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Gen Sobue - One of the best experts on this subject based on the ideXlab platform.

  • Postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy.
    Nutrition (Burbank Los Angeles County Calif.), 2020
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy
    Nutrition, 2004
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    Abstract Objective We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Methods Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. Results The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Conclusion This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • alcoholic neuropathy is clinicopathologically distinct from Thiamine Deficiency neuropathy
    Annals of Neurology, 2003
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Makoto Sugiura, Gen Sobue
    Abstract:

    Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of Thiamine-Deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting Thiamine Deficiency. Thirty-two patients with nonalcoholic Thiamine-Deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of Thiamine-Deficiency neuropathy (TDN), supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant Thiamine-Deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

  • postgastrectomy polyneuropathy with Thiamine Deficiency
    Journal of Neurology Neurosurgery and Psychiatry, 2001
    Co-Authors: Haruki Koike, K Misu, Naoki Hattori, Miyuki Ichimura, Masaaki Hirayama, Masaaki Nagamatsu, I Sasaki, Gen Sobue
    Abstract:

    OBJECTIVE—Polyneuropathy has been reported after gastrectomy performed to treat various lesions. Although Thiamine Deficiency is a possible cause of this neuropathy, the pathogenesis still remains to be clarified. Seventeen patients with peripheral neuropathy with Thiamine Deficiency after gastrectomy are described. METHODS—Seventeen patients with polyneuropathy after gastrectomy accompanied by Thiamine Deficiency were selected. Patients were restricted to those with total or subtotal gastric resection to treat ulcer or neoplasm. Patients who had undergone operations to treat morbid obesity were excluded. RESULTS—Intervals between the operation and onset of neuropathy varied from 2 months to 39 years. Most patients did not seem malnourished. Serum concentrations of B vitamins other than Thiamine were nearly normal. Symmetric motor-sensory polyneuropathy, predominantly involving the lower limbs, had progressed over intervals varying from 3 days to 8 years. Relative degrees of motor and sensory impairment also varied extensively. Some cases that progressed rapidly mimicked Guillain-Barre syndrome. Electrophysiological and pathological findings were those of axonal neuropathy. Substantial functional recovery from polyneuropathy was seen in most patients by 3 to 6 months after initiating Thiamine supplementation. Motor recovery was better than sensory recovery. CONCLUSIONS—Various symptoms were seen in patients with postgastrectomy neuropathy. Thiamine Deficiency should be considered in the differential diagnosis of motor-sensory polyneuropathy after gastrectomy.

Haruki Koike - One of the best experts on this subject based on the ideXlab platform.

  • Postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy.
    Nutrition (Burbank Los Angeles County Calif.), 2020
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • Myopathy in Thiamine Deficiency : Analysis of a case
    Journal of the Neurological Sciences, 2006
    Co-Authors: Haruki Koike, Naoki Hattori, Hirohisa Watanabe, Akira Inukai, Masahiro Iijima, Keiko Mori, Sobue
    Abstract:

    Abstract Background Tenderness in the limb muscles has been reported anecdotally in patients with beriberi neuropathy, but clinical effects of Thiamine Deficiency on skeletal muscle have received little attention. Objective To describe a patient with Thiamine Deficiency who manifested myopathic symptoms and responded well to Thiamine supplementation. Patient A 26-year-old woman with neuropathy and heart failure associated with Thiamine Deficiency also complained of myalgia and weakness, most troublesome in the proximal portions of the limbs. Results Serum creatine kinase, myoglobin, and aldolase concentrations were abnormally elevated. Magnetic resonance imaging of lower limb muscles demonstrated areas of high signal intensity in T2-weighted images and showed Gd-DTPA enhancement. A biopsy specimen from the quadriceps muscle showed myopathic changes without neurogenic changes. Abnormalities improved well with Thiamine administration. Conclusion Myopathy may occur in patients with Thiamine Deficiency.

  • postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy
    Nutrition, 2004
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    Abstract Objective We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Methods Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. Results The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Conclusion This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • alcoholic neuropathy is clinicopathologically distinct from Thiamine Deficiency neuropathy
    Annals of Neurology, 2003
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Makoto Sugiura, Gen Sobue
    Abstract:

    Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of Thiamine-Deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting Thiamine Deficiency. Thirty-two patients with nonalcoholic Thiamine-Deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of Thiamine-Deficiency neuropathy (TDN), supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant Thiamine-Deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

  • postgastrectomy polyneuropathy with Thiamine Deficiency
    Journal of Neurology Neurosurgery and Psychiatry, 2001
    Co-Authors: Haruki Koike, K Misu, Naoki Hattori, Miyuki Ichimura, Masaaki Hirayama, Masaaki Nagamatsu, I Sasaki, Gen Sobue
    Abstract:

    OBJECTIVE—Polyneuropathy has been reported after gastrectomy performed to treat various lesions. Although Thiamine Deficiency is a possible cause of this neuropathy, the pathogenesis still remains to be clarified. Seventeen patients with peripheral neuropathy with Thiamine Deficiency after gastrectomy are described. METHODS—Seventeen patients with polyneuropathy after gastrectomy accompanied by Thiamine Deficiency were selected. Patients were restricted to those with total or subtotal gastric resection to treat ulcer or neoplasm. Patients who had undergone operations to treat morbid obesity were excluded. RESULTS—Intervals between the operation and onset of neuropathy varied from 2 months to 39 years. Most patients did not seem malnourished. Serum concentrations of B vitamins other than Thiamine were nearly normal. Symmetric motor-sensory polyneuropathy, predominantly involving the lower limbs, had progressed over intervals varying from 3 days to 8 years. Relative degrees of motor and sensory impairment also varied extensively. Some cases that progressed rapidly mimicked Guillain-Barre syndrome. Electrophysiological and pathological findings were those of axonal neuropathy. Substantial functional recovery from polyneuropathy was seen in most patients by 3 to 6 months after initiating Thiamine supplementation. Motor recovery was better than sensory recovery. CONCLUSIONS—Various symptoms were seen in patients with postgastrectomy neuropathy. Thiamine Deficiency should be considered in the differential diagnosis of motor-sensory polyneuropathy after gastrectomy.

Naoki Hattori - One of the best experts on this subject based on the ideXlab platform.

  • Postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy.
    Nutrition (Burbank Los Angeles County Calif.), 2020
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • Myopathy in Thiamine Deficiency : Analysis of a case
    Journal of the Neurological Sciences, 2006
    Co-Authors: Haruki Koike, Naoki Hattori, Hirohisa Watanabe, Akira Inukai, Masahiro Iijima, Keiko Mori, Sobue
    Abstract:

    Abstract Background Tenderness in the limb muscles has been reported anecdotally in patients with beriberi neuropathy, but clinical effects of Thiamine Deficiency on skeletal muscle have received little attention. Objective To describe a patient with Thiamine Deficiency who manifested myopathic symptoms and responded well to Thiamine supplementation. Patient A 26-year-old woman with neuropathy and heart failure associated with Thiamine Deficiency also complained of myalgia and weakness, most troublesome in the proximal portions of the limbs. Results Serum creatine kinase, myoglobin, and aldolase concentrations were abnormally elevated. Magnetic resonance imaging of lower limb muscles demonstrated areas of high signal intensity in T2-weighted images and showed Gd-DTPA enhancement. A biopsy specimen from the quadriceps muscle showed myopathic changes without neurogenic changes. Abnormalities improved well with Thiamine administration. Conclusion Myopathy may occur in patients with Thiamine Deficiency.

  • postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy
    Nutrition, 2004
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    Abstract Objective We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Methods Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. Results The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Conclusion This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • alcoholic neuropathy is clinicopathologically distinct from Thiamine Deficiency neuropathy
    Annals of Neurology, 2003
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Makoto Sugiura, Gen Sobue
    Abstract:

    Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of Thiamine-Deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting Thiamine Deficiency. Thirty-two patients with nonalcoholic Thiamine-Deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of Thiamine-Deficiency neuropathy (TDN), supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant Thiamine-Deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

  • postgastrectomy polyneuropathy with Thiamine Deficiency
    Journal of Neurology Neurosurgery and Psychiatry, 2001
    Co-Authors: Haruki Koike, K Misu, Naoki Hattori, Miyuki Ichimura, Masaaki Hirayama, Masaaki Nagamatsu, I Sasaki, Gen Sobue
    Abstract:

    OBJECTIVE—Polyneuropathy has been reported after gastrectomy performed to treat various lesions. Although Thiamine Deficiency is a possible cause of this neuropathy, the pathogenesis still remains to be clarified. Seventeen patients with peripheral neuropathy with Thiamine Deficiency after gastrectomy are described. METHODS—Seventeen patients with polyneuropathy after gastrectomy accompanied by Thiamine Deficiency were selected. Patients were restricted to those with total or subtotal gastric resection to treat ulcer or neoplasm. Patients who had undergone operations to treat morbid obesity were excluded. RESULTS—Intervals between the operation and onset of neuropathy varied from 2 months to 39 years. Most patients did not seem malnourished. Serum concentrations of B vitamins other than Thiamine were nearly normal. Symmetric motor-sensory polyneuropathy, predominantly involving the lower limbs, had progressed over intervals varying from 3 days to 8 years. Relative degrees of motor and sensory impairment also varied extensively. Some cases that progressed rapidly mimicked Guillain-Barre syndrome. Electrophysiological and pathological findings were those of axonal neuropathy. Substantial functional recovery from polyneuropathy was seen in most patients by 3 to 6 months after initiating Thiamine supplementation. Motor recovery was better than sensory recovery. CONCLUSIONS—Various symptoms were seen in patients with postgastrectomy neuropathy. Thiamine Deficiency should be considered in the differential diagnosis of motor-sensory polyneuropathy after gastrectomy.

Masaaki Hirayama - One of the best experts on this subject based on the ideXlab platform.

  • Postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy.
    Nutrition (Burbank Los Angeles County Calif.), 2020
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • postgastrectomy polyneuropathy with Thiamine Deficiency is identical to beriberi neuropathy
    Nutrition, 2004
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Gen Sobue
    Abstract:

    Abstract Objective We assessed whether postgastrectomy polyneuropathy associated with Thiamine Deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of Thiamine status. Methods Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with Thiamine Deficiency were compared with those of 11 patients who had Thiamine-Deficiency neuropathy caused by dietary imbalance. Results The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Conclusion This study showed that Thiamine-Deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that Thiamine Deficiency can be a major cause of postgastrectomy polyneuropathy.

  • alcoholic neuropathy is clinicopathologically distinct from Thiamine Deficiency neuropathy
    Annals of Neurology, 2003
    Co-Authors: Haruki Koike, Naoki Hattori, Masaaki Hirayama, Masahiro Iijima, Keiko Mori, Makoto Sugiura, Gen Sobue
    Abstract:

    Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of Thiamine-Deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting Thiamine Deficiency. Thirty-two patients with nonalcoholic Thiamine-Deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of Thiamine-Deficiency neuropathy (TDN), supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant Thiamine-Deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

  • postgastrectomy polyneuropathy with Thiamine Deficiency
    Journal of Neurology Neurosurgery and Psychiatry, 2001
    Co-Authors: Haruki Koike, K Misu, Naoki Hattori, Miyuki Ichimura, Masaaki Hirayama, Masaaki Nagamatsu, I Sasaki, Gen Sobue
    Abstract:

    OBJECTIVE—Polyneuropathy has been reported after gastrectomy performed to treat various lesions. Although Thiamine Deficiency is a possible cause of this neuropathy, the pathogenesis still remains to be clarified. Seventeen patients with peripheral neuropathy with Thiamine Deficiency after gastrectomy are described. METHODS—Seventeen patients with polyneuropathy after gastrectomy accompanied by Thiamine Deficiency were selected. Patients were restricted to those with total or subtotal gastric resection to treat ulcer or neoplasm. Patients who had undergone operations to treat morbid obesity were excluded. RESULTS—Intervals between the operation and onset of neuropathy varied from 2 months to 39 years. Most patients did not seem malnourished. Serum concentrations of B vitamins other than Thiamine were nearly normal. Symmetric motor-sensory polyneuropathy, predominantly involving the lower limbs, had progressed over intervals varying from 3 days to 8 years. Relative degrees of motor and sensory impairment also varied extensively. Some cases that progressed rapidly mimicked Guillain-Barre syndrome. Electrophysiological and pathological findings were those of axonal neuropathy. Substantial functional recovery from polyneuropathy was seen in most patients by 3 to 6 months after initiating Thiamine supplementation. Motor recovery was better than sensory recovery. CONCLUSIONS—Various symptoms were seen in patients with postgastrectomy neuropathy. Thiamine Deficiency should be considered in the differential diagnosis of motor-sensory polyneuropathy after gastrectomy.

Molly M Mcmahon - One of the best experts on this subject based on the ideXlab platform.

  • metabolic acidosis and Thiamine Deficiency
    Mayo Clinic Proceedings, 1999
    Co-Authors: Susan A Romanski, Molly M Mcmahon
    Abstract:

    We describe a 19-year-old patient who was receiving home parenteral nutrition in whom lactic acidosis developed. A review of her home parenteral nutrition formula revealed the absence of multivitamins, most significantly Thiamine. After Thiamine administration, the acidosis resolved, and the patient experienced pronounced clinical improvement. Clinicians must be aware that Thiamine is essential for normal glucose metabolism and that Thiamine Deficiency can lead to lactic acidosis. Thiamine Deficiency should be included in the differential diagnosis of lactic acidosis. The recent shortage of intravenous multivitamin preparations has led to documented cases of lactic acidosis as a result of Thiamine Deficiency, and a previous shortage led to several deaths due to lactic acidosis as a consequence of Thiamine Deficiency. All patients receiving parenteral nutrition must also receive adequate vitamin supplementation.