PubMed Health⌕ Search

Biomedical subjects

P Velayutham

Publications and source records attributed to P Velayutham.

6 recordsLinked to original sources
PubMed2006

Juvenile hyperthyroidism: an experience.

OBJECTIVE: To analyze the clinical profile of juvenile hyperthyroidism at presentation, their treatment outcome; predictors of remission and relapse. METHODS: Retrospective analysis of medical records of 56 patients with juvenile hyperthyroidism seen over a period of 16 years. A cohort of 38 females and 18 males with mean (+/-SD) age of 14.9 +/- 3.4 years (range 3 to 18 years) was analyzed. RESULTS: Majority of patients was in the age group of 12-16 years. Common symptoms observed at presentation were weight loss (82.1%), excessive sweating (78.6%), heat intolerance (76.8%), increased appetite (73.2%) and diarrhea in 48.2%. In addition, accelerated linear growth was observed in 7.1% of patients. Goiter was present in 98.2% of children; 94.5% of which was diffuse and 4.8% was multinodular. The mean ((+/-SD) T3 was 4.8 +/- 3.4 ng/mL (N, 0.6-1.6), T4 was 218 +/- 98 ng/mL (N, 60-155) and TSH was 0.44 +/- 0.36 (N, 0.5-5.5 microIU/mL). TMA positivity seen in 36.9% of patients. All patients were treated with carbimazole; subsequently 4 patients required thyroidectomy and one required radioactive iodine ablation. Mean (+/-SD) duration of follow-up in our patients was 4.9 +/- 3 years, ranging between 1.6 to 16 years and mean (+/-SD) duration of treatment was 34.4 +/- 22.6 months (range 12 to 120 months). Mean (+/-SD) duration to achieve euthyroidism was 5.2 +/- 4.7 months, ranging between 1-33 months. On intention to treat analysis, remission with carbimazole was achieved in 47.6%, remaining patients failed to achieve remission with drug treatment. CONCLUSION: Graves disease is the commonest cause of juvenile hyperthyroidism. Carbimazole is safe, effective, cheap, and easily available form of therapy. It is occasionally associated with serious side effects but requires prolonged follow up.

Adolescent↗
PubMed2005

Effect of opiates on growth hormone secretion in acromegaly.

Morphine at doses of 5 mg and 10 mg does not stimulate growth hormone (GH) secretion in normal subjects, and its effect on GH secretion in acromegaly is not widely documented. We investigated the effect of 15 mg intravenous morphine on growth hormone in patients with active acromegaly compared to normal subjects (7 acromegalics and 5 controls). Their mean (+/- SEM) age was 30.5 +/- 7.6 years and 29.5 +/- 0.5 years, respectively. Basal and peak response of growth hormone after morphine was measured with simultaneous assay of cortisol to exclude the effect of stress. Mean (+/- SEM) basal growth hormone was 103.16 +/- 28.04 ng/ml in acromegalics compared to 4.51 +/- 1.43 ng/ml in controls. Morphine caused an elevation of growth hormone in both acromegalics and normal subjects (p < 0.05). However, the Delta (peak minus basal) response of growth hormone was comparable between the two groups. A concurrent fall in cortisol was noted after morphine in both the groups, excluding the effect of stress on growth hormone. We conclude that higher doses (15 mg) of morphine are required to stimulate GH secretion in normal subjects, and that opioids exert a positive modulating effect on growth hormone secretion in patients with active acromegaly suggesting partial autonomy of the pituitary tumor.

Acromegaly↗
PubMed2004

Idiopathic granulomatous hypophysitis presenting as non-functioning pituitary adenoma: description of six cases and review of literature.

The aim of this study was to analyse the complete profile and outcome of patients with idiopathic giant cell granulomatous hypophysitis. Six consecutive cases of idiopathic giant cell granulomatous hypophysitis were studied from 1993 to 2002. Headache and visual disturbances were the most frequent presenting symptoms. All patients had hypogonadism, four had hypoadrenalism and three were hypothyroid at presentation. None of them had diabetes insipidus preoperatively. A sellar mass with suprasellar extension on MRI with loss of the posterior pituitary 'bright spot' was a consistent observation in all patients. All patients underwent surgical excision of the mass lesion with histopathological confirmation of giant cell granulomatous hypophysitis. Other systemic granulomatous diseases were excluded by appropriate investigations. Postoperatively, all patients became hypothyroid and hypogonad, five patients had adrenal insufficiency, while two developed permanent diabetes insipidus. The clinical presentation of giant cell granulomatous hypophysitis is that of an expanding sellar mass lesion with a varying degree of endocrine dysfunction. Preoperative diagnosis of 'hypophysitis' is usually difficult; however, stalk thickening and loss of posterior pituitary 'bright spot' on MR imaging are clues to the diagnosis.

Adenoma↗
PubMed2003

Vitamin D deficiency masquerading as pseudohypoparathyroidism type 2.

A case of antiepileptic-induced vitamin D deficiency, who presented with hypocalcemia, hyperphosphatemia with increased tubular reabsorption of phosphate mimicking pseudohypoparathyroidism type 2, is reported. He showed remarkable improvement with calcium and vitamin D treatment with normalisation of serum calcium and phosphate with reestablishment of phosphaturic response.

Adult↗