Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 15-year-old girl developed acute lymphoblastic leukemia (ALL). The patient was treated according to the 13th protocol of the Tokyo Children's Cancer Study Group, and thereafter remained free of disease. However, at the age of 20, she complained of polyuria, polydipsia and amenorrhea. Hematological or meningeal relapse was ruled out on the basis of clinical and laboratory findings. The plasma concentrations of GH, TSH, LH, FSH, ACTH and ADH were low or below the detectable limits. There was no increase in urine osmolarity after water deprivation. Arginine, LH-RH, TRH and CRH tolerance tests revealed no or low responses of GH, LH/FSH, TSH, and ACTH/cortisol, respectively. Magnetic resonance imaging demonstrated thickening of the pituitary stalk, which was homogeneously enhanced by gadolinium administration. A biopsy specimen showed fibrosis and infiltration of CD8-positive T lymphocytes in a portion of the pituitary stalk, whereas the adenohypophysis was normal. In addition, no leukemic cells were observed in the samples. Thus, a diagnosis of lymphocytic infundibuloneurohyophysitis (LIN) was established. All the symptoms were improved by treatment with hydrocortisone, L-thyroxine, desamino-8-d-arginine vasopressin, estrogen and gestagen. This is the first reported case of ALL complicated by LIN.
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PMID:[Lymphocytic infundibuloneurohypophysitis during the first remission in acute lymphoblastic leukemia]. 1119 41

A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and still showed impaired water diuresis during glucocorticoid replacement therapy is reported. A 45-year-old woman was initially admitted for nausea, vomiting, and general malaise. Her serum sodium and plasma osmolality, ACTH and cortisol values were low, but her urine osmolality was high. Other pituitary hormone levels, thyroid hormone levels, and a computed tomogram of the pituitary gland were normal. The patient was treated with hydrocortisone and followed in the outpatient clinic; however, she was lost to follow up 18 months after admission. Three years later she presented with hypoglycemia and hyponatremia. Her serum or plasma ACTH, FT3, FT4, cortisol levels were low and her serum TSH level was high. Pituitary stimulation tests revealed a blunted response of ACTH to CRH and an exaggerated response of TSH to TRH. Plasma ADH was inappropriately high, and a water-loading test revealed impaired water diuresis and poor suppression of ADH. Although ADH was suppressed, impaired water diuresis was observed in the water loading test after hydrocortisone supplementation. Thyroxine supplementation completely normalized the water diuresis. Her outpatient clinic medical records revealed a gradual increase in TSH levels during follow up, indicating that she had developed hypothyroidism during glucocorticoid replacement therapy. The hyponatremia on the first admission was due to glucocorticoid deficiency, whereas the hyponatremia on the second admission was due to combined deficiencies of glucocorticoid and thyroid hormones.
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PMID:A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and impaired water diuresis during glucocorticoid replacement therapy. 1122 40

Paraneoplastic syndromes induced by inappropriate-ectopic production of hormones, cytokines and growth factors, therefore not mediated directly by local infiltration or metastatic spread, occur in approximately 10 per cent of patients with malignant disease in initial phase. Subjects with paraneoplastic syndromes often are affected by small occult tumors which may be diagnosed only at autopsy. Inappropriate secretion of peptide hormones is the commonest cause of paraneoplastic syndromes. On the basis of an up-to-date review of the literature, this article discusses pathogenetic mechanisms, diagnostic features and essential therapeutic measures concerning the syndromes of inappropriate ACTH/CRH, PTHrp, TRH/TSH, ADH and MSH secretion. Moreover, some of paraneoplastic syndromes, that are associated with production of cytokines and growth factors by either tumor- or non malignant host microenvironment -cells, are briefly outlined.
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PMID:[Paraneoplastic syndromes associated with urogenital tumours: an up-to-date review]. 1894 70

Stress is generally a natural phenomenon that affects behaviour, physiological processes, and neuroendocrine, neurochemical, neurological and immune responses. Many somatic and mental disorders are thought to result from chronic stress. Stress-induced gonadal dysfunction is not restricted to humans, but is observed in all higher animals. Stress-induced gonadal dysfunction comprises disturbances of the hypothalamic-pituitary-gonadal axis and of spermatogenesis. Various stressors induce changes in the secretion of neurotransmitters and hormones, such as CRH, ADH, beta-endorphins, somatostatin, VIP, PRL, GH, TSH, dopamine, serotonin, neuropeptide Y, melatonin, ACTH, glucocorticosteroids, catecholamines and androgens. In acute stress, testicular function is principally modified by cytokines and fluctuating concentrations of gonadotropins, while in chronic stress, hypogonadotropic hypogonadism and disruption of spermatogenesis of varying severity, including spermatogenetic arrest, are observed. In spite of the decades-long interest in the relationships between psychological stress and the function of male gonads, many questions in this area remain unanswered.
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PMID:Psychological stress and the function of male gonads. 2237 97