, and capsular induration were the more common genital lesions found in 25% of 163 DES-exposed males as compared to 6% in 168 control males. Semen analysis data on 39 subjects of the DES-exposed group and 25 subjects of the control group showed that 26% of the DES-exposed group produced an ejaculate volume under 1.5 ml; no such cases were observed in the control group. The average values for sperm density ant total motile spermatozoa per ejaculate, although in the normal range, were more than two times lower in the DES-exposed group as compared to the controls. A quality score of greater than 10 ("severely pathologic semen") was found in 28% of the DES-exposed group as compared to 0 in the control group. An association of pathologic semen quality with physical abnormalities was found only in the DES-exposed group. Two cases of azoospermia, one without genital abnormalities on physical examination and one with bilateral hypotrophic testes were observed so far in the DES-exposed group. Eighteen percent of 229 DES-exposed female patients had irregular menstrual cycles (oligomenorrhea) as compared to 10% of 136 controls. The history of pregnancy revealed a lower incidence of pregnancy in the DES-exposed group (18%) than in the control group (33%). Circumferential ridges of the vagina and cervix were seen in 40% of 229 DES-exposed females but in none of 136 controls. Colposcopic findings in the vagina revealed adenosis in 66.8% of the DES-exposed females and in 3.6% of the control group. Dysplastic lesions were more prevalent in the vagina and cervix of the DES-exposed subjects. No cases of cancer were observed in either the male or female offspring.

Cell Count↗
PubMed1975

Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.

The pattern of thyrotropin secretion was analyzed in seven euthyroid women, before and after withdrawal of long-term thyroid hormone, by serial measurements of thyroid 131l uptake, serum thyroxine, tri-iodothyronine, and thyrotropin concentrations, and the response to thyrotropin-releasing hormone. During exogenous hormone administration, 131l uptake was suppressed, and serum thyrotropin concentrations before and after administration of thyrotropin-releasing hormone were undetectable. After withdrawal of exogenous hormone, thyrotropin secretory function was transiently impaired, as indicated by undetectable basal thyrotropin concentrations together with absence of response to thyrotropin-releasing hormone, and subsequently by normal values of basal thyrotropin concentration and normal responses to releasing hormone while serum thyroxine and tri-iodothyronine concentrations were subnormal. Decreased thyrotropin reserve persisted for two to five weeks. Detectable values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal 131l uptake usually occurred concurrently in two to three weeks. Serum thyroxine concentration returned to normal at least four weeks after hormone withdrawal.

Adult↗
PubMed1975

Pituitary-thyroid responsiveness to intramuscular thyrotropin-releasing hormone based on analyses of serum thyroxine, tri-iodothyronine and thyrotropin concentrations.

To develop a test of pituitary-thyroid responsiveness to thyrotropin-releasing hormone that would obviate the need for measuring serum thyrotropin, we determined serum thyrotropin, thyroxine, and tri-iodothyronine concentrations before and at frequent intervals after the intramuscular administration of 2 mg of thyrotropin-releasing hormone in normal subjects and in patients with a variety of thyroid disorders. In specimens obtained four and five hours after administration of the hormone to normal subjects, serum thyroxine concentration increased 2.4 plus or minus 0.7 mug per 100 ml (mean plus or minus S.D.) over base-line values, the magnitude of increase being greater than 1.5 mug per 100 ml in 32 of 34 subjects. Serum thyroxine concentrations after administration of thyrotropin-releasing hormone did not increase in 11 hyperthyroid patients. Of 13 with hypothyroidism, increases in 12 were 0 to 0.7 mug per 100 ml; in one the increment was 1.2 mug per 100 ml. Measurement of the serum thyroxine response to intramuscular thyrotropin-releasing hormone will usually suffice to determine the integrity of the hypothalamic-pituitary-thyroid complex.

Adult↗
PubMed1975

The time course of changes in TRH responsiveness in man following a single dose of liothyronine.

The serum thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH, 100 mug i.v.) was evaluated prior to and at various times following the oral administration of single doses of liothyronine (100 mug) given at weekly intervals. The TSH response to TRH was mildly depressed when TRH was given 1 hr after liothyronine administration when the serum triiodothyronine (T3) concentration was strikingly elevated, was markedly reduced 16 and 24 hr after liothyronine, was essentially abolished 3 days after liothyronine when the serum T3 concentration was normal, and was normal 7 days after liothyronine administration. These findings suggest that the more prolonged suppression of TRH responsiveness, observed following the withdrawal of long-term excess endogenous or exogenous thyroid hormones, cannot be ascribed to the intrinsic duration of action of the hormone present at the time of withdrawal, but rather to the prolonged extent of the suppression itself.

Administration, Oral↗
PubMed1975

Diversion of peripheral thyroxine metabolism from activating to inactivating pathways during complete fasting.

In 9 euthyroid obese volunteers, as previously reported, 4 weeks of total caloric deprivation resulted in a striking decrease in serum 3,5;3'-triiodothyronine (T3) concentration. The present studies reveal that this decrease in serum T3 is accompanied by a proportionately similar increase in the serum concentration of 3,3',5' -T3 (reverse T3; rT3). In four additional obese volunteers given suppressive doses of sodium-Lthyroxine (T4) for 1 month prior to fasting, serum T3 concentration declined sharply during a 6-11 day period of fast, while rT3 concentration increased strikingly. Concentrations of both T3 and rT3 returned to control values during a 5 day period of refeeding. The findings indicate that caloric deprivation results in an alteration in peripheral T4 metabolism away from generation of T3 and toward the generation of rT3. Since the former is more active than T4, and the latter is essentially inactive, caloric deprivation appears to shunt peripheral T4 metabolism from activating to inactivating pathways.

Adult↗
PubMed1975

The effect of intramuscular thyrotropin-releasing hormone on the thyroid 131I uptake in man.

The effect of a single large intramuscular injections of TRH (2 mg) on the thyroid 131I uptake in normal man was assessed at varying intervals following the administration of TRH. When the 131I was given simultaneously with TRH, the 3- and 5-hour 131I uptake decreased. When the 131I was administered 8 hours after TRH, the thyroid 131I increased significantly. This response in uptake is similar to that observed in the rat following TSH stimulation. The present study defines the time course of the thyroid 131I uptake response to endogenous TSH stimulation.

Adult↗
PubMed1974

Hyperresponse to thyrotropin-releasing hormone accompanying small decreases in serum thyroid hormone concentrations.

To determine whether pituitary thyrotropin (TSH) responsiveness to thyrotropin-releasing hormone (TRH) is enhanced by small decreases in serum thyroxine (T4) and triiodothyronine (T3), 12 euthyroid volunteers were given 190 mg iodide po daily for 10 days to inhibit T4 and T3 release from the thyroid. Basal serum T4, T3, and TSH concentrations and the serum T4 and TSH responses to 400 mug TRH i.v. were assessed before and at the end of iodide administration. Iodide induced small but highly significant decreases in basal serum T4 (8.0+/-1.6 vs. 6.6+/-1.7 mug/100 ml; mean +/- SD) and T3 (128+/-15 vs. 110+/-22 ng/100 ml) and increases in basal serum TSH (1.3+/-0.9 vs. 2.1+/-1.0 muU/ml). During iodide administration, the TSH response to TRH was significantly increased at each of seven time points up to 120 min. The maximum increment in serum TSH after TRH increased from a control mean of 8.8+/-4.1 to a mean of 13.0+/-2.8 muU/ml during iodide administration. As evidence of the inhibitory effect of iodide on hormonal release, the increment in serum T3 at 120 min after TRH was significantly lessened during iodide administration (61+/-42 vs. 33+/-24 ng/100 ml). These findings demonstrate that small acute decreases in serum T4 and T3 concentrations, resulting in values well within the normal range, are associated both with slight increases in basal TSH concentrations and pronounced increases in the TSH response to TRH. These results demonstrate that a marked sensitivity of TSH secretion and responsiveness to TRH is applicable to decreasing, as well as increasing, concentrations of thyroid hormones.

Adult↗