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A case of nocturnal polyuria in olivopontocerebellar atrophy.
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We report a case of olivopontocerebellar atrophy without sleep apnea syndrome who presented nocturnal polyuria. It is considered that a disturbance in the circadian rhythm for arginine vasopressin secretion due to degeneration of suprachiasmatic nuclei and marked increase in the secretion of atrial
The effect of intranasal desmopressin on nocturnal waking in urination in multiple system atrophy patients with nocturnal polyuria.
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Nocturnal waking in urination (nocturia) is a common feature in patients with multiple system atrophy (MSA). Degeneration of arginine vasopressin (AVP) neurons in the suprachiasmatic nucleus in this disorder may lead to nocturnal polyuria, which has been treated with intramuscular desmopressin. We
Increase in 24-hour urine production/weight causes nocturnal polyuria due to impaired function of antidiuretic hormone in elderly men.
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OBJECTIVE
The goals of the present study were to evaluate whether the different function of endogenous antidiuretic hormone (arginine vasopressin; AVP) results in the difference in 24-h production/weight and to make indexes of lifestyle advice for patients with nocturia due to nocturnal polyuria
[A case of late-onset Pick's disease with polyuria].
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A 72-year-old male was admitted to our hospital with a 2-year history of polyuria, prosopagnosia and aphasia. He showed characteristic clinical features of Pick's disease such as stereotyped verbal output and behavior and personality changes. CT and MRI scans showed marked atrophy in the bilateral
Xanthoma disseminatum with neurological involvement and optic atrophy: improvement with cladribine.
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A 9-year-old boy presented with multiple hyperpigmented papules over flexors with polyuria, polydipsia and progressive loss of vision. Histopathology of papule suggested a diagnosis of non-Langerhans cell histiocytosis and systemic evaluation showed central diabetes insipidus and optic atrophy. With
Altered dipeptidyl peptidase-4 activity during the progression of hyperinsulinemic obesity and islet atrophy in spontaneously late-stage type 2 diabetic rats.
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Altered dipeptidyl peptidase-4 (DPP4) activity during the progression of late-stage type 2 diabetes was measured in Otsuka Long-Evans Tokushima fatty (OLETF) rats. Compared with OLETF rats subjected to 30% food restriction, food-satiated OLETF rats exhibited spontaneous hyperphagic obesity, insulin
[A case of multisystem Langerhans' cell histiocytosis with lung deterioration over 15 years].
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We report a case of multisystem Langerhans cell histiocytosis (LCH) with lung, bone and pituitary involvement. A 20-year-old man developed thirst, polydipsia and polyuria in 1983. He had right femur pain from 1988 and osseous LCH was diagnosed based on the operated specimen in 1989. From July 1990,
Diabetes Mellitus With Concurrent Cerebellar Degeneration and Necrosis in a Domestic Goose ( Anser anser domesticus).
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A 5-year-old sexually intact male Toulouse goose ( Anser anser domesticus) was presented for ataxia, polyuria, and polydipsia. The goose was cachectic and exhibited head tremors. Results of plasma biochemical analysis and point-of-care glucometry revealed persistent hyperglycemia. Despite supportive
Mutation in saposin D domain of sphingolipid activator protein gene causes urinary system defects and cerebellar Purkinje cell degeneration with accumulation of hydroxy fatty acid-containing ceramide in mouse.
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The sphingolipid activator proteins (saposins A, B, C and D) are small homologous glycoproteins that are encoded by a single gene in tandem within a large precursor protein (prosaposin) and are required for in vivo degradation of some sphingolipids with relatively short carbohydrate chains. Human
Nocturia, nocturnal polyuria, and sleep quality in the elderly.
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Nocturia is a common symptom in the elderly, which profoundly influences general health and quality of life. One consequence of nocturia is sleep deterioration, with increased daytime sleepiness and loss of energy and activity. Accidents, e.g., fall injuries, are increased both at night and in the
[DIDMOAD syndrome (diabetes insipidus, diabetes mellitus, optic atrophy, deafness) with cerebello-pontine atrophy].
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The case is reported of a 32-year old women of Dutch origin who presented with diabetes insipidus, diabetes mellitus, atrophy of the optic nerve, and dilatation of the urinary tract, the combination known as "DIDMOAD syndrome". Unusual features of this case were regional atrophy of the cerebellum
Moxibustion, an alternative therapy, ameliorated disturbed circadian rhythm of plasma arginine vasopressin and urine output in multiple system atrophy.
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Previously no alternative therapy approach has been made to ameliorate disturbed circadian arginine vasopressin rhythm (C-AVP-R) in multiple system atrophy (MSA). A 65-year-old man with MSA showed loss of C-AVP-R and nocturnal polyuria. We performed moxibustion at specific acupuncture points on the
[The Wolfram syndrome: diabetes mellitus, hypacusis, optic atrophy and short stature in STH deficiency].
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METHODS
A 43-year-old man was known for 3 years to have diabetes mellitus. For 2 months before admission he had symptoms of hyperglycaemia with polyuria, polydipsia, weight loss, as well as impairment of vision and declining fitness. In addition to bilateral deafness he was clearly of normally
Congenital central diabetes insipidus and optic atrophy in a Wolfram newborn: is there a role for WFS1 gene in neurodevelopment?
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BACKGROUND
Wolfram syndrome (WS) is an autosomal recessive neurodegenerative disorder characterized by diabetes mellitus (DM), optic atrophy (OA), central diabetes insipidus (CDI) and deafness (D). The phenotype of the disease has been associated with several mutations in the WFS1 gene, a nuclear
Senior-Loken syndrome (nephronophthisis and tapeto-retinal degeneration): a study of 8 cases from 5 families.
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The association of nephronophthisis and tapeto-retional degeneration was described by both Senior and Loken in 1961, but prior to 1974 only 28 cases had been published. This report describes 8 new cases in 27 members of 5 families. The severe juvenile type produces blindness in infancy and death
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