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Reader Reactions and Timely Responses from Experts

Volume 57 - Issue 3 - March 2017

Photo Quiz Answer: Squamous Cell Carcinoma, or Something Else?

To the Editor:

The “squamous cell carcinoma” in the December 2016 “Photo Quiz 360”1 and the answer published in the January 2017 issue2 looks like a typical keratoacanthoma, with a well-defined, raised rolled border and a keratin-filled central crater. Further evidence for this diagnosis is the rapid growth of the lesion. Surgical excision was the appropriate therapy with either diagnosis. However, a follow-up article, including a photomicrograph of the excisional specimen and the differential diagnosis, is indicated.

Yelva Lynfield, MD
Mendota Heights, Minnesota

References:

  1. Lam N-CV, Matalia NB. A truck driver with a skin lesion on his upper arm. Consultant. 2016;56(12):1093.
  2. Lam N-CV, Matalia NB. Last issue’s answer: squamous cell carcinoma. Consultant. 2017;57(1):48.

In Reply:

Thank you, Dr Lynfield, for your comment. I agree that keratoacanthoma would be an important differential diagnosis of this lesion, because it has the features you mentioned. However, in the primary care setting, it is best to presume a diagnosis of possible squamous cell carcinoma and proceed with definitive treatment, because keratoacanthoma cannot be reliably distinguished from squamous cell carcinoma in the clinical setting.

The final pathology report of the resected specimen showed “squamous cell carcinoma, well differentiated.” Since the time this lesion was removed, the patient subsequently has had 4 other lesions removed from his hands, neck, and arm, with pathology examination findings showing “squamous cell carcinoma, low grade” and “squamous cell carcinoma in situ with focal invasion.”

All these lesions were successfully removed with clear margins, and the patient is currently in good health.

Nguyet-Cam V. Lam, MD
Bethlehem, Pennsylvania

 

More on Hypertriglyceridemia and Atherosclerotic Disease

To the Editor:

The article on hypertriglyceridemia in association with low low-density lipoprotein cholesterol (LDL-C) levels1 in the January 2017 issue deserves comment.

Triglycerides (TGs) do not accumulate with the atherosclerotic disease (AtD) plaque to any significant degree. The link between high TGs and AtD is via high-density lipoprotein cholesterol (HDL-C) and LDL-C. If LDL-C levels are high enough or HDL-C levels are low enough, then the ratio between LDL-C and HDL-C is abnormal and leads to AtD. (Of course, if the patient smokes cigarettes, then AtD events can occur at any level of LDL-C or HDL-C. In general, this occurs early in life. Hypertension can similarly cause AtD events late in life.) If LDL-C levels are low enough, then in the absence of cigarette smoking or hypertension, AtD events usually do not occur. The main reasons for lowering high TG levels in this scenario are to avoid pancreatitis, nonalcoholic fatty liver disease, and (when combined with low HDL-C levels) future diabetes. (The Helsinki Heart Study2 showed little benefit of treatment with gemfibrozil in terms of cardiovascular risk reduction in participants with a TG level greater than 200 mg/dL unless their LDL-C to HDL-C ratio was 5.0 or greater.)

TG levels of the sort described in the article do not require treatment per se, only observational follow-up.

William E. Feeman Jr, MD
Bowling Green, Ohio

ReferenceS:

  1. Leonard EJ, Scuderi CB, Zenni MM. Familial hypertriglyceridemia with concomitant familial hypobetalipoproteinemia. Consultant. 2017;57(1):​12-15.
  2. Manninen V, Tenkanen L, Koskinen P, et al. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation. 1992;85(1):37-45.

In Reply:

We agree that hypertriglyceridemia does not contribute, to any real extent, to plaque formation in AtD. In our article, we stated that “the elevated TG level warrants more scrutiny for the sake of the liver over time and to a lesser extent the heart.”

Guidelines from the American Heart Association/American College of Cardiology1 and the National Cholesterol Education Program Adult Treatment Panel III2 do in fact identify LDL-C as the primary target of therapy and not very low-density lipoprotein cholesterol (VLDL-C) or TGs. The guidelines also recommend using combination therapy when the TG level is 500 mg/dL or above only to prevent pancreatitis and eruptive xanthomas, without clear benefit to cardiovascular event reduction.2

We also agree that elevated TGs indirectly contribute to coronary artery disease risk, mostly via the “poor company” TGs keep when elevated—low HDL-C levels, and small, dense (pattern B) LDL particles that are more atherogenic than their more buoyant counterparts, large (pattern A) LDL particles. There also is evidence that intermediate-density lipoproteins are quite atherogenic and are linked to VLDL-C metabolism.

TGs may also stimulate atherogenesis by other mechanisms such as the production of proinflammatory cytokines/interleukins, fibrinogen, and coagulation factors, as well as the impairment of fibrinolysis. These tend to contribute to the sclerosing of the arterial walls but not to plaque formation. Therefore, their roles in atherogenesis have a basic biologic plausibility. There is evidence from larger clinical trials that TG lowering may be cardioprotective independent of LDL-C lowering. There was clear cardiac event reduction in both the Veterans Affairs High-Density Lipoprotein Intervention Trial3 (secondary prevention) and in the Helsinki Heart Study4 (primary prevention) with TG lowering with gemfibrozil. Part of the benefit is from raising HDL-C levels, but it also is likely a result of a direct TG-lowering effect.

European Society of Cardiology/European Atherosclerosis Society dyslipidemia guidelines5 state that while a TG level below 150 mg/dL is desirable, the first step in management is to achieve the appropriate LDL-C target based on total cardiovascular risk. Pharmacologic therapy should only be considered in patients at high cardiovascular risk who also have a TG level above 200 mg/dL and who cannot reduce this level with lifestyle measures alone. Thus, we agree that LDL-C is the primary atherogenic risk target, and lowering the LDL-C level with statin therapy alone or statins in combination with ezetimibe (after acute coronary syndromes) or a proprotein convertase subtilisin/kexin type 9 inhibitor, is the correct treatment. TG lowering is still relegated to the “bench” to prevent pancreatitis, hepatic steatosis, secondary inflammatory processes, and eruptive xanthomas.

Evan J. Leonard, MS, PA-C; Christopher B. Scuderi, DO; and Martin M. Zenni, MD
Jacksonville, Florida

References:

  1. Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;​129(suppl 2):S1-S45.
  2. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Final Report. Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute; 2002. NIH publication 02-5215.
  3. Otvos JD, Collins D, Freedman DS, et al. Low-density lipoprotein and high-density lipoprotein particle subclasses predict coronary events and are favorably changed by gemfibrozil therapy in the Veterans Affairs High-Density Lipoprotein Intervention Trial. Circulation. 2006;113(12):​1556-1563.
  4. Frick MH, Elo O, Haapa K, et al. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med. 1987;317(20):1237-1245.
  5. Reiner Ž, Catapano AL, De Backer G, et al; European Association for Cardiovascular Prevention and Rehabilitation and ESC Committee for Practice Guidelines (CPG) 2008-2010 and 2010-2012 Committees. ESC/EAS guidelines for the management of dyslipidaemias: the Task Force for the Management of Dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur Heart J. 2011;​32(14):1769-1818.

 

February’s “Photo Essay” Article on Keratosis Follicularis: Correction

In February’s “Photo Essay,” the name of one of the authors of the case report on keratosis follicularis was inadevertently omitted from the byline. 

The corrected list of authors of the article is as follows: Jacqueline Bullock, BS, PA-S; Syed A. A. Rizvi, PhD; Jose Mendez, DO; Gerardo F. Ferrer, MD; Jose D. Suarez, MD; Jasmin Ahmed, BS; and Sultan S. Ahmed, MD.

Access the corrected article at www.consultant360.com/articles/collection-conditions-dermatologic-manifestations.

Michael Gerchufsky, ELS, CMPP
Managing Editor