Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient was a 16-month-old girl, born by mature natural delivery and weighing 3,320 g. Hirsutism was noted on birth. Development of pubic hair and hypertrophy of the labia minora were noted after 8 months. At the time of admission, the height was 80 cm and body weight 14.5 kg. Systemic obesity, facial acne, systemic hirsutism, low pitched voice and hypertrophied clitoris were observed. Androstenedione, dehydroepiandrosterone-sulfate and cortisol showed high levels in the blood, and the urinary 17-KS was obviously high, along with an increase in urinary 17-OHCS. The subject did not respond to either the dexamethasone inhibition test or ACTH load test. The abdominal CT revealed a tumor in the front upper position of the left kidney, and adrenal scintigraphy disclosed an obvious accumulation image in the adrenal gland on the left side. Based on the diagnosis of a left adrenal tumor, left adrenalectomy was performed. The tumor measured 5.0 x 4.5 x 3.7 cm, and weighed 57 g. Histopathologically it was diagnosed as adrenocortical adenoma. The infantile virilizing adrenocortical tumor is reported together with some discussion of the literature.
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PMID:[A case of infantile virilizing adrenocortical tumor]. 261 Jan 80

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.
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PMID:Pheochromocytoma associated with adrenocortical adenoma: case report and literature review. 372 Jun 79

The clinical response of 57 adult patients with Cushing's syndrome due to bilateral adrenocortical hyperplasia or adrenocortical adenoma is documented following resolution of hypercortisolaemia by various forms of treatment. Despite satisfactory biochemical remission of the disease the clinical result was far less satisfactory when assessed by persistence of obesity (55%), menstrual irregularity (41%), hypertension (29%) and insulin-dependent diabetes (22%). Myopathy, hirsuitism and psychological abnormalities persisted to a lesser extent. The mortality rate of the series over a 30 year follow-up period was 4 times that of a general population matched for sex, age and year of entry into the series. Cardiovascular disease was the cause of death in 85%. Irreparable cardiovascular disease is produced early in the course of hypercortisolaemia, emphasizing the vital importance of the earliest possible recognition and treatment of this disease.
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PMID:The clinical response to treatment in adult Cushing's syndrome following remission of hypercortisolaemia. 398 55

Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.
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PMID:[Diagnosis and treatment of adrenocortical tumors]. 631

A 48-year-old woman underwent jejunoileal bypass surgery for obesity while hypercalcemic. Three years later, she developed symptomatic osteomalacia impairing her daily activities. Bone biopsy confirmed the clinical diagnosis of osteomalacia, and treatment with 8000 U daily of vitamin D and milk resulted in striking improvement of clinical symptoms and resolution of her osteomalacia both chemically and histologically. The patient, however, again became hypercalcemic and a parathyroid adenoma was subsequently removed with restoration of serum calcium values to normal. Neither the occurrence and successful treatment of gross symptomatic osteomalacia consequent to jejunoileal bypass surgery, nor the obscuration of primary hyperparathyroidism by osteomalacia has been hitherto well documented in the United States.
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PMID:Symptomatic osteomalacia after jejunoileal bypass surgery in a patient with primary hyperparathyroidism. A study of the change in bone morphology and vitamin D metabolites before and during treatment. 660 88

A 37-year-old woman presented with acute psychosis and cognitive impairment. Skull x-ray showed an enlarged sella turcica with erosion of the floor. Endocrinologic workup suggested the diagnosis of Cushing's disease and hyperprolactinemia. She had no cushingoid feature, and the only physical sign was mild generalized obesity. She showed a paradoxic response to dexamethasone suppression, and underwent trans-sphenoidal resection of a pituitary macroadenoma. Electron microscopy showed the tumor to be a Crooke's cell adenoma. Results of immunohistochemical staining were positive only for ACTH and beta-endorphin. The neuropsychiatric manifestations resolved after surgery.
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PMID:Occult Cushing's disease presenting with acute psychosis. 671 82

Hypocycloidal tomograms of the sella turcica and serum prolactin concentrations were obtained in 146 women with amenorrhea, galactorrhea, or both to diagnose prolactin-secreting pituitary adenomas. Findings suggesting an adenoma, ie, abnormal tomogram and elevated serum prolactin concentration, were found in 24.6% (16/65) of previously unscreened patients and 59.2% (48/81) of prescreened patients. The combination of an abnormal tomogram and elevated prolactin level was relatively specific for an adenoma, as 91% (42/46) of women with these findings who underwent surgery had histologically confirmed tumors. Tumors occurred in women from 15 to 45 years of age, with amenorrhea or galactorrhea ranging from less than six months to more than 20 years in duration. Some women in this series also had obesity, rapid weight loss, polycystic ovarian syndrome, amenorrhea following discontinuance of oral contraceptive use, or emotional stress.
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PMID:Prolactin-secreting pituitary adenomas. III. Frequency and diagnosis in amenorrhea-galactorrhea. 719 Oct 13

We are presenting a series of 23 patients with Cushing disease selected from a larger study in which the ectopic production of ACTH (paraneoplastic or tumoral), adrenal adenoma or carcinoma were discarded. Sixteen were female and seven male. Diagnosis was fundamentally realized by clinical manifestations derived from hypercortisolism (obesity, muscular atrophy, diabetes, osteoporosis or polyglubulia). The polytomography demonstrated a deformed sella in 19 patients. Endocrine exams showed an alteration in rhythm of Cortisol and elevated levels of urinary metabolites. Others exams, Liddle Test, Metopirona Test, or stimulation of exogenic ACTH did not always permit diagnosis of pituitary adenoma. Plasmatic dosage of ACTH is the best test although results did not always agree with clinical manifestations. In each case we performed clinical treatment in preparation for surgery and later selective removal of adenoma or total pituitary ablation by transphenoidal approach. Of 21 patients, we found an adenoma during surgery in 15; the other 6 on whom we performed a total hypophysectomy, the pathological study showed an adenoma in 5 and a hyperemic gland with thick capillaries in 1. Another type of treatment was used on 2 due to their age. Nine patients were given post-operative radiotherapy. We conclude that microsurgery by transphenoidal approach offers the best possibilities for patients with Cushing disease.
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PMID:[Surgical treatment in Cushing's disease (authors' translation)]. 731 90

In 379 men less than age 75 years who underwent initial transurethral prostatectomy for benign prostatic hypertrophy specimen weights were compared with host ages, obesity, smoking habits and the presence of incidental cancer. Among 334 men 60 to 74 years old average specimen weights increased with increasing obesity from 20.3 to 36.6 gm. Underweight men in comparison with men at least 30% overweight demonstrated more small specimens (10 gm. or less, 24% versus 2%, p < 0.001) and fewer large specimens (50 gm. or more, 5% versus 26%, p < 0.005). This pattern was present in smokers and nonsmokers. Adenoma weights increased with increasing host age and were larger in nonsmokers of all age groups. Body habitus was similar in the prostatectomy patients and 290 office patients of similar age, suggesting no increase in obstructive uropathy among obese men despite the larger adenomas. These observations are compatible with different risk factors for the obstructing and nonobstructing components of benign prostatic enlargement.
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PMID:Larger prostatic adenomas in obese men with no associated increase in obstructive uropathy. 769 Apr 27


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