My middle age patient complains of night sweats for several months, but she has had no weight loss and does not appear ill. What could I be missing?

Night sweats (NS) is a common patient complaint, affecting about a third of hospitalized patients on medical wards1.  Despite its long list of potential causes, direct relationship between the often- cited conditions and NS is usually unclear2, its cause may remain elusive In about a third to half of cases in the primary care setting, and its prognosis, at least in those >65 y of age, does not appear to be unfavorable 2,3.

Selected commonly and less frequently cited conditions associated with NS are listed (Table)2-9.  Although tuberculosis is one of the first conditions we think of when faced with a patient with NS, it should be emphasized that NS is not common in this disease (unless advanced) and is rare among hospitalized patients as a cause of their NS1,9.

In one of the larger study of adult patients seen in primary care setting, 23% reported pure NS and an additional 18% reported night and day sweats5; the prevalence of NS in both men and women was highest in 41-55 y age group. In multivariate analyses, factors associated with pure NS in women were hot flashes and panic attacks; in men, sleep disorders. 

Table. Selected causes of night sweats

Commonly cited Less frequently cited
Neoplastic/hematologic (eg, lymphoma, leukemia, myelofibrosis)

Infections (eg, HIV, tuberculosis, endocarditis)

Endocrine (eg, ovarian failure, hyperthyroidism, orchiectomy, carcinoid tumor, diabetes mellitus [nocturnal hypoglycemia], pheochromocytoma)

Rheumatologic (eg, giant cell arteritis)

Gastroesophageal reflux disease

B-12 deficiency

Pulmonary embolism

Drugs (eg, anti-depressants, SSRIs, donepezil [Aricept], tacatuzumab)

Sleep disturbances (eg, obstructive sleep apnea)

Panic attacks/anxiety disorder



Diabetes insipidus


  1. Lea MJ, Aber RC, Descriptive epidemiology of night sweats upon admission to a university hospital. South Med J 1985;78:1065-67.
  2. Mold JW, Holtzclaw BJ, McCarthy L. Night sweats: A systematic review of the literature. J Am Board Fam Med 2012; 25-878-893.
  3. Mold JW, Lawler F. The prognostic implications of night sweats in two cohorts of older patients. J Am Board Fam Med 2010;23:97-103.
  4. Mold JW, Holtzclaw BJ. Selective serotonin reuptake inhibitors and night sweats in a primary care population. Drugs-Real World Outcomes 2015;2:29-33.
  5. Mold JW, Mathew MK, Belgore S, et al. Prevalence of night sweats in primary care patients: An OKPRN and TAFP-Net collaborative study. J Fam Pract 2002; 31:452-56.
  6. Feher A, Muhsin SA, Maw AM. Night sweats as a prominent symptom of a patient presenting with pulmonary embolism. Case reports in Pulmonology 2015.
  7. Rehman HU. Vitamin B12 deficiency causing night sweats. Scottish Med J 2014;59:e8-11.
  8. Murday HK, Rusli FD, Blandy C, et al. Night sweats: it may be hemochromatosis. Climacteric 2016;19:406-8.
  9. Fred HL. Night sweats. Hosp Pract 1993 (Aug 15):88.
My middle age patient complains of night sweats for several months, but she has had no weight loss and does not appear ill. What could I be missing?

Is diabetes mellitus (DM) an independent risk factor for venous thromboembolism (VTE)?

Although DM was originally thought to be an independent risk factor for DM1,2, more recent data suggest otherwise.

A population-based study involving residents of Olmsted County, Minnesota, calculated the incidence of VTE among patients with DM over a 25-year period and found it to be higher than that of controls .   However, in the same study, after controlling for hospitalization for major surgery or medical illness and nursing home confinement, no association between DM and VTE was found2  .  

A recent systematic review and meta-analysis of case-control and cohort studies involving over 1 million patients found no significant association between DM and VTE when controlled for common risk factors (eg, obesity, sedentary life style, smoking, hypertension, or dyslipidemia)3.  The authors concluded that DM and its complications are not independent risk factors for incident VTE.  

Thus, it appears that much of the risk of DVT in DM may be related to its comorbidities and the need for hospitalization, surgery or nursing home stay.


  1. Petrauskiene V, Falk M, Waernbaum I, et al. The risk of venous thromboembolism is markedly elevated in patients with diabetes. Diabetologia 2005;48:1017-21.
  2. Heit JA, Leibson CL, Ashrani AA, et al. Is diabetes mellitus an independent risk factor for venous thromboembolism? A population-based case-control study. Thromb Vasc Biol 2009; 29:1399-1405.
  3. Gariani K, Mavrakanas T, Combescure C, et al. Is diabetes mellitus a risk factor for venous thromboembolism? A systematic review and meta-analysis of case-control and cohort studies. Eur J Intern Med 2016;28:52-58.
Is diabetes mellitus (DM) an independent risk factor for venous thromboembolism (VTE)?

Should we treat asymptomatic candiduria?

This is a common scenario among our hospitalized patients with indwelling catheters, prior antibiotic therapy or diabetes mellitus who seem to have no clinical signs of infection. Fortunately, candidemia from urinary sources appears uncommon to rare, with up to nearly ½ of patients clearing their candiduria with removal of the indwelling catheter alone (1). The Infectious Diseases Society of America guidelines do not recommended treatment of asymptomatic candiduria unless the patient belongs to a group at high risk of dissemination, such as severely immunosuppressed or neutropenic patients, infants with low birth weight, and patients who will undergo urologic manipulation (2).  Supporting such recommendation is a retrospective long-term follow-up of patients with candiduria demonstrating no significant improvement in rates of recurrences of candiduria or candidemia with treatment (3).  Fluconazole is usually considered the first-line agent of choice when treatment is indicated.  

1. Kauffman CA. Candiduria. Clin Infect Dis 2005;41:S371-6.

2. Pappas PG, Kauffman CA, Andes D, et al. Clinical Practice Guidelines for the Management of Candidiasis: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis 2009; 48:503–35.

3. Revankar SG, Hasan MS, Revankar VS, et al. Long-term follow-up of patients with candiduria. Eur J Clin Microbiol Infect Dis 2011;30:137-140.

Should we treat asymptomatic candiduria?

Should we routinely use broad spectrum empiric antibiotic therapy in our diabetic patients with cellulitis of the lower extremities?

The short answer is “No”! The myth that diabetics with acute bacterial skin and skin structure infections should be routinely placed on antibiotics against gram-positives as well as gram-negatives and/or anaerobes probably originates from the extrapolation of data revolving around the frequent polymicrobial nature of diabetic foot infections.  These infections often originate from chronic ulcers and are complicated by deep tissue infection or gangrene (1), which is often not the case in our diabetic patients with cellulitis alone.  

In a recent study of the microbiology of cellulitis or cutaneous abscess in hospitalized patients, Staphylococcus and Streptococcus sp. accounted for 90% of cultured organisms in  diabetic patients, not significantly different than that of non-diabetics (1). This finding also supports national guidelines which do not recommend routine use of broader spectrum antibiotics in diabetics with cellulitis or cutaneous abscess (2).  This may be a good area to include in our antibiotic stewardship practices.

1. Jenkins TC, Knepper BC, Moore SJ, et al. Comparison of the microbiology and antibiotic treatment among diabetic and nondiabetic patients hospitalized for cellulitis or cutaneous abscess. J Hosp Med 2014;9:788-794.

2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis 2014;59:e10-e52.

Should we routinely use broad spectrum empiric antibiotic therapy in our diabetic patients with cellulitis of the lower extremities?