We present a case of thyrotoxic periodic paralysis (TPP) presenting with stroke symptoms as a harbinger of Grave’s disease. A 61-year-old female presented with symptoms of abdominal pain and fatigue two weeks prior to admission and reported acute diarrhoea and unintentional weight loss. Investigation revealed thyrotoxicosis with undetectable thyroid stimulating hormone (TSH), elevated free T4 and elevated thyroid stimulating immunoglobulin (TSI). On the third day of admission, while undergoing physical therapy, code stroke was called on account of the onset of right-side predominant acute flaccid paralysis of upper and lower extremities, right-side facial droop, dysarthria and hyporeflexia bilaterally. The patient was alert and fully oriented with stable vitals with no increased labour in breathing at room air. An emergent head and neck CT, angiography, and magnetic resonance imaging (MRI) were negative. Serum potassium was 2.7 mmol/l, requiring prompt replacement. The patient’s paralysis and dysarthria improved over the following three days with a complete reversal of symptoms following the correction of serum potassium. Thyrotoxic periodic paralysis can occur in association with any of the causes of hyperthyroidism. It is due to a significant intracellular shift of potassium, subsequently manifesting clinically with hypokalaemia and muscle paralysis.
Primary biliary cholangitis (PBC) is an inflammatory cholestatic disease that tends to worsen, leading to hepatic cirrhosis and portal hypertension. We present a case of a middle-aged female who presented with progressively worsening generalized itch; the examination was significant only for urticarial rash and facial swelling. Investigation revealed direct hyperbilirubinemia, mildly elevated transaminase, and significant elevation of alkaline phosphatase. A differential was performed with labs including antimitochondrial antibodies (AMA) for PBC, hepatitis panel, anti-smooth muscle antibodies for autoimmune hepatitis, and tissue transglutaminase IgA for celiac disease, all of which were unremarkable. The patient was empirically treated with ursodeoxycholic acid (UDCA). Given the excellent clinical response at the three-week follow-up to treatment despite negative AMA, further testing with anti-sp100 and anti-gp210 was pursued, which returned positive for anti-sp100, confirming the diagnosis of PBC.
Riedel's lobe is a rare anatomical variant of the liver morphology with a downward tongue-like projection of the anterior edge of the right lobe. It is usually detected incidentally with abdominal imaging performed for other indications. We present a case where we found Riedel's lobe incidentally, with invasive adenocarcinoma arising from close proximity. A 64-year-old female came in with encephalopathy and was found to have a distended abdomen with tenderness. Imaging revealed a complex lobular mass in the right hepatic lobe with an elongated extension of the right lobe inferiorly consistent with Riedel's lobe. The differential considered was malignancy versus abscess. CT-guided biopsy revealed invasive adenocarcinoma consistent with intrahepatic cholangiocarcinoma, which was further supported by the presence of portocaval lymph nodes. Various studies have tried to establish an association between Riedel's lobe and the occurrence of cancer arising from the surrounding structures, primarily from liver or metastasis. This case report adds to the current literature when such an association is being studied.
Long-acting (LA) cabotegravir/rilpivirine (CAB/RPV) is a complete regimen for the management of human immunodeficiency virus type 1 (HIV-1) infection to replace their oral antiretroviral therapy (ART) when they have been virologically suppressed. We present a case of successful achievement of undetectable HIV RNA viral load levels in an acquired immunodeficiency syndrome (AIDS) patient with long-standing virologic failure within two months of CAB/RPV LA initiation. This was later complicated by immune reconstitution inflammatory syndrome (IRIS) due to Mycobacterium avium-intracellulare (MAI) infection and hepatitis B virus (HBV) reactivation.
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