Lege Artis Medicinae

[Twenty Years for Talents]

GYIMESI Ágnes Andrea

APRIL 20, 2012

Lege Artis Medicinae - 2012;22(04)

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Further articles in this publication

Lege Artis Medicinae

[Were the Middle Ages an Age of Darkness? ]

GAÁL Csaba

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[Ethical Issues in Psychotherapy – Part I]

KOVÁCS József

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[The Illness of Franz Kafka and his Perception of the World ]

GERLINGER Lilla

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[What have we flawed and what went wrong?]

BALOGH Sándor

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[The diabetic foot syndrome: pathomechanism, clinical picture, current treatment and prevention]

JERMENDY György

[Diabetic foot syndrome is a characteristic late complication of diabetes mellitus. It can develop in patients with type 1 as well as type 2 diabetes mellitus, especially in case of a long duration of diabetes and sustained poor metabolic state. Diabetic neuropathy plays a pivotal role in the pathomechanism, but vascular symptoms might also contribute to the complex clinical picture. For making the diagnosis, evaluation of complaints, performing physical examination and using simple tests for identifying both distal, somatosensory neuropathy and potential angiopathy are of great importance. Therapeutic approaches aim to achieve proper glycaemic control, as well as to ameliorate symptoms of neuropathy, improve peripheral blood supply by medicines, angioplasty or intervention radiological methods, fight against infections and off-load the foot. Surgical intervention might also be necessary, and in severe cases, amputation might be needed. The diabetic foot syndrome increases mortality risk in patients with diabetes. Complaints related to diabetic foot syndrome are often resistant to treatment and tend to recur. Thus, prevention with long-term, good metabolic control and protection of the foot are of particular importance.]

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Sandhoff disease is a rare type of hereditary (autosomal recessive) GM2-gangliosidosis, which is caused by mutation of the HEXB gene. Disruption of the β subunit of the hexosaminidase (Hex) enzyme affects the function of both the Hex-A and Hex-B isoforms. The severity and the age of onset of the disease (infantile or classic; juvenile; adult) depends on the residual activity of the enzyme. The late-onset form is characterized by diverse symptomatology, comprising motor neuron disease, ataxia, tremor, dystonia, psychiatric symptoms and neuropathy. A 36-year-old female patient has been presenting progressive, symmetrical lower limb weakness for 9 years. Detailed neurological examination revealed mild symmetrical weakness in the hip flexors without the involvement of other muscle groups. The patellar reflex was decreased on both sides. Laboratory tests showed no relevant alteration and routine electroencephalography and brain MRI were normal. Nerve conduction studies and electromyography revealed alterations corresponding to sensory neuropathy. Muscle biopsy demonstrated signs of mild neurogenic lesion. Her younger brother (32-year-old) was observed with similar symptoms. Detailed genetic study detected a known pathogenic missense mutation and a 15,088 base pair long known pathogenic deletion in the HEXB gene (NM_000521.4:c.1417G>A; NM_000521:c.-376-5836_669+1473del; double heterozygous state). Segregation analysis and hexosaminidase enzyme assay of the family further confirmed the diagnosis of late-onset Sandhoff disease. The purpose of this case report is to draw attention to the significance of late-onset Sandhoff disease amongst disorders presenting with proximal predominant symmetric lower limb muscle weakness in adulthood.