Cases reported "diabetic neuropathies"

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21/323. Acute gastric dilatation accompanied by diabetes mellitus.

    A 72-year-old man with diabetic triopathy was hospitalized with methicillin resistant staphylococcus aureus pneumonia. Six hours after the admission, his abdomen was fully expanded. An abdominal X-ray showed gastric dilatation. After insertion of a gastric tube to extract gastric air, his abdomen was flat and gastric dilatation improved. A positive Schellong test and decreased coefficient of RR interval in electrocardiogram variation indicated autonomic neuropathy, which may explain the reason for gastric hypomotility. Acute gastric dilatation in this patient may have occurred due to gastric hypomotility as a result of diabetic autonomic neuropathy in addition to gastric motility inhibition resulting from gastric autonomic nerve stimulation by bacterial toxin. ( info)

22/323. Intravenous immunoglobulin therapy for diabetic amyotrophy.

    A 49-year-old woman with diabetes mellitus developed progressive weakness and atrophy of both thighs rendering her wheelchair-bound within two months. The neurological findings and electrophysiological test results were compatible with diabetic amyotrophy (DA). Immediately after intravenous immunoglobulin (IVIg) therapy (20 g x 3 days), she became able to walk with a cane. After the next course of the therapy, she could walk without assistance. This dramatic effect of IVIg therapy together with the recent observation of vasculitic neuropathy in DA indicates an inflammatory process in this condition, and gives support to this treatment for DA. ( info)

23/323. An unusual neuropathy in a diabetic patient: evidence for intravenous immunoglobin-induced effective therapy.

    We report the case of a 68-year old type-2 diabetic male patient who was admitted to hospital for progressive weakness in the right lower limb. Although his metabolic control was good, he lost more than 20 kg of weight. Despite intensive physio- and vitaminotherapy, his neurological condition kept on degrading with a severe amyotrophy and pain of the right thigh. He was unable to walk and to stand alone. Besides a yet known sensitive polyneuropathy, the electrophysiological study revealed an obvious motor involvement with signs of demyelination and axonal degeneration. Combined with the albuminocytologic dissociation observed in the cerebrospinal fluid, these specific clinical and electrophysiological features led us to postulate a diagnosis of inflammatory neuropathy. The patient underwent a treatment by methylprednisolone and immunoglobins that rapidly induced a striking improvement of his neurological condition. This case report illustrates that rare forms of neuropathy such as inflammatory neuropathies close to chronic inflammatory demyelinating polyneuropathy (CIDP) can occur in diabetic patients and superimpose on the more commonly described forms of neuropathies. It recalls the importance of recognizing CIDP-like neuropathies because unlike other forms of neuropathy, inflammatory neuropathies are perfectly curable. ( info)

24/323. Intra-articular neuropathic fracture of the calcaneal body treated by open reduction and subtalar arthrodesis.

    A novel pattern of neuropathic intra-articular calcaneal fracture in a diabetic patient is described. This fracture combined proximal retraction of the tuberosity and body along with hindfoot collapse and plantar ulceration. Following control of the acute Charcot process with total contact casting, surgical reduction and subtalar arthrodesis was performed to stabilize the hindfoot and decrease the risk of recurrent ulceration. After healing, the patient successfully resumed ambulation and presently uses extra-depth shoes for daily activities. Despite the risks of surgical treatment, this difficult fracture may be treated operatively to maintain plantigrade alignment and offer limb salvage for the neuropathic patient. ( info)

25/323. erythropoietin-dependent anaemia: a possible complication of diabetic neuropathy.

    We report the case of a 52-year-old woman with long-term type 1 diabetes mellitus, complicated with proliferative retinopathy, autonomic neuropathy and microalbuminuria and moderate renal failure. A normochromic, normocytic are generative anaemia had been diagnosed for three years. Clinical and biological investigations for the aetiology of anaemia remained normal or negative. Anaemia was associated with a concentration of erythropoietin (EPO) in the normal range, but inappropriately low regarding anaemia. Treatment with recombinant EPO induced a rapid increase in haemoglobin level and improved the patient's quality of life. The role of diabetic neuropathy in the genesis of anaemia, in conjunction with a modest renal impairment is discussed. ( info)

26/323. Neuropathic pain--from mice to men.

    The past decade has seen great progress in understanding the syndrome of neuropathic pain, its causes and in finding new drugs that promise great benefit. For example, an early outcome of the research has been the observation that the new drugs do not blunt normal pain sensation--a pattern beginning to find explanation through the realisation that neural pain circuits rewire themselves, both anatomically and biochemically, after nerve injury. In this article, we discuss a case of a known diabetic patient with intractable pain and the course of management provided by the use of novel tools and devices coming to the fore in this rapidly expanding specialty. ( info)

27/323. A suspected case of proximal diabetic neuropathy predominantly presenting with scapulohumeral muscle weakness and deep aching pain.

    A 48-year-old man with a 14-year history of type 2 diabetes with proliferative diabetic retinopathy and distal symmetrical diabetic polyneuropathy visited our hospital. Eight months later, he subacutely developed difficulty in both shoulder movement and trouble standing up from a squatting position. This was accompanied by severe bilateral shoulder and thigh pain. magnetic resonance imaging of the brain, cervical and lumbar spine, computed tomography of the shoulder and X-ray films of the cervical spine and shoulder revealed no abnormality. cerebrospinal fluid showed a mild elevation of protein (0.93 g/l) without cell infiltration. Antiganglioside antibodies and point mutation of mitochondrial dna at position 3243 were not found. Neuropathology of the sural nerve showed a moderate myelinated fiber loss, active axonal degeneration, but onion-bulb formation, endoneurial or epineurial vasculitis were not observed. electromyography revealed neurogenic changes in the proximal upper limb muscles. Nerve conduction studies revealed mild bilateral slowing in nerve conduction velocity in both of the upper and lower limbs. The diagnosis of this patients was suspected to be a proximal diabetic neuropathy (diabetic amyotrophy). The pain and muscle weakness had persisted more severely in the shoulder than in the thigh throughout the clinical course. His unbearable symptoms could be partially alleviated by an administration of a selective serotonin reuptake inhibitor, fluvoxamine maleate. Proximal diabetic neuropathy is a rare disabling type of neuropathy, which is characterized with subacute bilateral muscle weakness and wasting in the proximal part of the lower limbs. The involvement of the scapulohumeral region observed in this case is very unusual in proximal diabetic neuropathy. ( info)

28/323. Opioids in non-cancer pain: a life-time sentence?

    There is continuing reluctance to prescribe strong opioids for the management of chronic non-cancer pain due to concerns about side-effects, physical tolerance, withdrawal and addiction. Randomized controlled trials have now provided evidence for the efficacy of opioids against both nociceptive and neuropathic pain. However, there is considerable variability in response rates, possibly depending on the type of pain, the type of opioid and its route of administration, the time to follow-up, compliance and the development of tolerance. Five patients were selected with nociceptive or neuropathic pain in whom other pharmacological or physical therapies had failed to provide satisfactory pain relief. They received transdermal fentanyl (starting dose 25 microg/h) for at least 6 weeks. Transdermal fentanyl dosage was titrated upwards as required. Transdermal fentanyl provided adequate pain relief in patients with nociceptive pain (diabetic ulcer, osteoporotic vertebral fracture, ankylosing spondylitis) or neuropathic pain with a nociceptive component (radicular pain due to disc protrusion, herpetic neuralgia). The duration of treatment ranged from 6 weeks to 6 months for four cases. In the case of ankylosing spondylitis, treatment was carried out for 2 years, stopped and then restarted successfully. There were no withdrawal effects or addictive behaviour on treatment cessation, regardless of duration of the treatment. In conclusion, strong opioids may provide prolonged effective pain relief in selected patients with nociceptive and neuropathic non-cancer pain. Transdermal fentanyl treatment can often be temporary and can easily be stopped following adequate pain relief without withdrawal effects or any evidence of addictive behaviour. ( info)

29/323. Mononeuropathy of the deep palmar branch of the ulnar nerve. A case occurring in a diabetic woman.

    A diabetic woman developed mononeuropathy of the deep palmar branch of the ulnar nerve six months following repetitive palmar trauma. The illness was initially incorrectly diagnosed as motor neuron disease, emphasizing the importance of accurate diagnosis of diseases that cause wasting of intrinslc muscles in the hand. ( info)

30/323. Increased platelet aggregation in diabetic patients with microangiopathy despite good glycemic control.

    The pathogenesis of diabetic micro- and macroangiopathy cannot be fully explained by hyperglycemia alone. To clarify diabetic complications mediated by increased platelet activity, we have studied platelet aggregation and its second messenger molecules such as protein kinase c (PKC), RhoA, and phosphatidylinositol 3-kinase (PI3- kinase), in six diabetic patients with diabetic retinopathy and other diabetic complications in spite of good glycemic control. Their HbA(1c) levels throughout the observation period had been less than 6% with diet treatment alone, despite which diabetic retinopathy developed to the pre-proliferative stage during 2-8 years observation. Low-dose thrombin (< 0.5 U/ml)-stimulated platelet aggregation in the diabetic patients was enormously elevated compared with healthy control subjects. PKC, RhoA and PI3-kinase activities in the cytosol- and membrane-associated fractions were examined in the platelets from the two patients (Cases 2 and 4). Platelet membrane-associated RhoA and PI3-kinase activity in Case 2 were increased before the stimulation. Platelet RhoA and PI 3-kinase activities in Case 4 were increased after the stimulation with low-dose thrombin (0.01 U/ml). Membrane-associated immunoreactive PKC alpha, but not PKC beta in Cases 2 and 4 was elevated. Although platelet hyperactivity in these four patients was observed, PKC and RhoA in mononuclear leukocytes from these patients were not different from healthy subjects. Membrane-associated PKC alpha and RhoA immunoreactivities also increased in the other three cases. These results suggest that hyperreactivity of PKC alpha may lead to increased RhoA and PI3-kinase activities and platelet hyperfunction in diabetic patients with good glycemic control, and that raised platelet PKC alpha may be implicated in the pathogenesis of diabetic complications. ( info)
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