Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

POEMS syndrome is a rare systemic multi-organ disease usually reported in Japanese patients. The clinical course is slow with a 5-year survival of 60%. Death is caused by polyneuropathy and or anasarka. We observed four cases in our ward (all males, aged 39, 57, 54 and 54 years) who all presented at least four characteristic clinical signs. Gynecomasty together with impotency was seen in all patients. All had hypogonadism and borderline hyperprolactinaemia. Hyperoestrogenism was seen in two. In three patients, rare endocrinopathies were part of the POEMS syndrome. One patient had diabetes mellitus. The clinical course was variable and a function of the effectiveness of plasmocyte dyscrasia therapy. Little work has been done on endocrinopathies in POEMS syndrome. In most cases, gonadotrope function is impaired with gynecomasty and impotency in men, amenorrhoea in women. Generally the hypogonadism is hypogonadotropic. Hyperoestrogenism is frequent and prolactin levels are normal or high with an exaggerated response to thyroid releasing hormone stimulation. The aetiology of POEMS syndrome is unknown. Current research is based on an immunologic theory based on the discovery of high levels of interleukin 6 in POEMS patients with or without Castleman's disease. The cytokine would affect the different organs and lead to clinical expression. Corticosteroids are usually effective in most patients, particularly in reducing the oedema and controlling the polyneuropathy.
 ...
PMID:[Endocrine diseases in POEMS syndrome. Apropos of 4 cases]. 797 57

Several hormonal alterations have been described in patients with chronic renal failure. However, there are few epidemiological studies on uremia-associated endocrine derangements, in particular in patients undergoing peritoneal dialysis (PD). A cross-sectional descriptive study was performed to assess the prevalence of hormonal dysfunctions affecting pituitary secretions in the whole population of patients in the PD unit of our hospital. The total population included 69 patients, 66 on continuous ambulatory PD and 3 on continuous cycling PD. There were 31 men and 38 women, the mean age was 55 years (range 23-82 years), and the mean duration of PD was 32 months (range 1-161 months). There were 27 (39.1%) patients with diabetes mellitus (7 type I and 20 type II). Clinical records were reviewed for hormonal alterations affecting the pituitary and its target glands. The whole population had available data on the pituitary-thyroid axis. The following diagnoses and prevalences were found: hypothyrotropic hypothyroidism 4 (5.8%), subclinical hypothyroidism 4 (5.8%), primary hypothyroidism 8 (11.6%), and low T3 syndrome 11 (15.9%). The remaining pituitary hormones were available in 20 patients. Hyperprolactinemia was found in 7 (35%) patients and abnormally increased growth hormone levels in 6 (30%). Gonadotropin levels were normal for the age of the women and showed a tendency to be increased in most of the men. Corticotropin levels were normal in all patients with available data. There was no relationship between the high prevalence of diabetes mellitus in our population and the remaining hormonal derangements found. These results suggest that there is a non-negligible prevalence of pituitary abnormalities in uremic patients undergoing PD.
 ...
PMID:Pituitary dysfunctions in uremic patients undergoing peritoneal dialysis: a cross sectional descriptive study. 853 9

The hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator presides over the pulsatile and feedback-regulated activities of the pituitary-gonadal axis. Awakening of synchronous activity of the GnRH neuronal ensemble in the earliest stages of puberty heralds the onset of full activation of the reproductive axis in girls and boys. Progression from prepuberty to adulthood in boys is directed by marked (30-fold) amplitude enhancement of pulsatile luteinizing hormone (LH) secretion, as assessed by an ultrasensitive immunofluorometric assay and deconvolution analysis. There is a much less apparent rise in LH secretory burst frequency (approximately 1.3-fold increase). Consequently, human puberty is an amplitude-driven neuroendocrine maturational process. However, less is known about pulsatile follicle-stimulating hormone (FSH) release in puberty. Multiple pathophysiologies that result in hypogonadotropic hypogonadism can converge on a final common mechanism of attenuated hypothalamic GnRH pulse generator output and hence reduced LH (and FSH) secretion. Disturbances may take the form of reduced GnRH pulse frequency and/or attenuated GnRH secretory burst mass. When the pathophysiology of hypogonadism originates exclusively in a failed GnRH pulse generator, then either treatment of the primary disease process where possible (e.g., by refeeding in starvation, improved metabolic control in diabetes mellitus, dopamine agonist treatment in hyperprolactinemia, etc) and/or treatment with pulsatile GnRH (e.g., in Kallmann's syndrome, isolated hypothalamic lesions, etc.) can provide relevant therapeutic options in children and adults.
 ...
PMID:Neuroendocrine mechanisms mediating awakening of the human gonadotropic axis in puberty. 879 95

The frequency of biopsies with different types of mastitis among all patients with benign breast diseases in twenty years was 3%. About 2/3 of the patients were younger than 50 years, the average age was 46.7 years. Comparing the frequency of the different types of mastitis the puerperal mastitis is very rare in contrast to the increasing non-puerperal and granulomatous inflammatory breast lesions. The diagnosis "granulomatous mastitis" is one of exclusion. Both non-infectious and infectious causes must be considered. The origin of the granulomatous mastitis often is unknown, but it is supposed to be an autoimmune localized response due to the retained and extravasated fat and protein rich secretions in the ducts in cases of hyperprolactinemia (drug induced or by microprolactinomas) or hormonal imbalances characterized by epitheloid cell granulomas with giant cells microabscesses around lipid drops, but without necroses. An idiopathic type of granulomatous mastitis concerns young women in relationship to parturition with a similar histological pattern predominantly of the lobules. Special types of mastitis are the B-lymphocytic autoimmune mastitis associated with a longstanding insulin-dependent diabetes mellitus type I, the sarcoidosis, panniculitis and the rare but very different infectious diseases with breast involvement. Particularly in cases without features of secretory activity a carefully bacterioscopic and microbiologic work-up of fresh material from the surgical specimens is necessary for a final diagnostic report.
 ...
PMID:[Mastitis. Classification, histopathology and clinical aspects]. 915 1

More than thirty types of tumors in the sellar region can mimic pituitary adenoma on, magnetic resonance imaging. When they exist, clinical manifestations are not necessarily highly contributive to diagnosis. Headache, visual impairment, signs of antepituitary insufficiency or possible dysmenorrhea with galactorrhea attributed to hyperprolactinemia due to compression of the dopaminergic axis are not specific and may be misleading. Clinical signs of diabetes insipidis and polyphagia are however suggestive of non-pituitary tumors. Consequently, high-resolution imaging (MRI) and sometimes particular diagnostic circumstances (post partum for hypophysitis for example, or breast cancer for metastasis) orient the diagnosis. More rarely tumor enlargement, for example in certain germ cell tumors, provides a clue.
 ...
PMID:[Intra-sellar non-adenomatous expansive process]. 920 62

The cardinal clinical features of PCOS are hirsutism and menstrual irregularity from anovulation. Obesity occurs in approximately 50% of hyperandrogenic anovulatory women, some of whom also have non-insulin-dependent diabetes mellitus. Underlying these clinical findings are several biochemical abnormalities, including LH hypersecretion, hyperandrogenism, acyclic estrogen production, decreased SHBG capacity, and hyperinsulinemia, all of which contribute to increased ovarian production of androgens, particularly T. A fundamental mechanism of ovarian hyperandrogenism in PCOS is LH hypersecretion. Whether the central nervous system is a possible locus for initiating LH hypersecretion remains unclear, because exaggerated LH secretion is temporarily reversed by induced ovulatory cycles or physiologic luteal concentrations of progesterone. On the other hand, desynchronization of pulsatile LH secretion from sleep in girls with PCOS and an exaggerated (e.g., masculinized) early LH response to GnRHa testing in women with hyperandrogenic anovulation and congenital adrenal virilizing disorders suggest that events occurring before puberty, perhaps during fetal life, may irreversibly alter neuroendocrine function. Hyperinsulinemia from insulin resistance is an important regulatory mechanism governing ovarian hyperandrogenism. Hyperinsulinemia in hyperandrogenic anovulatory women potentiates ovarian hyperandrogenism by enhancing LH secretion; potentiating 17-hydroxylase and, to a lesser extent, 17,20-lyase activity; and suppressing SHBG capacity. It is a key component of hyperandrogenic anovulation caused by a type of insulin resistance that in independent and additive to that of obesity alone. Although the mechanisms governing insulin action on ovarian steroidogenesis are unknown, abnormalities of intracellular insulin signaling or cytochrome P450c 17[alpha] activity may render the 17-hydroxylase/17,20-lyase enzyme complex more sensitive to insulin. Hyperinsulinemia in hyperandrogenic anovulatory women is accompanied by upper-body obesity characterized by an increased amount of abdominal fat. Upper-body obesity is an important independent risk factor for CVD and diabetes. Although genetic and environmental factors affect fat distribution, sex steroids, particularly androgens, regulate lipid metabolism, suggesting yet another link between the hormonal and metabolic abnormalities of hyperandrogenic anovulation. A careful history and physical examination guide the extent of diagnostic testing. Slowly progressive hirsutism with anovulation of peripubertal onset usually reflects hyperandrogenic anovulation. This type of clinical presentation requires an evaluation to rule out other endocrinopathies (e.g., virilizing tumors, adult-onset CAH, hyperprolactinemia, and Cushing's syndrome). Virilization or severe rapidly progressive hirsutism requires immediate investigation to rule out a possible virilizing tumor. The ultimate goals of therapy for hyperandrogenic anovulatory women are to normalize the endometrium, antagonize androgen action at target tissues, reduce insulin resistance, and correct anovulation, if necessary.
 ...
PMID:Polycystic ovary syndrome. 942 64

Programs of psychocorrection for application in endocrinology in cases of diabetes type I and II, hyperprolactinemia and menopause are described. Programs took into consideration the severity of somatic state and specificity of psychologic problems of the patients. Dynamic psychodiagnostic observations of the patients both before and after the course of treatment as well as the comparison with analogous groups of patients which were not treated by means of psychotherapy revealed significant positive psychologic changes under influence of psychocorrection and general improvement of the somatic state.
 ...
PMID:[Experience with group psychocorrection in somatic diseases]. 946 36

The immune system is still regarded by many as autonomous, and prolactin (Prl) has traditionally been considered as a lactogenic hormone. Over the last 10 years, the total number of publications considering Prl is decreasing, while the number of those investigating its role in immunity sustainly increased. In addition to the pituitary gland, Prl-like peptides can be produced by activated leukocytes and fibroblasts. Elevated serum levels of Prl in (rat) adjuvant arthritis, (murine) collagen type II-induced arthritis, (murine and human) systemic lupus erythematosus (SLE), and (murine and rat) autoimmune type I diabetes may influence the outcome of the disease. It is suggested that mild hyperprolactinemia is a risk factor for the development of autoimmunity. This can occur under certain circumstances, for example adrenocortical deficiency or postpartum. In human SLE, Prl appears to favor the production of anti-double stranded DNA. While glucocorticoids would damp the immune reactivity, Prl constitutes a stimulatory link between the neuroendocrine and immune systems. Future directions should include: 1) multicenter projects for evaluation of the therapy with Prl-inhibiting compounds in SLE, considering for example the HLA-DRB1 *0301 status; and 2) the regulation of extra-pituitary Prl-like cytokines ("proliferins") (e.g., in rheumatoid arthritis synovium) and their role in the production of catabolic enzymes.
 ...
PMID:Prolactin in autoimmune diseases. 952 Oct 87

We report a case of pyodermia chronica glutealis complicated by acromegalic gigantism associated with hyperprolactinemia. The serum prolactin, growth hormone, adrenocorticotropic hormone, and 11-deoxycortisol levels were elevated, but the estradiol and dehydroepiandrosterone-sulphate levels were within normal limits. However, the testosterone level was very low. Histopathologically, we found sinus tracts and scarring in a specimen from the buttocks. We could not immunohistochemically detect clear androgen, growth hormone, or prolactin receptors at any site. The patient was a man with a height of 197 cm and weight of 140 kg, he had clinical features of active acromegaly such as excessive sweating and increased thickness of soft tissue. He was also diagnosed with diabetes mellitus. Under such conditions, bacteria could easily grow and lesions might have been aggravated by the heavy pressure from his weight, a possible causes of his pyodermia chronica glutealis.
 ...
PMID:Pyodermia chronica glutealis complicated by acromegalic gigantism. 960 82

We report a rare case of Klinefelter's syndrome (KS) with mixed connective tissue disease (MCTD), diabetes mellitus (DM) and several endocrine disorders. A 57-year-old man presented with polyarthritis and tapering fingers with Raynaud's phenomenon on admission. In addition to a karyotype of 47, XXY, a marked restrictive change in respiratory functional test, a myogenic pattern in electromyogram, the positive tests for anti-RNP antibody indicated that this was a case of KS complicated with MCTD. The patients also presented DM with insulin resistance, hyperprolactinemia, slight primary hypothyroidism and hypoadrenocorticism. The mechanism for these coincidences remains to be elucidated.
 ...
PMID:Klinefelter's syndrome accompanied by mixed connective tissue disease and diabetes mellitus. 1056 40


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>