Multiple myeloma is a plasma cell dyscrasia characterized by abnormal bone marrow clonal plasma cells, histological confirmation of plasmacytoma, monoclonal protein in serum or urine, and evidence of endorgan damage. Organ involvement in multiple myeloma manifests as CRAB (hyperCalcemia, Renal insufficiency, Anemia, lytic Bone lesions). Cutaneous complications in multiple myeloma have been reported in many different phenotypes such as cryoglobulinemia rash, bruising, amyloid deposition, and squamous cell carcinoma. However, cutaneous metastasis of multiple myeloma is very rare with fewer than 100 cases described in the literature so far. Here, we present a case of biopsy-confirmed primary cutaneous multiple myeloma. Our case has other less common features of multiple myeloma such as renal amyloidosis and a coexisting malignant melanoma. This case report describes a unique presentation of multiple myeloma to understand the disease better.

We present the case of a male patient, initially treated for myxedema coma secondary to Hashimoto's thyroiditis, who was discharged on levothyroxine and a low-dose steroid taper but was re-admitted for the treatment of status epilepticus. During the second admission, the patient developed encephalopathy and cognitive dysfunction. Thyroid peroxidase (TPO) antibodies (Abs) were elevated and the patient was treated with high-dose steroids with clinical improvement. The patient was determined to have Hashimoto's encephalopathy (HE) due to the clinical picture as well as the response to high-dose glucocorticoid therapy. Cerebrospinal fluid (CSF) analysis demonstrated elevated protein, immunoglobulin G (IgG) index, and IgG synthesis rate; however, albumin index was elevated, indicating a disrupted blood-brain barrier. We suggest that HE be considered in the differential diagnosis for patients presenting with seizures, coma, stroke-like symptoms, behavior changes, and unexplained encephalopathy. After ruling out more common pathologies, HE should be considered by testing for anti-TPO Abs.

The hepatocellular function can be evaluated using aspartate aminotransferase (AST) and alanine aminotransferase (ALT) which are biochemical markers of the liver. Whenever there is an ischemic, toxic, or inflammatory injury to the liver, necrosis of the hepatocytes occurs and these biochemical markers are released into the circulation, showing an acute elevation in serum levels.In this case report, we discuss the unique clinical presentation of a female patient who came to the Emergency Room (ER) with acute onset chest pain with laboratory findings of elevated serum aminotransferases and cholestatic markers and was ultimately diagnosed with chronic cholecystitis.The usual clinical presentation associated with extremely elevated levels of liver enzymes can be one of three cases: acute viral hepatitis, toxin-induced liver injury, or acute ischemic insult to the liver. However, our patient was diagnosed with chronic cholecystitis despite her unique initial presentation of acute, severe transaminitis.While one may find elevated liver enzyme levels in acute cholecystitis, owing to the sudden nature of the inflammatory process, chronic cholecystitis is not known to cause high levels of serum amino transaminases or fulminant liver failure.Our case report indicates a diverse phenotype of chronic cholecystitis with an unusual presentation of acute, severe transaminitis. It helps expand the differential diagnoses of acute elevation of liver function tests (LFTs). Further studies are needed to explore the pathology behind chronic cholecystitis in order to understand its impact on liver damage.

Systemic sclerosis (SSc) is a rare connective tissue disorder with a complex pathogenesis involving vascular dysfunction, small vessel proliferation as well as alterations of innate and adaptive immunity. Gastrointestinal (GI) involvement in SSc is almost universal and affects nearly 90% of the patients. Of all the GI manifestations, 30%–75% are oesophageal abnormalities, including gastro-oesophageal reflux disease, reflux oesophagitis and Barret’s oesophagus. The incidence of gastric manifestations is about 22% with a common presentation of gastric antral vascular ectasia (GAVE). However, autoimmune atrophic gastritis (AIG) is not a known manifestation of SSc. Our case has a unique presentation of the coexistence of GAVE and AIG. We have conducted a thorough literature review to study a possible association of AIG and SSc and understand the pathology of SSc.