Hashimoto's Thyroiditis and Graves' Disease in One Patient: The Extremes of Thyroid Dysfunction Associated with Interferon Treatment.

Autoimmune thyroid disease associated with interferon therapy can manifest as destructive thyroiditis, Graves' Hyperthyroidism, and autoimmune (often subclinical) hypothyroidism, the latter persisting in many patients. There are scare reports of a single patient developing extremes of autoimmune thyroid disease activated by the immunomodulatory effects of interferon. A 60-year-old man received 48 weeks of pegylated interferon and ribavirin therapy for chronic HCV. Six months into treatment, he reported fatigue, weight gain, and slowed cognition. Serum thyroid stimulating hormone (TSH) was 58.8 mIU/L [0.27-4.2], fT4 11.1 pmol/L [12-25], and fT3 4.2 pmol/L [2.5-6.0] with elevated anti-TPO (983 IU/mL [<35]) and anti-TG (733 U/mL [<80]) antibodies. He commenced thyroxine with initial clinical and biochemical resolution but developed symptoms of hyperthyroidism with weight loss and tremor 14 months later. Serum TSH was <0.02 mIU/L, fT4 54.3 pmol/L, and fT3 20.2 pmol/L, with an elevated TSH receptor (TRAb, 4.0 U/L [<1.0]), anti-TPO (1,163 IU/mL) and anti-TG (114 U/mL) antibodies. Technetium scan confirmed Graves' Disease with bilateral diffuse increased tracer uptake (5.9% [0.5-3.5%]). The patient commenced carbimazole therapy for 6 months. Treatment was ceased following spontaneous clinical and biochemical remission (TSH 3.84 mIU/L, fT4 17pmol/L, fT3 4.5 pmol/L, and TRAb <1 U/L). This raises the need to monitor thyroid function closely in patients both during and following completion of interferon treatment.

Artifactual Hypoglycaemia in Systemic Sclerosis and Raynaud's Phenomenon: A Clinical Case Report and Short Review.

Background. Artifactual hypoglycaemia, defined as a discrepancy between glucometer (capillary) and plasma glucose levels, may lead to overtreatment and costly investigations. It is not infrequently observed in patients with Raynaud's phenomenon due to vascular capillary distortion, yet this is clinically underappreciated. Case Report. We report a 76-year-old woman with systemic sclerosis and Raynaud's phenomenon, who presented with upper gastrointestinal bleeding and found to have concomitant persistent hypoglycaemia (1.0-2.7mmol/L) on a point-of-care glucometer in the absence hypoglycaemic symptoms. She underwent a 2-week hospital admission, repeated glucose monitoring, hydrocortisone replacement and dextrose infusions, with consequent hyperglycaemia on plasma measurements. Clinically, she did not satisfy Whipple's triad and radiological investigations failed to identify pituitary or pancreatic pathology. A 72-hour fast was negative for hyperinsulinaemia or exogenous insulin use and her sulphonylurea metabolite urinary screen was negative. Discussion. Treatment of low capillary blood glucose is usually met with clinical impetus to treat, even when hypoglycaemic symptoms are lacking. The correct diagnosis may have been achieved had there been an observation of her cold hands, scleroderma facies, and consideration of the likely distorted peripheral microvasculature. Early identification of this presumably rare clinical scenario may have prevented overtreatment, altered methods of monitoring, and avoided unnecessary investigations.

Variant Guillain-Barré Syndrome in a Patient with Non-Hodgkin's Lymphoma.

We report a 72-year-old female patient with diffuse large B cell non-Hodgkin's lymphoma (NHL) with previous treatment with standard chemotherapy presenting as an acute, ascending, sensorimotor polyneuropathy. Nerve conduction studies and lumbar puncture supported a rare, but ominous, axonal variant of Guillain-Barré Syndrome (GBS) known as acute motor and sensory axonal neuropathy (AMSAN), which is distinguished from the more common, acute demyelinating forms of GBS. Previous reports have largely focused on toxicities secondary to chemo- or radiotherapy as a major contributor to the development of acute neuropathies in malignancy. Clinicians should also be mindful of direct neoplastic invasion or, less commonly, paraneoplastic phenomenon, as alternative mechanisms, the latter possibly reflecting immune dysregulation in particularly aggressive lymphomas. At the time of writing, this is the first report in the literature of an axonal variant of GBS in a patient with diffuse large B cell NHL. A discussion regarding common and uncommon neuropathies in haematological malignancies is made, with a brief review of the anecdotal evidence supporting a paraneoplastic association with GBS or its variant forms in the setting of lymphoma.