Hemifacial Spasm as the Presenting Manifestation of Type 3c
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Type 3c diabetes mellitus (T3cDM), or pancreatogenic diabetes mellitus, may occur because of a variety of exocrine pancreatic diseases, mainly acute or chronic pancreatitis, pancreatic trauma, malignancy, hemochromatosis, and cystic fibrosis. Among these, chronic pancreatitis is the most common cause. The pathophysiology includes impaired hormonal regulation of glucose homeostasis and activation of hepatic gluconeogenesis, leading to glycemic instability. Authors herein report a case of a 31-year-old patient, with a history of chronic pancreatitis, who presented with hemifacial spasm. The patient was found to have hyperglycemia and eventually diagnosed as T3cDM, which responded remarkably to insulin.

A 31-year-old non-smoker and non-alcoholic man presented to the emergency department with abdominal pain. He also complained of intermittent twitching surrounding his eyelids for the last three months, which had aggravated recently for the last 12 days. He had a history of pancreatitis six years ago, which had been managed conservatively. He did not visit for any further follow-up, as he was asymptomatic except involuntary weight loss and passage of foul-smelling oily diarrhea for last 1 month, suggestive of steatorrhea. Family history and drug history were non-contributory. The patient was afebrile and normotensive. On physical examination, intermittent twitching involving muscles on the right side of the face, including the eyelid, was observed.

The arterial blood gas analysis, serum ketones and serum osmolarity were within normal limits. C-peptide levels were low (0.4 ng/mL). Complete blood cell count, renal, hepatic and thyroid function tests, and lipid profile, were within normal limits. A magnetic resonance imaging of the brain as well as a magnetic resonance angiography revealed no significant findings, thus ruling out any structural, cerebrovascular, metabolic or demyelinating etiology.

Relevant tests for detection of pancreatic exocrine insufficiency were positive. Pancreatic islet cells and glutamic acid decarboxylase (GAD)-65 autoantibodies were negative. Antinuclear antibody, antineutrophil cytoplasmic antibody, HIV, VDRL, and hepatitis C virus serology were also negative. The absence of hilar lymphadenopathy as well as normal serum levels of angiotensin-converting enzyme and calcium ruled out neurosarcoidosis.

A multi-detector computed tomography scan of the abdomen revealed pancreatic atrophy, duct dilatations and calcifications, suggestive of chronic pancreatitis. A bedside capillary blood glucose measurement revealed hyperglycemia (332 mg/dL). Fasting and post-prandial blood glucose were 210 mg/dL and 320 mg/dL, respectively. HbA1c was estimated to be 8.6%. A diagnosis of pancreatogenic diabetes mellitus (type 3c) was made on the backdrop of chronic pancreatitis. The patient was treated with premixed insulin [Insulin isophane/NPH (70%) and human insulin/soluble insulin (30%)]. Hemifacial spasm disappeared with achieving euglycemia and did not recur.

Source: https://tremorjournal.org/articles/10.5334/tohm.611/
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