Squamous Cell Carcinoma of the External Auditory Canal Presenting as a Persistent Ear Infection: A Case Report and Imaging Features.

Squamous cell carcinoma (SCC) is the most common malignant tumor involving the temporal bone but generally very rare. The temporomandibular joint (TMJ), middle cranial fossa, and facial nerve canal are uncommon areas for the tumor to spread. We present the case of primary SCC of the temporal bone in a 63-year-old male presenting for otorrhea, otalgia, facial weakness, and facial pain after failing outpatient antibiotic therapy for an ear infection. Initial inpatient workup was significant for a hypertensive emergency, leukocytosis, and acute kidney injury. Opacification of cavities (i.e., left middle ear, external auditory canal (EAC)), destructive bony changes (i.e., mastoiditis, erosion of facial nerve canal, and TMJ), and invasion of the middle cranial fossa due to a soft tissue mass were noted on CT and MRI. Operative biopsy showed moderately differentiated SCC. The patient received treatment at the hospital consisting of antibiotics and supportive treatment. Plans for an outpatient PET scan and chemoradiotherapy per consultants' recommendations were arranged. The patient was discharged with appropriate medications and outpatient referrals and underwent infuse-a-port placement. Overall, this case describes some key points given the limited studies thus far. It demonstrates certain imaging characteristics of SCC of the temporal bone in the setting of a chronic ear infection. The malignancy spreads to the posterior TMJ wall and the temporal lobe, which very few cases have shown. The tumor also invades specifically the mastoid and tympanic segments of the facial nerve canal. This may be one of the first cases to showcase these features given the rarity of their simultaneous occurrence.

Urinary Ammonium in Clinical Medicine: Direct Measurement and the Urine Anion Gap as a Surrogate Marker During Metabolic Acidosis.

Ammonium is the most important component of urinary acid excretion, normally accounting for about two-third of net acid excretion. In this article, we discuss urine ammonium not only in the evaluation of metabolic acidosis but also in other clinical conditions such as chronic kidney disease. Different methods to measure urine NH4+ that have been employed over the years are discussed. The enzymatic method used by clinical laboratories in the United States to measure plasma ammonia via the glutamate dehydrogenase can be used for urine ammonium. The urine anion gap calculation can be used as a rough marker of urine ammonium in the initial bedside evaluation of metabolic acidosis such as in distal renal tubular acidosis. Urine ammonium measurements, however, should be made more available in clinical medicine for a precise evaluation of this important component of urinary acid excretion.

Urinary Angiotensinogen in Patients With Type 1 Diabetes With Microalbuminuria: Gender Differences and Effect of Intensive Insulin Therapy.

Introduction: Angiotensinogen (AOG) is the precursor of peptides of the renin angiotensin system (RAS). Because insulin up-regulates transcriptional factors that normally repress kidney AOG synthesis, we evaluated urinary AOG (uAOG) in patients with type 1 diabetes (T1D) and microalbuminuria who are receiving either intensive or conventional insulin therapy. Methods: Urine samples from participants of the Diabetes Control and Complications Trial (DCCT) were used for the following: (i) uAOG/creatinine measurements in 103 patients with microalbuminuria and 103 patients with normoalbuminuria, matched for age, gender, disease duration, and allocation to insulin therapy; and (ii) uAOG/creatinine measurements from patients with microalbuminuria allocated to intensive insulin therapy (n = 58) or conventional insulin therapy (n = 41) after 3 years on each modality. Results: uAOG was higher in patients who started with microalbuminuria than in those with normoalbuminuria (6.65 vs. 4.0 ng/mg creatinine, P < 0.01). uAOG was higher in females than in males with microalbuminuria (11.7 vs. 5.4 ng/mg creatinine, P = 0.015). uAOG was lower in patients with microalbuminuria allocated to intensive insulin therapy than in conventional insulin therapy (3.98 vs. 7.42 ng/mg creatinine, P < 0.01). These differences in uAOG were observed though albumin excretion rate (AER) was not significantly different. Conclusion: In patients with T1D and microalbuminuria, uAOG is increased and varies with gender and the type of insulin therapy independently of AER. This suggests that AOG production is increased in females and it is decreased by intensive insulin therapy. The reduction in uAOG with intensive insulin therapy, by kidney RAS downregulation, may contribute to the known renoprotective action associated with intensive insulin and improved glycemic control.