Biomedical subjects

M Sparagana

Publications and source records attributed to M Sparagana.

13 recordsLinked to original sources

PubMed1988

Late recurrence of benign pheochromocytomas: the necessity for long-term follow-up.

Two patients who had removal of seemingly benign pheochromocytomas had recurrences 10 and 14 years later despite normal catecholamine excretion for 7 and 9 years postoperatively. The first patient returned with a myocardial infarction and an apparently solitary recurrence; the second patient with a stroke and metastatic disease. Both patients had recurrence of hypertension and increased catecholamine excretion. They were given phenoxybenzamine and are doing satisfactorily 7 and 9 years after their recurrences. Such patients should be followed after surgery for 15 or more years for early detection of recurrences. Prompt therapy should reduce the risk of undesirable complications.

Adrenal Gland Neoplasms↗

PubMed1988

Positive iodine-131 6 beta-iodomethyl-19-norcholesterol (NP-59) adrenal images can precede return of adrenocortical function after o,p' DDD treatment.

A patient with bilateral adrenal hyperplasia, due to the ectopic adrenocorticotrophic hormone (ACTH) syndrome, received a 3-month course of treatment with 1,1 dichloro-2(o-chlorophenyl)-2-(p-chlorophenyl)ethane (o,p' DDD), which caused adrenal hypofunction requiring steroid therapy. Eleven months later, Cushing's syndrome recurred. His CT scan showed a left adrenal gland that was enlarged and a normal-sized right adrenal gland. However, the NP-59 image showed increased uptake by both glands. Venous effluent was sampled from each adrenal vein. The plasma cortisol level from the left gland was 1392 ng/ml, and that from the right gland was 667 ng/ml. The latter value was not significantly different from the values obtained at peripheral sites (517-744 ng/ml). In the course of recovery from o,p' DDD damage, the ability of the adrenal gland to take up NP-59 may be restored before the return of its biosynthetic and secretory functions. Serial NP-59 adrenal images can anticipate the recurrence of Cushing's syndrome after adrenolytic therapy, thereby permitting early retreatment.

19-Iodocholesterol↗

PubMed1988

Episodic ectopic ACTH syndrome associated with pulmonary infarctions.

The etiology of the ectopic ACTH syndrome, associated with certain tumors, is unclear. The ectopic ACTH syndrome was diagnosed in our patient by the characteristic clinical and laboratory findings. Shortly after admission, pulmonary infarctions were documented by lung scans and computed tomography. After treatment with anticoagulants, his plasma ACTH level and its suppressibility became normal. There was no evidence of a tumor. The ectopic ACTH syndrome recurred one year later in conjunction with another episode of pulmonary infarctions. During anticoagulant therapy his infarctions cleared and his plasma ACTH level normalized. In the five years since the onset, no tumor has been found, and plasma ACTH level remains normal and suppressible. We propose that our patient's pulmonary infarctions stimulated pulmonary ACTH production, leading to Cushing's syndrome.

ACTH Syndrome, Ectopic↗

PubMed1987

An unusual pheochromocytoma associated with an androgen secreting adrenocortical adenoma. Evaluation of its polypeptide hormone, catecholamine, and enzyme characteristics.

Our patient had a left suprarenal mass. His blood pressure was normal, but his urinary catecholamines (CA), vanillylmandelic acid (VMA), total metanephrines (TMn) and 5-hydroxyindolacetic acid (5HIAA) were elevated. In addition, he had elevated, nonsuppressible urinary 17-ketosteroids (17KS) and androsterone, but his urinary 17-hydroxycorticoids (17OHCS) and free cortisol were normal, as were his plasma cortisol and ACTH. After resection of the suprarenal mass, the patient's urinary hormone values reverted to normal. The mass contained a pheochromocytoma and an adrenocortical adenoma. The pheochromocytoma was unusual in that it contained very little norepinephrine (NE) and dopamine (DA) and an abundance of epinephrine (E) despite normal enzyme concentrations. Electron micrographs showed primarily E granules with few of the NE-type. The immunoperoxidase histochemical stains for vasoactive intestinal peptide (VIP) and serotonin (S) were strongly positive. The patient's blood pressure may have been normal because his pheochromocytoma secreted E, VIP, or S. The associated adrenocortical adenoma produced no symptoms and was probably coincidental.

Adenoma↗

PubMed1987

Tumor-induced osteomalacia: long-term follow-up of two patients cured by removal of their tumors.

Two patients with mesenchymal tumors had osteomalacia associated with marked hypophosphatemia and renal phosphate wasting. Their serum calcium and parathyroid hormone levels were normal. The first patient also had aminoaciduria and glucosuria in addition to phosphaturia. Both patients were treated with very large doses of vitamin D2 and phosphate without improvement in the osteomalacia or normalization of the serum phosphate. Complete removal of a low-grade fibrosarcoma in the second patient and removal of an ossifying fibroma in the first patient resulted in a cure in both patients despite no further therapy with vitamin D or phosphate. The excessive aminoaciduria and glucosuria of the first patient also remitted. During a 14-year follow-up period, there has been no evidence of tumor recurrence, hypophosphatemia, or osteomalacia in either patient. The levels of 1,25-dihydroxycholecalciferol remain within the normal range in both patients.

Adult↗

PubMed1987

Primary hypogonadism associated with o,p' DDD (mitotane) therapy.

Mitotane is a drug which is concentrated largely in adipose tissue and the adrenal glands. It has a remarkable specificity for the adrenal cortex and can produce necrosis of that organ; consequently, it has been used as a therapeutic agent for adrenocortical carcinoma. Because of the similarity between adrenocortical and testicular tissue, mitotane could be expected to cause testicular damage; however, there is sparse support for this in the literature. We recently studied a patient who developed impotency due to primary testicular failure at the time that he was treated with mitotane. A testicular biopsy, performed about four months after the drug was discontinued, showed normal appearing Leydig cells and atrophy of the seminiferous tubules with the picture of a maturation arrest. In the four and one half years since he last received mitotane, the patient's libido has slowly improved and his plasma testosterone, gonadotropins and LH response to gonadotropin-releasing hormone have become essentially normal. We propose that mitotane can be cytotoxic to the testis as it is to the adrenal cortex.

ACTH Syndrome, Ectopic↗

PubMed1979