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MBBS, MD (Pathology),
Sanjay Gandhi institute of trauma and orthopedics,
Bengaluru.
On Aug 2018




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Dr. Mamta Gupta
Consultant
(Ex HOD Obs &Gynae, Hindu Rao Hospital and associated NDMC Medical College, Delhi)
Aug 2018




Dr. Rajendra Kumar Ghritlaharey

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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011




Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
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Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011
Anuradha

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.


Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020

Important Notice

Case report
Year : 2023 | Month : July | Volume : 17 | Issue : 7 | Page : ED14 - ED16 Full Version

Parathyroid Adenoma Associated with Granulomatous Inflammation- A Case Report


Published: July 1, 2023 | DOI: https://doi.org/10.7860/JCDR/2023/61072.18182
Shyama Manojkumar Chag, Keyuri Bharat Patel, Krishna Maheshkumar Panchal

1. Assistant Professor, Department of Pathology, Pramukh Swami Medical College, Shree Krishna Hospital, Bhaikaka University, Anand, Gujarat, India. 2. Professor, Department of Pathology, Pramukh Swami Medical College, Shree Krishna Hospital, Bhaikaka University, Anand, Gujarat, India. 3. Senior Resident, Department of Pathology, Pramukh Swami Medical College, Shree Krishna Hospital, Bhaikaka University, Anand, Gujarat, India.

Correspondence Address :
Shyama Manojkumar Chag,
HASH Arpan Society, V V Nagar Main Road, Behind Walmiki Bunglows, Anand-388001, Gujarat, India.
E-mail: shyamamc@charutarhealth.org

Abstract

Parathyroid adenoma is a benign neoplasm derived from the parenchymal cells of a parathyroid gland. Most patients present with unknown aetiology. Inflammatory disorders of the parathyroid gland are poorly defined and necrotising granulomatous inflammation of the parathyroid gland is very rare and its co-existence with a functioning adenoma of the parathyroid is indeed a unique presentation. Hereby, the author presents a case of a 47-year-old female who presented with generalised weakness and joint pain with radiological and biochemical evidence of hyperthyroidism. The patient had undergone a nuclear Tc-99m sestamibi parathyroid scan which was suggestive of parathyroid adenoma and was operated for the same. Routine histopathological examination was suggestive of parathyroid adenoma with chronic granulomatous inflammation. However, diagnostic possibilities of inflammatory aetiologies are numerous and each has presented its characteristics, and theories have always focused on disorders of the parathyroid gland which can occur probably due to autoimmune and non infectious aetiology. Hypercalcaemia can be caused by many causes. However, parathyroid adenoma with co-existent granulomatous inflammation is a rare finding. Sometimes it is not possible to find the exact cause of granulomatous inflammation as in the present case.

Keywords

Hypercalcaemia, Hyperparathyroidism, Hypertension

Case Report

A 47-year-old female presented to the Department of Otorhinolaryngology with complaints of generalised weakness and joint pain for six to eight months. The patient was relatively asymptomatic before eight months then she developed weakness, joint pain, and weight loss of weight (10 kg). She was diagnosed with diabetes mellitus one year back, while had hypertension and hypothyroidism for five years. She was on a combination of Dapagliflozin 10 mg and Metformin 500 mg with Vildagliptin 50 mg medication for diabetes, amlodipine 5 mg for hypertension, and levothyroxine 75 μg for hypothyroidism.

On general examination, no remarkable findings were noted. On systemic examination, no abnormalities were present in the head and neck region. Ultrasonography (USG) for the thyroid and parathyroid gland showed a well-defined hypoechoic nodule noted posterior to a mid-pole of the left lobe of the thyroid with a well-defined capsule, which was not separate from thyroid parenchyma and measured 1.3×0.7×0.5 cm. Tc-99m sestamibi parathyroid scan showed an increased area of radiotracer concentration in the region of the posterior aspect of the lower pole of the left thyroid lobe, suggestive of parathyroid adenoma involving the posterior aspect of the lower pole of the left lobe of the thyroid gland. On laboratory investigations, the complete blood count and coagulation profile were within the normal physiological range. Biochemical testing showed high Parathyroid Hormone (PTH) levels of 57.8 pg/mL and serum calcium level 10.60 mg/dL.

The patient underwent excision for the parathyroid adenoma. The histopathological analysis of the frozen section showed nodules of chief cells, oxyphil cells, and clear cells arranged in glands, trabeculae and nest pattern separated by fibrous septae. Occasional clusters showed mild nuclear atypia. After routine processing on Haematoxylin and Eosin (H&E)-stained section showed nodules of chief cells, oxyphil cells, and clear cells arranged in glands, trabeculae and nest pattern separated by fibrous bands with the presence of many well-formed granulomas compromised of epithelioid cells, histiocytes, lymphocytes, foreign body and Langhans giant cells with a central area of necrosis. The focal lobule shows infiltration of mature adipocytes in parathyroid parenchyma (Table/Fig 1),(Table/Fig 2),(Table/Fig 3),(Table/Fig 4).

Thus, the final diagnosis was parathyroid adenoma with chronic granulomatous inflammation of the left lower parathyroid gland. After the excision of the gland, the PTH level was reduced to 31.0 pg/mL and the serum calcium level 8.3 mg/dL.

Discussion

Parathyroid adenoma is a benign neoplasm of the parathyroid gland, typically involving one gland. It occurs in women and men in a ratio of 3:1. They can develop at any age, but most cases occur in patients in the fourth decade. It accounts for over 85% of cases of Hyperparathyroidism (HPT) (1). Hypercalcaemia is usually associated with either PTH-dependent or PTH-independent processes as well as infections like Tuberculosis (Tb), leprosy, disseminated candidiasis, systemic fungal infections, and non infective conditions like inflammatory bowel disease and foreign body granulomas. Granulomatous diseases can cause hypercalcaemia due to increased 1α-hydroxylase enzymatic activity in tissue macrophages which leads to elevated levels of 1,25- dihydroxy vitamin D3 (1,25(OH)2D) which is resistant to feedback control (2),(3).

The index patient had PTH-mediated hypercalcaemia due to granulomatous processes involving the parathyroid gland which posed significant diagnostic challenges. Clinical research shows that parathyroid adenoma with associated granulomatous inflammation is a rare presentation, but studies have shown chronic inflammation can cause hyperfunctioning. The parathyroid gland is weakly antigenic, so it is rare to encounter granulomatous inflammation due to probable tuberculous infection of the parathyroid gland (Table/Fig 5) (4),(5),(6),(7). Few of them presented as chronic granulomatous inflammation and all cases with primary hyperparathyroidism presented with concomitant adenoma. Few cases reported the presence of granulomatous inflammation but special tests and special stain for acid-fast bacilli are negative which excludes sarcoidosis.

In addition, the index patient had primary hyperparathyroidism associated with end-stage renal disease and diabetes mellitus which are an immunocompromised state that explains the occurrence of chronic inflammation. Activation of osteoclasts in primary hyperparathyroidism leads to increased bone resorption associated with vitamin D 1,25(OH)2D3- mediated granulomatous disorders. However, evaluation of 1,25(OH)2D3 levels was not performed in this patient, but serum calcium decreased to 8.3 mg/dL and serum PTH decreased to 31.0 pg/mL after the removal of parathyroid adenoma. This could be explained by the causal association of granulomatous inflammation in the parathyroid gland and hyperfunctioning of the parathyroid gland associated with an immunocompromised state.

The current case presented with routine high PTH levels and calcium levels, but histopathological examination suggested associated granulomatous inflammation, which was found to have an incidental finding in microscopy.

Conclusion

The present case sheds light on the significance of Granulomatous inflammation with parathyroid adenoma as a rare presentation. It is not clear whether parathyroid adenoma-associated hyperfunctioning contributed to the chronic inflammation, but it might show immunocompromised state can be associated with any chronic inflammation.

References

1.
Marcocci C, Cetani F. Clinical practice. Primary hyperparathyroidism, N Engl J Med. 2011;365(25):2389-97. [crossref][PubMed]
2.
Rados DV, Furlanetto TW. An unexpected cause of severe and refractory PTH- independent hypercalcaemia: Case report and literature review. Arch Endocrinol Metab. 2015;59(3):277-80. [crossref][PubMed]
3.
Zouras S, Surya A, Abusahmin H, Hassan M, Humphreys E, Nagaraja P, et al. Granulomatous disease of unusual sites causing hypercalcaemia: Two case reports. AACE Clin Case Rep. 2019;5(1):e44-e49. [crossref][PubMed]
4.
Kabbaj DE, Oualim Z. Parathyroid gland tuberculosis associated with secondary hyperparathyroidism in hemodialysis patient. Saudi J Kidney Dis Transplant. 2010;21(4):742-43.
5.
Anaforoglu I, Siviloglu C, Livaoglu A, Algün E. Granulomatous infiltration of a parathyroid adenoma presenting as primary hyperparathyroidism in a woman: A case report. J Med Case Reports. 2010;4:400. [crossref][PubMed]
6.
Jacob PM, Sukumar GC, Nair A, Thomas S. Parathyroid adenoma with necrotizing granulomatous inflammation presenting as primary hyperparathyroidism. Endocr Pathol. 2005;16(2):157-60. [crossref][PubMed]
7.
Singh HP, Narang V, Sood N, Puri H. Parathyroid adenoma associated with granulomatous inflammation: A curious cause of hypercalcaemia. J Clin Diagn Res. 2016;10(4):ED21-ED22.[crossref][PubMed]

DOI and Others

DOI: 10.7860/JCDR/2023/61072.18182

Date of Submission: Oct 31, 2022
Date of Peer Review: Dec 21, 2022
Date of Acceptance: Mar 01, 2023
Date of Publishing: Jul 01, 2023

AUTHOR DECLARATION:
• Financial or Other Competing Interests: None
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. Yes

PLAGIARISM CHECKING METHODS:
• Plagiarism X-checker: Nov 01, 2022
• Manual Googling: Jan 06, 2023
• iThenticate Software: Feb 16, 2023 (4%)

ETYMOLOGY: Author Origin

EMENDATIONS: 8

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