CIDP, Hashimoto’s Thyroiditis and Nephropathy: Autoimmune Syndrome Complex?

Raghavendra, S; Saran, Sonal; Somashekar, R.; Ashalatha, R; Shankar, S K

doi:10.1017/s0317167100007186

Cited by 11 publications

(6 citation statements)

References 17 publications

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“…Recent studies have shown that HCV infection is often associated with the appearance of autoimmune diseases, including SLE, SS, and thyroid disease, and can cause peripheral neuropathy even in the absence of cryoglobulinemia (11,12). Most peripheral neuropathy in patients with HCV infection is the axonal type of symmetrical sensorimotor neuropathy or multifocal mononeuropathy.…”

Section: Discussionmentioning

confidence: 99%

Acute Combined Central and Peripheral Demyelination Showing Anti-Aquaporin 4 Antibody Positivity

et al. 2012

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Neuromyelitis optica spectrum disorder (NMOSD) is characterized by optic neuritis or transverse myelitis with anti-aquaporin 4 (AQP4) antibodies (1). We herein present the case of a patient with NMOSD who also was affected with peripheral neuropathy. A 58-year-old woman developed gait disturbance and sensory impairment in the lower limbs. She exhibited longitudinally extensive transverse myelitis with anti-AQP4 antibodies. Nerve conduction studies showed demyelinating changes. Laboratory findings showed hepatitis-C virus (HCV) infection. Her peripheral neuropathy improved after immunotherapy. There have been no previous reports of NMO or NMOSD associated with neuropathy. The HCV infection or undetermined humoral factors other than the anti-AQP4 antibodies may have caused her peripheral neuropathy.

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Section: Discussionmentioning

confidence: 99%

Acute Combined Central and Peripheral Demyelination Showing Anti-Aquaporin 4 Antibody Positivity

et al. 2012

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“…Interestingly, there was also a report on an adult patient with Hashimoto's thyroiditis who developed isolated peripheral nervous system involvement consisting of chronic inflammatory demyelinating polyneuropathy; in that case neurophysiological tests indicated prolonged sensory and motor terminal latencies, slowing of conduction block in nerve segments and absent F-waves. 13 To the best our knowledge, peripheral nerve involvement in HE was reported in only one case in the pediatric literature. Salpietro et al 16 reported a 13-year-old girl with HE who developed distal neuropathy.…”

Section: Discussionmentioning

confidence: 95%

“…12 A comorbidity of HE and sensorimotor polyneuropathy has been rarely reported in the literature. 13,14 In the adult literature, isolated reduction of sensory nerve action potential amplitudes was reported in a patient with a diagnosis of HE. 15 In that case the authors concluded that there was an involvement of the dorsal root ganglia, namely a sensory ganglioneuropathy.…”

Section: Discussionmentioning

confidence: 99%

A case of steroid-resistance Hashimoto's encephalopathy presenting with sensorimotor polyneuropathy

et al. 2018

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Hashimoto's encephalopathy (HE) is a rare, auto-immune disease characterized by symptoms of acute or subacute encephalopathy associated with increased anti-thyroid antibody levels. The course of most HE cases is relapsing and remitting, which is similar to that of vasculitis and stroke. Steroids are the first line treatment in HE. In steroid non-responders other immunomodulatory therapies or plasmapheresis could be applied. We report a case of steroidresistance HE with sensorimotor polyneuropathy, as a rare presentation of this disorder. Our case showed that HE may present with sensorimotor polyneuropathy; therefore HE should be considered in the differential diagnoses of polyneuropathy.

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“…Case Reports in Endocrinology Importantly, in previous studies, over one-third of patients affected by hypothyroidism had residual polyneuropathy after 12 months of adequate thyroid replacement therapy [2], with a reported case of severe hypothyroid neuropathy which had only resolved after 6 years of thyroid hormone replacement [17]. Previous reports have pointed to an association between Hashimoto's thyroiditis and autoimmune demyelinating neuropathies such as Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy, likely due to an underlying shared genetic susceptibility to autoimmune conditions [18][19][20][21][22]. e significant clinical improvement in our patient's distal weakness together with partial improvement in his NCS findings after 12 months of thyroxine therapy and the absence of other systemic involvements make the presence of an autoimmune demyelinating neuropathy a less likely diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Severe Hypothyroidism Complicated by Myopathy and Neuropathy with Atypical Demyelinating Features

Brzozowska

Banthia

Thompson

et al. 2021

Case Reports in Endocrinology

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Autoimmune hypothyroidism may result in a wide range of neuromuscular disorders. The frequently observed neurological manifestations of acquired hypothyroidism include mild to moderate myopathy and sensorimotor neuropathy, which usually resolve by clinical and electrophysiological criteria, in adults treated with thyroid hormone replacement. We report a case of a 30-year-old male with severe hypothyroidism secondary to chronic autoimmune thyroiditis who presented with a 2-year history of progressive fatigue, upper and lower limb weakness, myalgia, and intermittent paraesthesia. His neurological exam demonstrated proximal and distal muscle weakness, lower limb areflexia, and relatively intact sensory modalities. The patient’s biochemistry revealed unusually and profoundly raised the thyroid stimulating hormone (TSH) level of 405.5 mIU/L (reference range (RR): 0.27–4.2 mIU/L) and creatine kinase (CK) level of 20,804 U/L (RR: 45–250 U/L), while his nerve conduction studies (NCS) demonstrated severe sensorimotor polyneuropathy with both axonal and demyelinating features. Thyroid hormone replacement therapy over the first 3 months resulted in biochemical normalization of his extremely deranged thyroid function tests (TFTs) and CK levels. At 12 months, despite maintaining euthyroidism and noticeable improvement in strength, his nerve conduction studies (NCS) demonstrated the continued absence of distal motor and sensory responses in his lower limbs with only partial improvement in sensory amplitudes and conduction velocities in his upper limbs. This report highlights the potential for severe neuromuscular consequences from advanced and chronic autoimmune hypothyroidism. The patient’s myopathy has resolved over a period of three months with prompt normalization of CK levels. Concerningly, the patient achieved significant but incomplete recovery from his mixed axonal and demyelinating neuropathy with residual mild distal weakness and areflexia in his lower limbs and persistent motor and sensory impairments on his NCS. The severity and incomplete resolution of our patient’s neurological manifestations emphasize the importance of early diagnosis and the need for prompt therapeutic intervention for hypothyroidism.

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CIDP, Hashimoto’s Thyroiditis and Nephropathy: Autoimmune Syndrome Complex?

Cited by 11 publications

References 17 publications

Acute Combined Central and Peripheral Demyelination Showing Anti-Aquaporin 4 Antibody Positivity

Acute Combined Central and Peripheral Demyelination Showing Anti-Aquaporin 4 Antibody Positivity

A case of steroid-resistance Hashimoto's encephalopathy presenting with sensorimotor polyneuropathy

Severe Hypothyroidism Complicated by Myopathy and Neuropathy with Atypical Demyelinating Features

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