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Biomedical subjects

K M Shakir

Publications and source records attributed to K M Shakir.

At least 19 recordsLinked to original sources
PubMed2000

Dual X-ray absorptiometry total body bone mineral content and bone mineral density in 18- to 22-year-old caucasian men.

Eighty-six healthy, young Caucasian 18-year-old men with no known disease or bone injury were recruited to this study at the United States Naval Academy. Change in bone mineral density (BMD) of the hip, lumbar spine, and distal tibia, and total body bone mineral content (TBMC) was measured by dual-energy X-ray absorptiometry (DXA). BMD and TBMC of these men were measured within 2 months (67 +/- 3 days) of entering the Academy, and, at the end of their first, second, and fourth years. Hip BMD was unchanged during the study period (p > 0.05). Lumbar spine BMD increased 3% (p < 0.001) and distal tibia BMD increased 5% (p < 0.001). TBMC showed a 7.5% increase over the study period. In this group of young men, gain in BMD and TBMC is greatest to age 21 years, with minimal further increase after age 21. The significance of this rise in bone mass during early adulthood on risk for osteoporotic fractures in later life or its impact on exercise-related bone injuries is unknown and warrants further examination.

Absorptiometry, Photon↗
PubMed2000

Anemia: a cause of intolerance to thyroxine sodium.

Usual causes of intolerance to thyroxine sodium include coronary artery disease, advanced age, untreated adrenal insufficiency, and severe hypothyroidism. We describe 4 patients with iron deficiency anemia and primary hypothyroidism. After treatment with thyroxine sodium, these patients developed palpitations and feelings of restlessness, which necessitated discontinuation of the thyroid hormone. After the anemia was treated with ferrous sulfate for 4 to 7 weeks, they were able to tolerate thyroxine sodium therapy. Iron deficiency anemia coexisting with primary hypothyroidism results in a hyperadrenergic state. In such patients, we postulate that thyroid hormone administration causes palpitations, nervousness, and feelings of restlessness. Correction of any existing pronounced anemia in hypothyroid patients who are intolerant to thyroxine sodium therapy may result in tolerance to this agent.

Adult↗
PubMed1998

Time interval between the last dose of propylthiouracil and I-131 therapy influences cure rates in hyperthyroidism caused by Graves' disease.

PURPOSE: To examine the effects of propylthiouracil (PTU) pretreatment on the outcome of initial I-131 therapy for Graves' disease. DESIGN: A retrospective chart review was done. PATIENTS AND METHODS: The authors studied 106 patients in an outpatient nuclear medicine setting who were given initial I-131 therapy for Graves' disease from September 1989 to March 1993 and followed for at least 6 months after therapy. These patients were divided into groups based on whether they had ever received PTU or, if they had received PTU, the length of time between the last dose of PTU and the I-131 therapy dose. Measured failure rates of initial I-131 therapy were based on recurrent or continued hyperthyroidism. RESULTS: Treatment failure rates increased markedly from 2.5% in non-PTU-treated patients (n = 80) to 23.1% (n = 26) in patients pretreated with PTU (P = 0.003). Although not significant, two PTU-pretreated subgroups showed a trend toward increased failure rates. The failure rate was 15.4% (n = 13) in patients whose last dose of PTU was 7-14 days before I-131 therapy, and it increased further to 30.8% (n = 13) in patients whose last dose of PTU was within 1 week of I-131 therapy. CONCLUSIONS: PTU pretreatment within 2 weeks of I-131 treatment is a strong independent risk factor in failure rates after initial I-131 therapy in patients with Graves' disease. Patients should be free of PTU for 2 weeks before I-131 therapy if they are able to tolerate it, otherwise the dose of I-131 may need to be adjusted upward to diminish the risk that the initial I-131 therapy will fail.

Adult↗
PubMed1998

Parathyroid carcinoma: report of three cases and review of the literature.

Parathyroid carcinoma is a rare endocrine malignancy characterized by the exaggerated metabolic effects of the parathyroid glands. The preoperative differential diagnosis between parathyroid carcinoma and primary hyperparathyroidism is often difficult because many of the signs and symptoms are very similar. Intraoperative differentiation is obscured by the strict anatomic and histologic criteria required for diagnosis of parathyroid carcinoma. We have encountered three patients with parathyroid carcinoma during the last 10 years and managed them successfully. Two of them presented with recurrence of hypercalcemia, one 11 years after and the other 3 years after the primary operation for hyperparathyroidism; both patients were eventually diagnosed with parathyroid carcinoma. The third case was suspected as primary hyperparathyroidism preoperatively but confirmed as carcinoma subsequent to histologic examination.

Adult↗
PubMed1997

Ferrous sulfate-induced increase in requirement for thyroxine in a patient with primary hypothyroidism.

Recent studies have shown that under experimental conditions ferrous sulfate may reduce the gastrointestinal absorption of orally administered levothyroxine sodium in patients with primary hypothyroidism. We describe a patient who became hypothyroid while taking ferrous sulfate. The hypothyroid status was corrected by increasing the dose of levothyroxine. Subsequently, when ferrous sulfate was discontinued, the patient became hyperthyroid while taking the higher dose of thyroid hormone preparation. Since both hypothyroidism and iron deficiency anemia may coexist, additional thyroid function testing is recommended in patients treated concurrently with ferrous sulfate and L-thyroxine.

Administration, Oral↗
PubMed1996

Pseudocarcinoid syndrome associated with hypogonadism and response to testosterone therapy.

OBJECTIVE: To characterize a disorder of episodes of flushing and increased levels of 5-hydroxyindoleacetic acid (5-HIAA) in men with secondary hypogonadism who respond to testosterone therapy. MATERIAL AND METHODS: We present detailed case reports of three male patients who had flushing, secondary hypogonadism, and increased urinary 5-HIAA levels and describe their clinical and laboratory features before and after treatment with testosterone. In addition, six male patients with hypogonadism (three with primary and three with secondary hypogonadism) without flushing were assessed. RESULTS: The three patients with flushing and secondary hypogonadism (serum total testosterone 5.45 +/- 0.63 nmol/L, free testosterone 89.3 +/- 7.0 pmol/L, follicle-stimulating hormone 3.85 +/- 0.58 IU/L, and luteinizing hormone 4.41 +/- 0.98 IU/L) had increased urinary 5-HIAA levels (98.5 +/- 12.2 micromol/24 h) but normal blood serotonin levels (9.66 +/- 1.58 micromol/L). During a pentagastrin-calcium stimulation test, serum calcitonin and blood serotonin values were normal in patients with secondary hypogonadism and flushing. Detailed investigation showed no evidence of a carcinoid tumor. Urinary 5-HIAA levels became normal (16.6 +/- 1.73 micromol/24 h) after treatment with testosterone. When testosterone therapy was discontinued in two patients, flushing and increased urinary 5-HIAA levels recurred. Furthermore, flushing and the elevated urinary 5-HIAA values resolved when testosterone treatment was reinitiated. The six patients with hypogonadism without flushing had normal urinary 5-HIAA levels (14.9 +/- 3.31 micromol/24 h). CONCLUSION: Male patients with flushing and increased urinary 5-HIAA levels should undergo assessment for hypogonadism after screening for carcinoid tumor. If hypogonadism is diagnosed, resolution of flushing and normalization of 5-HIAA may be achieved with testosterone treatment. We suggest that pseudocarcinoid syndrome associated with hypogonadism be the descriptive label used for this combination of clinical features.

Aged↗
PubMed1995

Galactorrhea caused by esophagitis.

A case of galactorrhea caused by painful esophagitis, a previously unreported etiology, is presented. The galactorrhea promptly resolved with appropriate treatment of the esophagitis. It is proposed that the mechanism of production of galactorrhea is similar to that seen with chest wall lesions. This cause should be kept in mind when evaluating unusual causes of galactorrhea.

Adult↗
PubMed1995

Nicotinic acid decreases serum thyroid hormone levels while maintaining a euthyroid state.

OBJECTIVE: To evaluate the effects of nicotinic acid on serum thyroid hormone levels in the absence of systemic illness or hepatic dysfunction. DESIGN: We determined the effect of treatment with nicotinic acid on serum thyroid hormone levels in one female and four male patients (mean age, 44.4 years) with hyperlipidemia. MATERIAL AND METHODS: In the five study patients, we measured serum lipids in conjunction with serum thyroxine (T4), triiodothyronine (T3) resin uptake, T3, free T4, thyroid-stimulating hormone (TSH), and thyroxine-binding globulin before, during, and after treatment with nicotinic acid. RESULTS: Serum lipid levels responded appropriately to nicotinic acid treatment. Thyroid function studies done a mean of 1.3 years (range, 0.5 to 3.5) after initiation of nicotinic acid therapy (mean daily dose, 2.6 +/- 0.7 g) revealed significant decreases in serum levels of total T4 (21%), free T4 index (16%), T3 (13%), and thyroxine-binding globulin (23%) (P < 0.02), whereas no significant changes were noted in free T4, T3 resin uptake, and TSH levels. During the course of treatment, the patients, who were carefully questioned, had no symptoms of hypothyroidism. Hypothyroidism was further excluded in three patients who had a normal serum TSH response to administration of thyrotropin-releasing hormone. In two patients, measurements of thyroid function returned to pretreatment levels after discontinuation of nicotinic acid therapy. No patient had significant abnormalities in liver-associated enzymes or evidence of systemic illness during the course of treatment. CONCLUSION: These results suggest that nicotinic acid decreases serum thyroid hormone concentrations while maintaining a euthyroid state. This effect may be mediated through reduction in thyroxine-binding globulin, but other mechanisms may also be involved.

Adult↗
PubMed1994

Normal gastric inhibitory polypeptide response to oral glucose in hypothyroidism.

Although the action of gastric inhibitory polypeptide (GIP) on the beta cells of the pancreas is well documented, the effect of this hormone on insulin secretion in patients who are hypothyroid has not been studied. Hypothyroid patients demonstrate increased serum immunoreactive insulin levels in response to oral glucose when compared with euthyroid subjects. We postulated that a delayed and exaggerated response of GIP could account for the hyperinsulinaemic response. Nine thyroidectomized patients (aged 44.9 +/- 3.6 years) who were otherwise healthy but undergoing re-evaluation for recurrence of thyroid carcinoma, were given a 75 g oral glucose tolerance test (OGTT). These subjects were studied 6 weeks after thyroid hormone replacement had been stopped and while on hormone treatment. The serum glucose and plasma GIP responses to oral glucose were similar in the euthyroid and hypothyroid states. The serum insulin response as well as the areas under the curve for insulin following OGTT were significantly elevated (P < 0.01) during hypothyroidism. Solid-phase gastric emptying times studied in six patients who were euthyroid and hypothyroid were not different (35 +/- 12 versus 36 +/- 14 min respectively). None of the subjects had detectable levels of serum thyroglobulin, microsomal or parietal cell antibodies. In summary, we have confirmed a hyperinsulinaemic response to an OGTT and normal solid-phase gastric emptying rates in this form of hypothyroidism. We did not find significant differences in serum glucose or GIP responses and postulate this as evidence of resistance to the effects of endogenous insulin. The mechanism of alterations in carbohydrate tolerance in the hypothyroid state continue to remain unknown.

Adult↗
PubMed1994

Changes in triiodothyronine mark severe pain syndrome: a case report.

Non-thyroidal illness is classically associated with a low total triiodothyronine (T3) level. Episodes of severe recurrent dental pain unassociated with fever or systemic infection in a patient was marked 2 to 3 weeks later by low T3 levels (56 ng/ml). Other thyroid and metabolic tests were normal. T3 levels returned to normal on resolution of pain. Recurrence of a transient, mild episode of pain was not associated with a low T3 2 weeks after its onset. We suggest that T3 levels may be markers for severe pain and suffering or disturbances responsible for pain and suffering in patients receiving analgesics.

Biomarkers↗