Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wolfram's syndrome, also known as DIDMOAD syndrome, includes juvenile diabetes mellitus and optic atrophy variously associated with diabetes insipidus and deafness. We describe the neurological findings in 5 patients with Wolfram's syndrome. All patients had a neurological examination and were subjected electrophysiological and brain imaging including CT scan and, in one patient, MRI. There were two pairs of brothers and a sporadic case with paternal consanguinity suggesting recessive inheritance. Neurological abnormalities were found in four patients including dysarthria, seizures, anosmia, nystagmus, ataxia and changes in the electroencephalograms, electroretinograms and evoked potentials. In contrast with previous reports, four patients had abnormal brain CT scan with prominent atrophy of the brainstem. In the patient studied with NMR, severe brainstem and cerebellar atrophy was found. These neuroradiological findings are reminiscent of those described in olivopontocerebellar atrophy and are in agreement with previous pathological studies. We conclude that Wolfram's syndrome includes phenotypical manifestations of olivopontocerebellar atrophy. This reinforces the opinion that olivopontocerebellar atrophy is a nonspecific syndrome of varied causes.
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PMID:[Neurologic manifestations in Wolfram's syndrome]. 833 58

A 76 years old patient suffering from insulin dependent diabetes presents a multiple, bilateral and asymmetric cranial neuropathy involving on the left side the cranial nerves VIII, IX with a participation of the efferent autonomic fibers of the nerves VII and IX (xerostomia) and the nerve XII, and involving on both sides the nerves VII and X. Like it is known from literature the nerve XI was spared, probably because of the more caudal emergence from the brainstem. The disease was preceded by a violent otalgia on the left side which was initially interpretated as a malignant external otitis. This affection was associated with an inflammatory syndrome that was easily monitored by the blood sedimentation rate. The course was favorable but marked by fluctuations of the neurological deficits. The MRI shows a pachymeningitis localised at the beginning in the medial fossa and on the cerebellar tentorium, later on the left parieto-occipital convexity. The diagnosis of a focal idiopathic pachymeningitis was confirmed by excluding different other affections like inflammatory, tumoral and infectious diseases, by using MRI examinations, CSF analysis and especially meningeal biopsy. It is a rare inflammatory disease of unknown origin with potentially persistent neurological deficits. We discuss the differential diagnosis and the therapeutical possibilities, which consist in a long term immunosuppression with corticosteroids and azathioprine.
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PMID:[Neuritis of multiple cranial nerves in idiopathic focal pachymeningitis]. 886 57

We report the case of a 36-year-old female patient with insulin dependent diabetes who developed hypothyroidism of pituitary origin after giving birth. She had low levels of free T4 and TSH with no response to i.v. TRH. Antimicrosome antibodies were increased (1/25000), suggesting Hashimoto's thyroiditis. The other hormones were normal except for a low level of growth hormone and insulin growth factor 1. There were no antibodies against the pituitary. MRI of the pituitary was normal. We suspect a vascular origin for this partial pituitary deficiency.
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PMID:[Combined deficiency of thyroid stimulating hormone and growth hormone in a diabetic patient with Hashimoto thyroiditis]. 961 34

Previous studies have shown both increased and decreased regional cerebral glucose metabolism-blood flow (rMRGlu-rCBF) values in diabetes. We sought to elucidate the influence of diabetes on rMRGlu-rCBF in 57 patients with pure cerebral microangiopathy. Sixteen of 57 patients had diabetes requiring therapy (11 NIDDM, 5 IDDM). Using a special head-holder for exact repositioning, rMRGlu (PET) and rCBF (SPET) were imaged and measured in slices, followed by MRI. White matter and cortex were defined within regions of interest taken topographically from MRI (overlay). Diabetic and non-diabetic microangiopathy patients were compared to 19 age-matched controls. The diabetic patients showed significantly lower rMRGlu-rCBF values in all regions than controls, whereas non-diabetic patients did not. There were no significant NIDDM-IDDM differences. rMRGlu-rCBF did not depend on venous blood glucose levels at the time of the PET examination. However, analysis of variance with the factors diabetes, atrophy and morphological severity of microangiopathy showed that lowered rMRGlu-rCBF in the diabetic group was due to concomitant atrophy only (P < 0.005), while neither diabetes nor microangiopathy had any influence on rMRGlu-rCBF (all P > 0.2). These results were confirmed by multivariate factor analysis. It can thus be concluded that a supposed decrease in rMRGlu-rCBF in diabetes mellitus is in fact only an artefact produced by the concomitant atrophy. All previous studies failed to correct for atrophy, and a critical reappraisal is required.
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PMID:Influence of diabetes mellitus on regional cerebral glucose metabolism and regional cerebral blood flow. 1071 98

Diabetic muscle infarction is a rare complication of diabetes mellitus. However, idiopathic compartment syndrome in the diabetic patient is even a rarer disease, which has been reported only in three cases up to date. The disease seems to occur in patients affected by type 1 diabetes mellitus with a history of poorly controlled glucose levels. MRI aids in the diagnosis by delineating the edema of the muscle. However, definitive diagnosis is made using the Stryker needle unit. Treatment is accomplished by immediate two-incision fasciotomy. We present a case where a 34 yr-old female with a long standing history of poorly controlled Type 1 diabetes mellitus presented with a painful right lower extremity and was diagnosed with compartment syndrome. In our patient, a single incision fasciotomy to release the pressure was sufficient and might be considered as an alternative and less morbid procedure in the diabetic patient with already poorly healing tissues. We conclude that the muscle infarction in these patients is from diffuse microangiopathic disease leading to muscular infarction and fluid accumulation in the cells causing a decrease in the space in the compartment in question causing compartment syndrome.
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PMID:Review and case report of idiopathic lower extremity compartment syndrome and its treatment in diabetic patients. 1117 20

We present the case of a young man with recently manifesting type I diabetes mellitus who progressively developed clinical and radiological signs and symptoms of cervical posterior column myelopathy with eventually spontaneous and complete recovery as concerns both clinical symptomatology and MRI abnormalities.
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PMID:Transient myelopathy of the cervical posterior columns in a young man with recently diagnosed diabetes mellitus. 1171 69

Movement disorders such as chorea and ballism rarely occur in diabetes mellitus. We report the case of 26-year-old man with a 13-year-history of type 1 diabetes mellitus. He presented with a right side hemichorea. Brain CT-scan and MRI showed an infarction of the head of the caudate nucleus and the anterior part of the putamen. Presence of microangiopathy affecting retina, kidneys and peripheral nerves suggest a similar involvement of the lenticulo-striatal arteries. Hemichorea and hemiballism usually occur in older patients presenting type 2 diabetes mellitus. Non-ketotic hyperglycaemia is the common cause in such situation. Striatal infarct, as seen in our patient, is rarely reported.
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PMID:[Hemichorea caused by striatal infarct in a young type 1 diabetic patient]. 1188 23

Type 1 diabetes is the clinical manifestation of aberrant leukocytic infiltration of the pancreatic islets; it is usually diagnosed only very late in disease progression, after the critical autoimmune phenomena have mostly played out. A noninvasive means of directly monitoring the evolution of islet infiltrates would have important research and clinical applications. We have exploited fluorescence and MRI of long-circulating magnetofluorescent nanoparticles to visualize micro-vascular leakage, as an indicator of inflammation, in pancreata of mouse models of type 1 diabetes ex vivo or in vivo. We could detect the onset and evolution of insulitis in vivo and in real time, permitting us to study the natural history of diabetes in individual animals.
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PMID:Imaging inflammation of the pancreatic islets in type 1 diabetes. 1530 47

One of the most complex and most difficult congenital anomalies is spina bifida. Peter Van Forest was the first one who noticed this anomaly in 1587, and Recklinghausen, in 1886, classified spina bifida to types and suggested surgical procedures for its management. Earlier name, spina bifida, is currently more and more replacing with a term "defect of neural tube" (NTDs), or even more, "spinal dysraphia". Anomaly can appear at any level of spinal cord (cervical, thoracal, lumbar and sacral) and posterior localization is more often than the anterior one. Contrary to the open spinal dysraphism that can be perceived immediately, closed spinal dysraphism is very deceiving anomaly, and therefore, it must be treated properly as soon as it is diagnosed. Because of its seclusion, the term usually used is "occult spinal dysraphism (OSD)". The incidence of this anomaly is unknown, but it has been reported that it is more common among female children. Etiology of OSD is also unknown, but some of its risk factors are as follows: previous pregnancy with NTD, partner with NTD, type 1 diabetes mellitus, usage of anticonvulsives, a lack of folates in mother's nutrition. Prenatal diagnose of OSD is practically impossible. Skin changes, orthopedic, urological and neurological problems, suggest considering this complex anomaly. X-ray, ECHO, MRI, as well as neuropsychological examination corroborate diagnosis. At the same time, the diagnosis (once it is confirmed) represents the indication for neurosurgical treatment.
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PMID:[Occult spinal dysraphia]. 1561 81

A major stumbling block for research on and treatment of type 1 diabetes is the inability to directly, but noninvasively, visualize the lymphocytic/inflammatory lesions in the pancreatic islets. One potential approach to surmounting this impediment is to exploit MRI of magnetic nanoparticles (MNP) to visualize changes in the microvasculature that invariably accompany inflammation. MNP-MRI did indeed detect vascular leakage in association with insulitis in murine models of type 1 diabetes, permitting noninvasive visualization of the inflammatory lesions in vivo in real time. We demonstrate, in proof-of-principle experiments, that this strategy allows one to predict, within 3 days of completing treatment with an anti-CD3 monoclonal antibody, which NOD mice with recent-onset diabetes are responding to therapy and may eventually be cured. Importantly, an essentially identical MNP-MRI strategy has previously been used with great success to image lymph node metastases in prostate cancer patients. This success strongly argues for rapid translation of these preclinical observations to prediction and/or stratification of type 1 diabetes and treatment of individuals with the disease; this would provide a crucially needed early predictor of response to therapy.
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PMID:Noninvasive imaging of pancreatic inflammation and its reversal in type 1 diabetes. 1611 Mar 29


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