A 65‐year‐old woman was transferred to us with 3 weeks of bandlike, nonexertional lower chest tightness associated with severe dizziness on standing and palpitations. She had difficulty ambulating because of leg weakness and pain with tactile stimuli and noted a weak right hand grasp. She had severe weight loss over 5 months (35 pounds), chronic constipation, and depressed mood. She was recently diagnosed with diabetes mellitus (DM) and started on repaglinide but revealed later that she had had elevated blood sugar as high as 300 over the last 7 years. Prior to transfer she was ruled out for coronary artery disease (echocardiogram, stress test, and cardiac catheterization), stroke (brain CT and US Doppler of carotids) , and malignancy (body imaging with colonoscopy), She was cachectic (BM1 18) with significant orthostatic hypotension (supine BP 145/72, sitting BP 107/68), Neurologic examination was positive for hyperalgesia, muscle atrophy with weakness (proximal > distal) in all extremities, and right partial ulnar neuropathy. Deep tendon reflexes were globally decreased. MRI spine ruled out compressive radiculopathy. Paraneoplastic antibodies, aldolase, vitamin E and B12 levels, ACTH stimulation test, and heavy metal screen were negative. HbA1c was 6.2. EMG revealed a sensorimotor polyneuropathy because of axon loss along with thoracic and lumbosacral polyradiculopathy. Radionuclide hemodynamic testing, tilt table, and autonomic reflex testing including QSART (quantitative sudomotor axon reflex) testing indicated autonomic dysfunction. Her revelation of chronic uncontrolled DM and severe weight loss and tests confirming a diffuse neuropathy strongly indicated a diagnosis of diabetic neuropathic cachexia. She was started on nutritional supplementation and insulin. Her hyperalgesia and orthostasis responded to neurontin and midodrine.
Diabetic neuropathic cachexia is a rare complication of uncontrolled DM predominantly seen in elderly men with a few cases reported in women. It is characterized by severe sensorimotor peripheral neuropathy with superimposed diffuse thoracic and lumbosacral polyradiculopathy, autonomic dysfunction, depression, and severe weight loss. The dramatic manifestations can lead to extensive testing looking for paraneoplastic neurologic syndromes or cardiac disease. Contrary to the common “glove‐and‐stocking” neuropathy of DM, this shows recovery of nerve function in tandem with weight gain over an average of 1‐2 years. Mainstays of treatment remain stringent DM control, medications for neuropathic pain including antidepressants, and aggressive nutritional and physical therapy.
Diabetic neuropathic cachexia is a disabling condition that can present as a perplexing diagnostic challenge. Awareness regarding this disease entity can help channel resources for appropriate testing and effective management
M. Patel, none; S. Manda, none; A. Ramaswamy, none.