Changes in bone mineral density and bone turnover markers in patients undergoing hematopoietic stem cell transplant.

INTRODUCTION: Hematopoietic stem cell transplant (HSCT) is frequently complicated by endocrine abnormalities and loss of bone mass. This prospective study was conducted to evaluate the bone loss post-HSCT. MATERIALS AND METHODS: A total of 50 patients was evaluated pretransplantation, and 25 had HSCT (17 males, 8 females; 19 allogenic, 6 autologous). Bone mineral density (BMD) and bone markers were measured at baseline, 3-6 months and 12 months. RESULTS: The mean age and body mass index were 25.1 ± 16.3 years and 19.4 ± 4.5 kg/m(2), respectively. There were 15 adults (60%), and 10 adolescents (40%). There was a significant decline in BMD from the baseline at total femur (-8.7%; P < 0.0001), femoral neck (-5.0%; P = 0.003), femoral trochanter (-6.0%; P = 0.001), and Ward's triangle (-9.9%; P < 0.0001) at 6 months posttransplantation. From the 6 months to 12 months, there was a significant improvement in BMD at above sites except at Ward's triangle. The decline in BMD was nonsignificant at the whole body (-0.3%, P = 0.748) and the lumbar spine (-2.7%, P = 0.130) at 6 months posttransplant. Younger patients with allogenic graft and steroid use are more likely to have significant loss of BMD at hip posttransplant. Serum osteocalcin decreased, and N-telopeptide increased at 3-6 months, which return to baseline at 1-year posttransplant. CONCLUSIONS: A significant bone loss is observed at 6 months in patients with post-HSCT. The bone loss occurs predominantly at cortical bone. There is recovery of bone mass at 12 months posttransplant except at Ward's triangle. Bone loss after HSCT is multifactorial.

Pituitary oncocytoma presenting as Cushing's disease.

A 19-year-old girl presented with classical features of Cushing's syndrome. Endocrinal evaluation was consistent with pituitary source of ACTH; but imaging showed normal pituitary. Bilateral inferior petrosal sinus sampling confirmed the diagnosis. A successful remission was achieved after adenomectomy by transphenoidal route. Histopathological examination was consistent with pituitary oncocytoma and immunohistochemistry was positive for synaptophysin, chromogranin, neuron specific enolase, S-100, ACTH, prolactin, and GH.

Hidden diagnosis of multiple endocrine neoplasia-1 unraveled during workup of virilization caused by adrenocortical carcinoma.

Multiple endocrine neoplasia-1 (MEN1) is an autosomal dominant syndrome with classic triad of parathyroid hyperplasia, pancreatic neuroendocrine tumors, and pituitary adenomas. Other recognized manifestations include carcinoid, cutaneous or adrenocortical tumors. It is commonly presented with clinical features related to parathyroid, pancreas or pituitary lesions. Here, we have presented a case that had virilization and biochemical Cushing's syndrome due to adrenocortical carcinoma as presenting feature of MEN1. Cushing's syndrome in MEN1 is an extremely rare and usually late manifestation and most cases are due to corticotropin-producing pituitary adenomas. Although Cushing's syndrome generally develops years after the more typical manifestations of MEN1 appear, it may be the primary manifestation of MEN1 syndrome particularly when related to adrenal adenoma or carcinoma.

Nelson's syndrome presenting as bilateral oculomotor palsy.

Nelson's syndrome refers to a clinical spectrum arising from progressive enlargement of pituitary adenoma and elevated adrenocorticotrophic hormone after total bilateral adrenalectomy for Cushing's disease comprising of hyperpigmentation, visual field defects which can be life threatening. We report here a 50-year male presenting with rapid onset of Nelson's syndrome with an unusual finding of bilateral oculomotor palsy mistakenly treated as ocular myasthenia.

Evaluation of thyroid and adrenal functions in patients with hyponatremia.

BACKGROUND: Hyponatremia is frequently detected as a cause in patients admitted to command Hospital Kolkata with altered sensorium. We evaluated these patients to rule out two common endocrine causes as etiological factors i.e. hypothyroidism and hypoadrenalism. METHOD: We studied 100 patients over a period of two years in all seasons who were admitted to hospital with altered sensorium and found to have hyponatremia as a cause, after ruling out other causes of altered sensorium as per inclusion and exclusion criteria. They were subjected to thyroid and adrenal evaluation in addition to detailed history, clinical examination and lab evaluation as per study protocol. RESULTS: Total 100 patients were enrolled in the study. The age of patients varied from 31 years to more than 70 years. Majority of patients were between the age group of 41-60 years (49 patients. Males were predominant in the study. Only 8 patients were detected to have hypothyroidism requiring replacement therapy and only 2 patients had adrenal insufficiency. 48 patients had drug induced hyponatremia and 42 idiopathic hyponatremia. No seasonal variation was noted. CONCLUSION: Thiazide diuretic intake as antihypertensive drug was found to be a major cause of hyponatremia. Most of the patients in this group were using thiazide diuretics. In idiopathic group the cause of hyponatremia can be hypothesized as multifactorial. The hot and humid climate of Kolkata and other coastal regions made them more vulnerable to develop hyponatremia. Hypothyroidism and hypoadrenalism were not found to be major causes of unexplained hyponatremia.

Pituitary calcification masquerading as pituitary apoplexy.

Pituitary calcification occurs commonly in lactotroph or somatotroph adenoma but rare in chomophobe or gonadotroph adenoma. On imaging, it can mimic hemorrhage, hence may masquerade pituitary apoplexy if patient present with neurological manifestations. We present a case of pituitary calcification which mimicked pituitary apoplexy.

Combined granulomatous and lymphocytic hypophysitis presenting as pituitary incidentaloma in a middle-aged woman.

We report a case of 41-year-old lady who presented with chronic headache of 6-month duration and a sellar mass with a suprasellar extension on imaging, which was interpreted as pituitary macroadenoma. She had normal pituitary function and visual perimetry. On clinical examination and imaging it was provisionally diagnosed as pituitary incidentaloma due to hypophysitis and she was advised steroid therapy, but underwent transnasal resection of the tumor against suggestion. Histopathological examination revealed combined granulomatous and lymphocytic hypophysitis most likely of autoimmune in origin. Definitive diagnosis of hypophysitis can be made only on histopathological examination. As most cases of autoimmune hypophysitis are surgically treated, patients should be assessed on individual basis for requirement of steroids in postoperative period.

Medical management of pheochromocytoma: Role of the endocrinologist.

Pheochromocytoma is a rare tumor arising from chromaffin cells in adrenal medulla or other paraganglia in the body, which may be associated with many genetic syndromes and mutation. The role of endocrinologist is in biochemical diagnosis of suspected cases; its anatomic and functional localization with the help of imaging like CT, MRI, and nuclear scanning; preoperative control of hypertension; and postoperative follow-up of cases that have undergone surgical resection. Familial and genetic screening of cases and their family is important to detect occult cases. Endocrinologist will also play a role in cases with malignant pheochromocytoma in assessment of metastasis, control, chemoradiotherapy, and follow-up.

Adult hypopituitarism: Are we missing or is it clinical lethargy?

Hypopituitarism, a disease of varied etiologies, is a serious endocrine illness that requires early recognition and prompt treatment to avoid its severe deleterious effects. In adults it is often missed due to non-specific symptoms of growth hormone deficiency and hypogonadism or mild deficiencies of other pituitary hormones. In some it may present with acute onset of symptoms suggestive of acute adrenal (corticotropin) insufficiency or symptoms due to mass lesion in/or around pituitary. High index of suspicion is required to seek hypopituitarism in patients with non-specific symptoms such as fatigue and malaise. Treatment of isolated hormone deficiency, partial or panhypopituitarism, has gratifying results although they require lifelong treatment and follow-up.

Prevalent and Emerging Therapies for Osteoporosis.

Osteoporosis and fractures associated with it constitute a real and serious socio-medical problem, which only recently has come to the forefront of social consciousness. With increasing number of exservicemen and their dependents, osteoporosis management has become very important in our setup. Currently available pharmacological therapies for prevention of fragility fractures are limited in scope, efficacy and acceptability to patients. Oral bisphosphonates are the standard treatment for osteoporosis which are associated with significant gastrointestinal side effects and thus poor patient compliance. Newer regimens, including intravenous (IV) formulations of bisphosphonates, have successfully come in vogue with greater patient compliance and equal or better benefits. The real need in osteoporosis treatment is for additional anabolic drugs. The only currently approved anabolic agent for treating osteoporosis is teriparatide (recombinant human parathyroid hormone 1-34), which stimulates new bone formation. Considerable efforts are being made to develop new, more effective treatment for osteoporosis. These novel drugs under trial include those primarily inhibiting osteoclastic bone resorption (like bisphosphonates) such as inhibitors of receptor activator of nuclear factor-kappa B ligand (RANKL) signalling, cathepsin K inhibitors, c-Src kinase inhibitors, integrin inhibitors, chloride channel inhibitors and the drugs with osteo-anabolic actions such as orally active parathyroid hormone (PTH) analogues, calcium sensing receptor antagonists, PTH-related peptide analogues and agents that induce osteoblast anabolism via pathways involving key, recently identified, molecular targets (wnt low-density lipoprotein receptor-related protein-5 signalling; sclerostin antibodies).

Efficacy and Toxicity Profile of Methotrexate Chloroquine Combination in Treatment of Active Rheumatoid Arthritis.

BACKGROUND: The present study was conducted to study the efficacy and toxicity profile of methotrexate chloroquine combination in treatment of active rheumatoid arthritis. METHODS: 24 patients of rheumatoid arthritis confirming to revised American Rheumatism Association (ARA) criteria were studied prospectively for twenty months. Clinical evaluation was made every 3 months. Clinical disease variables measured at each visit were number of joints with swelling, number of joints with tenderness and pain, duration of morning stiffness and physician and patient assessment of disease activity. Blood counts, liver function tests and other adverse effects due to drugs were monitored every 2 months. RESULTS: 10 patients demonstrated more than 50% improvement. 4 patients withdrew from study, 2 because of excessive nausea and vomiting and 2 because of noncompliance. Other side effects noted were hyperpigmentation, photosensitivity, skin rashes, raised transaminases and stomatitis. CONCLUSION: Methotrexate chloroquine combination has good efficacy and toxicity profile. Gastrointestinal side effects are most common and usually responsible for the discontinuation of the drugs.