HIV

Besides malignancy, what other causes of cachexia should we usually consider in our hospitalized patients?

FA Manian MD, MPH, , , Leave a comment

Although cachexia , a loss of >5% body weight over 12 months,  has been reported in about 30% of patients with cancer, many other chronic conditions  commonly encountered in our hospitalized patients may also be a culprit.  In fact, cachexia is not infrequent in CHF (20%), COPD (20%), kidney failure (40%), or rheumatoid arthritis (10%) (1,2).  We also shouldn’t overlook HIV and tuberculosis as a cause.

Cachexia is a multifactorial disease which does not fully reverse with nutritional support.  Numerous mediators have been implicated, including cytokines such as tumor-necrosis factor-α, and interleukin [IL]-1 and -6, as well as transforming growth factors such as myostatin and activin A (2). 

In patients with CHF, angiotensin II appears to be a key mediator, associated with insulin resistance, depletion of  ATP in skeletal muscles, poor appetite, reduction in insulin-like growth factor-1 (IGF-1), and an increase in glucocorticoid and IL-6 levels.  All these factors contribute to “cardiac cachexia” through muscle wasting, reduced food intake and lower muscle regeneration. 

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References

  1. Morely JE, Thomas DR, Wilson M-M G. Cachexia: pathophysiology and clinical relevance. Am J Clin Nutr 2006;83:735-43. https://www.ncbi.nlm.nih.gov/pubmed/16600922
  2. Yoshida T, Delafontaine P. Mechanisms of cachexia in chronic disease states. Am J Med Sci 2015;35:250-256. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587350/
Besides malignancy, what other causes of cachexia should we usually consider in our hospitalized patients?

My 65 year old patient has had several bouts of bacterial pneumonia in the past 2 years. Her total serum immunoglobulins are within normal range. Could she still be immunodeficient?

FA Manian MD, MPH, , , , , , , Leave a comment

Absolutely! Besides HIV infection which should be excluded in all patients with recurrent bouts of bacterial pneumonia irrespective of age, “selective polysaccharide antibody deficiency”, also known as “specific antibody deficiency” or SAD, should also be excluded (1-3). SAD in adults with recurrent pneumonia is not rare, having been reported in about ~8% of such patients (4).  

Think of SAD when your adult patient presents with recurrent bouts of bacterial pneumonia  despite having normal serum total immunoglobulin (IgG, IgA, and IgM) levels and IgG subtypes (1-3).  These patients have a normal response to tetanus toxoid (a protein) but cannot mount adequate antibody response against polysaccharide antigens of pathogens such as pneumococcus.  

One way to diagnose SAD in a suspected patient is through vaccination with 23-valent pneumococcal polysaccharide vaccine (PPSV23).  In patients with low baseline antibody titers to many of the capsular types of pneumococcus included in the PPSV23,  a suboptimal response (defined by the lab) 4 weeks after vaccination with PPSV23 is suggestive of SAD. Remember that if your patient has already been vaccinated with the 13 valent pneumococcal conjugate vaccine (PCV13), you can only evaluate for the response to serotypes included in the  PPSV23 only.

Although there are no randomized-controlled studies and treatment should be individualized, immunoglobulin replacement may reduce the risk of future bouts of pneumonia in SAD (2-3). 

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References

1. Cohn JA, Skorpinski E, Cohn JR. Prevention of pneumococcal infection in a patient with normal immunoglobulin levels but impaired polysaccharide antibody production. Ann Allergy Asthma Immunol 2006;97:603-5. https://www.ncbi.nlm.nih.gov/pubmed/17165266

2. Cheng YK, Kecker PA, O’Byrne MM, Weiler CR. Clinical and laboratory characteristics of 75 patients with specific polysaccharide antibody deficiency syndrome. Ann Alergy Asthma Immunol 2006;97:306-311. https://www.ncbi.nlm.nih.gov/pubmed/17042135

3. Perez E, Bonilla FA, Orange JS, et al. Specific antibody deficiency: controversies in diagnosis and management. Front Immunol 207;8:586. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5439175/pdf/fimmu-08-00586.pdf

4. Ekdahl K, Braconier JH, Svanborg C. Immunoglobulin deficiencies and impaired immune response to polysaccharide antigens in adult patients with recurrent community acquired pneumonia. Scand J Infect Dis 1997;29:401-7. https://www.ncbi.nlm.nih.gov/pubmed/9360257

 

My 65 year old patient has had several bouts of bacterial pneumonia in the past 2 years. Her total serum immunoglobulins are within normal range. Could she still be immunodeficient?

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?

FA Manian MD, MPH, , , , , , , , , , , Leave a comment

Yes!  Although we often associate oral candidiasis with thrush or pseudomembranous white plaques, another common form of oral candidiasis seen in hospitalized patients is “acute atrophic candidiasis” (AAC), also referred to as “antibiotic sore mouth” because of its association with use of broad spectrum antibiotics (1,2). 

Despite the absence of thrush, patients with AAC often have erythematous patches on the palate, buccal mucosa and dorsum of the tongue. Common symptoms include burning sensation in the mouth (especially with carbonated drinks in my experience), dry mouth and taste buds “being off” (2).  

Aside from antibiotics, other predisposing factors for AAC include corticosteroids, HIV disease, uncontrolled diabetes mellitus, iron deficiency anemia, and vitamin B12 deficiency.

So next time you see a hospitalized patient with new onset sore, burning mouth that wasn’t present on admission, think of antibiotic sore mouth!

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References

1. Stoopler ET, Sollecito TP. Oral mucosal diseases. Med Clin N Am 2014;98:1323-1352. https://www.ncbi.nlm.nih.gov/pubmed/25443679

2. Millsop JW, Fazel N. Oral candidiasis. Clin Derm 2016;34:487-94. https://www.ncbi.nlm.nih.gov/pubmed/27343964

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?