MON-142 Neuropathy in a Patient with Diabetes Mellitus: Not Always a Diabetic Disease

Diabetic neuropathy (DN) is the most common form of neuropathy in patients with diabetes mellitus (DM). Although DN is very common, other etiologies for neuropathy can exist or co-exist in patients with DM. DN might be nonspecific and mimic neuropathies seen in other diseases. Therefore, its proper...

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Veröffentlicht in:Journal of the Endocrine Society 2019-04, Vol.3 (Supplement_1)
Hauptverfasser: Baranski Lamback, Elisa, Regazzi Avelleira, Joao Carlos, Oliveira, Ricardo, Zagury, Roberto
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Oliveira, Ricardo
Zagury, Roberto
description Diabetic neuropathy (DN) is the most common form of neuropathy in patients with diabetes mellitus (DM). Although DN is very common, other etiologies for neuropathy can exist or co-exist in patients with DM. DN might be nonspecific and mimic neuropathies seen in other diseases. Therefore, its proper diagnosis requires a thorough history and exclusion of secondary causes such as leprosy. Due to increase in world-wide travel and migration, and because the transmission pathways of Mycobacterium leprae are not fully understood, it is now crucial to be aware of tropical diseases, such as leprosy, not generally seen or recognized in non-endemic countries. We report a case of 74-year old man with a 5-year history of DM who complained of feet paresthesia over the last four years, more pronounced on the left foot and progressively worse. Good glycemic control was achieved since diagnosis with Metformin. Microvascular complications were absent. Renal and thyroid function were normal as well as vitamin B12 levels. The patient denied alcohol or drug abuse, and did not have peripheral arterial disease, cancer, or use any neurotoxic drug. On examination of the lower limbs, deep tendon reflexes diminished. A mildly decreased vibration perception and numbness on the lower left limb were also observed. No other finding was present (normal pin-prick, normal gait and proprioception), nor did he present with muscle weakness. Amitriptyline and thioctic acid were prescribed with no clinical response. During the last year, multiple hyperpigmented anesthetic cutaneous lesions emerged in his legs and back. He subsequently developed a left foot drop and autonomic dysfunction. A diagnosis of borderline tuberculoid leprosy and type 1 reaction were established and a planned 12-month multidrug therapy (MDT) initiated. After six months of MDT, at last follow-up, the patient’s sensory neuropathy showed mild improvement. Resolution of autonomic symptoms was seen and nearly complete clearing of the skin lesions. In conclusion, leprosy and DM can cause progressive and irreversible nerve damage with similar clinical patterns. But, in cases of asymmetric neuropathy in a patient with DM, leprosy must be ruled out first before ascribing DM as the cause of the neuropathy. A thorough epidemiological history is mandatory to avoid misdiagnosis. If leprosy is not recognized and consequently left untreated, patients are at risk for permanent nerve damage. Leprosy is a potentially curable disease, cont
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Although DN is very common, other etiologies for neuropathy can exist or co-exist in patients with DM. DN might be nonspecific and mimic neuropathies seen in other diseases. Therefore, its proper diagnosis requires a thorough history and exclusion of secondary causes such as leprosy. Due to increase in world-wide travel and migration, and because the transmission pathways of Mycobacterium leprae are not fully understood, it is now crucial to be aware of tropical diseases, such as leprosy, not generally seen or recognized in non-endemic countries. We report a case of 74-year old man with a 5-year history of DM who complained of feet paresthesia over the last four years, more pronounced on the left foot and progressively worse. Good glycemic control was achieved since diagnosis with Metformin. Microvascular complications were absent. Renal and thyroid function were normal as well as vitamin B12 levels. The patient denied alcohol or drug abuse, and did not have peripheral arterial disease, cancer, or use any neurotoxic drug. On examination of the lower limbs, deep tendon reflexes diminished. A mildly decreased vibration perception and numbness on the lower left limb were also observed. No other finding was present (normal pin-prick, normal gait and proprioception), nor did he present with muscle weakness. Amitriptyline and thioctic acid were prescribed with no clinical response. During the last year, multiple hyperpigmented anesthetic cutaneous lesions emerged in his legs and back. He subsequently developed a left foot drop and autonomic dysfunction. A diagnosis of borderline tuberculoid leprosy and type 1 reaction were established and a planned 12-month multidrug therapy (MDT) initiated. After six months of MDT, at last follow-up, the patient’s sensory neuropathy showed mild improvement. Resolution of autonomic symptoms was seen and nearly complete clearing of the skin lesions. In conclusion, leprosy and DM can cause progressive and irreversible nerve damage with similar clinical patterns. But, in cases of asymmetric neuropathy in a patient with DM, leprosy must be ruled out first before ascribing DM as the cause of the neuropathy. A thorough epidemiological history is mandatory to avoid misdiagnosis. If leprosy is not recognized and consequently left untreated, patients are at risk for permanent nerve damage. Leprosy is a potentially curable disease, contrary to DM. 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Although DN is very common, other etiologies for neuropathy can exist or co-exist in patients with DM. DN might be nonspecific and mimic neuropathies seen in other diseases. Therefore, its proper diagnosis requires a thorough history and exclusion of secondary causes such as leprosy. Due to increase in world-wide travel and migration, and because the transmission pathways of Mycobacterium leprae are not fully understood, it is now crucial to be aware of tropical diseases, such as leprosy, not generally seen or recognized in non-endemic countries. We report a case of 74-year old man with a 5-year history of DM who complained of feet paresthesia over the last four years, more pronounced on the left foot and progressively worse. Good glycemic control was achieved since diagnosis with Metformin. Microvascular complications were absent. Renal and thyroid function were normal as well as vitamin B12 levels. The patient denied alcohol or drug abuse, and did not have peripheral arterial disease, cancer, or use any neurotoxic drug. On examination of the lower limbs, deep tendon reflexes diminished. A mildly decreased vibration perception and numbness on the lower left limb were also observed. No other finding was present (normal pin-prick, normal gait and proprioception), nor did he present with muscle weakness. Amitriptyline and thioctic acid were prescribed with no clinical response. During the last year, multiple hyperpigmented anesthetic cutaneous lesions emerged in his legs and back. He subsequently developed a left foot drop and autonomic dysfunction. A diagnosis of borderline tuberculoid leprosy and type 1 reaction were established and a planned 12-month multidrug therapy (MDT) initiated. After six months of MDT, at last follow-up, the patient’s sensory neuropathy showed mild improvement. Resolution of autonomic symptoms was seen and nearly complete clearing of the skin lesions. In conclusion, leprosy and DM can cause progressive and irreversible nerve damage with similar clinical patterns. But, in cases of asymmetric neuropathy in a patient with DM, leprosy must be ruled out first before ascribing DM as the cause of the neuropathy. A thorough epidemiological history is mandatory to avoid misdiagnosis. If leprosy is not recognized and consequently left untreated, patients are at risk for permanent nerve damage. Leprosy is a potentially curable disease, contrary to DM. 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Although DN is very common, other etiologies for neuropathy can exist or co-exist in patients with DM. DN might be nonspecific and mimic neuropathies seen in other diseases. Therefore, its proper diagnosis requires a thorough history and exclusion of secondary causes such as leprosy. Due to increase in world-wide travel and migration, and because the transmission pathways of Mycobacterium leprae are not fully understood, it is now crucial to be aware of tropical diseases, such as leprosy, not generally seen or recognized in non-endemic countries. We report a case of 74-year old man with a 5-year history of DM who complained of feet paresthesia over the last four years, more pronounced on the left foot and progressively worse. Good glycemic control was achieved since diagnosis with Metformin. Microvascular complications were absent. Renal and thyroid function were normal as well as vitamin B12 levels. The patient denied alcohol or drug abuse, and did not have peripheral arterial disease, cancer, or use any neurotoxic drug. On examination of the lower limbs, deep tendon reflexes diminished. A mildly decreased vibration perception and numbness on the lower left limb were also observed. No other finding was present (normal pin-prick, normal gait and proprioception), nor did he present with muscle weakness. Amitriptyline and thioctic acid were prescribed with no clinical response. During the last year, multiple hyperpigmented anesthetic cutaneous lesions emerged in his legs and back. He subsequently developed a left foot drop and autonomic dysfunction. A diagnosis of borderline tuberculoid leprosy and type 1 reaction were established and a planned 12-month multidrug therapy (MDT) initiated. After six months of MDT, at last follow-up, the patient’s sensory neuropathy showed mild improvement. Resolution of autonomic symptoms was seen and nearly complete clearing of the skin lesions. In conclusion, leprosy and DM can cause progressive and irreversible nerve damage with similar clinical patterns. But, in cases of asymmetric neuropathy in a patient with DM, leprosy must be ruled out first before ascribing DM as the cause of the neuropathy. A thorough epidemiological history is mandatory to avoid misdiagnosis. If leprosy is not recognized and consequently left untreated, patients are at risk for permanent nerve damage. Leprosy is a potentially curable disease, contrary to DM. Other etiologies for neuropathy can exist in patients with DM.</abstract><cop>Washington, DC</cop><pub>Endocrine Society</pub><doi>10.1210/js.2019-MON-142</doi><oa>free_for_read</oa></addata></record>
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title MON-142 Neuropathy in a Patient with Diabetes Mellitus: Not Always a Diabetic Disease
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