Semaan G. Kosseifi

The Association Between Obstructive Sleep Apnea Syndrome and Microvascular Complications in Well-Controlled Diabetic Patients

BACKGROUND Obstructive sleep apnea syndrome (OSAS) may promote hyperglycemia and insulin resistance. OBJECTIVE We studied the link between sleep apnea and microvascular diabetic complications in veterans with type 2 diabetes mellitus (DM-2). DESIGN A retrospective electronic chart of all veterans referred for sleep studies over a 1-year period was reviewed. Ninety-eight patients with a glycosylated hemoglobin < 6.5% were included in the study. The degree of glycemia (HbA1c) and presence of macro- and microvascular complications were compared with OSAS variables. METHOD Statistical analysis examined bivariate associations between OSAS variables and metabolic syndrome parameters. RESULTS The apnea hypopnea index was significantly related to diabetic microvascular complications, particularly retinopathy. Oxygen desaturation was significantly and inversely related to microalbuminuria, microvascular complications, retinopathy, and HbA1c. CONCLUSIONS Sleep apnea is associated with microvascular complications even in well-controlled DM-2 veterans. CLINICAL IMPLICATIONS Screening for OSAS should be considered in patients with DM-2.

Adalimumab-induced acute myelogenic leukemia.

Newer biological treatment strategies have been developed in the last decade with some promising outcomes. Their safety, however, has been questioned lately with multiple reports of increased risk for malignancies and infectious complications. These reports render their use suboptimal. We report a 44-year-old woman receiving adalimumab (Humira) for advanced juvenile rheumatoid arthritis who then developed acute myelogenic leukemia.

Peritoneal tuberculosis: modern peril for an ancient disease.

Extrapulmonary manifestations of Mycobacterium tuberculosis (MTB) in general, and tuberculous peritonitis (TBP) in particular, have posed complex diagnostic challenges for centuries. Peritoneal tuberculosis is a very rare manifestation of MTB with subtle clinical findings that may result in a significant diagnostic delay, often of more than four months. As the incidence of tuberculosis is declining in developed nations, clinicians may overlook the need to establish an early diagnosis and prompt therapy for this disorder. We present a case of peritoneal tuberculosis and a review of the literature.

Actinomycosis esophagitis in a patient with persistent dysphagia

Many causes of esophagitis exist in immunocompromised patients. Uncommon pathogens must be considered to facilitate timely and appropriate therapy. A limited number of cases of esophageal actinomycosis have been reported. This report describes an unusual case of esophageal actinomycosis in a patient with persistent dysphagia. The broad differential may have delayed definitive diagnosis in the case study patient. Biopsy and culture are essential for accurate diagnosis. Although actinomycosis is a rare disease, it should be included in the differential diagnosis of patients presenting with oral or esophageal complaints. It may also be considered as an opportunistic infection in immunocompromised patients. The treatment of choice is parenteral penicillin G, 18 to 24 million units for 2 to 6 weeks followed by oral therapy for 6–12 months.1

Reduction of amiodarone pulmonary toxicity in patients treated with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers

Background: Amiodarone (AM) is a widely used anti-arrhythmic medication. Its utility is, however, limited by adverse side effects. The mechanism of amiodarone-induced toxicity (APT) in the lungs is attributed primarily to stimulation of the angiotensin enzyme system leading to lung cell apoptosis and cell death. This mechanism has been demonstrated by in vitro and in vivo experimental animal studies. To date, however, no in vivo human studies have confirmed this mechanism for APT. Purpose: This study was undertaken to determine whether angiotensin converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB) offer a protective effect against APT in humans. Demonstration of a protective effect of an ACE-I or ARB would suggest that stimulation of the angiotensin enzyme system may be a key process in APT. Design: An 8-year retrospective analysis of all patients on AM therapy at the James H. Quillen Veterans Affairs Medical Center was undertaken. Results: A total of 1000 patients on AM were identified. One-hundred-and-seventeen were excluded from the study. Five-hundred-and-twenty-four patients were simultaneously on an ACE-I or ARB. The remaining 359 patients were not. Pulmonary toxicity attributed to AM was identified in five and 14 patients with and without concomitant ACE-I or ARB therapy, respectively. The APT rate for the entire patient sample was 2.2%. APT occurred in 1% of patients on an ACE-I or ARB and in 3.9% of patients not taking an ACE-I or ARB. This observed difference in percentage of APT was statistically significant. Conclusion: The concomitant use of ACE-I or ARB in patients taking AM appears to offer a protective effect against APT. This observation suggests that the stimulation of the angiotensin enzyme system may play an important role in APT in humans.

Respiratory Failure in a 70-Year-Old Veteran

In Western countries the incidence of amyotrophic lateral sclerosis (ALS) is 1.89 per 100,000 per year and the prevalence is 5.2 per 100,000. The incidence of ALS is lower among African, Asian, and Hispanic ethnicities when compared to Caucasians. The mean age of onset for sporadic ALS is about 60 years and there is a slight male predominance (male to female ratio of 1.5 to 1). Approximately two thirds of patients with ALS have the spinal form of the disease with symptoms presenting in the extremities. Patients typically have evidence of both lower motor neuron degeneration (atrophy, weakness, and fasciculations) and upper motor neuron degeneration (spasticity, weakness, and hyperreflexia). Patients with limb onset ALS typically complain of focal muscle weakness and wasting. The symptoms may start either distally or proximally in the upper and/or lower limbs. Gradually spasticity develops in the weakened atrophic limbs, affecting manual dexterity and gait. Patients with bulbar onset ALS typically present with dysarthria and dysphagia for solid or liquids. Limb symptoms can develop simultaneously with bulbar onset. In the vast majority of patients, limb weakness will occur within 1–2 years of bulbar onset ALS symptoms. A case of bulbar and sporadic limb ALS in a 70-year-old veteran, presenting with right diaphragmatic paralysis and respiratory failure, is presented.