|Year : 2021 | Volume
| Issue : 2 | Page : 119-121
Diabetic gustatory sweating
S Sheetal1, S Amith Kumar2
1 Department of Neurology, Pushpagiri Institute of Medical Sciences and Research Centre, Thiruvalla, Kerala, India
2 Department of Neurology, Lourdes Hospital, Kochi, Kerala, India
|Date of Submission||08-Nov-2020|
|Date of Decision||06-Dec-2020|
|Date of Acceptance||12-Dec-2020|
|Date of Web Publication||15-Apr-2021|
Dr. S Sheetal
16 FG, The Edge, Skyline Apartments, Thirumoolapuram, Thiruvalla - 689 115, Kerala
Source of Support: None, Conflict of Interest: None
Gustatory sweating refers to facial sweating after ingestion of food or drink. Gustatory sweating may develop as a symptom of autonomic dysfunction in patients with diabetes. It is reported in long-standing diabetes mellitus with associated complications such as neuropathy and nephropathy. We hereby report the case of a man, with long-standing diabetes, with associated neuropathy, who developed this symptom during an episode of tight control in glycemic status.
Keywords: Autonomic, diabetic nephropathy, diabetic neuropathy, gustatory sweating, type 2 diabetes mellitus
|How to cite this article:|
Sheetal S, Kumar S A. Diabetic gustatory sweating. Curr Med Issues 2021;19:119-21
| Introduction|| |
Gustatory sweating refers to facial sweating after ingestion of food or drink. It has been reported diversely in previous literature. It may occur as a physiological response to eating very spicy food or as an idiosyncratic reaction to a specific food product like chocolate or cheese. It has also been reported to occur following disease, trauma or surgery in the head and neck region. Frey's syndrome or auriculotemporal syndrome refers to the gustatory sweating developing after parotid surgery and is unilateral. Gustatory sweating may also be seen as a part of autonomic neuropathy in long-standing diabetes mellitus. It is reported in diabetic patients with complications such as neuropathy and nephropathy. It is characterized by profuse symmetrical sweating in the face, precipitated by eating, irrespective of the type of food. We hereby report the case of a man, with long-standing diabetes, with associated neuropathy, who developed this symptom during an episode of tight control in glycemic status. Informed written consent from the patient was obtained for reporting this case.
| Case Report|| |
A 64-year-old man, with a history of type 2 diabetes mellitus for the past 20 years, was on insulin, metformin, and vildagliptin. His blood sugars were poorly controlled. His baseline HbA1c value was 10.2. He had numbness and paresthesia over both feet up to the knees for the past 2 years. He also had a history of systemic hypertension and dyslipidemia. He developed effort dyspnea 2 months back, underwent treadmill test which was positive, and underwent coronary angiogram (CAG). His CAG revealed tight occlusion of the right coronary, and he underwent angioplasty for the same. During this time, since his blood sugars were not controlled, he was initiated on empagliflozin, a sodium-glucose co-transporter-2 (SGLT2) inhibitor. During the subsequent 2 weeks, his fasting blood sugar values were well controlled. He then noticed an unusual symptom, which he did not have previously. Every time he sat down to eat, within the first few seconds of starting eating, he developed profuse sweating over the scalp and back of the neck [Figure 1]. This would last for around 10 min. Initially, he thought that it was due to spicy foods. Hence, he tried taking nonspicy foods. However, every time he started eating, he developed profuse sweating, only over the scalp and back of the neck, irrespective of the type of food. The symptom was so troublesome to him that he started keeping a towel on the table during eating. His spouse reported that he was not enjoying his meals since he would try to finish the meal quickly to reduce this embarrassing symptom. He did not have these symptoms on taking liquids. He also reported postprandial bloating and fullness. He did not have any bowel or bladder symptoms. He had no history of trauma/surgery in the parotid region in the past. On examination, he had a pulse rate of 88/min and blood pressure (BP) of 140/90 mm of Hg. There was no postural fall in BP. He had hyperpigmentation over his legs bilaterally. Fundus examination showed features of diabetic retinopathy. On motor system examination, he had no weakness, ankle jerk was absent bilaterally, and plantars were bilaterally flexor. On sensory examination, he had graded sensory loss over bilateral lower limbs, up to the knees, vibration was impaired up to the knees, and position sense was impaired in the toes, bilaterally. Romberg test was positive. Laboratory investigations revealed a normal hemogram, renal biochemistry was normal, and there was no proteinuria. Nerve conduction study showed severe sensory-motor axonal neuropathy involving bilateral upper and lower limbs. A probable diagnosis of diabetic gustatory sweating was considered.
|Figure 1: Sweat drops seen over the scalp. This picture was taken while the patient was having rice and curry.|
Click here to view
| Discussion|| |
Diabetic gustatory sweating had been reported as early as 1973 by Watkins in six patients with long-standing insulin-dependent diabetes mellitus, with severe complications related to diabetes, such as retinopathy and nephropathy. Hayes and Tulloch have reported gustatory sweating in a patient with diabetes during an episode of poor glycemic control. In our patient, this symptom developed after achieving good glycemic control. His symptoms started after initiation of an SGLT2 inhibitor, however, whether this is causal or incidental cannot be established. SGLT2 inhibitors act by inhibiting SGLT2 in the proximal convoluted tubule of the kidneys to prevent reabsorption of glucose and facilitate its excretion in urine. SGLT2 inhibitors also induce natriuresis, however, it has been reported to be transient and is not reported to cause sustained reductions in plasma volume. Although SGLT2-induced hypovolemia activating compensatory sympathetic mechanism inducing sweating seems a plausible theory, SGLT2 inhibitors are reported to elicit inhibitory effects on sympathetic nervous system activity. There are no reports in the literature regarding the development of this symptom on starting SGLT2 inhibitors. More studies would be required in this field for elucidating a causal relationship. Treatment-induced neuropathy of diabetes is another condition which develops with initiation of intensive glycemic control. It is a painful acute neuropathy that affects autonomic and small somatosensory nerve fibers. Although our patient developed autonomic symptoms in the form of gustatory sweating, he had no symptoms of painful neuropathy. Diabetic gustatory sweating has been reported in patients with associated complications such as retinopathy, neuropathy, and nephropathy. Our patient was also noted to have features of retinopathy and neuropathy, as was reported in other patients. Shaw et al., in their study on 196 patients, observed that 69% of patients with nephropathy and 36% of those with neuropathy reported gustatory sweating. Shaw et al. have also emphasized that it is often very closely linked with diabetic nephropathy, however, our patient had no evidence of nephropathy.
The term gustatory sweating has been used diversely in previous literature. Frey's syndrome, or auriculotemporal syndrome which develops as a reaction to trauma, infection, or surgery, is marked by asymmetry and localized involvement in the distribution of the auriculotemporal nerve. It is felt that it develops due to aberrant reinnervation of postganglionic parasympathetic neurons to nearby denervated sweat glands and cutaneous blood vessels. This should be distinguished from diabetic gustatory sweating, where there is symmetric involvement on both sides of the face. In diabetic gustatory sweating, the mechanism hypothesized is axonal degeneration with abnormal sprouting from contiguous axons. Watkins has been proposed that during the development of diabetic neuropathy, abnormal connections may develop between the parasympathetic fibers of the vagus nerve and sudomotor tracts of the superior cervical sympathetic ganglion, thereby diverting the stimuli to the sympathetic cholinergic axons destined for the face. However, Stuart has proposed that diabetic gustatory sweating is merely physiological sweating, greatly exaggerated by diabetic neuropathy. In our patient, the extensive, symmetric involvement on both sides of the scalp and neck cannot be explained satisfactorily by axonal degeneration and aberrant connections. It also seems unlikely that advanced glycation-mediated nerve injury, which occurs in a length-dependent fashion, would involve the head and neck in a patient without first impairing orthostatic tone. Hence, this may be a physiological sweating response greatly exaggerated by diabetic neuropathy, as suggested by Stuart. It has been reported to be provoked by cheese, salty, or spicy food. However, in our patient, it was seen with all types of food. The treatment reported to be most successful is topical glycopyrrolate in moderate-to-severe symptoms of diabetic gustatory sweating, and it is reported to be safe, convenient, and effective.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Watkins PJ. Facial sweating after food: A new sign of diabetic autonomic neuropathy. Br Med J 1973;1:583-7.
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